E

N
D
O
C

/e
14 R
I
S,
AM

N
O
O
R

L
O
G
Y
 PRECOCIOUS PUBERTY (PP) E
Type Causes
N
D
Central isosexual PP (True PP)
O
Idiