Endocrinology PDF

ENDOCRINOLOGY
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GENERAL FEATURES OF ENDOCRINOLOGY 1
ENDOCRINOLOGY
CONTENTS
GENERAL FEATURES OF ENDOCRINOLOGY ................................................................................................................... 7
PHYSIOLOGY OF ENDOCRINOLOGY ............................................................................................................................... 7
FEATURES OF PHYSIOLOGY OF ENDOCRINOLOGY .................................................................................................... 7
SECOND MESSENGERS .............................................................................................................................................. 7
RECEPTORS PHYSIOLOGY .......................................................................................................................................... 8
LOCATION OF RECEPTORS ........................................................................................................................................ 9
GROUP I LIPOPHILIC RECEPTORS ............................................................................................................................ 10
GROUP II HYDROPHILIC HORMONES (BIND TO CELL MEMBRANE) ........................................................................ 10
G PROTEIN COUPLED RECEPTOR............................................................................................................................. 10
NITRIC OXIDE........................................................................................................................................................... 11
PITUITARY GLAND ....................................................................................................................................................... 12
DEVELOPMENT OF PITUITARY GLAND .................................................................................................................... 12
ANATOMY OF PITUITARY GLAND ............................................................................................................................ 12
PHYSIOLOGY OF PITUITARY GLAND ........................................................................................................................ 13
GROWTH HORMONE .............................................................................................................................................. 14
GIGANTISM ............................................................................................................................................................. 14
ACROMEGALY ......................................................................................................................................................... 14
DWARFISM .............................................................................................................................................................. 15
PROLACTIN .............................................................................................................................................................. 15
HYPERPROLACTINEMIA ........................................................................................................................................... 15
PITUITARY TUMOURS.............................................................................................................................................. 16
PITUITARY APOPLEXY .............................................................................................................................................. 16
SHEEHAN SYNDROME ............................................................................................................................................. 17
SYNDROME OF INAPPROPRIATE SECRETION OF ADH ............................................................................................. 17
DIABETES INSIPIDUS ................................................................................................................................................ 18
POLYURIA ................................................................................................................................................................ 18
THYROID GLAND ......................................................................................................................................................... 19
DEVELOPMENT OF THYROID ................................................................................................................................... 19
ANATOMY OF THYROID .......................................................................................................................................... 19
PHYSIOLOGY OF THYROID ....................................................................................................................................... 19
THYROID HORMONES ............................................................................................................................................. 20
HYPERTHYROIDISM ................................................................................................................................................. 20
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ENDOCRINOLOGY
HYPOTHYROIDISM .................................................................................................................................................. 21
CRETINISM .............................................................................................................................................................. 22
STRUMA OVARY ...................................................................................................................................................... 22
THYROTOXICOSIS .................................................................................................................................................... 22
GRAVE’S DISEASE .................................................................................................................................................... 23
GOITRE .................................................................................................................................................................... 23
PENDRED SYNDROME ............................................................................................................................................. 24
THYROIDITIS ............................................................................................................................................................ 24
HASHIMOTO’S THYROIDITIS .................................................................................................................................... 25
DE QUERVAIN THYROIDITIS .................................................................................................................................... 25
THYROID NODULE ................................................................................................................................................... 25
MALIGNANCY OF THYROID GLAND ......................................................................................................................... 26
FOLLICULAR CARCINOMA ....................................................................................................................................... 27
PAPILLARY CARCINOMA .......................................................................................................................................... 28
MEDULLARY CARCINOMA ....................................................................................................................................... 29
ANAPLASTIC CARCINOMA ....................................................................................................................................... 29
ANTITHYROID DRUGS.............................................................................................................................................. 30
THYROID SURGERY .................................................................................................................................................. 30
THYROID STORM ..................................................................................................................................................... 31
THYROID IMAGING.................................................................................................................................................. 31
THYROGLOSSAL CYST .............................................................................................................................................. 31
CALCIUM METABOLISM .............................................................................................................................................. 32
GENERAL FEATURES OF CALCIUM METABOLISM ................................................................................................... 32
DEVELOPMENT OF PARATHYROID GLAND .............................................................................................................. 32
ANATOMY OF PARATHYROID GLAND ..................................................................................................................... 32
PHYSIOLOGY OF PARATHYROID GLAND .................................................................................................................. 33
CALCIUM ................................................................................................................................................................. 33
PARATHROMONE .................................................................................................................................................... 34
CALCITONIN ............................................................................................................................................................ 34
HYPERPARATHYROIDISM ........................................................................................................................................ 34
OSTEITIS FIBROSIS CYSTICA ..................................................................................................................................... 35
PARATHYROID HYPERPLASIA .................................................................................................................................. 35
PARATHYROID ADENOMA ...................................................................................................................................... 35
PRIMARY HYPERPARATHYROIDISM ........................................................................................................................ 36
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ENDOCRINOLOGY
SECONDARY HYPERPARATHYROIDISM ................................................................................................................... 36

TERTIARY HYPERPARATHYROIDISM ........................................................................................................................ 36
HYPOPARATHYROIDISM .......................................................................................................................................... 36
PSEUDOHYPOPARATHYROIDISM ............................................................................................................................ 37
PSEUDOPSEUDOHYPOPARATHYROIDISM ............................................................................................................... 37
VITAMIN D............................................................................................................................................................... 37
VITAMIN D INTOXICATION ...................................................................................................................................... 38
FEATURES OF RICKETS............................................................................................................................................. 38
DIAGNOSIS OF RICKETS ........................................................................................................................................... 39
TREATMENT OF RICKETS ......................................................................................................................................... 39
VITAMIN D RESISTANT RICKETS .............................................................................................................................. 39
OSTEOMALACIA ...................................................................................................................................................... 39
FEATURES OF OSTEOPOROSIS................................................................................................................................. 40
CAUSES OF OSTEOPOROSIS .................................................................................................................................... 40
DIAGNOSIS OF OSTEOPOROSIS ............................................................................................................................... 41
TREATMENT OF OSTEOPOROSIS ............................................................................................................................. 41
HYPERCALCEMIA ..................................................................................................................................................... 42
HYPERCALCEMIC CRISIS .......................................................................................................................................... 43
TUMOUR LYSIS SYNDROME .................................................................................................................................... 43
TETANY .................................................................................................................................................................... 43
DRUGS OF CALCIUM METABOLISM ........................................................................................................................ 44
ENDOCRINE PANCREAS ............................................................................................................................................... 44
GENERAL FEATURES OF ENDOCRINE PANCREAS .................................................................................................... 44
PHYSIOLOGY OF ENDOCRINE PANCREAS ................................................................................................................ 44
NESIDIOBLASTOSIS .................................................................................................................................................. 45
HYPERGLYCEMIA AND HYPOGLYCEMIA .................................................................................................................. 45
CAUSES OF DIABETES MELLITUS ............................................................................................................................. 45
GENERAL FEATURES OF DIABETES MELLITUS ......................................................................................................... 46
TYPES OF DIABETES MELLITUS ................................................................................................................................ 46
TYPES OF MODY ...................................................................................................................................................... 47
DIABETES IN PREGNANCY ....................................................................................................................................... 47
COMPLICATIONS OF DIABETES MELLITUS .............................................................................................................. 48
DIABETIC KETOACIDOSIS ......................................................................................................................................... 48
NON KETOTIC HYPEROSMOLAR COMA ................................................................................................................... 48
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ENDOCRINOLOGY
JOINT MANIFESTATIONS OF DIABETES ................................................................................................................... 48

EYE MANIFESTATIONS OF DIABETES ....................................................................................................................... 49
RENAL MANIFESTATIONS OF DIABETES .................................................................................................................. 50
DIAGNOSIS OF DIABETES MELLITUS ........................................................................................................................ 50
TREATMENT OF DIABETES MELLITUS...................................................................................................................... 51
ALPHA GLUCOSIDASE INHIBITORS .......................................................................................................................... 51
THIAZOLIDONEDIONES ........................................................................................................................................... 52
BIGUANIDES ............................................................................................................................................................ 52
MEGLITINIDE ........................................................................................................................................................... 53
EXENATIDE .............................................................................................................................................................. 53
SULPHONYLUREAS .................................................................................................................................................. 53
FEATURES OF INSULIN ............................................................................................................................................ 54
TYPES OF INSULIN ................................................................................................................................................... 55
ACTION OF INSULIN ................................................................................................................................................ 55
ADRENAL GLAND......................................................................................................................................................... 56
GENERAL FEATURES OF ADRENAL GLAND .............................................................................................................. 56
ANATOMY OF ADRENAL GLAND ............................................................................................................................. 57
PHYSIOLOGY OF ADRENAL GLAND .......................................................................................................................... 57
ADRENAL TUMOUR ................................................................................................................................................. 58
ADRENAL HYPERPLASIA .......................................................................................................................................... 58
ADRENAL CARCINOMA ........................................................................................................................................... 58
FEATURES OF CUSHING SYNDROME ....................................................................................................................... 59
MANAGEMENT OF CUSHING SYNDROME .............................................................................................................. 59
ECTOPIC ACTH PRODUCTION .................................................................................................................................. 60
FEATURES OF CONN SYNDROME ............................................................................................................................ 60
HYPERALDOSTERONISM ......................................................................................................................................... 60
FEATURES OF ADDISON’S DISEASE ......................................................................................................................... 60
MANAGEMENT OF ADDISON’S DISEASE ................................................................................................................. 61
WATERHOURSE FRIEDRICHSON SYNDROME .......................................................................................................... 61
GENERAL FEATURES OF CONGENITAL ADRENAL HYPERPLASIA .............................................................................. 61
TYPES OF CONGENITAL ADRENAL HYPERPLASIA .................................................................................................... 62
MANAGEMENT OF CONGENITAL ADRENAL HYPERPLASIA ..................................................................................... 62
GENERAL FEATURES OF STEROID DRUGS ............................................................................................................... 63
INDICATIONS OF STEROIDS ..................................................................................................................................... 64
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ENDOCRINOLOGY
SIDE EFFECTS OF STEROID DRUGS .......................................................................................................................... 64

NEUROBLASTOMA .................................................................................................................................................. 64
CAUSES OF PHEOCHROMOCYTOMA ....................................................................................................................... 65
FEATURES OF PHEOCHROMOCYTOMA ................................................................................................................... 65
EXTRA ADRENAL PHEOCHROMOCYTOMA .............................................................................................................. 66
DIAGNOSIS OF PHEOCHROMOCYTOMA ................................................................................................................. 66
TREATMENT OF PHEOCHROMOCYTOMA ............................................................................................................... 67
PINEAL GLAND ............................................................................................................................................................ 67
MULTIPLE ENDOCRINE NEOPLASIA ............................................................................................................................. 68
GENERAL FEATURES OF MULTIPLE ENDOCRINE NEOPLASIA .................................................................................. 68
MEN I ...................................................................................................................................................................... 68
MEN IIA ................................................................................................................................................................... 68
MEN IIB ................................................................................................................................................................... 68
POLYGLANDULAR SYNDROME ................................................................................................................................ 69
CARCINOID .................................................................................................................................................................. 69
FEATURES OF CARCINOID ....................................................................................................................................... 69
MANAGEMENT OF CARCINOID ............................................................................................................................... 70
OBESITY ....................................................................................................................................................................... 70
WEIGHT GAIN AND WEIGHT LOSS .............................................................................................................................. 72
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ENDOCRINOLOGY
KEY TO THIS DOCUMENT
Text in normal font – Must read point.

Asked in any previous medical entrance
examinations
Text in bold font – Point from Harrison’s

text book of internal medicine 18th
edition
Text in italic font – Can be read if

you are thorough with above two.
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ENDOCRINOLOGY
GENERAL FEATURES OF ENDOCRINOLOGY
System favors oscillatory responses Positive feedback system

Paracrine regulation Somatostatin release inhibits Insulin release
C21 Cortisol, Progesterone
C19 Androgen
Somatostatin secreted by D cell
Melatonin is secreted by Pineal gland
Endocrine manifestations produced by Ketoconazole
Investigation of choice for Primary and Metastatic Somatostatin Receptor Scintigraphy
Neuroendocrine Tumour (except Insulinoma)
Best imaging modality for neuroendocrinal tumours Radionucleide scan
Lifelong treatment is necessary in Myxedema, Addison’s disease, Juvenile diabetes
PHYSIOLOGY OF ENDOCRINOLOGY
FEATURES OF PHYSIOLOGY OF ENDOCRINOLOGY
Hormone synthesized as peptide precursor Insulin, PTH, rennin, angiotensin II

NOT a peptide hormone Progesterone
Which hormone has NO Intracellular Storage Calcitriol
Vasodilator ANP
Hormone NOT acts by increasing protein synthesis Vasopressin
SECOND MESSENGERS
Bio organic computer Protein kinase and phosphatase

Transmission of regulatory signals through ECF Synaptic signals through neurotransmitters, endocrine
signals through hormones, G protein coupled receptors
NOT an example for transmission of Direct contact through gap junctions
regulatory signals
Various cells respond differentially to second Different enzyme composition
messenger because they have
Used for cell signaling NO
Second messengers are Substance that increase or decrease function
Secondary messengers cAMP, IP3, DAG, cGMP
Acts as second messenger Ca++
Intraneuronal second messenger Calmodulin
Hormone using phospholipase C as messenger Angiotensin II
NOT a second messenger Guanylate cyclase
Production of cAMP from ATP requires Adenyl cyclase
Membrane bound enzyme catalyzing formation of cyclic Adenylate cyclase
AMP from ATP
Membrane bound enzyme that catalyses formation of Adenylate cyclase
cAMP from ATP
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PHYSIOLOGY OF ENDOCRINOLOGY 8
ENDOCRINOLOGY
cAMP acts through Activation of protein kinase

All known effects of cyclic AMP in eukaryotic cells result Activation of protein kinase
from
Secondary derivative of biologically important Cyclic AMP
nucleotides
cAMP mediates Glucagon, LH, FSH
cAMP mediates Corticotrophin, Dopamine, Glucagon
Decrease in cAMP is caused by Alpha 2 receptor
Adenyl cyclase is inhibited by Somatostatin
Cyclic AMP is inactivated by Phosphodiesterase
NOT using cAMP as second messenger Vasopressin
NOT mediated by cAMP Estrogen
NOT using cAMP as second messenger Vasopressin, Growth hormone
cGMP as second messenger for ANP, NO
cGMP act on Atrial natriuretic peptide
Secretion of atrial natriuretic peptide Increased in central venous pressure
increases when there is
Cyclic GMP is a second messenger of Insulin
Second messenger is produced from Phosphatidyl Inositol
A phosphorylated derivative is acted upon by Phosphatidylinositol
Phospholipase C as a part of second messenger system
Substances act to increase release of Ca++ from Inositol triphosphate
endoplasmic reticulum
Calcium release from endoplasmic reticulum is Inositol triphosphate
triggered by
Inositol triphosphate and diacyl glycerol Phosphatidyl inositol 4,5 bisphosphate
are derived from (PIP2)
RECEPTORS PHYSIOLOGY
Membrane receptor For specific action, Molecular transport

Intracellular receptor Mainly on nuclear surface, Steroids act on them
Intracellular receptor Vitamin D3, Cortisone, Thyroxine, Androgen
Steroid receptor superfamily belongs to Zinc finger motif
Steroid receptor superfamily present in Vitamin D3, Thyroxine
Lipophilic acting on nuclear receptor Thyroxine
Cytoplasmic receptor Cortisol
NOT highly specific binding with single Glucocorticoid
type of nuclear receptor
Acts through tyrosine kinase receptor Insulin
Receptors which are transcription factors Estrogen, glucocorticoids, Vitamin D
Steroids bind to Cytosolic receptors and heat shock proteins
Binds to steroid receptors Steroids, Transcriptional factors, Steroid response
element
Belongs to steroid receptor super family Vitamin D3 receptor, thyroid receptor, retinoid receptor
Does NOT bind to steroid receptors Transcriptional mediators
Steroid hormone do NOT have attachment site for Transcription repressors
Receptors on cell membrane that activates ion channel Nicotinic cholinergic, GABA A receptors
after binding with agonists
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ENDOCRINOLOGY
Does NOT act by intracellular receptor Insulin

Does NOT have intracellular receptor Adrenaline
NOT have cell surface receptor Thyroxine
Which DOES NOT have Cell membrane receptor Steroids
True about receptor action Binding sites are non specific and one drug can displace
other
Operating time of following receptor is in milliseconds Ligand gated ion channels
C terminal end of androgen receptor is concerned with Ligand binding
Receptor mediated action NOT seen in General anesthetics
Receptor blocking agent has Increased Affinity for receptor and Intrinsic activity
Adrenaline, noradrenaline and dopamine acts through Seven pass receptor
Dopamine, norepinephrine, serotonin all have the 7 pass receptor
following type of receptors
GABA B is associated with G protein coupled receptor
GH, prolactin and erythropoietin are JAK STAT receptor
associated with
EDF, PGDF and insulin receptors are Tyrosine kinase receptor
associated
Aldosterone receptor NOT present in Liver
Mineralocorticoid receptor NOT found in Liver
LOCATION OF RECEPTORS
Muscarinic receptors M1 – gastric glands, M2 – AV node, M3 –

smooth muscle, ocular system, endocrine
glands
Nicotinic receptors Nm – neuromuscular junction, Nn –
ganglia, adrenal medulla
Alpha adrenergic receptors Alpha 1 – vascular smooth muscle,
prostatic urethra, dilator papillae. Alpha
2 – blood vessels, brain
Beta adrenergic receptors Beta 1 – heart, JG cells. Beta 2 – bronchus,
GIT, bladder, uterus, liver, skeletal muscle
spindle, blood vessles. Beta 3 – adipose
tissue, coronary vessels
Vasopressin receptors V1 – vascular smooth muscle, platelets. V2
– collecting duct. V3 – pituitary
Histamine receptors H1 – smooth muscles and endothelial cells,
H2 – parietal cells, H3 – CNS, H4 – Mast
cells, eosinophils, T cells, dendritic cells
Serotonin receptors 5HT1B/1D – constriction of cranial
vessels, 5HT3 – vomiting, 5HT4 - peristalsis
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ENDOCRINOLOGY
GROUP I LIPOPHILIC RECEPTORS
CYTOPLASMIC RECEPTORS NUCLEAR RECEPTORS

Glucorticoids & Mineralocorticoids Thyroid Hormones
Androgen,Estrogen
Retinoic acid
Vitamin D3 (1,25(OH) 2 D2
GROUP II HYDROPHILIC HORMONES (BIND TO CELL MEMBRANE)
C-AMP C-GMP Ca/IP3/DAG Kinase/Phosphatase

CRH ANF Oxytocin Growth Hormone
FSH NO M1,M3 Prolactin
TSH V1(Vascular smooth Insulin
muscle)
LH GnRH EGF
Adrenaline GHRH FGF
D1 to D5 Angiotensin IGF I & II
II(Vascular
&Smooth muscle)
MSH PDGF NGF
ACTH Substance P PDGF
Alpha 2 adrenergic Gastrin Erythropietin
Beta adrenergic CCK M-CSF
Parathromone TRH
V2 Alpha 1 adrenergic
Glucagon 5HT2
HCG H1
Angiotensin
II(Epithelium)
Somatostatin
Calcitonin
Lipotropin
5HT1
H2
M2
G PROTEIN COUPLED RECEPTOR
Small G proteins Rab, ras, rho/rac

G protein G channels, Phosphorylase formation, Made up of 3
units, Related to ras oncogene
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ENDOCRINOLOGY
G protein activation leads to Generation of second messenger

Metabotropic receptor Single sub unit structure, interact with G
protein, effects are for long period
G protein coupled receptor is Metabotropic receptor
G protein coupled receptor G proteins act as inhibitory and excitatory because of
difference in alpha subunit
In G protein coupled receptor, amino Extracellular side
terminal end faces
In G protein couples receptor, carboxy Cytoplasmic side
terminal end faces
Carboxy terminal end is associated with Alpha, beta and gamma
Normally GDP is associated with Alpha
G protein receptor complex Interacts with transmembrane domain, GTP to GDP,
Adenyl cylase activation leads to increased CAMP,
Helical structure, Binds to ligand at cell surface
G protein acts as inhibitory and excitatory because of Alpha subunit
difference in
Action of alpha subunit of G protein Breakdown of GTP to GDP
If there is Gs alpha sub unit gain of function mutation Increased cAMP
Gs Stimulates adenyl cyclase, increases
protein kinase A. eg beta1 and beta2
Gi Inhibits adenyl cyclase. Example alpha 2
Gq Activates phospholipase C which in turn
increases protein kinase C. example alpha
1
Gh Activates phosphodiesterase. Example
rods and cones
NITRIC OXIDE
Nitric oxide Free radical, Vasodilator, Oxidizing agent, Catalyst

Nitric oxide Vasodilator, Derived from arginine
Nitric oxide cGMP, regulate vascular tone, penile erection, low
concentration in cigarette smokers
Nitric oxide Formed from L-arginine by NO synthetase, causes
vasodilatation of all vessels, used in portal
hypertension, interacts with Hb, used in erectile
dysfunction, used in pulmonary hypertension, caused
systemic hypotension, Least systemic effect, Better
ventilation perfusion match
Molecules from which nitric oxide can be Arginine, amyl nitrite, isosorbide dinitrite
released in vivo
Endothelial relaxing factor is Nitric oxide
EDRF is Nitric oxide
Nitric oxide is produced in Endothelium
Nitric oxide synthase requires NADPH, FAD, FMN, Heme iron
Calcium independent/ inducible nitric oxide synthase NOS 2
Inducible form of nitric acid synthase is Macrophage
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PITUITARY GLAND 12
ENDOCRINOLOGY
present mainly in
Mechanism of action of nitric oxide cGMP
Causes release of NO from endothelial cell ADP, acetylcholine
Nitric Oxide does NOT act via Membrane bound receptor
Primary action of nitric oxide in gastrointestinal tract Smooth muscle relaxation
Inhaled gas used to prevent pulmonary artery pressure Nitric oxide
in adults and infants
Nitric oxide produces its antiaggregatory action by cGMP
increasing levels of
Inhaled gas used to decrease pulmonary artery pressure Nitric oxide
in infants and adults
Increasing nitric oxide Glycerine trinitrate, sodium nitroprusside, hydralazine
Release of NO is associated with Hydralazine, Nitroprusside, Nitroglycerine
PITUITARY GLAND
DEVELOPMENT OF PITUITARY GLAND
Pituitary gland arises from Ectoderm

Adenohypophysis arise from Roof of Stomodeum
Anterior Pituitary develops from Craniopharyngeal tube, Rathke’s Pouch
rd
Posterior pituitary develops from Floor of 3 ventricle in the region of Infundibulum
Diverticulum from floor of diencephalon Posterior pituitary
form
Oncocytes are associated with Kidney, Salivary glands, endocrine glands
Oncocytes are NOT seen in Pineal gland
ANATOMY OF PITUITARY GLAND
Weight of pituitary gland 600 mg

Pituitary gland Situated deep in sella, Sphenoidal air cells lie inferior to
it, Supplied by a branch of internal carotid artery
Type of cells in neurohypophysis Pituicytes
Most abundant cells in pituitary Somatotroph
Most earliest cells in pituitary Corticotrophs
Most resistant cells in pituitary Thyrotrophs
Least found cells in Pituitary Thyrotrophs
Pituitary related to each side by Cavernous sinus
Pituitary inferiorly related by Sphenoid air cells
Pituitary separated from optic chiasma by Diaphragmatic sella
Arterial supply of Pituitary Superior & Inferior Hypophyseal artery – branch of
Internal Carotid artery
Endocrine gland having portal circulation Hypophysis cerebri
Venous drainage from neurohypophysis is routed Portal vessels to adenohypophysis, Inferior hypophyseal
through veins to dural venous sinuses, Capillaries to median
eminence and hypothalamus
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PITUITARY GLAND 13
ENDOCRINOLOGY
NOT a route of Venous drainage from neurohypophysis Superior hypophyseal veins to ventricular tachycytes
Pituitary bright spot is due to High phospholipid content of posterior pituitary
Herring body Posterior pituitary
Best view to visualize pituitary fossa on X-ray skull Lateral skull view
Best view for detecting sella turcica on X ray Lateral view
J shaped sella is seen in Mucopolysacchroidoses, Achondroplasia, Optic chiasma
glioma, Neurofibromatosis I, Hydrocephalus
PHYSIOLOGY OF PITUITARY GLAND
Pituitary has no control over Adrenal medulla

Sequence of acquired pituitary hormone loss GH – FSH/LH – TSH - ACTH
FSH & LH are produced by Anterior Pituitary
Acidophilic Cells Growth hormone, Prolactin
Basophilic cells of pituitary secrete TSH, ACTH, LH
Alpha and beta subunits seen in LH, HCG
ACTH level highest during Early morning
Prolactin produced by Anterior Pituitary
Lactation is mediated by Prolactin
Oxytocin differs from vasopressin at Position 3 and 8
Vasopressin receptors V1 – vascular smooth muscle, V2 – collecting duct, V3 –
anterior pituitary
Vasopressin acts on Intramedullary collecting duct
Vasopressin acts by Water transport across collecting duct
Vasopressin acts via IP3 - DAG
Vasopressin is under control of Caudal ventrolateral medulla
ADH Postoperative increase in secretion, Neurosecretion,
Increased secretion when plasma osmolality is high, Act
on distal tubule and increase permeability
Increases ADH secretion Fluoxetine
Vasopressin is inhibited by Alcohol
Administration of exogenous vasopressin does NOT Renal hyposensitivity to ADH
increase urine osmolality
NOT true about ADH Increased secretion when plasma osmolality is low
NOT a function of vasopressin Increasing thirst
Deficiency of vasopressin results in Inability of kidney to concentrate urine
Conivaptan Non selective V1 and V2 blocker
Selective V1 blocker Relcavaptan, nelivaptan
Selective V2 blocker Lixivaptan, mozavaptan, tolvaptan
Myoepithelial cells are found in Salivary gland, mammary gland, parotid
Factor essential for myoepithelial cell contraction Oxytocin
Ejection of milk from breast Oxytocin
Hormone responsible for stimulating milk let down Oxytocin
reflex
Neurophysin is found in Oxytocin
Initial Investigation for Hyperpituitarism Serum IGF-1
Septooptic dysplasia is associated with HESX1 gene
Obese female, hypertension, chronic headache, normal Empty sella syndrome
pituitary function
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PITUITARY GLAND 14
ENDOCRINOLOGY
MC endocrinal abnormality associated No abnormality

with empty sella
Transection of pituitary stalk Diabetes insipidus, hyperprolactinemia, hypothyroidism
NOT occur after transection of pituitary stalk Diabetes mellitus
GROWTH HORMONE
Somatomedin mediates Deposition of chondroitin sulphate

Most physiological effects of growth hormone mediated Somatomedin
by
NOT a neurotransmitter Somatomedin
Anabolic action of protein is mediated by Growth hormone
Potent stimulator of growth hormone Arginine
Growth hormone secretion inhibited by Hyperglycemia
9 year old boy, growth retardation propensity to Growth hormone deficiency
hypoglycemia. Short stature, micropenis, increased fat
and high pitched voice. Bone age 5 years.
Growth hormone deficiency is associated with Obesity, micropenis, doll like facies
Deficiency of growth hormone Proportionate dwarfism, Symptomatic hypoglycemia,
Delayed tooth eruption, Sexual infantilism
Insulin provocative test is useful in differentiation of Hypopituitarism
short stature as a result of
TRH stimulation test is useful in diagnosis of disorders Growth hormone
of
Tests for growth hormone L-arginine test, L-dopa test
Laron syndrome Growth hormone insensitivity, growth failure
Growth hormone releasing factor Lung
(GRFoma)
GIGANTISM
Gigantism occur in Enuch

NOT a feature of gigantism Mental retardation
ACROMEGALY
MC cause of Acromegaly GH Producing pituitary adenoma

Acromegaly is due to excess of Growth hormone
Depressed nasal bridge NOT seen in Acromegaly
Hypoglycemia is NOT a feature of Acromegaly
Paradoxical response to GH release to TRH is seen in Acromegaly
Heel pad thickness is increased in Acromegaly
MC cause of increased heel pad thickness Heel injury
Acromegaly is associated with Increased GH, somatomedin C
Confirmatory investigation for acromegaly Glucose induced GH suppression
TRH stimulating test useful in diagnosing Acromegaly, Hyperthyroidism
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PITUITARY GLAND 15
ENDOCRINOLOGY
Serum IGF-1 test for Acromegaly

Drug of choice in acromegaly Octreotide
Drug used for Acromegaly Pegvisomant (GRH receptor Antagonist)
True about Octreotide Used in secretory diarrhea
Long acting octreotide Sandostatin
Side effect of octreotide Delays gall bladder emptying
NOT true about octreotide An absorbent
Octreotide NOT used in Glioma
Octreotide NOT used in Glucoganoma
NOT true about octreotide Effective orally
DWARFISM
Etiology of Nutritional dwarfism Chronic malnutrition

Disproportionate Dwarfism Hypothyroidism
PROLACTIN
Prolactin is secreted by Anterior Pituitary

Only hormone for which no stimulator has been Prolactin
isolated
Normal prolactin level 10 – 25 microgram/L
Normal prolactin level in a woman of reproductive age 25 ng/ml
Milk production Secretion by contraction of lactiferous sinus,
Neuroendocrine part of posterior pituitary is involved,
Oxytocin involved, Affected by emotion
Increased prolactin associated with Increased estradiol
Prolactin Decreases gonadotrophin action
TRH stimulates release of TSH, GH, Prolactin
Hyperprolactinemia is associated with Amenorrhoea, Galactorrhea, Infertility
Prolactin secretion is increased by Chlorpromazine
Prolactin secretion NOT increased by Dopamine
Hormone secretion inhibited by Dopamine Prolactin
Prolactin secretion of decreased by L- DOPA, Bromocriptine
Secretion of prolactin affected by Dopamine
Prolactin antagonist Dopamine
Prolactin secretion inhibited by Bromocriptine
Secretion of prolactin affected by Dopamine
Prolactin deficiency is tested by TSH test
HYPERPROLACTINEMIA
Causes of Hyperprolactinoma Chronic renal failure, Thyrotoxicosis, Metoclopramide

Hyperprolactinemia caused by Methyldopa, phenothiazines, metoclopramide
Investigation of choice for hyperprolactinemia Prolactin estimation
Gynaecomastia is NOT seen in Hypoprolactinemia
NOT true about hyperprolactinemia Elevated prolactin levels are always
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PITUITARY GLAND 16
ENDOCRINOLOGY
associated with adenoma
PITUITARY TUMOURS
Pituitary tumour 10% of brain tumours, erodes sella and extends into
surrounding area, differentiated by RETICULIN stain
MC type of Pituitary adenoma Prolactinoma
MC Pituitary tumour Prolactinoma
30 year old woman, secondary amenorrhoea for 3 years Prolactinoma
along with galactorrhoea
NOT true about prolactinoma in pregnancy Macroadenoma>1% associated with bad prognosis
Middle age female increasing visual loss, breast Serum prolactin
engorgement, irregular menses. investigation of choice
26 year female, prolactin 65 ng/L second month Routine obstetric care
Treatment of Choice for Prolactinoma Bromocriptine (oral dopamine agonist)
MC cause of Panhypopituitarism Pituitary adenoma
Galactorrhoea Inappropriate secretion of milk containing fluid from
breast
Amenorrhoea, Galactorrhoea, Bitemporal hemianopia Prolactin secreting Pituitary macroadenoma
Amenorrhoea, galactorrhoea, increased prolactin. CT Pituitary adenoma
scan reveal
Loss of erection, low testosterone, high prolactin Pituitary adenoma
Tumour less than 1 cm Microadenoma
Percentage of conversion of microadenoma to 5%
macroadenoma
Visual defect caused by tumor of Pituitary gland Bitemporal hemianopia
pressing Optic chiasma
Lactational amenorrhoea is due to Prolactin induced inhibition of GnRH
Weak Giants Pituitary adenoma
Expansion & Ballooning of sella Pituitary Adenoma
Enamel like superstructure is seen in Craniopharyngioma
Somatotrophic adenoma Eosinophilic staining
NOT a feature of pituitary eosinophilic Adrenal hypercortisolism
adenoma
Gold standard investigation for pituitary Contrast enhanced MRI
adenoma
Earliest method of diagnosing pituitary tumors CT scan
Best way to distinguish between pituitary tumor from Petrosal sinus sampling
ectopic ACTH producing tumor
Most preferred approach for pituitary surgery at Trans sphenoidal
present time
PITUITARY APOPLEXY
Hypocalcemia seen in Hypopituitarism

Associated with pituitary apoplexy Diabetes mellitus, sickle cell anemia, hypertension
NOT a cause of pituitary apoplexy Hyperthyroidism
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PITUITARY GLAND 17
ENDOCRINOLOGY
SHEEHAN SYNDROME
Postpartum pituitary necrosis Sheehan’s syndrome

Empty sella, amenorrhea, failure of lactation Sheehan syndrome
NOT a cause of primary amenorrhoea Sheehan syndrome
Most effective drug in Sheehan’s syndrome Corticosteroids
Drug essential in Sheehan syndrome Cortisone
Loss of libido in postpartum necrosis best treated with Low dose testosterone
SYNDROME OF INAPPROPRIATE SECRETION OF ADH
Free water clearance regulated by ADH

Circulatory form of ADH Free form
Form of ADH circulating in plasma Free form
ADH acts on Medullary Collecting duct
For concentration of urine by ADH, absorption of water Collecting duct
occurs from
When NaCl injected into internal carotid artery, it Supraoptic nucleus
causes release of ADH by stimulating
Greatest stimulator of ADH secretion Hyperosmolality
ADH is stimulated by Angiotensin II, Standing, Hyperosmolarity
Concentration of urine due to Angiotensin II, Aldosterone, ADH, ANP
SIADH is due to Excess ADH
MC cause of SIADH Ectopic ADH by Small Cell Cancer
Malignant tumour producing ACTH, ADH Oat cell cancer
SIADH secretion is seen in Lung abscess, vinca alkaloids, bronchial adenoma
SIADH caused by Vincristine, vinblastine, cyclophosphamide
SIADH Hyponatremia, Low Plasma osmality, High urine
Osmolality, Hyponatremia
SIADH Increased urine Na+, Increased urine osmolality
SIADH Na+ < 135, Uric acid < 4 mg/dl, K+ normal
Syndrome of inappropriate ADH is characterized by Hyponatremia and urine sodium excretion > 20 mEq/L
Inappropriate ADH secretion Water intoxication, expanded fluid volume,
hypomagnesemia, concentrated urine
Findings in SIADH Increased urine Na+, Increased urine osmolality
Hyponatremia with Isovolemia SIADH
SIADH associated with Hypogammaglobulinemia
Finding in SIADH Normal Blood Pressure
Edema Does NOT occur in SIADH (excess Vasopressin)
NOT seen in SIADH Low BP due to volume depletion
SIADH NOT associated with Interstitial nephritis
Treatment of SIADH Fludrocortisones, demeclocycline, hypertonic saline
Drug of choice for SIADH Demeclocycline
Vasopressin antagonist act on Medullary collecting duct
Treatment of SIADH V2/V1a antagonist (Conivaptan)
NOT used in SIADH Desmopression
Drug NOT used in SIADH Desmopressin
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PITUITARY GLAND 18
ENDOCRINOLOGY
DIABETES INSIPIDUS
Normal serum osmolality 285 - 295 mosm/L

Normal urine osmolality 350 - 1000 mosm/L
MC cause of diabetes insipidus in pregnancy Severe pre eclampsia
Causes of diabetes insipidus Head injury, Histiocytosis, Viral encephalitis
Nephrogenic diabetes is caused by Hypokalemia, sarcoidosis, hypercalcemia
NOT a cause of diabetic insipidus Multiple sclerosis
Inheritance of Diabetes insipidus X linked recessive
Central diabetes insipidus Low urine osmolality, Normal to high serum osmolality
Nephrogenic diabetes Renal tubule unresponsive to ADH
A child is crying excessively even after being given feed. Diabetes insipidus
He is passing large quantities of urine and reportedly
getting dehydrated. Urine examination shows no
proteinuria and a specific gravity of 1004. most likely
diagnosis
Diabetes insipidus is associated with Increased serum osmolality, Decreased urine osmolality
Diabetes insipidus associated with Hypernatremia
Diabetes insipidus Water deprivation test is required
Hypertonic contraction of fluid volume is caused by Diabetes insipidus
Recessive Nephrogenic diabetes Aquaporin 2
X linked nephrogenic diabetes V2 receptor
Urinary Osmolality in Diabetes Insipidus 30 mmol/L
Hyponatremia NOT seen in Diabetes insipidus
Diagnosis of diabetes insipidus require Water deprivation test
Hickey hare test Diabetes insipidus
Drug of choice for lithium induced diabetes mellitus Amiloride
Treatment of lithium induced diabetes insipidus Thiazide diuretics, K+ sparing diuretics
Main stay of treatment for nephrogenic diabetes Thiazide or amiloride diuretics, Salt restriction
insipidus
Drug of choice for central /neuogenic diabetes insipidus Desmopressin
Chlorpropamide is used in Central diabetes insipidus
NOT used for diabetes insipidus Furosemide
Drug NOT used in diabetes insipidus Furosemide
POLYURIA
Polyuria is caused by Hypercalcemia, primary hyperaldosteronism,

nephrogenic diabetes insipidus
9 year old female polyuria, polydipsia, metabolic Cystinosis
acidosis, on slit lamp examination crystal deposits are
seen in cornea
Cerebral salt wasting syndrome Polyuria, hypotension, dystautonomia
Head injury, raised ICT, put on ventilator and started on High output due to diuretics
IV fluids and diuretics. 24 hours later urine output 3.5
litres. sodium 156 mEq/L, osmolarity 316 mOsm/kg
Decreased serum and urine osmolality along with Psychogenic polydipsia
reduced serum sodium
Investigations done in women with polyuria > 6L/day Water deprivation test, Plasma and urine osmolality
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THYROID GLAND 19
ENDOCRINOLOGY
High urine osmolality > 300 along with increased Solute diuresis/high output due to diuretics
sodium
NOT true about treatment of primary Desmopressin is safely used in treatment
polydipsia
THYROID GLAND
DEVELOPMENT OF THYROID
Gland derived from foramen caecum Thyroid

Thyroid develops from Endoderm of thyroglossal duct
Thyroxine synthesis 11 weeks of gestation
ANATOMY OF THYROID
Average Weight of Thyroid gland 18 – 20 gm

Iodine uptake is seen in Thyroid, Salivary gland, Mammary gland
Iodine uptake seen in Thyroid, salivary gland, Mammary gland
nd th
Isthumus of thyroid is across tracheal ring 2 to 4
True about blood supply of thyroid gland Superior thyroid artery is a branch of external carotid
artery, Inferior thyroid artery is a branch of
thyrocervical trunk, Parathyroid arteries are usually a
branch of inferior thyroid artery
Superior thyroid artery is related to External Laryngeal Nerve
st
Inferior thyroid artery arise from Thyrocervical trunk of 1 part of subclavian artery
NOT true about thyroid ima Thyroid ima artery is invariably a branch of arch of aorta
Middle thyroid vein drains into Internal jugular vein
Recurrent laryngeal artery is in close association with Inferior thyroid artery
Lymphatics directly into blood stream Thyroid
Method of choice to detect thyroid size USG
accurately
PHYSIOLOGY OF THYROID
Thyroid hormones are synthesized from Tyrosine

Thyroid hormone in blood is transported by Albumin, Thyroid binding globulin, Thyroid binding
prealbumin (Transthyretin)
Relation between normal thyroid weight with dietary Inversely
iodine content
Iodophores are mixtures of Iodine and surface acting agents
Thyroid peroxidase is NOT involved in Secretion of Thyroglobulin into Colloid
Epiphyseal closure is mediated by Thyroxine
Bruit heard in which pole of thyroid Upper pole
Isotopes used in thyroid I 131, I123,Technetium 99
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THYROID GLAND 20
ENDOCRINOLOGY
Amount of I 131 used in thyroid scan 50 millicurie

Dose of I 131 used in thyroid scan 1 millicurie
I 131 emits Beta radiation
THYROID HORMONES
Thyroid hormone T3 is more avidly bound to nuclear receptors than T4,

T4 has maximum plasma concentration, T3 is more
active than T4, T4 has longer half life than T3
Concentration of T4 & T3 T4 > T3
Half life of T4 & T3 T4 > T3
Thyroid hormone tightly bound to Plasma protein T4
Thyroid hormone tightly bound to nuclear receptor T3
Highest affinity for receptor T3
Highest T3:T4 ratio in Brain
Major fate of T4 Reverse T3
Thyroxine Increased lipolysis, Increased BMR, Increased O2
consumption, Increased myocardial contractility
NOT true about thyroid hormones T4 shorter half life than T3
Subunit unique to TSH Beta
Normal value of TSH 0.34 to 4.25 mIU/L (microIU/ml)
Action of thyroid hormones on Increases heart rate, increases stroke
cardiovascular system volume, decreases peripheral resistance
Thyroid hormones Decreases cholesterol level, negative
nitrogen balance, vitamin utilization
HYPERTHYROIDISM
Occurrence of hyperthyroidism following administration Jod Basedow effect

of supplemental iodine to subjects with endemic iodine
deficiency goiter
Jod Basedow Disease Iodine Induced Hyperthyroidism
Most earliest & Consistent feature of Hyperthyroidism Cardiac Manifestation
Tachycardia in hyperthyroidism is caused by stimulation β1 receptor
of
Hyperthyroidism Diarrhoea and heat intolerance
Moebius sign Inability to converge eyes in Hyperthyroidism
Von grafe sign Lagging behind upper eyelid
Plummer nail Hyperthyroidism
Best initial screening test for hyperthyroidism Serum TSH and T4 estimation
Most sensitive test for hyperthyroidism Free thyroxine index
Hyperthyroidism is diagnosed by T3,T4,TSH
Decreased T3,T4,TSH it cannot be Hyperthyroidism
Treatment of Hyperthyroidism & Functioning Thyroid Iodine 131
Cancer
Best treatment of hyperthyroidism in young female Surgical treatment
having retrosternal extension
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THYROID GLAND 21
ENDOCRINOLOGY
Treatment of hyperthyroidism in Propylthiouracil with T3

pregnancy
HYPOTHYROIDISM
Incidence of hypothyroidism 1 in 4000

MC Neonatal Disease Screened Neonatal Hypothyroidism
MC cause of Hypothyroidism in Iodine Sufficient areas Autoimmune Hypothyroidism (Hashimoto’s Thyroiditis)
of the world
MC cause of Neonatal Hypothyroidism Thyroid Gland Dysgenesis
MC cause of Endemic Goitre/Hypothyroidism Iodine Deficiency
MC cause of Acquired hypothyroidism Autoimmune thyroiditis
MC cause of congenital hypothyroidism Thyroid dysgenesis
MC cause of congenital hypothyroidism Defective hormone synthesis
Causing hypothyroidism PAS, Lithium, Amiodarone
Hypothyroidism caused by Lithium, Hemochromatosis, Scleroderma
Drug causing hypothyroidism Ethionamide
Drugs causing thyroid dysfunction Amiodarone, Lithium, Cholestyramine
Wolff Chaikoff effect is due to Inhibition of organic binding of iodine
Iodine associated hypothyroidism is common in Women
Myxedema is characterized by Hypercapnea, Hypotension, Hypoglycemia
Common presentation of juvenile hypothyroidism Growth retardation, Mental retardation with in 2 years,
Umbilical hernia
Commonest feature of hypothyroidism in children Cold extremities
Disproportionate dwarfism Hypothyroidism
Hypothyroidism in infant Delayed closure of fontanelle
Thyroid dysgenesis Not associated with palpable goitre
Dry skin is seen in Hypothyroidism
Hung up reflux (delayed ankle jerk Hypothyroid
relaxation)
Normocytic normochromic anemia Hypothyroidism
Reversible dementia Hypothyroidism
Chromatin positive seminiferous tubule dysfunction Hypothyroidism
Associated with hypothyroidism High triglycerides
Dense Metaphyseal Band Hypothyroidism
Epiphyseal dysgenesis, Wormian bone, Growth Hypothyroidism
retardation, Mental Retardation, Cold Intolerance
Hypothyroidism in pregnancy is associated with Recurrent abortion, Polyhydramnios, Preterm labour
Hypothyroidism in pregnancy least likely associated PIH
with
Amiodarone induced thyroid dysfunction Hyperthyroidism is common in iodine deficient areas,
amiodarone inhibits deiodinase activity, amiodarone
therapy is associated with initial reduction of serum T4
levels
False regarding amiodarone High incidence of torsa des pointes
Epiphyseal dysgenesis Hypothyroidism
TSH and TRH deficiency Micropenis, convulsions, hypoglycemia
Symptom NOT associated with Hypothyroidism Increased Appetite
NOT a feature of hypothyroidism in newborn Mental retardation
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THYROID GLAND 22
ENDOCRINOLOGY
Hypothyroidism with increased TSH level is NOT seen in Sheehan syndrome

NOT associated with hypothyroidism Low cholesterol
NOT a feature of congenital hypothyroidism Hyperthermia
True marker of iodine deficiency Neonatal hypothyroidism
Most sensitive parameter in monitoring iodine Neonatal hypothyroidism
deficiency control programme in a community
Blood specimen for neonatal thyroid screening is Cord blood
obtained from
Ideal place to collect blood sample for TSH in newborn Cord blood at the time of birth
th
Ideal place & time to collect blood sample for TSH Heel pad on 4 day of birth
estimation for neonatal thyroid screening
Single most test for Hypothyroidism Increased TSH
Screening test for Neonatal Hypothyroidism TSH and T4 assays on heel prick blood sample
MC Investigation for Hypothyroidism Serum TSH
Primary hypothyroidism T3,T4 decrease, TSH increase
Thiocyanates and perchlorates act by Inhibiting uptake of iodine into acinar cell
Antithyroid action of Lugol’s iodine is by inhibition of Iodine uptake
Treatment of hypothyroidism in patient with ischemic Low dose of levothyroxine
heart disease
Radio iodine cause euthyroid state in 2 months
Absolute contraindication for radioiodine treatment Pregnancy, breast feeding
Complication of therapy with radioiodine therapy Hypothyroidism
Hypothyroidism following Thyroidectomy occurs within 2-5 days
CRETINISM
Cretinism Prolonged physiological jaundice, Common in iodine

deficiency endemic areas, Delayed skeletal
development, Short limbs and short stature
Endemic cretinism Strabismus, Spastic diplegia
Hypothyroid cretinism Deafness with facial palsy
No social smile, no eyebrows, protruded tongue Cretinism
NOT a feature of cretin Hyperpyrexia
NOT a feature of Sporadic cretinism Aplasia of thyroid
NOT a feature of cretinism Hyperpyrexia
STRUMA OVARY
Struma ovary associated with Hyperthyroidism

Struma ovary is composed entirely of Mature thyroid tissue
THYROTOXICOSIS
MC cause of Thyrotoxicosis Grave’s Disease

Jose Badesow effect Thyrotoxicosis in elderly
Apathetic thyrotoxicosis Masked presents with fatigue and weight loss
Thyrotoxicosis Pretibial myxedema, Glycosuria, Unilateral
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THYROID GLAND 23
ENDOCRINOLOGY
exophthalmos
Thyrotoxicosis associated with Soft non ejection systolic murmur, Irregularly irregular
pulse, Scratching sound in systole
Thyrotoxicosis is associated with Fine tremor
Dancing carotid Thyrotoxicosis
Stellwag sign Infrequent blinking in Thyroid Ophthalmopathy (strange
look)
Darlympe sign Upper sclera is seen
Von Grafe sign Lid lag
Thyrotoxicosis in which serum thyroglobulin level is NOT Thyrotoxicosis factitia (self administration of thyroid
increased hormone)
NOT a CVS finding in thyrotoxicosis Early diastolic murmur
NOT a cardiovascular finding in elderly thyrotoxicosis Early diastolic murmur
patient
NOT seen in primary thyrotoxicosis Myopathy
NOT associated with thyroid storm Surgery of thyrotoxicosis
NOT a feature of thyrotoxicosis Hair loss
20 year old girl, 9 month history of neck swelling, Thyroid scan
thyrotoxic symptoms.T4 increased decreased TSH,
palpable 2 cm nodule. next investigation
Drug of choice for treatment of thyrotoxicosis during Propylthiouracil
pregnancy
Treatment of choice in childhood thyrotoxicosis Carbimazole
Childhood Thyrotoxicosis Carbimazole
Management of fetal thyrotoxicosis Propylthiouracil to fetus
Absolute contraindication of treatment of I131
thyrotoxicosis in pregnancy
5% guanethidine is used for treatment of Thyrotoxic ophthalmopathy
NOT given in thyrotoxicosis complicating pregnancy Lugol’s iodine
In thyrotoxicosis beta blocker do NOT control Oxygen consumption
GRAVE’S DISEASE
MC cause of Proptosis in adults (25-50 years) Graves Ophthalmopathy

Type of hypersensitivity in Grave’s disease Type II hypersensitivity
Mechanism of autoimmunity in Grave’s Abnormal expression of MHC class II
disease molecules
Orange skin appearance is seen in Grave’s disease
Skin of Grave’s disease patient Warm and moist
Extraocular muscle commonly affected in Grave’s Inferior rectus
disease
Management of Grave’s disease with eye Total thyroidectomy
signs
GOITRE
Goiter is said to be endemic, if its 10%

prevalence is greater than
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THYROID GLAND 24
ENDOCRINOLOGY
One year old child, short stature, lethargy, constipation, Thyroid dyshormogenesis
palpable goiter, low T4 and elevated TSH
Goiter more than 5% of population Endemic goiter
Mineral leading to endemic goiter Iodine
MC Presentation of Endemic Goitre Diffuse Goitre
Uptake of radioiodine in endemic goiter Increased
Thoracic extension of cervical goiter is approached Neck
through
MC Presentation of Retrosternal Goitre Dyspnoea
Retrosternal tumor Bluish discolouration of face, Edema of face, Occur in
thyroid tumors
Plunging goiter is Retrosternal goitre
Efficiency of a goiter control programme can be Neonatal thyroxine levels
assessed using
Therapy of choice for diffuse toxic goiter in a patient of Radio iodine
age 45 years
A newborn with a large goiter enough to cause dyspnea Tracheostomy
is treated with
Treatment of respiratory distress due to swelling in Open immediately
neck few hours after thyroidectomy
Swelling of neck following thyroidectomy, most likely Respiratory obstruction
resulting complication
Iodised oil used to prevent Goitre Poppy seed oil
Can be used for treatment of goiter Burnt sea weed
PENDRED SYNDROME
Inheritance of Pendred syndrome Autosomal recessive

Pendred syndrome is due to defect in Chromosome 7q
Pendred syndrome Diffuse colloid goiter, Nodular goiter, Mental
retardation, Bilateral sensorineural deafness
Pendred Syndrome Congenital Sensorineural Deafness, Goitre
Goiter in pendred syndrome at Puberty
THYROIDITIS
Fever and pain in thyroid gland Increased ESR

I131 uptake in acute thyroiditis Initially increase and then decrease
A young patient has a midline tender swelling in neck Subacute thyroiditis
occurring after an attack of sore throat. diagnosis is
Depressed radioactive uptake is seen in Subacute thyroiditis, Factitious thyroiditis
Thyroid antibodies are NOT seen in Tuberculous thyroiditis
Thyroiditis NOT presenting with ophthalmic features Reidel’s thyroiditis
Bilateral proptosis, heat intolerance, palpitations. Reidel’s thyroiditis
UNLIKELY diagnosis
Reidel thyroiditis Hypothyroid
Ophthalmic signs are absent in Reidel’s Thyroiditis
Suppurative thyroiditis Euthyroid
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THYROID GLAND 25
ENDOCRINOLOGY
Treatment of chronic lymphocytic Thyroxine

thyroiditis
Only reason to operate in thyroiditis To overcome pressure on trachea and esophagus
HASHIMOTO’S THYROIDITIS
MC cause of Thyroiditis Hashimoto’s Thyroiditis

Hashimoto’s thyroiditis Transient thyroiditis
Hashimoto’s thyroiditis Follicular destruction, increase in lymphocytes,
Oncocytic metaplasia
Hurthle/Askansky Cells Hashimoto’s thyroiditis
Anti microsomal, Anti Thyroglobulin antibody Hashimoto’s Thyroiditis
In Hashimoto’s disease serum antibodies are mainly Thyroglobulins
against
In hashimoto’s thyroiditis, there is infiltration of Leucocytes
Hashimoto’s thyroiditis associated with Hypothyroidism
NOT true about Hashimoto’s thyroiditis Orphan annie eyed nucleus
NOT true about Hashimoto’s thyroiditis Anti thyroid nuclear antibodies
DE QUERVAIN THYROIDITIS
MC cause of Painful Thyroid Subacute Granulomatous Thyroid

Dequervain thyroididtis/Subacute Thyroiditis Viral Origin
De quervain thyroiditis also known as Granulomatous thyroiditis
De Quervan’s thyroiditis Pain, increased ESR, fever, Depressed radioactive
thyroid iodine uptake, Tend to regress spontaneously,
Associated with enlargement of thyroid
Subacute thyroiditis is associated with Hyperthyroidism
NOT a feature of De Quervain disease Autoimmune etiology
NOT true about de Quervian thyroiditis Increased uptake of radioactive iodine, Autoimmune
etiology
THYROID NODULE
nd
MC Solitary Thyroid Nodule Benign Colloid Nodule, 2 Follicular Adenoma
Hard thyroid nodule, vocal cord paralysis Carcinoma
Solitary nodule thyroid Common in female, Thyroidectomy done
Solitary nodule of thyroid in a non endemic area Adenoma
Plummer disease Toxic nodular goitre
65 year old man presents with signs and Toxic multinodular goitre
symptoms of thyrotoxicosis, his radio
iodine scan and 24 hour uptake show a
patchy pattern but normal amount of
radioiodine uptake
Fetal adenoma Follicular adenoma of thyroid
Next Investigation after TFT Thyroid Scan
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THYROID GLAND 26
ENDOCRINOLOGY
Investigation of choice in discrete thyroid swelling FNAC

Investigation of choice for Solitary Thyroid Nodule FNAC
Feature of thyroid nodule on USG suggestive of Hypoechogenecity, nonhomogenous, microcalcification
malignancy
Features of thyroid nodule suggestive of malignancy on Hypoechogenecity, Non homogenous,
USG Microcalcification
Toxic adenoma on scan appear as Hot nodule
Hot nodule Never malignant
Percentage of Malignancy in Cold Nodule thyroid 75% (cold nodule NOT always indicate malignancy)
False about thyroid nodule Cold nodule diagnostic of malignancy
25 year old woman, recurrent headache and sweating, Serial 24 hours test for catecholamines, metanephrines,
mother had renal calculi and died after having a neck VMA excretion
mass, thyroid nodule. no clinical signs of thyrotoxicosis,
before performing thyroid surgery
Treatment of choice for hyperfunctioning solitary nodule Radioiodine ablation
Treatment of choice of toxic adenoma in 52 year old Radioactive iodine
male
Indication of surgery in case of thyroid swelling Cosmetic, Pressure symptoms, Swelling with symptoms
Treatment of solitary toxic nodular goiter Lobectomy
Treatment of multinodular goiter Subtotal thyroidectomy
Treatment of choice of cold nodule in thyroid Hemithyroidectomy
Swelling of thyroid gland. Cold nodule, USG. Non cystic Hemithyroidectomy
solid mass. management
Most Appropriate Operation for Solitary Nodule in One Hemithyroidectomy
Lobe of Thyroid
Treatment of solitary nodule showing follicular Near total thyroidectomy
adenoma
Near total thyroidectomy means Lobectomy + isthumectomy + subtotal
lobectomy
26 year woman, palpable thyroid nodule, needle biopsy Total thyroidectomy and modified neck dissection on
demonstrates amyloid in stroma of lesion, cevical the side of enlarged lymph node
lymphadenopathy is palpated on same side of lesion
NOT true about management of thyroid nodule 4 cm size always resected
Management of cyst having cystic and Lobectomy
solid components
MALIGNANCY OF THYROID GLAND
Smoking is NOT a risk factor for Thyroid

MC cause of Metastasis of Thyroid gland Breast
MC Thyroid cancer metastasing to Bone Hurthle Cell Carcinoma
Radiation exposure during infancy linked to Carcinoma thyroid
Latent aberrant thyroid Metastatic foci from primary in thyroid
Lateral aberrant thyroid is associated Papillary carcinoma thyroid
with
Thyroid carcinoma Usually euthyroid
Low risk in thyroid carcinoma Women < 40 years, Papillary carcinoma < 5 cm
Malignancies that does not take up iodine Medullary carcinoma thyroid, hurthle cell
carcinoma
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THYROID GLAND 27
ENDOCRINOLOGY
Distant metastasis to lung in thyroid Children

cancer is common in
Prognostic scales for thyroid cancer AGES, MACIS, TNM, DNA ploidy
Hurthle cell carcinoma Derived from oxyphilic cells, high
mortality, treated by total thyroidectomy
and central neck node dissection
Recurrence in hurthle cell cancer is 99m Tc sestambi scanning
monitored by
Malignant lymphoma of thyroid In patients with tracheal compression,
isthumectomy is the most appropriate
form of biopsy
Thyroid lymphoma mostly arise from Hashimoto’s thyroiditis
patients with
NOT a histological variant of thyroid neoplasm Merkel cell
NOT true about lymphoma of thyroid Slow growing
Headache flushing, patient relative died of thyroid Measurement of catecholamines
tumour
Features of thyroid carcinoma Hypoechoic, microcalcification, majority
shows invasion into thyroid storm
Feature of thyroid NOT suggestive of malignancy Hyperechogenecity
Neoadjuvant chemotherapy NOT used in Thyroid carcinoma
Treatment of differentiated thyroid cancer I 131
Lady, Nodular thyroid left side of neck, Presence of Dissection with Postoperative radiotherapy
multiple lymphnodes in neck. Best treatment
Patient operated for thyroid surgery for thyroid Open wound sutures in the ward
swelling, later in evening developed difficulty in
breathing, swelling in neck. immediate management
FOLLICULAR CARCINOMA
MC cause of Adenomatoid cancer Follicular Carcinoma

Follicular carcinoma of thyroid is mostly due to Nras
mutation
Follicular thyroid carcinoma is associated PAX8
with
PPAR gamma is associated with Follicular adenoma, follicular carcinoma
Change of follicular adenoma to follicular 3p deletion
carcinoma
Age group for follicular carcinoma 50 years
thyroid
Thyroid carcinoma with pulsatile vascular skeletal Follicular carcinoma
metastasis
Malignancy developing in case of long standing goiter Follicular carcinoma
Hurthle cell tumor is Follicular carcinoma
Cancer developing from long standing MNG Follicular, anaplastic
Carcinoma thyroid with blood borne metastasis is Follicular
Route of spread of follicular carcinoma of thyroid Hematogenous
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THYROID GLAND 28
ENDOCRINOLOGY
Lymph node metastasis least commonly seen in Follicular carcinoma thyroid

Follicular carcinoma and adenoma differentiated by Vascular Invasion
Most critical factor in distinguishing Integrity of capsule
follicular adenoma from follicular
carcinoma
Psammoma bodies NOT seen in Follicular carcinoma thyroid
FNAC is NOT useful in Follicular carcinoma
Radio iodine is used in treatment of Follicular carcinoma
PAPILLARY CARCINOMA
MC genetic alteration in papillary thyroid cancer BRAF

Rearrangement of RET is associated with Papillary carcinoma thyroid
Chernobyl gas tragedy is associated with papillary carcinoma thyroid
Syndromes associated with papillary Gardner syndrome, cowden syndrome
carcinoma thyroid
Age group for papillary carcinoma 30 – 40 years
thyroid
Common histology of thyroid cancer Papillary type
Carcinoma arising from thyroglossal cyst Papillary
Thyroid carcinoma having best prognosis Papillary
Occult thyroid carcinoma with nodal metastasis Papillary
Papillary carcinoma usually present as Single nodule with lymph node
Carcinoma caused by Radiation Papillary
Features of Papillary carcinoma Radiation, secondaries to Lymph nodes
Compared to follicular carcinoma, papillary carcinoma Bilaterality, Local recurrence common, Increased
has lymphnode metastasis
Thyroid status in a patient with papillary Euthyroid
carcinoma thyroid
Papillary carcinoma Encapsulated, Mostly multifocal
Orphan Annie nucleus Papillary carcinoma thyroid
Psammoma bodies, Dystrophic calcification Papillary carcinoma thyroid
Variants of papillary carcinoma thyroid Columnar, Diffuse sclerosing, insular
Variant of papillary carcinoma with poor Tall cell variant
prognosis
NON aggressive variant of papillary carcinoma Follicular variant
Least malignant thyroid cancer Papillary
NOT true about papillary carcinoma of thyroid Always unifocal
FNAC needle size 22-26
FNAC 22 – 23 for Desmoplastic lesions
FNAC 25 Routine
FNAC 27 Children and sensitive lesions
Radioiodine destroys neoplastic cells predominantly in Beta rays
papillary carcinoma thyroid by
2 cm thyroid nodule, papillary carcinoma in a 50 year Near total thyroidectomy with modified neck dissection
old man
Treatment of Choice for Papillary carcinoma Thyroid Near total thyroidectomy with Radioiodine &
with bony metastasis Radiotherapy
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THYROID GLAND 29
ENDOCRINOLOGY
Best treatment of cervical node involvement in papillary Radical neck dissection

carcinoma thyroid
Prophylactic neck dissection on opposite Papillary carcinoma thyroid
side is NOT indicated in
MEDULLARY CARCINOMA
RET proto oncogene encodes for Tyrosine kinase receptor on cytoplasmic

membrane
RET ligand is identified as Glial cell line derived neurotrophic factor
(GDNF)
RET Chromosome 10
NOT a differentiating thyroid cancer Medullary carcinoma
Point mutation of RET Medullary carcinoma thyroid
Medullary carcinoma thyroid is common Superior pole
in
Medullary carcinoma thyroid is Osteoblastic skeletal metastasis
associated with
Most aggressive medullary carcinoma of MEN IIB
thyroid is associated with
Thyroid carcinoma secreting ACTH Medullary carcinoma
Ectopic ACTH secretion is associated with Medullary carcinoma thyroid
All Thyroid cancer From Follicular Cells EXCEPT Medullary carcinoma thyroid from parafollicular cells (c
cells)
ACal Medullary Carcinoma Thyroid
RET Protooncogene Medullary carcinoma
Medullary carcinoma of thyroid arise from Parafollicular cells
Multiple submucosal neuroma associated with Medullary carcinoma thyroid
Amyloid like stroma Medullary carcinoma
Thyroid carcinoma associated with hypocalcemia Medullary carcinoma
MC Presentation of Medullary Carcinoma Thyroid Diarrhoea
Medullary carcinoma of thyroid NOT associated with Antibodies
Most important predictor of medullary CEA
carcinoma thyroid
Treatment of medullary carcinoma thyroid Surgery only
Treatment of Medullary carcinoma Total thyroidectomy
Treatment of medullary carcinoma with lymph node Total thyroidectomy with radiotherapy
metastasis
Palpable thyroid nodule demonstrating amyloid stroma, Total thyroidectomy and modified neck dissection on
cervical lymphnode on the same side of lesion the side of enlarged lymph node
NOT true about diagnosis of medullary carcinoma Histological mitochondria is essential for diagnosis
thyroid
ANAPLASTIC CARCINOMA
Mutated p53 is associated with Anaplastic carcinoma
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THYROID GLAND 30
ENDOCRINOLOGY
Most Malignant Thyroid Cancer Anaplastic

Sudden increase in size of Long standing goiter Anaplastic carcinoma
Anaplastic carcinoma Elderly, Lymphatic infiltration common, P53 mutation,
Distant metastasis common, Some degree of
differentiation to papillary and follicular type
A patient with long standing multinodular goiter Anaplastic carcinoma
develops hoarseness of voice also the swelling
undergoes sudden increased in size
NOT a differential diagnosis of Solitary nodule of Anaplastic carcinoma
Thyroid
Treatment of Choice for Anaplastic carcinoma Thyroid Palliative/symptomatic
infiltrating Trachea & Sternum
Treatment of Anaplastic Carcinoma of thyroid Total thyroidectomy
ANTITHYROID DRUGS
Anti thyroid drugs improve symptoms in 2 weeks

Anti thyroid drugs cause euthyroid state 4 weeks
Anti thyroid drugs Can be used up to day of surgery
Plasma half life of carbimazole 8 hours
Side effects of carbimazole Choanal atresia, Scalp defect, Neck swelling
NOT a side effect of carbimazole Cleft lip or palate
Methimazole is differentiated from propylthiouracil in Less frequent dosage schedule
that
Safely used in pregnancy Propylthiouracil
Conversion of T4 to T3 inhibition by Propylthiouracil
Fastest acting thyroid hormone inhibitor Potassium iodide
False about iodine Contraindicated in hyperthyroidism
THYROID SURGERY
External Laryngeal Nerve Close to Superior Thyroid Ligated Nearer to Gland

Artery
Recurrent Laryngeal Nerve Close to Inferior Thyroid Ligated Away from Gland
Artery
MC cause of Right Recurrent Laryngeal Nerve Palsy Thyroid Surgery
Sudden increase in size of thyroid swelling along with Hemorrhage within the cyst
pain. Most likely cause
NOT a cause of stridor after thyroid surgery Hypocalcemia
NOT a complication of hemithyroidectomy Hypocalcemia
NOT a life threatening complication of thyroid surgery Hypocalcemia
NOT a cause of rise in end tidal CO2 during thyroid Anaphylaxis
surgery
A patient undergoes thyroid surgery, following which Oral Ca and vitamin D
she develops perioral tingling. Blood ca 8.9 mEq
Hematoma after thyroid surgery Immediate Evacuation
Tension hematoma deep to cervical fascia Usually due to slippage of ligature of
superior thyroid artery
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THYROID GLAND 31
ENDOCRINOLOGY
Patient presents with a neck swelling and respiratory Open immediately

distress few hours after a thyroidectomy surgery. next
management would be
A 50 year old male is suffering from severe dyspnoea Open the operative site
after thyroid surgery. Treatment of choice
In postoperative room after thyroid surgery, patient Remove the stitch and take the patient to OT
developed sudden respiratory distress, dressing was
removed and it was found to be slightly blood stained
and wound was bulging. first thing to be done
Most dangerous complication in a patient who had Respiratory obstruction
undergone thyroid surgery and develop hematoma at
the operative site
THYROID STORM
Thyroid storm is due to Inadequate control of thyroid toxicity

Mortality of thyroid storm 10 – 20%
Thyroid storm does NOT occur in Surgery for thyroiditis
NOT a treatment of thyroid storm Radioactive iodine
NOT used in management of thyroid storm Reserpine
THYROID IMAGING
Investigation for Thyroid Imaging Iodine 123

MC used Radionucleide for Thyroid Imaging Tc 99 Pertechnate
Advantages of USG in thyroid lesion Locating the swelling, Nature of cystic swelling,
Accuracy in detecting lesion
THYROGLOSSAL CYST
MC site of thyroglossal cyst Subhyoid

Hyoid bone is closely associated with Thyroglossal cyst or fistula
NOT true about thyroglossal cyst Incision and drainage is the treatment of choice
Surgery for Thyroglossal cyst Sistrunk operation
Carcinoma that does NOT arise from Medullary carcinoma thyroid
thyroglossal cyst
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CALCIUM METABOLISM 32
ENDOCRINOLOGY
CALCIUM METABOLISM
GENERAL FEATURES OF CALCIUM METABOLISM
Corrected calcium concentration is calculated by adding 0.8 mg/dl to the total calcium level for every decrement
in serum albumin of 1.0 g/dl
Calmodulin Calcium binder in cell
NOT regulated by calcium or calmodulin Hexokinase
Which is associated with Hypercalcemia William’s Syndrome
Osteoid formation is normal in Scurvy, Osteoporosis, secondaries bone
Fraying and cupping of metaphyses of long bone in Rickets, Metaphyseal dysplasia, Hypophosphatemia
children
Costochondral junction swelling Chondrodystrophy, Scurvy, Rickets
Protrusio acetabuli Osteoporosis, Rheumatoid arthritis, Paget’s disease
Raised alkaline phosphatase Sarcoidosis, secondaries, paget’s disease
Increased alkaline phosphatase Primary hyperparathyroidism, Chronic renal failure,
Paget’s disease, Rickets, Osteomalacia,
hypophosphatemia
Hypophosphatemia is seen in Rickets, hyperparathyroidism
Basal Ganglia Calcification Hyperparathyroidism, Perinatal hypoxia, Fahr’s
syndrome
Soft tissue calcification occurs in Scleroderma, Hyperthyroidism, Hypervitaminosis D
Short fourth metacarpal Albright Hereditary osteodystrophy,
Turner syndrome
Hot spots in bone scan Hyperparathyroidism, Osteoblastic secondaries,
Metastatic nodes
Sclerosis of bone Secondaries from prostate, Fluorosis, Osteopetrosis
Sclerotic lesion in bone Osteopetrosis, Melorheostosis, Caffey disease
Sclerotic lesion of bone is NOT seen in Osteitis fibrosa
DEVELOPMENT OF PARATHYROID GLAND
Parathyroid develops from Branchial pouch

th
Cell of parafollicular region derived from 5 brachial pouch, Ultimobrachial body
th
Superior parathyroid glands are derived from 4 branchial pouch
rd
Inferior parathyroid gland develops from 3 branchial pouch
ANATOMY OF PARATHYROID GLAND
Parathyroid gland Four in number, Superior glands are more constant in

position and lie at the level of inferior border of cricoids
cartilage, Color distinguish it from thyroid gland
Parathyroid gland looks like Jaundiced tongue of humming bird
Blood supply of Parathyroid gland Inferior Thyroid artery
Position of superior parathyroid Inferior border of Cricoid cartilage level
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ENDOCRINOLOGY
Identification of Parathyroid gland Brownish yellow colour

Location of inferior parathyroid Location is more variable than superior
Site of ectopic parathyroid Superior parathyroid
Site of undescended gland may be at Angle of mandible
NOT true about parathyroid gland Parasympathetic secretomotor supply
Most sensitive in identifying missed Sestambi scan
parathyroid
Treatment of multiglandular hyperplasia Removal of two and half glands
Treatment of primary Removal of three and half glands
hyperparathyroidism in MEN
PHYSIOLOGY OF PARATHYROID GLAND
Investigation for locating parathyroid gland Tc Thallium substraction scan
CALCIUM
Trade off hypothesis is implicated in Calcium

homeostasis of
Most abundant human cation Ca++
Active form of calcium Free ionized calcium
Normal Serum Calcium in children 8.8 – 10.8 mg/dl
Normal Serum Calcium 9 – 10.5 mg/dl
Calcium Absorbed in upper small intestine, Absorption increased
by acidic pH
Calcium absorption is from Proximal small intestine
Absorption of calcium increased by Acidic pH
Increased calcium intake cause Iron deficiency
Osteoclasts are inhibited by Calcium
Relation between magnesium and serum calcium Direct relation
Decreased extracellular calcium leads to Decreased membrane stability
Hormone not having role in Calcium metabolism Thyroxine
Calcium level falls to normal after cortisone Addisonian crisis, metastatic calcification, vitamin D
administration overdose
Post operative normocalcemia 24 – 72 hours
Organ NOT involved in calcium metabolism Spleen, Lung
Small ca++ binding protein that modifies activity of Calmodulin
many enzymes and other proteins in response to
changes of Ca++ concentration
Pentagastrin test measures Serum calcium
Calcium spark Local changes in intracellular calcium concentration
Function of Phospholamban Collects calcium into Sarcoplasmic reticulum
Lusiotrophic effect (relaxation of heart) is associated with Phopholamban
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ENDOCRINOLOGY
PARATHROMONE
Peptide hormone Parathromone

PTH 84 amino acids
Parathromone is a Peptide Hormone
Parathromone Vit D absorption increase, Mobilizes calcium from bone,
Increases intestinal absorption of calcium
Parathromone Stimulate 1,25 D3 formation, Increases resorption of
bone
Normal Serum Parathromone 9 – 65 pg/ml
Expected in a patient whose diet has been low in Increased parathromone secretion
calcium for 8 weeks
Serum calcium increased by Parathromone
NOT an action of parathromone Absorption of phosphorus increase
Jansen’s disease Mutation in PTH/PTHrP receptor, autosomal dominant, gain
of function
CALCITONIN
Osteoclast are inhibited by Calcitonin

Osteoclast has specific receptor for Calcitonin
Medullary carcinoma secretes Calcitonin
NOT produced by Neuron Calcitonin
Calcitonin is a Peptide hormone
Function of Calcitonin Decrease Calcium, Decrease Phosphate
Hypocalemia due to calcitonin by Decreased bone resorption
Calcitonin causes hypoglycemia by Inhibiting bone resorption
Pain in Paget’s disease is relieved by Calcitonin
Intranasal calcitonin used for Post menopausal osteoporosis, Paget’s disease
HYPERPARATHYROIDISM
MC cause of hyperparathyroidism Single adenoma

Subtle presentation of hyperparathyroidism Asymptomatic hypercalcemia
Symptoms of hyperparathyroidism Constipation and muscle weakness , Anorexia and
weight loss, Polydipisia and polyuria
Subperiosteal resorption of thickness of bone of skull Hyperparathyroidism
increased in
Sub periosteal erosion of middle phalanges at radial Hyperparathyroidism
aspect is characteristic of
Cod Fish Vertebra, Osteomalacia, Osteoporosis Hyperparathyroidism
Hyperparathyroidism Brown tumor (MC Mandible)
Absence of lamina dura in alveolus Hyperparathyroidism
Hourglass vertebrae, Triradiate pelvis Hyperparathyroidism
Tufting of terminal phalanges Hyperparathyroidism
Pathognomic of hyperparathyroidism Subperiosteal resorption of phalanges
50 year old man, multiple pathological fractures. Ca Hyperparathyroidism
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ENDOCRINOLOGY
11.5 mg/dl. Phosphate 2.5 mg/dl. Alkaline phosphatase

940 IU/dl.
Soft tissue calcification with hypercalcemia is observed Hyperparathyroidism
in
Hyperparathyroidism associated with Brown tumour, Cyst, Osteoporosis
Hyperparathyroidism Increased calcium, Decreased phosphate
Subcutaneous calcification Hyperparathyroidism
Rugger jersey spine Renal osteodystrophy
Rugger jersey spine in CRF is due to Hyperparathyroidism
NOT true about hyperparathyroidism Commonly after thyroidectomy
Pseudotumour cerbri is NOT a complication of Hyperparathyroidism
Soft tissue calcification does NOT occur in Hyperparathyroidism
In hyperparathyroidism, bone erosion is NOT seen in Jaws
Resorption of terminal phalanx NOT seen in Hyperparathyroidism
Sclerosis of bone NOT seen in Hyperparathyroidism
NOT associated with hyperparathyroidism Osteopetrosis
NOT a marker for hyperparathyroidism Calcitonin
NOT a feature of hyperparathyroidism Osteosclerosis
NOT a feature of hyperparathyroidism Anuria
X ray of which bone is diagnostic in Skull, Phalanges
hyperparathyroidism
OSTEITIS FIBROSIS CYSTICA
Osteitis fibrosa cystica is due to Parathyroid adenoma

Features of osteitis fibrosa cystica Fracture, Increased serum calcium, Increased alkaline
phosphatase
PARATHYROID HYPERPLASIA
Parathyroid hyperplasia All four glands are involved

Treatment of parathyroid hyperplasia Removal of 3 ½ gland
PARATHYROID ADENOMA
MC cause of raised serum calcium Parathyroid adenoma

MC Site of Parathyroid adenoma Inferior Parathyroid Gland
NOT a common site of metastatic calcification Parathyroid
Differentiate parathyroid adenoma from hyperplasia Indentifying hyperplasia of all glands at surgery in
parathyroid hyperplasia
Sestambi scan is used in Parathyroid adenoma
Investigation of choice in parathyroid pathology Tc thallium substraction scan
Investigation for Parathyroid Location MIBI + CT Scan
Treatment of parathyroid adenoma Removal of adenoma
75 year old woman present with myocardial infarction Ultrasound guided alcohol injection in the mass
after 6 weeks with mild CHF, past H/o neck surgery for
parathyroid adenoma 5 years ago, ECG shows slow
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ENDOCRINOLOGY
atrial fibrillation. Serum calcium 13 mg/dl, urinary Ca++

300 mg/24 hours. small mass in paratracheal position
behind right clavicle
Treatment of choice for parathyroid Total thyroidectomy with modified radical
carcinoma neck dissection (if nodes are positive),
radiotherapy
PRIMARY HYPERPARATHYROIDISM
MC cause of Primary Hyperparathyroidism Solitary Parathyroid Adenoma

MC cause of Asymptomatic Hypercalciuria in 3rd to 5th Primary Hyperparathyroidism
decade
Asymptomatic hypercalcemia in a 30 year old young Primary hyperparathyroidism
male
Primary hyperparathyroidism Hyperplasia, Adenoma, MEN 1
NOT true about Primary Hyperparathyroidism Increased Serum Phosphate
Initial screening for Primary hyperparathyroidism Serum PTH
Increased alkaline phosphatase Primary hyperparathyroidism
SECONDARY HYPERPARATHYROIDISM
MC cause of Secondary Hyperparathyroidism Renal Failure

Secondary hyperparathyroidism due to vitamin D Hypophosphatemia
deficiency shows
45 year old man, known case of CRF develop rugger Secondary hyper parathyroidism
jersy spine. probable cause
Most characteristic finding of secondary Osteitis fibrosa cystica
hyperparathyroidism
Associated with secondary hyperparathyroidism Chronic renal failure, Rickets, Osteomalacia, vitamin D
deficiency, Medullary carcinoma thyroid
NOT associated with secondary hyperparathyroidism Osteoporosis
Secondary hyperparathyroidism NOT seen in Osteoporosis

Secondary hyperparathyroidism NOT seen in Parathyroid adenoma
TERTIARY HYPERPARATHYROIDISM
Tertiary hyperparathyroidism Secondary hyperparathyroidism following chief cell

adenoma
Tertiary parathyroidism Autonomic dysfunction
HYPOPARATHYROIDISM
Parathyroid insufficiency presents after 2 – 5 days after thyroid surgery

MC cause of Hypoparathyroidism Surgical Removal of Parathyroid Gland
MC presentation of hypoparathyroidism beyond Seizure
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ENDOCRINOLOGY
neonatal period
Intracerebral Punctate calcification Hypoparathyroidism
Low calcium and high phosphate Hypoparathyroidism
Osteoporosis is NOT a complication of Hypoparathyroidism
PSEUDOHYPOPARATHYROIDISM
Pseudohypoparathyroidism is due to Receptor of bone and kidney

defect in
Pseudohypoparathyroidism Decreased formation of cAMP
Pseudohypoparathyroidism Increased PTH, Decreased Serum calcium, Increased
phosphate, Albright’s hereditary osteodystrophy,
Heterotopic calcification
Albright hereditary osteodystrophy is associated with Pseudohypoparathyroidism type Ia,
pseudopseudohypoparathyroidism, Gs alpha subunit
deficiency
Response to urinary cAMP to PTH decreased in Pseudohypoparathyroidism type Ia, Ib
Response to urinary cAMP to PTH is normal in Type II pseudohypoparathyroidism and
pseudopseudohypoparathyroidism
Hyperphosphatemia, short metacarpal, cataract Pseudohypoparathyroidism
PSEUDOPSEUDOHYPOPARATHYROIDISM
Pseudopseudohypoparathyroidism is due Bone receptor only (paternal imprinting

to defect in in kidney only)
Serum PTH in pseudopseudohypoparathyroidism Normal
VITAMIN D
Vitamin D 25 hydroxylation occurs in liver, 1 alpha hydroxylation

in kidney. In absence of sunlight, minimum daily
requirement is 400 – 600 IU
NOT an antioxidant Vitamin D
Active form of vitamin D 1,25 (OH)2 vitamin D
Anti rachitic vitamin is activated in Kidney
Vitamin D is biologically activated in Kidney
Site at which 1,25 hydroxylation of vitamin D takes Proximal convoluted tubule
place in kidney is
Essential for Vitamin D metabolism Parathromone
Action of vitamin D Stimulate absorption of calcium
Vitamin D deficiency Increased phosphate in urine, Increased alkaline
phosphatase
Least useful investigation for hyperphosphatemia Vitamin D levels
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ENDOCRINOLOGY
VITAMIN D INTOXICATION
Vitamin D intoxication Nausea and vomiting, Muscular weakness, Anorexia,

Metastatic calcification
Abnormality of bone associated with excess of Vitamin A and vitamin D
Raised calcium and phosphorus seen in Vitamin D intoxication
Dense metaphyseal band Hypervitaminosis D
FEATURES OF RICKETS
MC age group for rickets Less than 4 years

Splaying and cupping of metaphysic of long bones in a Rickets, Metaphyseal dysplasia, Hypophosphatasia
child
Osteomalacia/Rickets associated with Neurofibroma, Osteoblastoma, Hemangiopericytoma
NOT a cause of osteomalacia/Rickets Ewing’s sarcoma
Rickets is NOT seen in Hypocalcemia
Basic pathological defect in rickets Defective osteoclastic resorption of uncalcified osteoid
and cartilage
Basic defect in rickets Defective mineralization
Defective mineralization of epiphyseal plate in a Rickets
growing child
Defective mineralization of proximal zone of cartilage of Rickets
epiphysis
Osteoid without Mineralisation Rickets
Rickets of vitamin D deficiency is associated with Ricketiorosary at costochondral junction produced by
subluxation of sternal plate
Widened physis, cupped & frayed metaphysis Rickets
Early sign of rickets Craniotabes
Nutritional rickets Decreased calcification of growing bone
Ricketic rosary Rickets, scurvy, chondrodystrophy
Features of rickets in infancy Craniotabes, Rachitic rosary, Wide open fontanelles
Rickets is associated with Deficient calcification of Osteoid
Flaring of anterior ends of ribs Rickets
Rickets Pot belly, Craniotabes
Type of rickets with elevated serum Renal osteodystrophy
phosphorus
Trefoil pelvis is associated with Rickets
Hot cross bun skull Rickets
Paint brush metaphysis Rickets
Quant’s Sign Rickets, T Shaped Depression In Occipital Bone
Quant sign (T shaped depression in occipital bone) Rickets
In nutritional rickets, changes occur at Metaphysis
Bony lesion in rickets is due to Reduced dietary calcium absorption
NOT a feature of Rickets Widening of Joint space
NOT a feature of rickets in infancy Bow legs
NOT a presentation of Rickets in infant Bow legs
NOT a feature of Rickets Gunstock deformity
NOT true about rickets Early development of teeth
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ENDOCRINOLOGY
DIAGNOSIS OF RICKETS
Rickets Serum phosphate reduced, alkaline phosphate

increased, hyperphosphaturia
Laboratory diagnosis of Rickets Decreased Calcium, Decreased Phosphate, Increased
Alkaline Phosphatase
Metabolic indicator of Rickets Increased alkaline phosphatase
Persistent biochemical marker of rickets Serum alkaline phosphatase
Biochemical abnormality in nutritional rickets Hypocalcemia
Best biochemical marker of Active rickets Serum calcium
Alkaline phosphatase in Rickets Increased
Classical X ray feature of Rickets Cupping and Fraying
Earliest radiological change in Rickets Absence of normal zone of provisional calcification
Radiological feature of rickets Splaying and cupping of metaphysic, Ricketic rosary,
Flaring of anterior end of ribs
Rickets is characterized by Decrease in calcium content of bone, widening of
growth cartilage, beading of ribs
Earliest evidence of healing in rickets is provided by Radiological examination of growing bone end
Earliest evidence of healing in rickets is provided by Radiological examination of growing bone
TREATMENT OF RICKETS
Treatment of vitamin D deficiency rickets Vitamin D3 is given at a dose of 50-150 mg/dl
VITAMIN D RESISTANT RICKETS
Vitamin D resistant rickets is also known as Hypophosphatemic rickets

Hypophosphatemic type of Vitamin D Resistant Rickets X-linked dominant
Vitamin D resistant rickets Defect in proximal tubular absorption
Vitamin D resistant rickets Metaphyseal widening
Vitamin D resistant rickets is NOT associated with Osteoporosis
Treatment of vitamin D resistant rickets Large doses of vitamin D
OSTEOMALACIA
Commonest cause of osteomalacia in our country Dietary deficiency of vitamin D and calcium
Cause of osteomalacia Phenytoin, Malabsorption, Indoor stay
Drug induced osteomalacia is caused by Phenytoin
A diet deficient in calcium will most commonly result in Osteomalacia
Common finding in osteomalacia Low serum phosphate
Osteomalacia is associated with Increased deposition of uncalcified osteoid
Characteristic finding in osteomalacia Decreased serum calcium and phosphate
Most characteristic finding in Osteomalacia Increased deposition of Osteoid with decreased
Mineralisation
In osteomalacia Mineralization of bone is deficient
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ENDOCRINOLOGY
Milkman fracture Pseudofracture in adults

Pseudofracture Osteomalacia
Loosers zone Osteomalacia
Osteomalacia is associated with Increase in osteoid maturation time
Decreased S.Calcium, Decreased Phosphate, Increased Vitamin D Deficiency Osteomalacia
Alkaline Phosphatase, Increased PTH
Osteomalacia Increased alkaline phosphatase, looser’s zone, increases
osteoid formation, decresed mineralization
Renal osteodystrophy differs from nutritional and Hyperphosphatemia
genetic form of osteromalacia in having
Osteomalacia Serum calcium low or normal, Serum phosphate is low,
Alkaline phosphatase is raised
Raised alkaline phosphatase, raised parathromone level Vitamin D deficiency
along with low calcium and low phosphate level
Biochemical changes in osteomalacia Serum Ca normal or decreased, Decreased 1,25 (OH) 2D
NOT a diagnostic feature of osteomalacia Increased serum calcium
NOT a radiological feature of osteomalacia Lytic lesion
Osteomalacia in pregnancy and lactation is best treated Vitamin D and calcium
by
FEATURES OF OSTEOPOROSIS
Osteoporosis according to WHO T -2.5

Areas in which T < 2.5 in osteoporosis Lumbar spine, femoral neck, total hip
Osteoporosis is most likely associated with Asian, white, smoke
MC form of osteoporosis Involutional osteoporosis
Osteoporosis Decreased Bone mass
Decreased bone mass per unit volume Osteoporosis
Bone density decreased in Osteoporosis
Osteoporosis Normal Ca, normal phosphate, normal alkaline
phosphatase
Osteoporosis Commonly presents with fracture, Codfish vertebra
MC manifestation of osteroporosis Compression fracture of spine
MC site of fracture of bone in senile osteoporosis Vertebra
NOT associated with osteoporosis Fracture clavicle
CAUSES OF OSTEOPOROSIS
Osteoporosis Hypervitaminosis D, Lead Poisoning

Osteoporosis seen in Thyrotoxicosis, Rheumatoid arthritis, Steroid therapy,
Chronic heparin therapy, Old age, Hyperparathyroidism,
Sarcoidosis, Cushing’s disease, Menopause
Risk factors for osteoporosis Smoking, COPD
Osteoporosis is seen after chronic use of Glucocorticoids
MC cause of medication mediated osteoporosis Glucocorticoids
Causing osteoporosis in long term usage GnRH analogue
Drugs causing osteoporosis Lithium, Dilantin, Heparin
Axial Osteoporosis Cushing’s Syndrome
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ENDOCRINOLOGY
Osteoporosis is NOT seen in Hypoparothyroidism

Does NOT cause osteoporosis Fluoride
Osteoporosis NOT seen in Hypoparathyroidism, Hypothyroidism
DIAGNOSIS OF OSTEOPOROSIS
Gold standard for diagnosis of osteoporosis Dual energy X ray absorptiometry

Bone density is best studied by DEXA
Gold standard for assessing bone mineral density Dual energy X ray absorptiometry
70 year female is on treatment with Alendronate for DEXA
severe osteoporosis. Now she complains of pain in right
thigh. What is the next investigation to be performed?
TREATMENT OF OSTEOPOROSIS
Bisphosphonates act by Decreasing osteoclast mediated resorption of bone

Serious adverse effect of bisphophonate Acute renal failure
st
1 Bisphosphonate Approved Etindronate
Unique Administration Technique, Once Yearly i.v/Once Zolendronate, Idandronate
Monthly Oral/Most potent
Zolendronate Normalizes 90 % of BMD test (if steroid used for more than 3
months)
Most Potent Drug for Treatment & Prevention of Bisphosphonates
Osteoporosis
Drug of choice for Steroid induced Osteoporosis Bisphosphonates
Prevention of Steroid Induced Osteoporosis Risendronate
Treatment of Postmenopausal Osteoporosis Alendronate, Risendronate
Drug of choice for senile osteoporosis Estrogen
Useful in treatment of osteoporosis Calcium
65 year female presented with osteoporosis, treatment Calcium, oestrogen, progesterone
started with
Treatment of postmenopausal osteoporosis Estrogen, Alendronate, Calcitonin
Agents decrease bone resorption in osteoporosis Alendronate, Etindronate, Strontium
48 year female, severe menorrhagia, underwent Estrogen
hysterectomy, wishes to take hormone replacement
therapy. Physical examination and breast normal. X ray
osteoporosis
SERM used for treatment of osteoporosis Raloxifene
Useful for osteoporosis Raloxifene
Calcium content of bone is increased in Estrogen supplementation in post menopausal women
SERM useful for osteoporosis Raloxifene
Advantages of using raloxifen over estrogen in Reduces fracture rate, avoids endometrial hyperplasia,
postmenopausal woman no increase in incidence of carcinoma breast
Agent increasing osteoblastic new bone formation in Teriparatide
osteoporosis
Does NOT decrease bone resorption in osteoporosis Teliparatide
Monoclonal antibody against RANKL receptor used in Denosumab
treatment of osteoporosis
Denosumab is used for Osteoporosis in postmenopausal women
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ENDOCRINOLOGY
Both antiresorptive and bone formative Strontium ranelate

Both decreased bone resorption and increased bone Strontium ranelate
formation
NOT used in treatment of Osteoporosis Progestins
Drug NOT used in treatment of Osteoporosis Steroids
Bisphosphonates NOT used in Vitamin D intoxication
Bisphosphonates is NOT used for Hypervitaminosis D
NOT used for treatment of postmenopausal Vitamin C
osteoporosis
NOT appropriate is treatment of Norethindrone (progestin)
osteoporosis
HYPERCALCEMIA
MC Paraneoplastic Syndrome Hypercalcemia

Hypercalciuria Hyperparathyroidism, Vitamin D intoxication,
Sarcoidosis
Hypercalcemia Lithium therapy, chronic renal failure, multiple
myeloma
Vitamin A deficiency, Lithium therapy, Multiple Hypercalcemia
myeloma, Sarcoidosis, Milk alkali disease,
Hyperparathyroidism, Breast cancer, Hodgkin’s
lymphoma, TPN, Thiazide diuretic, pheochromocytoma
Hypercalcemia may be caused by Trimethoprim
Furosemide do not cause Hypercalcemia
NOT true about Osteoporosis Hypercalcemia
NOT a complication of total thyroidectomy Hypercalcemia
PTH like substance produced by Squamous cell carcinoma
Hypercalcemia associated with malignancy is most Parathyroid hormone related protein
often mediated by
Hypercalcemia associated with malignancy is most Parathromone hormone related protein
often mediated by
Hypercalcemia in breast cancer is mostly due to Bone secondaries
MC cause of Asymptomatic hypercalciuria in 1st decade Familial Hypercalciuric Hypercalcemia
Milk alkali syndrome may be caused by ingestion of Calcium carbonate
Burnett syndrome Chronic form of milk alkali disease
Polyuria, pain abdomen, nausea, vomiting, altered Hypercalcemia
sensorium, bronchogenic carcinoma
NOT a feature of Hypercalcemia Diarrhoea
Treatment of hypercalcemia Gallium nitrate, Plicamycin, Etindronate, Mitramycin,
Calcitonin, Pamridonate, IV fluid with furosemide.
Normal saline
Principal treatment for Hypercalcemia To restore Hydration
Pralidonate is used in treatment of Hypercalcemia
NOT a dietary management of idiopathic hypercalciuria Reduced calcium diet
Hypercalcemia is NOT treated by Tamoxifen
NOT used for acute hypercalcemia Gallium nitrate, bisphosphonates
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ENDOCRINOLOGY
HYPERCALCEMIC CRISIS
MC cause of Hypercalcemic Crisis Ca Breast

Hypercalcemic crisis is treated by Phosphate
Treatment of parathyroid crisis Parathyroidectomy for removal of adenoma,
Thyrocalcitonin
TUMOUR LYSIS SYNDROME
Tumor lysis syndrome Common with Burkitt’s lymphoma, treated by allopurinol,

rasburicase
Tumour Lysis syndrome is characterized by Hyperkalemia, Hyperuricemia, Hypocalcemia
NOT seen in tumour lysis syndrome Hypercalcemia
TETANY
Causes of hypocalcemia Protamine, heparin, glucagon

Common cause of Hypocalcemia Acute pancreatitis, Massive soft tissue infection
Hypocalcemia occurs as a side effect of Thiazide
Pancreatitis, Phenytoin therapy, Loop diuretic cause Hypocalcemia
Seen in diuretic phase of ATN Hypocalcemia
Operation that may cause of hypocalcemia Thyroidectomy
NOT a cause of stridor after thyroidectomy within 2 Hypocalcemia
hours
NOT a complication of hemithyoridectomy Hypocalcemia
Features of Hypocalcemia Numbness and tingling of circumoral region,
hyperactivity tendon reflexes, QT interval prolongation,
carpopedal spasm
Signs of Hypocalcemia Chovstek Sign, Trousseau Sign (Carpopedal Spasm),
Erb’s Sign – Muscle contraction by subthreshold
stimulation, Peroneal Sign – Tapping over Peroneal
Nerve causes Plantar Flexion
Sudden decrease in serum calcium is associated with Increased excitability of muscle and nerve
Hypocalcemia causes increased Decreasing threshold for action potential
excitability of nerve and muscle by
Patient undergoing LSCS following prolonged labour Hypocalcemia
under subarachnoid block developed carpopedal
spasm. Lignocaine was used, diagnosis
Hypocalcemia in immediate post op period following Increased uptake by bone
excision of parathyroid adenoma is due to
NOT true of hypocalcemia Inverse relation with Mg++ level
NOT a manifestation of hypocalcemia Diminished DTR
Perioral tingling after thyroid surgery IV calcium gluconate and serial monitoring
Management of chronic hypocalcemia Thiazides, Elemental calcium, Vitamin D analogues
Etiology of tetany Hypocalcemia, alkalosis, hyperventilation
Gastric tetany due to Decreased calcium absorption
Tetany Seen in Hypoparathyroidism
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ENDOCRINE PANCREAS 44
ENDOCRINOLOGY
NOT an etiology of Tetany Hyperkalemia

Hyperexcitability in tetany is due to Low calcium causes increased permeability to Na+
Treatment of 10 kg weight infant presented with tetany IV calcium gluconate with cardiac monitoring
First thing to be administered in a baby presenting with Calcium gluconate
tetany
Treatment of tetany Calcium Gluconate
Management of post thyroidectomy patient developing IV calcium gluconate
tetany
DRUGS OF CALCIUM METABOLISM
Bone resorption enhanced by PGE2

Second messenger IP3 leads to release of Calcium
Mode of administration of palidronate IV
Calcitriol Increased calcium absorption from intestine
Calcitriol Suppressive action of PTH
Paricalcitol Suppressive action on PTH without or less hypercalcemia
Cinacalcet Reduces PTH and calcium, acts on calcium sensing receptor
Fastest acting calcium lowering agent Calcitonin
Bisphosphonates are NOT used in Vitamin D excess
ENDOCRINE PANCREAS
GENERAL FEATURES OF ENDOCRINE PANCREAS
Endocrine pancreas Insulin, Glucagon, Somatostatin, Pancreatic polypeptide

NOT secreted by endocrine pancreas Chymotrypsin
Mechanism protecting normal pancreas from Proteolytic enzymes secreted in inactive form
autodigestion
Inhibitor of Glucagon secretion Somatostatin
Glucagon by Alpha cells
Delta cells of pancreas secrete Somatostatin (D cells)
D cells of pancreas secrete Somatostatin
Lanreotide Autogel, slow release somatostatin
G cells Gastrin
F cells secrete Pancreatic polypeptide
PHYSIOLOGY OF ENDOCRINE PANCREAS
Glucagon secretion is stimulated by Gastrin

Products of preproglucagon on L cells of GLP 1, GLP 2, Glicentin
small intestine
Glucagon stimulates Insulin release
Glucagon stimulates glycogenolysis only in Liver
Glucagon does NOT stimulate Skeletal muscle
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ENDOCRINOLOGY
glycogenolysis in
NESIDIOBLASTOSIS
Nesidioblastosis Hypoglycemic episodes may be seen, histopathology

show hyperplasia of islet cells, diazoxide may be used
for treatment, Proliferation of primitive cells of islets of
langerhans
Nesidioblastosis Disease of children and infants
HYPERGLYCEMIA AND HYPOGLYCEMIA
Hormone that can cause hyperglycemia Thyroxine

without known effects on glycogen or
gluconeogenesis
Drug causing both hyper and Pentamidine
hypoglycemia
Early morning hyperglycemia with increased glucose of Insufficient insulin
3.00 am
Dawn phenomenon Morning hyperglycemia due to insufficient insulin
Hyperglycemia caused by GH, Cortisol, Catcholamines, Glucagon
Drug causing hyperglycemia Beta blockers
Hyperglycemia may be caused by Chlorthiazides, corticosteroids, theophylline
Pancreatic hormone associated with hyperglycemia Glucagon
Hyperglycemia NOT associated with Indomethacin
Hypoglycemia is caused by Alcohol
Hypoglycemia Hypopituitarism, Fibroma, Soft tissue sarcoma,
Hepatocellular carcinoma, Uremia, Addison’s disease
Hypoglycemia caused by Alcohol intoxication
Fasting hypoglycemia Glucose 6 phosphatase deficiency, Uremia, Glycogen
synthase deficiency
Causes of fasting hypoglycemia Glucose 6 phosphatase deficiency, glycogen synthase
deficiency, uremia
Defense in hypoglycemia Glucagon, glucose, epinephrine
Associated with increased awareness of Long term diabetes mellitus, poorly
hypoglycemia controlled diabetes mellitus, switching
from sulfonylurea to insulin
Hypoglycemia is NOT associated with Appropriate for gestational age
Released in surgical stress Adrenaline, ACTH, Epinephrine, Cortisol, GH
Stress induced hyperglycemia due to Glucocorticoids, GH, Epinephrine
Released in stress Vasopressin, Adrenaline
NOT released in surgical stress Insulin
CAUSES OF DIABETES MELLITUS
Diabetes mellitus is present in Ataxia telangiectasia, myotonic dystrophy, fanconi’s
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ENDOCRINOLOGY
anaemia
Commonest cause of juvenile onset diabetes in India Fibrocalcific pancreaticopathy
Associated with peripheral artery disease, coronary Insulin deficiency
artery disease, stroke
NOT a cause for Diabetes Mellitus Hypothyroidism
GENERAL FEATURES OF DIABETES MELLITUS
Glucose intolerance caused by Thiazides, Propanolol, Furosemide, Phenytoin

MC cause of Death in Diabetes Mellitus Myocardial Infarction
Mauriac syndrome Diabetes, Obesity, Dwarfism
Diabetes mellitus diagnosed when Fasting blood sugar more than 125 and 2 hour
postprandial blood sugar more than 199
Enzyme deficient in diabetes mellitus Glucokinase
Mc congenital anomaly associated with Diabetes Sacral agenesis
Mellitus
Malformation specific for maternal insulin dependent Caudal regression
diabetes mellitus
Cataract in Diabetes due to accumulation of Sorbitol
Snow Flake Cataract Diabetes Mellitus
Suggesting diabetes mellitus rather than appendicitis in Nocturnal enuresis over preseding 4 weeks
children
Fat associated with Insulin resistance of Obesity Central Abdominal Fat
CSF glucose is increased in Diabetes Mellitus
Factor limiting synthesis of Triglycerides in adipose Alpha Glycerophosphate
tissue in Diabetes
Fructose metabolism is NOT affected in Diabetes Fructokinase is NOT affected by Insulin
Mellitus because
TYPES OF DIABETES MELLITUS
HLA associated Type I diabetes

Type I Diabetes mellitus DR3/DR4
Type I DM Family history is about 15%, Time of onset is NOT
predictable
Predictive marker for Type I Diabetes Islet cell antibodies
HLA protective for type I diabetes HLA B1Q602
Hyperactive enzyme in type I diabetes Pyruvate carboxylase
mellitus
35 genes are involved in pathogenesis of Type II diabetes mellitus
NIDDM Increased levels of insulin in blood
Unique feature of Type II DM Inability to respond to Insulin
Type II diabetes mellitus Increased level of insulin in blood
Type II diabetes may Require insulin treatment
AIAPP Type II diabetes
Characteristic of type II diabetes mellitus Insulin resistance
Characteristic feature of long standing type II DM Islet amyloid protein (amylin)
Islet cell focal fibrosis with deposition of Type II diabetes mellitus
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ENDOCRINOLOGY
amylin
Localized amyloid deposit in pancreas Type II diabetes mellitus
Cause of diarrhea in type II diabetes Intestinal dysmotility
Grandfather diabetic father NOT diabetic DM type II
Both father and grandfather diabetic MODY
Maturity onset diabetes of young Autosomal dominant
MODY Vertical transmission through atleast two successive
generation is essential for diagnosis
The most common MODY type is HNF1 alpha
Mitochondrial Diabetes Early hypoglycemia, associated with weight gain,
hearing loss
TYPES OF MODY
MODY 1 HNF 4 alpha

MODY 2 Glucokinase
MODY 3 HNF 1 alpha
MODY 4 IPF 1
MODY 5 HNF 1 beta
MODY 6 Neuro D1
DIABETES IN PREGNANCY
Commonest congenital anomaly seen in pregnant Neural tube defects

woman with diabetes mellitus
NOT true about diabetes in pregnancy Insulin resistance improves with pregnancy
Congenital disease in diabetes mellitus Due to free radical injury, 6-10% associated with major
congenital anomaly, insulin can be given
NOT seen in gestational diabetes Malformations
Gestational diabetes is associated with Early labour, Hyperemesis, Spontaneous abortion
Major risk factor for Neural tube defects maternal diabetes
Best Indicator to assess lung maturity in IDM Presence of Phosphatidyl Glycerol
GDM is best diagnosed at Second trimester
Babies of diabetic mother will be Large
NOT a complication in newborn to diabetic mother Hyperglycemia
Least common anomaly in diabetic Pregnancy Caudal Regression Syndrome
Large for date baby may be due to Beckwith syndrome, Diabetic mother, Genetic
predisposition
MC congenital malformation seen in a diabetic Cardiac defect
pregnant woman
Useful investigation in first trimester to identify risk of Glycosylated Hb
fetal malformation in diabetic
Predict Chances of Abnormality in Diabetic Mother Glycosylated Hb
Detect Abnormal fetus in Diabetic Mother USG
Use of insulin during pregnancy Insulin does NOT cross placenta, during pregnancy
insulin requirement increases and cannot be met with
sulfonylurea
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ENDOCRINOLOGY
COMPLICATIONS OF DIABETES MELLITUS
Characteristic complication of diabetes mellitus Retinopathy and Neuropathy

Microvascular complication of Diabetes Diabetic Retinopathy
Diabetic complication associated with Cardiovascular complications
legacy effect
Hyperglycemic hyperosmolar state is NOT Acidosis
associated with
NOT a neonatal complication of diabetes Omphalitis
NOT a life threatening complication of diabetes mellitus Emphysematous appendicitis
DIABETIC KETOACIDOSIS
Diabetic patient blood glucose 600 mg/dl, Na 122 Blood Na level increase
mEq/L was treated with insulin. After giving insulin
blood glucose reduced to 100 mg/dl.
Starvation and diabetes mellitus can lead to Increase in glucagon insulin ratio, Increase in blood
ketoacidosis. which of the following features is in favour glucose, Increase in cAMP
of ketoacidosis due to diabetes mellitus
Blood glucose in DKA 250 - 300 mg/dl
DKA is associated with Initial hyperkalemia
Ketone body maximum in DKA b-Hydroxy butyric acid
Feature of Diabetic ketoacidosis Decreased bicarbonate
Orbital mucormycosis is a complication of Diabetic ketoacidosis
NOT seen in DKA Bradycardia
Treatment of DKA Insulin, 0.9% saline, 5% dextrose
Treatment of Choice for Diabetic Ketoacidosis Insulin
Glucose is added to saline, if plasma glucose comes to 200 mg/dL
Insulin is discontinued when glucose level is 150 – 250 mg/dL
Most effective correction of acidosis in diabetic Iv insulin
ketoacidosis
What happens if insulin alone is given in diabetic Hypokalemia
ketoacidosis
In Diabetic Ketoacidosis, When Normal Saline is When Blood Glucose Reaches 250 mg%
changed to 5% Glucose
On successful treatment Hyperchloremic acidosis
NON KETOTIC HYPEROSMOLAR COMA
Non Ketotic hyperosmolar coma Type II diabetes, elderly, insidious onset

Glucose Level in Non Ketotic hyperosmolar coma Greater than that of DKA
JOINT MANIFESTATIONS OF DIABETES
MC cause of Neuropathic joint Diabetes

MC Joint involved in Diabetes Mellitus Tarsal & Tarsometatarsal
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ENDOCRINOLOGY
Diabetic patient, swelling of knee joint, associated with Neuropathic joint

sclerosis without deformity, loose bodies are seen in
aspiration
Amputation contraindicated in diabetes Fore foot amputation
Syme’s amputation is contraindicated in Diabetic foot
Site of Diabetic foot ulcer Head of Metatarsal
MC site of diabetic ulceration Plantar surface of foot
NOT a etiopathogenesis of diabetic foot Myelopathy
Site of diabetic foot ulcer Heel, Head of metatarsal
Foot ulcer in diabetic mellitus Macroangiopathy
Diabetic gangrene due to Ischemia, Increased blood glucose, Altered defence by
host and neuropathy
Diabetic gangrene NOT due to Vasospasm
NOT a feature of Diabetic gangrene Microangiopathy
Off label use of mexiletine Diabetic neuropathy
EYE MANIFESTATIONS OF DIABETES
Causes of Non healing corneal ulcer Diabetes mellitus, Dacryocystitis, Raised IOP
Fluctuation of Refractory Error Diabetic Cataract
35 year insulin dependent diabetic mellitus patient on Cataract
insulin for past 10 years. gradually progressive painless
loss of vision
MC cause of vitreous hemorrhage in adults Diabetes
MC cause of vitreous hemorrhage Diabetes mellitus
MC cause of Rubeosis iridis Diabetes mellitus
MC cause of Visual loss in Non Proliferative Diabetic Maculopathy
Retinopathy
MC cause of Visual Loss in Proliferative Diabetic Vitreous Hemorrhage
Retinopathy
MC cause of Spontaneous Vitreous Hemorrhage in Proliferative Diabetic Retinopathy (Neovascularisation)
Adults
Sudden loss of vision patient with diabetic retinopathy Vitreous hemorrhage
MC cause of Black Floaters in Diabetics Vitreous Hemorrhage
MC cause of Visual impairment in diabetics Maculopathy
Circinate retinopathy is seen in Diabetes mellitus, Hypertension, Elderly woman
Tractional retinal detachment Diabetes mellitus
Isolated 3rd nerve palsy with papillary sparing Diabetes
Diabetic Retinopathy MORE COMMON in Type I Diabetes Mellitus (Insulin Dependent)
60 old man has both HTN and DM for 10 years, reduced Diabetic retinopathy
vision in one eye, central bleed on fundus examination
Microaneurysms are seen in Diabetic retinopathy
Earliest symptom of Diabetic retinopathy Microaneurysm
Hallmark of proliferative diabetic retinopathy Neovascularisation
Diabetic Papillopathy Swelling of disc with telangiectasia
MC Nerve palsy in Diabetic Retinopathy Occulomotor
NOT a feature of diabetic retinopathy Arteriolar dilatation
Does NOT take part in pathogenesis of macular edema Retinal pigment epithelium dysfunction
in diabetic retinopathy
Most Important Predictor of Diabetic Retinopathy Duration
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ENDOCRINOLOGY
Screening strategy for prevention of blindness form High risk screening

diabetic retinopathy according to NPCB
Ophthalmic examination of child with type I diabetes After 5 years
mellitus
A case of NIDDM with diabetes for one year should As early as possible
have ophthalmic examination
ERDS Early treatment for diabetic retinopathy study
Treatment of diabetic macular edema Ruboxistaurium, Pyridazinones, Benfotiamine
Intraocular lens is contraindicated in Young diabetes, One eyed, Overt corneal dystrophy
Treatment of advanced proliferative diabetic Reattachment of detached or torn retina, removal of
retinopathy with extensive vitreoretinal fibrosis and epiretinal membrane, Vitrectomy
tractional retinal detachment
Clinically significant diabetic macular edema with non Pars plana vitectomy
progressive diabetic retinopathy treated with macular
grid photocoagulation. still has vitreomacular traction
In diabetes mellitus, following lens extraction Delayed wound healing, Hyphema, Infection
RENAL MANIFESTATIONS OF DIABETES
Causes of Papillary Necrosis Diabetes, Sickle cell disease, NSAIDs

Middle aged diabetic female, flank pain and fever. On Xanthogranulomatous kidney
USG kidney was irregular and showed fat density lesion
with calculi
MC cause of nephrotic range proteinuria in an adult Diabetes mellitus
Most reliable indicator of diabetic nephropathy Overt proteinuria
Urinary excretion of glucose with normal concentration Renal glycosuria
of glucose
Renal glycosuria is associated with SGLT – 2 protein
Alimentary glycosuria Following starvation, thyrotoxicosis,
following gastrectomy
Most characteristic finding in diabetic nephropathy Nodular glomerulosclerosis
Pathological changes in diabetic nephropathy Kimmelstein Wilson lesion (diffuse glomerular
sclerosis), Basement membrane thickening, Fibrin caps
and capsular drops
Glycogen Accumulation in Proximal Convolute tubule in Armani-Ebstein Cell
Diabetic Nephropathy
False positive microalbuminuria Urinary infection
Retard progression of renal disease proteinuria in Enalapril
diabetic
Drugs used to retard progression of renal disease ACE inhibitors, ARBs
Diabetic nephropathy Pancreatic transplantation may improve proteinuria in
early stages
Pancreatic transplantation is usually performed with Kidney transplantation
DIAGNOSIS OF DIABETES MELLITUS
Impaired glucose tolerance Fasting glucose < 126 g/dl, Plasma glucose 140 - 200
after 2 hours after a 75 g oral glucose load
Test performed when diagnosis of diabetes in doubt Oral glucose tolerance test
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ENDOCRINOLOGY
Oral glucose tolerance in children is done with 1.75 gm/kg glucose

Minimum fasting blood glucose for diabetes mellitus 126 mg/dl
After 5 days, a man undergoes oral GTT GH levels are increased, Decreased insulin, Decreased
glucose tolerance, Glucagon level is increased, Increase
in FFA
Estimated average glucose is based on HbA1c
HbA1c level explains Long term status of blood sugar
Diagnosis of diabetes HbA1c > 6.5%
Glycosylated Hb assesses Response to insulin in DM
Cut off for one hour glucose challenge test 140 mg/dl
Most important test to be done in a comatose patient Serum creatinine, Blood Ph
with blood glucose of 750 mg/dl will be
Genetic study will NOT reveal Diabetes mellitus
Serum fructosamine can NOT be used for Screening of diabetes
Fructosamine is a glycated form of Albumin
TREATMENT OF DIABETES MELLITUS
Best advice given to patient of newly diagnosed type II Exercise

diabetes mellitus
Microvascular Complication Prevention Aldolase Reductase Enzyme Inhibitor, Tolestat
Weight Neutral antidiabetic Drug Gliptin, Pramlitide
Antidiabetic drugs safely used in renal failure Glimepride, Rosiglitazone, Repaglinide
Which is Insulin Secretogogue Repaglinide
Pramlitide Amylin analogue for both type I and type II diabetes mellitus
Gliptin Dipeptidyl peptidase 4 inhibitor
Cholestyramine Binds to bile acids and decreases its reabsorption,
Inhibits intestinal glucose absorption, Inhibits hepatic
gluconeogenesis
Imeglimin Oral anti diabetic agent, activator of
AMP kinase
Sergliflozine Renal glucose transport inhibitor
Colesevalem is used in treatment of Diabetes
Drug used in diabetes Acetohexamide
Exenatide is used in Type 2 diabetes
Hypoglycemic drug causing B12 deficiency Metformin
Treatment of hypoglycemia on treatment with acarbose Glucose
and insulin
Propanolol is contraindicated in diabetes mellitus due Masks hypoglycemic symptoms
to
Intensive management of diabetes NOT needed for DM with acute MI
ALPHA GLUCOSIDASE INHIBITORS
Only oral hypoglycemic agent in type I Alpha glucosidase inhibitor

diabetes
Alpha glucosidase inhibitor Reduces intestinal absorption of carbohydrates,
effective in both type I and II DM, can be used with
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ENDOCRINOLOGY
other oral hypoglycemic agents

Alpha glucosidase inhibitor Miglitol
Acarbose Reduce only POSTPRANDIAL glucose, Alpha glucosidase
inhibitor, Reduces fibrinogen level
Prevention of Post Prandial Diabetes Mellitus Acarbose
Does NOT increase insulin sensitivity Acarbose
Does NOT cause hypoglycemia Acarbose
NOT true about acarbose It reduces both pre and post prandial glucose
Does NOT cause hypoglycemia Acarbose
NOT true about alpha glucosidase inhibitor Hypoglycemia is a common and serious adverse effect
THIAZOLIDONEDIONES
Mechanism of action of Glitazones Increased peripheral utilization of glucose

Black box warning Rosiglitazone
Troglitazone is used in Type II diabetes mellitus
Pioglitazone Metabolized in liver by CYP3A4, Selective agonist for
nuclear peroxisome proliferator activated receptor
gamma, Avoided in patients with cardiovascular disease
Pioglitazone PPAR gamma agonist, metabolized in liver,NOT given in
case of diastolic dysfunction
PPAR gamma receptors are highest in Adipocytes
NOT true about pioglitazone Should be avoided in patient with cardiovascular
disease
Oral hypoglycemic agent least likely to cause Rosiglitazone
hypoglycemia
Common side effect of thiazolidonedione Water retention with weight gain
BIGUANIDES
Biguanides Don’t stimulate insulin release, decrease hepatic

glucose production, can be combined with
sulfonamides
Lactic acidosis may be due to Biguanides
Death from lactic acidosis in diabetes mellitus is Phenformin
associated with therapy of
Hyperosmal non ketotic coma can be precipitated in Phenformin
diabetic patient by
Lactic acidosis common with Phenformin
Danger in lactic acidosis Acidosis
When lactic acid is produced in response Excreting carbon dioxide through lungs
to injury, body minimizes pH change by
Cohen woods classification is used to know Lactic acidosis
the cause of
Metformin Increases Insulin sensitivity
Macrovascular Complication Prevention Metformin
Drug to be discontinued on the day of surgery Metformin
NOT true about Metformin Acts by increasing insulin secretion
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ENDOCRINOLOGY
NOT true about metformin Increases insulin secretion

Therapeutic dose monitoring NOT advised for Metformin
Does NOT cause weight gain in diabetes Metformin
Diarrhea is side effect of Metformin
Chronic usage of Metformin causes deficiency of Vitamin B12
MEGLITINIDE
Meglitinides Act by stimulating insulin release, decrease postprandial

hyperglycemia, hypoglycemia is less common than
sulfonylurea
NOT true about nateglinide Decreases insulin resistance
Benzoic acid derivative stimulates insulin secretion Repaglinide
during meals used in treatment of Diabetes mellitus
Postprandial hypoglycemia may be controlled by Repaglinide
New drug effective in controlling post prandial blood Repaglinide
sugar
EXENATIDE
GLP – 1 Most potent incretin from L cells in small intestine,

stimulates insulin secretion
GLP – 1 analogue Exenatide, Liraglutide
Exenatide Decreases glucagon secretion, GLP1 analogue, given
subcutaneously, type II diabetes mellitus
Exenatide Used for type 2 DM, GLP 1 analgogue, Decreases
glucagon, Given SC
Liraglutide Contraindicated in medullary carcinoma of thyroid
SULPHONYLUREAS
Sulfonylurea produce hypoglycemia by Increasing insulin release, increasing insulin receptors,

sensitization of cells to islets of glucose
Sulfonylurea act by Increasing insulin secretion from pancreas
Sulfonylureas act by Closing K+ channel
NOT a criteria for starting sulfonylurea Total pancreatectomy
Tolbutamide acts by Increasing insulin secretion
NOT a second generation hypoglycemic Tolbutamide
Lactic acidosis is NOT seen in Tolbutamide
Dilutional hyponatremia is caused by Chlorpropamide
Flushing is common in oral hypoglycemic drug with Chlorpropamide
alcohol
NOT true about chlorpropamide Short acting
Antidiabetic drug with anorectic effect Glipizide
Monotherapy of which can hypoglycemia Glibenclamide
Hypoglycemia is most common with Glyburide
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ENDOCRINOLOGY
FEATURES OF INSULIN
Nobel Price for sequencing insulin aminoacids Sanger

DNA Sequencing
Insulin A chain has 21 aminoacids and B chain has 30 aminoacids
Insulin is a Polypeptide
Insulin secreted with this molecule in 1:1 ratio C peptide
Insulin secretion begins at 12 weeks
rd
In fetus, insulin secretion begins by 3 month
During fetal life maximal growth is caused by Insulin
Hormone using an enzyme receptor for its action Insulin
NOT a local hormone Insulin
Insulin is secreted by Beta cells
α sub unit of Insulin To bind Insulin
β subunit of insulin Signal transduction
Insulin Stability Zinc
Facilitates action of Insulin Role of Chromium
For both Type I & Type II Diabetes Insulin
Maximal HbA1c Reduction Insulin
Insulin acts through Tyrosine Kinase
Growth factors promote cell growth by acting on Tyrosine kinase
Insulin in certain tissue mediated through cGMP
Insulin Required for transport of glucose, aminoacid, Na+, K+
NOT a mechanism of action of Insulin Inhibition of Na+ K+ ATPase
In seriously ill patient, addition of aminoacid in diet Increased secretion of insulin
results in a positive nitrogen balance. mechanism for
this
Effect of catecholamines on insulin secretion Inhibit insulin secretion via alpha 2 adrenergic
receptors, stimulate secretion via beta adrenergic
receptor, net effect is inhibitory
Insulin secretion seen in Glucose, Vagal stimulation, Acetylcholine
Insulin secretion is increased by Gastrin, Secretin, CCK, Glucagon, Growth hormone,
Glucocorticoids
Insulin secretion NOT increased by VIP
Does NOT stimulate insulin production Somatostatin
Insulin secretion inhibited by Epinephrine
Insulin secretion is inhibited by Epinephrine, Somatostatin, Propanolol
Insulin secretion is inhibited when glucose 90 mg/dl
concentration is below
Insulin resistance is increased by Anti TNF alpha
Glucose level at which glucose secretion 80 mg/dl
occurs
NOT an indication of newer insulin Diabetic kidney disease
NOT a side effect of insulin Albuminuria
NOT used in treatment of insulin induced hypoglycemia Adrenaline
NOT a complication of Insulin therapy Hyperglycemia
Recombinant human insulin made by CDNA of pancreatic cell
Initial step in production of human insulin in genetic Obtaining insulin mRNA from β–cells of pancreas
engineering
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ENDOCRINOLOGY
After rich carbohydrate meal, Insulin secretion GLP-1 amide

stimulated by
Decreased blood glucose, increased insulin, normal C Accidental exogenous insulin administration
peptide
Insulin resistance Cushing syndrome, Werner syndrome, Ataxia
telangiectasia
Acanthosis nigricans is associated with Insulin resistance
Insulin resistance syndrome does NOT include Hyperuricemia
Insulin stress assay estimates Growth hormone
Effect of smoking on skin Reduced absorption in skin due to
vasoconstriction
Sliding scale regimen of insulin is used in Hospitalized diabetic patients
TYPES OF INSULIN
Least antigenic type of insulin Humulin

Human insulin differs from beef insulin by 1 amino acid residue
Rapid and short acting Insulin Lispro, Aspart, Glulisine
Long acting insulin Ultralente
Longest acting insulin Protamine zinc insulin
Longest duration of insulin is obtained with Protamine zinc insulin
Long acting insulin preparations frequently Subcutaneous route
administered by
Insulin analogue Designer product, easily adjusted according to need,
more powerful than insulin
st
1 Prepared Human Recombinant Insulin, Longest Insulin Glargine
Insulin, Only Insulin Prepared in Acidic Ph, Cannot be
mixed with other Insulin
Lispro insulin Action is faster and shorter in duration than regular
insulin, It is given 15 minutes prior to meal
Absorption of lispro insulin Delayed by mixing with NPH
NOT an advantage of monocomponent insulin Longer duration of action
Exubera Inhaled insulin
ACTION OF INSULIN
Hormone using an enzyme for its action Insulin

Insulin increase activity of Glucokinase, Glycogen synthase, Acetyl co A
carboxylase
Insulin causes K+ entry into cells
Mechanism of action of insulin on target cells Insulin binds to a receptor molecule on the outer
surface of plasma membrane which activates tyrosine
kinase that is cytosolic domain of receptor
Mechanism of insulin resistance in Liver
Increased insulin Decreased glucagon, Increased intracellular potassium,
Hypoglycemia, Enhanced fatty acid synthesis
Increased ratio of insulin to glucagon cause Decreased levels of cyclic AMP
Low insulin glucagon ratio favours Glucose 6 phosphatase
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ADRENAL GLAND 56
ENDOCRINOLOGY
Lack of Insulin leads to Increased production of 3 hydroxy butyrate

NOT done by insulin Ketogenesis
NOT an action of insulin Gluconeogenesis, Ketogenesis
Rapid infusion of insulin cause Hypokalemia
NOT an adverse effect of insulin Hyperglycemia
Glycogen synthetase is increased by Insulin
Insulin acts on glucose metabolism by Increased permeability across cell membrane against
glucose gradient
Insulin increases glucose entry into skeletal muscle, Increasing the number of GLUT 4 in muscle and adipose
adipose tissue and liver cells by tissue and glucokinase in liver cells
Insulin promote transport of glucose in Hepatocytes, Muscles, Adipose tissue
Glucose mediated insulin release through ATP dependent K+ channels
Action of Insulin on Glycolysis Promotes
Glucose mediated insulin release in ATP dependent calcium channels
Insulin mediated glucose uptake GLUT 4, Adipose tissue, Skeletal muscle , Heart
Glucose transporter in myocyte GLUT 4
Insulin mediated glucose uptake GLUT 4
Insulin facilitate glucose uptake in Heart
Insulin decreases gluconeogenesis by Inactivating pyruvate carboxylase
Synthesis of pyruvate carboxylase is repressed by Insulin
Insulin does NOT increase activity of Pyruvate carboxylase
Phosphorylase B is maintained in an inactivated state by Insulin
In muscle phosphorylase b is inactivated by ATP
Phosphorylase b is maintained in an inactivated state by Insulin
NOT an action of insulin Gluconeogenesis
Role of insulin in lipid metabolism Activates lipoprotein lipase, Activates acetyl coA
carboxylase, Decreases free fatty acid level
Insulin promotes lipogenesis by Decreasing cAMP, Increased transport of glucose into
cells, Increased transport of acetyl coA carboxylase
Insulin causes lipogenesis by Increasing acetyl co A carboxylase activity, increases the
transport of glucose into cells, decreases intracellular
cAMP level
Insulin on Triglyceride synthesis Increases
Insulin neuritis Painful neuropathy associated with
initiation of insulin treatment
ADRENAL GLAND
GENERAL FEATURES OF ADRENAL GLAND
Essential endocrine gland Adrenals

Maximum vitamin C is found in Adrenal cortex
Adrenal reserve is best tested by infusion of ACTH
Precursor of ACTH Proopiomelanocortin
Receptor for ACTH Melanocortin 2 receptor
Metyrapone test for ACTH deficiency
NOT true about adrenal medulla Secretes epinephrine and excess of norepinephrine
Hepatomegaly, abdominal distension, jaundice, anemia, Wolman disease
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ADRENAL GLAND 57
ENDOCRINOLOGY
adrenal calcification
Deficient enzyme in Wolman disease Acid lysosomal lipase
Metabolite accumulating in Wolman’s disease Cholesteryl ester
Stippled calcification of adrenals Wolman’s disease
Medical adrenalectomy Mitotane
Mitotane and metyrapone inhibit 11 beta hydroxylase
Glycyrrhizic acid Inhibition of 11 beta HSD II
Nelson syndrome most likely seen after Adrenalectomy
Secondaries to adrenal, common site of primary Lung
Best modality for imaging adrenal gland Ultrasound
in neonates
ANATOMY OF ADRENAL GLAND
Derived from both ectoderm and endoderm Suprarenal gland

Middle Zone of Adrenal Cortex Zona Fasciculata
Suprarenal gland IVC and liver form anterior relation of right suprarenal
gland, Medial border is related to left inferior phrenic
artery, Middle suprarenal artery is branch of abdominal
aorta, Right suprarenal gland drains IVC, left suprarenal
gland drains left renal vein
Suprarenal gland IVC and liver form anterior relation of right suprarenal
gland, medial border is related to left inferior phrenic
artery, middle suprarenal artery is a branch of
abdominal aorta
Relation of Right Suprarenal gland include Right Lobe of Liver,Inferior Vena cava
Suprarenal gland get blood supply from Aorta, Renal artery, Inferior phrenic artery
Suprarenal gland does NOT get blood supply from Superior mesenteric artery
Central vein of right suprarenal gland Inferior vena cava
Right adrenal vein Short and difficult to ligate
PHYSIOLOGY OF ADRENAL GLAND
Adrenal gland Secrete more epinephrine and 20% norepinephrine,

Chromaffin granules are seen in pheochromocytoma,
Adrenal medulla hormones NOT essential for life
Adrenal cortex Glomerulosa secretes aldosterone,
fasciculata secretes cortisol and reticularis
secretes sex hormone
Zone of adrenal cortex that never undergo Zona glomerulosa
atrophy after hypophysectomy
Stem cell property in adrenal gland Zona glomerulosa (changes in reticularis,
so left during adrenalectomy)
Rate limiting enzyme in adrenaline synthesis Tyrosine hydroxylase
Tyrosine hydroxylase is inhibited by Parachlorophenylalanine
Hormones by adrenal medulla Norepinephrine, Epinephrine, Dopamine
Adrenal medulla does NOT secrete Cortisol
ACTH is increased in Glucocorticoids, CAH, Adrenal hypoplasia
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ADRENAL GLAND 58
ENDOCRINOLOGY
Epinephrine action on liver Glycogenolysis

Epinephrine stimulates Lipolysis, Glycolysis, Gluconeogenesis
Cortisol on metabolism Increased gluconeogenesis, Increased proteolysis,
Increased protein anabolism in liver
Secretion of cortisone in highest in 6 am to 8 am
Hepatic gluconeogenesis stimulated by Cortisol
Diurnal variation in eosinophil count is due to Cortisol
Cortisol does NOT increase Eosinophil
Site of production of aldosterone in body Zona glomerulosa
Aldosterone escape Chronic exposure to aldosterone causes decrease in Na+
excretion, few days after that Na+ excretion is normal
Escape phenomenon is due to Increased ANP
Excess aldosterone NOT associated with Hyperkalemia
Increased aldosterone does NOT lead to Metabolic acidosis
Aldosterone antagonist causes Hypovolemia, hyponatremia, hyperkalemia
Aldosterone antagonist NOT used in treatment of Gynecomastia
ADRENAL TUMOUR
Investigation of choice for adrenal mass CT

Adrenal adenoma and carcinoma distinguished by MRI
CT scan features of adrenal adenoma Calcification is rare, low attenuation, homogenous
density and well defined borders(regular margins)
To be ruled out in incidentaloma Cushing disease, Metastasis, Adrenal adenoma
Carcinoma, Adrenal hyperplasia
Indication of surgery in case of adrenal incidentaloma Size > 5 cm, Bilateral adrenal metastasis, Functional
tumor
Incidental finding in CT scan a 3 cm adrenal mass, Adrenalectomy
should NOT be done
Adrenal histoplasmosis Adrenal glands are symmetrically enlarged
NOT a feature of Von Hippel Lindeau syndrome Adrenal adenoma
ADRENAL HYPERPLASIA
Adrenal cortical hyperplasia from adrenal tumor CT scan

NOT correct of bilateral adrenal hyperplasia CT diagnostic
ADRENAL CARCINOMA
Adrenal carcinoma associated with Von Hippel lindeau

ENSAT staging for Adrenal carcinoma
Management of adrenocortical carcinoma Berrutti regimen (Mitotane)
Bilateral adrenalectomy is NOT useful in Adrenal carcinoma
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ADRENAL GLAND 59
ENDOCRINOLOGY
FEATURES OF CUSHING SYNDROME
MC Endocrinopathy Cushing Syndrome

MC cause of Cushing’s Syndrome Administration of Exogenous Corticosteroids
MC cause of Cushing’s syndrome Iatrogenic
Main cause of endogenous Cushing syndrome ACTH pituitary tumour
MC of endogenous Cushing syndrome in Adrenal carcinoma
children
Commonest cause of Cushing syndrome Hyperplasia
Cushing syndrome is a feature of Adrenal carcinoma, Oat cell carcinoma of lung, Pituitary
adenoma
Cushing syndrome is due to excess of Cortisol
Earliest manifestation of Cushing syndrome Loss of diurnal variation
Striae are commonly seen in Cushing’s Syndrome
Metabolic acidosis is seen in Cushing’s Syndrome
Basophils are decreased in Cushing’s syndrome
Cushing’s disease (different from Cushing’s syndrome) Increased ACTH and increased cortisol
associated with
Cushing syndrome Oligomenorrhoea, Insulin resistance, Centripetal
obesity, Violaceous stria, Proximal myopathy, Edema,
DM, HT
Cushing syndrome Increased aldosterone, Increased epinephrine, Edema
Feature of Cushing’s syndrome caused by Decreased ACTH, increased cortisol,
adrenal adenoma decreased DHEAS
Crooke hyaline body in present in Basophil cells of pituitary gland in cushing syndrome
Polyuria is NOT caused by Cushing syndrome
NOT seen in Cushing’s syndrome Hypoglycemia
NOT a feature of Cushing’s disease Episodic hypertension
NOT true about Cushing’s Syndrome Hyperkalemia
Pseudo Cushing syndrome is associated Obesity, alcoholism, depression
with
MANAGEMENT OF CUSHING SYNDROME
Most appropriated investigation for diagnosing cushing Plasma cortisol

syndrome
Pasireotide diaspartate is a new drug for Somatostatin analogue
Cushing disease which acts via
Treatment of Patient with Cushing’s disease when Bilateral Adrenalectomy
Pituitary surgery has failed
During bilateral adrenalectomy for Cushing’s disease, Ligation of left adrenal vein
intraoperative dose of hydrocortisone given after
Treatment of choice for Cushing’s disease Selective transsphenoidal resection
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ADRENAL GLAND 60
ENDOCRINOLOGY
ECTOPIC ACTH PRODUCTION
Ectopic ACTH production associated with Hypokalemic hypochloremic metabolic alkalosis

Ectopic ACTH production Small cell carcinoma of lung
Carcinoma lung associated with Ectopic ACTH production
FEATURES OF CONN SYNDROME
Conn syndrome Diastolic hypertension without edema, Proximal

myopathy
Conn syndrome associated with Hypertension, muscle weakness, hypokalemia
Conn’s syndrome commonly associated with Cortical adenoma
Features of Conn syndrome Low K+
Spironolactone bodies Aldosterone adenoma
NOT a feature of Conn syndrome Anasarca
NOT a feature of Conn syndrome Raised rennin level
Respiratory alkalosis is NOT seen in Conn Syndrome
NOT a feature of Conn syndrome Edema
HYPERALDOSTERONISM
MC cause of Hyperaldosteronism Conn’s Syndrome (Adrenocortical Adenoma-Left sided

MC)
Hyperaldosteronism causes Hypokalemia
Increased aldosterone Metabolic alkalosis, Hypernatremia, Hypertension,
Hypokalemia
Glucocorticoid remediable aldosteronism Response of aldosterone secretion by
ACTH stimulation is sustained
Primary Hyperaldosteronism Renin secretion depressed
Characteristic feature of Primary Hyperaldosteronism Hypokalemia
NOT a feature of Primary hyperaldosteronism Pedal edema
Hyperaldosteronism does not cause Metabolic acidosis
NOT a feature of hyperaldosteronism Very high Na+ in plasma
Secondary Hyperaldosteronism High plasma rennin activity
Aldosterone synthesis inhibited by Hypernatremia
Screening test for mineralocorticoid excess Aldosterone rennin ratio
FEATURES OF ADDISON’S DISEASE
Causes of primary adrenal insufficiency Autoimmune polyglandular syndrome I(defect in

autoimmune regulator(AIRE), autoimmune polyglandular
syndrome 2
MC cause of adrenal insufficiency in HIV CMV
Drugs causing Addison’s disease Ketoconazole, Aminoglutethimidine
Allgrove syndrome (Triple A syndrome) Addison’s diseae, Achalasia, Alacrima
MC cause of Addison’s Disease in India Tuberculosis
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ADRENAL GLAND 61
ENDOCRINOLOGY
MC cause of Addison’s disease Autoimmune adrenalitis

Acute adrenal insufficiency Weakness, vomiting, fever, hypotension, hypoglycemia,
hyperkalemia
Adrenal insufficiency Asthenia, Hyperpigmentation, Abdominal pain ,
Decreased sodium potassium ratio, Decreased ECF,
Increased plasma rennin activity, HYPERCALCEMIA
Palpation on the costovertebral angle produces pain Rogoff sign
and tenderness in acute adrenal insufficiency
Hyperpigmentation seen in Primary adrenocortical insufficiency
Addisonian pigmentation Involves moles, scars, palmar creases. Decreased
fibrosis
Adrenal & ear pinna Calcification Addison’s Disease
NOT a feature of Addison’s disease Hypokalemia
Addison disease is NOT characterized by Hyperglycemia
NOT true about Addisonian hyperpigmentaion Does NOT involve oral mucosa
Addison’s disease NOT associated with Low rennin levels
NOT a feature of Addison’s disease Hypertension
Chronic adrenal insufficiency NOT characterized by Weight gain
MANAGEMENT OF ADDISON’S DISEASE
Cosyntropin test for Adrenal insufficiency

Water load test is helpful in diagnosis of Addison’s disease
Most diagnostic test in Addison disease ACTH stimulation test
Drug given in Addison’s disease Hydrocortisone
WATERHOURSE FRIEDRICHSON SYNDROME
Waterhouse Friedrichsen syndrome is caused by Neisseria mengitidis

Waterhouse Friedrichsen Syndrome Primary Acute Adrenal Insufficiency due to Hemorrhage
associated with Neisseria Infection, MC Complication of
Meningococcal Meningitis
Pathological change in Waterhouse Friedrichson Adrenal Cortex
Syndrome is marked in
management of Waterhouse Friedrichson syndrome Penicillin G
GENERAL FEATURES OF CONGENITAL ADRENAL HYPERPLASIA
Defect protein in congenital lipoid adrenal hyperplasia STAR protein (steroidogenic acute regulatory protein)
MC mutation in congenital adrenal hyperplasia CYP21A2
MC cause of female pseudohermaphroditism Adrenal cortical tumour
20 year female, oligomenorrhoea, facial hair, raised free Adrenal hyperplasia
testosterone level
Apparent mineralocorticoid excess is due to 11 beta hydroxysteroid dehydrogenase
Acquired cause of 11 beta hydroxysteroid dehydrogenase Liquorice containing glycyrrhizic acid
deficiency
CAH associated with Hypoglycemia, Hyponatermia, Hyperkalemia
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ADRENAL GLAND 62
ENDOCRINOLOGY
10 month baby, previously normal, suddenly developed Familial glucocorticoid deficiency

distress in crib. Hyperpigmentation in external genitalia.
Blood glucose 30 mg%
Ketosteroids appear in urine in Congenital adrenogenital syndrome
Gender identity disorder with good prognosis Congenital adrenal hyperplasia
TYPES OF CONGENITAL ADRENAL HYPERPLASIA
Male pseudohermophroditism 5 alpha reductase deficiency, 17 hydroxylase deficiency,

Gonadal dysgenesis
21 alpha hydroxylase deficiency Most common cause of CAH in children, Affected
female present with ambiguous genitalia, Affected
males present with precocious puberty
Commonest cause of primary amenorrhoea with 21 hydroxylase deficiency
ambiguous genitalia in a female patient with 46XX
chromosome
1 month baby, frequent vomiting and failure to thrive. 21 hydroxylase deficiency
Moderate dehydration. sodium 122 mEq/L and
potassium 6.1 mEq/L
10 day male pseudohermophrodite 46XY BP 110/80 17 hydroxylase deficiency
mm hg
Baby girl ambiguous genitalia 21 hydroxylase deficiency 46XX
of salt wasting type. karyotype
5 year old girl with hypertension and virilization, 11 beta hydroxylase
hypokalemia
Female child, virilisarion, hypertension, low plasma 11 beta hydroxylase deficiency
rennin
MANAGEMENT OF CONGENITAL ADRENAL HYPERPLASIA
Neonatal screening for congenital adrenal Heel prick blood for 17 hydroxy
hyperplasia progesterone
4 week old female child normal genitalia, severe Aldosterone
dehydration, hyperkalemia and hyponatremia,
measurement of
5 year old boy pubic hair, tall and has increased Increase 11 deoxycortisol
pigmentation of his genitalia and phallic enlargement.
130/90 mm Hg. Measurement
5 year old boy precocious puberty BP 130/80 mm Hg. 11-deoxycortisol
diagnosis by estimation of
Which is Elevated in 3β-HSD deficiency DHEA
Treatment of virilising adrenal hyperplasia Cortisone
Drug used for CAH Dexamethasone
Drug used for fetal therapy for congenital adrenal Dexamethasone
hyperplasia
Which of the following drug is used for treatment of Ketoconazole
Adrenal hyperplasia
Appropriate advice to mother with previous history of To start steroid as soon as pregnancy confirmed
delivering a child with CAH
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ADRENAL GLAND 63
ENDOCRINOLOGY
GENERAL FEATURES OF STEROID DRUGS
Steroids Inhibits release of arachidonic acid from vessel wall

through action on phosholipase A, Inhibit vascular
membrane permeability, Increase glucose synthesis in
liver
Steroids Prevent deiodination
Present intracellularly in muscle cell Corticosteroid
Does NOT belong to steroid receptor superfamily Epinephrine receptor
Glucocorticoids act in inflammation by Increasing lipocortin
Anti-inflammatory action of corticosteroids due to Breakdown of phospholipid
blockage of
Adrenal suppression due to steroid therapy It does NOT occur in patients receiving inhaled steroids
Adrenal suppression due to steroid therapy Should be suspected in anyone receiving >5 mg
prednisolone daily
At same concentration, which form of steroid is more Ointment
potent
All natural glucocorticoids have Mineralocorticoid effect
Most potent topical corticosteroid Betamethasone valerate cream 0.5%
Most potent mineralocorticoid Aldosterone
Compared to hydrocortisone, maximum glucocorticoid Dexamethasone
action
Corticosteroid with maximum sodium retaining Fludrocortisones
potential
Mineralocorticoid replacement Fludrocortisone
Corticosteroid given by inhalational route Beclomethasone
Steroid used as aerosol Beclomethasone
Best inhalational steroid with least systemic effects Beclomethasone
NOT true about beclomethasone Effective in acute asthma
Maximum glucocorticoid activity Dexamethasone
Most potent glucocorticoid activity Betamethasone
Least potent glucocorticoid activity Cortisone
Glucocorticoid with maximum Hydrocortisone
mineralocorticoid activity
Glucocorticoid with mineralocorticoid activity seen in Cortisol
Corticosteroid needs least systemic monitoring Budesonide
Least mineralocorticoid activity Methyl prednisolone
Least mineralocorticoid activity Dexamethasone
NO mineralocorticoid activity Prednisolone
Steroid NOT used topically Prednisolone
Longest half life having intermediate acting Triamcinolone
glucocorticoid
Steroid with only glucocorticoid activity Triamcinolone
Retention of sodium is a side effect of Triamcinolone
Least glucocorticoid activity Triamcinolone
Ozurdex 7% Dexamethasone
Glucocorticoid receptor blocker Mifepristone
Selective mineralocorticoid activity DOCA
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ADRENAL GLAND 64
ENDOCRINOLOGY
NOT a long term therapy of steroids Pot belly

Adrenal steroids contraindicated in Severe hypotension, osteoporosis, diabetes mellitus
Steroid are NOT contraindicated in Eczematous skin disease
INDICATIONS OF STEROIDS
Indication for use of corticosteroids Loeffler’s syndrome

Steroids indicated in Collagen diseases
Corticosteroids are indicated in E.coli septicemia
Steroids are used in Severe typhoid fever
SIDE EFFECTS OF STEROID DRUGS
Teratogenicity of prednisone Oral cleft

Retarded bone growth Steroid therapy
Commonest complication of topical steroids Glaucoma
Prolonged use of steroids may cause Decrease in bone matrix protein
If steroid given to Pregnant female Cleft Palate
Corticosteroid in children cause Reduction in behavior
Side effects of steroids due to its mineralocorticoid Hypertension
component
One of the common side effects of Oropharyngeal candidiasis
beclomethasone dipropionate
Dependent on maternal or fetal corticosteroid Induction of thymic involution, production of
surfactant, functional thyroid
Systemic steroid does NOT cause Glaucoma
NOT a side effect of corticosteroids Muscular hypertrophy, Reduced appetite
NOT a side effect of steroids Osteomalacia
NOT an adverse effect of tropically administered Intertrigo
steroids
NOT a side effect of steroid Photosensitivity
NOT a side effect of steroid Hypoglycemia
NEUROBLASTOMA
Gene amplification is associated with Neuroblatoma

n-myc gene is associated with Neuroblastoma
Primary neurogenic tumor Neuroblastoma
Commonest intraabdominal tumor below 2 years Neuroblastoma
Commonest tumor of lumbar region in children Neuroblastoma
Childhood tumor most commonly metastasizes to bone Neuroblastoma
MC neonatal malignant tumor Neuroblastoma
MC malignant neoplasm of infancy Neuroblastoma
Neuroblastoma originates from Adrenals, Mediastinum, Neck
Metabolites excreted in urine in neuroblastoma HVA, VMA, Catecholamines
Catecholamines are secreted by Neuroblastoma
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ADRENAL GLAND 65
ENDOCRINOLOGY
MC presentation of Neuroblastoma Lytic lesion in skull with suture diastasis

Hutchinson type of secondaries in skull form Neuroblastoma
Hutchinson secondaries Orbital secondaries in neuroblastoma
Robert’s secondaries Liver secondaries in neuroblastoma
Bilateral adrenal enlargement with stippled calcification Neuroblastoma
1 year child with abdominal mass and calcification of X Neuroblastoma
ray
Neuroblastoma in children Hypertension, Hepatomegaly, Proptosis
Child coming with proptosis, multiple skeletal limb Neuroblastoma
secondaries and sutural separation
1 year child, swelling in left flank, episodes of flushing Neuroblastoma
and diarrhea, sweating and bone pain
16 year girl, abdominal lump. bone scan needed in Neuroblastoma
Neuroblastoma Associated with mild hypertension, Treatment is
excision and post operative radiotherapy
Neuroblastoma Most common extracranial solid tumour of childhood,
>50% present with metastasis at the time of diagnosis,
often encase aorta and its branches at the time of
diagnosis
Calcification near kidney in 6 month child Neuroblastoma
Oposclonus myoclonus phenomena Neuroblastoma
Opsoclonus myoclonus phenomena is associated with Neuroblastoma, lung cancer, breast cancer
Opsomyoclonus is a clinical feature of Neuroblastoma
Increase in AFP Neuroblastoma
MIC 2 is a marker of Ewing’s sarcoma
NOT seen in neuroblastoma Splenomegaly
NOT seen in neuroblastoma Flexner Winter Steiner rossette
Good prognosis in Neuroblastoma associated with trkA expression
Good prognosis Hyperploidy
Prognosis of Stage IV-S neuroblastoma Good
Bad prognosis of neuroblastoma Age>1 year
Bad prognosis is associated with Tyrosine kinase B, n - myc
CAUSES OF PHEOCHROMOCYTOMA
Pheochromocytoma associated with VHL, MEN IIA

Pheochromocytoma associated with Medullary carcinoma of thyroid, Von hippel landau
disease, Sturge Weber syndrome, Neurofibromatosis
Pheochromocytoma is associated with Sipple syndrome
NOT associated with pheochromocytoma Prader Willi syndrome
FEATURES OF PHEOCHROMOCYTOMA
Great masquerader Pheochromocytoma

Pheochromocytoma like symptoms Chemodectoma, ganglioneuroma
First described pheochromocytoma syndrome NF1
Pheochromocytoma 10% bilateral, 10% extrapyramidal, 10% malignant
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ADRENAL GLAND 66
ENDOCRINOLOGY
Commonest cause of paroxysmal hypertension Pheochromocytoma

MC Site of Phaeochromocytoma Adrenal Medulla
Catecholamines Phaeochromocytoma
In Pheochromocytoma, increased excretion of Urinary VMA
Fasting hyperglycemia is almost always seen in Pheochromocytoma
Pheochromocytoma predominantly secretes Norepinephrine
Catecholamines in pheochromocytoma is Neural stimulation
not by
Predominant sign of pheochromocytoma Episodic hypertension
Vannilylmandelic acid is increased in Pheochromocytoma
Pheochromocytoma is bilateral in 10%
Pheochromocytoma elaborates Norepinephrine, epinephrine and dopamine
Pheochromocytoma Increased hematocrit, Orthostatic hypotension,
Imparied glucose tolerance
MC manifestation of Pheochromocytoma Hypertension
Pheochromocytoma in MEN II syndrome Multicentric, bilateral adernal
Malignancy in pheochromocytoma is indicated by Metastasis
Pheochromocytoma does NOT arise from Chest wall but arise from mediastinum and neck
NOT true about Pheochromocytoma 10% asymptomatic
NOT an indication for ACE inhibitors Pheochromocytoma
NOT a feature of pheochromocytoma Wheezing
NOT true about pheochromocytoma 90% malignant
NOT a feature of pheochromocytoma Low cortisol levels, Hypocalcemia
NOT associated with pheochromocytoma Rhabdomyolysis
NOT increased in pheochromocytoma 5 HIAA
EXTRA ADRENAL PHEOCHROMOCYTOMA
MC Extraadrenal site of Phaeochromocytoma Organ of Zuckerkandl (Paravertebral Sympathetic

Chain)
Extraadrenal pheochromocytoma secrete Norepinephrine exclusively
MEN associated pheochromocytoma Epinephrine
secrete
Extraadrenal pheochromocytoma Less than 100 gm
DIAGNOSIS OF PHEOCHROMOCYTOMA
FNAC is contraindicated in Phaeochromocytoma

MIBG is used for diagnosing Phaeochromocytoma
Adrenal Phaeochromocytoma CT Scan
Extraadrenal Phaeochromocytoma MIBG scan
Phaeochromocyoma – sensitive investigation Urine Fractionated Metanephrine
Phaeochromocyoma – specific investigation Plasma Free Metanephrine
Diagnosis of pheochromocytoma High performance liquid chromatography
of urinary catecholamines and
metanephrine (drugs interfere this test, so
drugs should be discontinued 2 weeks
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PINEAL GLAND 67
ENDOCRINOLOGY
before this test

Diagnosis of pheochromocytoma Liquid chromatography tandem mass
spectroscopy (minimal drug interference)
Diagnosis of pheochromocytoma Plasma free metanephrine, urinary total
metanephrine
Any Surgery in a pheochromic patient. investigations Estimation of urinary metanephrines, VMA and
catecholamines
Most useful test for diagnosis of pheochromocytoma 24 hour metanephrine
Most sensitive for evaluation of pheochromocytoma MRI
MRI signs of pheochromocytoma Swiss cheese pattern
High sensitivity imaging test for DOPA PET
pheochromocytoma
Pheochromocytoma localized by CT scan
TREATMENT OF PHEOCHROMOCYTOMA
Averbuch’s chemotherapy for Pheochromocytoma

Pheochromocytoma is treated by Alpha followed by beta blockers
Ideal drug employed in preoperative preparation for Phenoxybenzamine
surgical excision of pheochromocytoma
Management of intraoperative hypertensive crisis while Sodium nitroprusside
operating pheochromocytoma
NOT given in patient with pheochromocytoma Atenolol
Treatment of choice for Adrenalectomy
Pheochromocytoma
Anesthetic agent contraindicated in Halothane
surgery for pheochromocytoma
Treatment of recurrent I131 MIBG ablation
pheochromocytoma
NOT needed for pheochromocytoma Termination of pregnancy
PINEAL GLAND
Melatonin is secreted by Pineal gland

Brain sand Pineal gland
Exposure to darkness leads to increased melatonin Increasing serotonin N acetyl transferase
secretion. It is brought about by
Melatonin secretion is increased by IV infusion of tryptophan and epinephrine
Commonest tumor of pineal gland in adult Germ cell tumor
Diencephaly syndrome Pinealoma, diabetes insipidus,
exophthalmos
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MULTIPLE ENDOCRINE NEOPLASIA 68
ENDOCRINOLOGY
MULTIPLE ENDOCRINE NEOPLASIA
GENERAL FEATURES OF MULTIPLE ENDOCRINE NEOPLASIA
RET (Point Mutation) MEN 2A, 2B, Familial Medullary Carcinoma Thyroid
Medullary carcinoma of thyroid associated with MEN II
MEN Syndrome associated with Medullary Carcinoma
NOT associated with MEN II Parathyroid adenoma
NOT associated with MEN II Islet cell hyperplasia
Intermittent headache, hyperthyroidism, thyroid nodule Measure urine VMA and aspiration of thyroid nodule
MEN I
Chromosome associated with MEN I syndrome Chromosome 11q13

MEN I syndrome (Wermer syndrome) Pituitary tumour, Parathyroid tumour, Pancreatic
tumour
Most commonly involved in MEN 1 Parathyroid
Second most commonly involved in MEN I Enteropancreatic (gastrinoma, insulinoma)
36 year old female, hyperparathyroidism, pituitary MEN I
adenoma, islet cell tumour, cutaneous angiofibroma
Intractable peptic ulceration with renal stones MEN I syndrome
Calcium excess associated with MEN I
Carcinoid tumor of MEN I are of Foregut type
MEN I does not include Medullary carcinoma thyroid
NOT involved in MEN I Adrenal
NOT a component of Werner syndrome Adrenal
MEN IIA
MEN IIA syndrome (Sipple syndrome) Parathyroid Hyperplasia, Medullary Carcinoma of

Thyroid, Phaeochromocytoma
MEN IIA does NOT include Pituitary Adenoma
NOT a feature of MEN IIA Pituitary tumour
MEN IIB
MEN IIB Wagenmann Froboese Syndrome Medullary Carcinoma Thyroid, Pheochromocytoma,

Mucosa Neuroma
Medullary carcinoma in MEN IIB is More aggressive than that of MEN II A
NOT a component of MEN II B Parathyroid hyperplasia
20 year male, chronic constipation, headache, MEN IIB
palpitations, marfanoid habitus, neuroma of tongue,
medullated corneal nerve fibres, 2*2 cm nodule in
thyroid gland
NOT associated with MEN IIB Hyperparathyroidism
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CARCINOID 69
ENDOCRINOLOGY
POLYGLANDULAR SYNDROME
Polyglandular syndrome type I Autosomal recessive, stars in childhood,mucocutaneous

candidiasis, hypoparathyroidism, adrenal insufficiency
Polyglandular syndrome type II Polygenic inheritance, adults, female predisposition
Polyglandular syndrome type II Adrenal insufficiency, thyroiditis, type I diabetes
Polyglandular syndrome II (Schmidt syndrome) Adrenocortical insufficiency and Grave’s disease
associated with
NOT used for polyglandular syndrome type II Insulin
CARCINOID
FEATURES OF CARCINOID
Smoking is a protective factor for Lung carcinoid

Omeprazole May induce carcinoid tumour in rats
Carcinoid syndrome is associated with Serotonin, tachykinin, motilin,
prostaglandin
Common sites of carcinoid Bronchus, rectum, small intestine
Carcinoid syndrome is common in Midgut
MC site of carcinoid tumour Distal ileum
st nd
MC Site of Carcinoid tumour GIT/Intestine, 1 Ileum, 2 Rectum
MC site of GIT carcinoid tumour Appendix
MC Site of Small Bowel Carcinoid Ileum
MC tumour occurring in appendix Carcinoid
Carcinoid tumour common in Appendix
Maximum Malignant Potential Carcinoid Pancreas
Carcinoid with maximum metastasis Pancreas
Carcinoid tumor in which site have least potential for Lung
malignancy
Feature of lung carcinoid Rarely produce carcinoid syndrome
Carcinoid syndrome does NOT manifest in Bronchial carcinoma
Does not metastasize, does not cause Esophagus
syndrome
Does not cause syndrome Liver and rectum
Carcinoid with syndrome Testis and ovary
Carcinoid tumor without syndrome Testis, ovary, liver
Multiple secondary type of lesion in liver, NOT Small arterioles
responding to diarrhea and flushing. Most preferably
due to lesion in
Gastric carcinoid Type I – atrophic gastritis, type II – gastrinoma, type III –
without hypergastrinemia
Type I and type II gastric carcinoid Hypergastrinemia
Type III gastric carcinoid Hypogastrinemia
Cardiac Calcification Carcinoid Syndrome
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OBESITY 70
ENDOCRINOLOGY
Carcinoid syndrome produce valvular disease in Tricuspid

Pathological finding in carcinoid heart syndrome Fibrous endocardial thickening of right ventricle,
tricuspid valve, pulmonary valve
Part of heart commonly affected in carcinoid syndrome Inflow tract of RV
Ovarian tumour associated with flushing & cyanosis Carcinoid
Pellagra like dermatitis Carcinoid syndrome
Least role in flushing Serotonin
Paroxysmal hypotension Carcinoid syndrome
Diarrhea in carcinoid is associated with Flushing, steatorrhea, watering stool
Metabolite increased in urine in carcinoid 5-HIAA
Foregut carcinoid Low seratonin level, Argentaffin negative
Carcinoid is commonly associated with Intestinal obstruction
Percentage of carcinoid syndrome 90%
associated with metastasis to liver
Appendiceal carcinoid are more common in Females
Typical carcinoid Increased levels of 5 HIAA
Atypical carcinoid Elevated levels of urinary 5 HT
KCC II (Kulchitsky) Atypical carcinoid
Characteristic pathologic finding in carcinoid syndrome Fibrous endocardial thickening of Right ventricle,
tricuspid valve and pulmonary valve
NOT seen in carcinoid syndrome Constipation
NOT true about gastrointestinal carcinoid Rectum is spared
5 Hydroxy indole acetic acid in urine in Carcinoid
Single most prognostic factor for small intestine carcinoid Liver metastasis
MANAGEMENT OF CARCINOID
Stain for carcinoid Chromograffin B

Treatment of carcinoid 5HT3 antagonists
Drugs used in treatment of carcinoid Tropisetron, lanreotide, interferon alpha
syndrome
Drug NOT used in treatment of carcinoid Sumatriptan (5-HT receptor agonist)
Carcinoid Appendix if tumor size > 2cm at base Right Hemicolectomy
OBESITY
Overweight in children >85 percentile

Obesity in children >95 percentile
Internationally accepted method of measuring obesity BMI
Normal BMI for Asian population 18.5 – 22.9
Overweight if BMI >25
Obese if BMI >30
BMI to classify obesity should be >30
BMI > 40 Extremely obese
Morbid obesity is more than 45
Appetite is increased by Neuropeptide Y, melanin concentrating hormone, agouti
related peptide, orexin, endocannabinoid
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OBESITY 71
ENDOCRINOLOGY
Deficiency of leptin causes Obesity

Leptin Satiety hormone (inhibits hunger), paradoxically
increased in obesity
NOT a cause of microvesicular fatty liver Obesity
Decreased basal metabolic rate seen in Obesity
Pickwickian syndrome Obesity, somnolence, hypercapnia, polycythemia
Obesity is associated with Frochlich, Prader willi, Lawrence Moon Biedl Syndrome
Syndromes associated with obesity Ahlstrom syndrome, Cohen syndrome, Carpenter syndrome
Obesity associated with Osteoarthritis, Hypertension, Gall stones
Least common association with morbid obesity Rheumatoid arthritis
Obesity NOT associated with Pancreatitis
NOT a feature of Lawrence Mood Biedl Diabetes insipidus
syndrome
NOT a significant anesthetic problem in morbidly obese Decreased cardiac output relative to total body mass
patient
Body Mass Index/Quetelet Index Weight in Kg
(Height in m)2
Pondreal Index Height in cm
3
Body Weight in Kg
Broca Index, Ideal Body Weight Height in cm – 100
Weight height index used to calculate BMI Broca index
Corpulence index is a measure of Obesity In adults in India
Corpulence index Measurement of obesity
Abdominal fat accumulation is assessed by Waist to hip ratio
Height independent indices of obesity Corpulence index
Waist circumference in obesity Men > 90 cm, women >80 cm
Height is NOT included in Corpulence index
Sites for measuring skin fold thickness Mid triceps, mid biceps, sub scapular,
supra iliac
NOT a site for measuring skin fold thickness Anterior abdominal wall
Densitometry Underwater weighing
Radiocontrast is NOT contraindicated in Obesity
Main treatment of hypoventilation with obesity Weight loss
Done to reduce obesity Regular exercise with some amount of food
Zone diet is recommended in Obesity
Drug of first choice in weight reduction Fenfluramine
programmes
Drugs used for obesity Orlistat, Sibutramine, Olestra
Lorcaserin is used in management of Obesity
Caralluma fimbriata is used in treatment Obesity
of
Restrictive bariatric surgeries Vertical band gastroplasty (prototype), lap adjustable
silicon banding
Restrictive malabsorptive bariatric surgeries Rouex en Y bye pass, bilopancreatic division, bilopancreatic
division with duodenal switch
NOT a primarily restrictive operation for morbid obesity Switch duodenal operation
Bariatric surgical procedure does NOT include Ileal transposition
NOT a restrictive operation for morbid obesity Duodenal switch
NOT a bariatric surgical procedure Ileal transposition
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WEIGHT GAIN AND WEIGHT LOSS 72
ENDOCRINOLOGY
WEIGHT GAIN AND WEIGHT LOSS
Weight gain is seen in Cushing syndrome, Hypothyroidism-myxedema,

Insulinoma
Weight loss is seen in Pheochromocytoma, Hyperthyroidism, Diabetes
mellitus, Adrenal insufficiency, Uremia
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ENDOCRINOLOGY

SECONDARY HYPERPARATHYROIDISM ................................................................................................................... 36

JOINT MANIFESTATIONS OF DIABETES ................................................................................................................... 48

SIDE EFFECTS OF STEROID DRUGS .......................................................................................................................... 64

KEY TO THIS DOCUMENT

Text in normal font – Must read point.

Text in bold font – Point from Harrison’s

Text in italic font – Can be read if

GENERAL FEATURES OF ENDOCRINOLOGY

System favors oscillatory responses Positive feedback system

FEATURES OF PHYSIOLOGY OF ENDOCRINOLOGY

Hormone synthesized as peptide precursor Insulin, PTH, rennin, angiotensin II

Bio organic computer Protein kinase and phosphatase

cAMP acts through Activation of protein kinase

Membrane receptor For specific action, Molecular transport

Does NOT act by intracellular receptor Insulin

Muscarinic receptors M1 – gastric glands, M2 – AV node, M3 –

GROUP I LIPOPHILIC RECEPTORS

CYTOPLASMIC RECEPTORS NUCLEAR RECEPTORS

GROUP II HYDROPHILIC HORMONES (BIND TO CELL MEMBRANE)

C-AMP C-GMP Ca/IP3/DAG Kinase/Phosphatase

G PROTEIN COUPLED RECEPTOR

Small G proteins Rab, ras, rho/rac

G protein activation leads to Generation of second messenger

Nitric oxide Free radical, Vasodilator, Oxidizing agent, Catalyst

DEVELOPMENT OF PITUITARY GLAND

Pituitary gland arises from Ectoderm

ANATOMY OF PITUITARY GLAND

Weight of pituitary gland 600 mg

PHYSIOLOGY OF PITUITARY GLAND

Pituitary has no control over Adrenal medulla

MC endocrinal abnormality associated No abnormality

Somatomedin mediates Deposition of chondroitin sulphate

Gigantism occur in Enuch

MC cause of Acromegaly GH Producing pituitary adenoma

Serum IGF-1 test for Acromegaly

Etiology of Nutritional dwarfism Chronic malnutrition

Prolactin is secreted by Anterior Pituitary

Causes of Hyperprolactinoma Chronic renal failure, Thyrotoxicosis, Metoclopramide

associated with adenoma

Hypocalcemia seen in Hypopituitarism

Postpartum pituitary necrosis Sheehan’s syndrome

SYNDROME OF INAPPROPRIATE SECRETION OF ADH

Free water clearance regulated by ADH

Normal serum osmolality 285 - 295 mosm/L

Polyuria is caused by Hypercalcemia, primary hyperaldosteronism,

Gland derived from foramen caecum Thyroid

Average Weight of Thyroid gland 18 – 20 gm

Thyroid hormones are synthesized from Tyrosine

Amount of I 131 used in thyroid scan 50 millicurie

Thyroid hormone T3 is more avidly bound to nuclear receptors than T4,

Occurrence of hyperthyroidism following administration Jod Basedow effect

Treatment of hyperthyroidism in Propylthiouracil with T3

Incidence of hypothyroidism 1 in 4000

Hypothyroidism with increased TSH level is NOT seen in Sheehan syndrome

Cretinism Prolonged physiological jaundice, Common in iodine

Struma ovary associated with Hyperthyroidism

MC cause of Thyrotoxicosis Grave’s Disease

MC cause of Proptosis in adults (25-50 years) Graves Ophthalmopathy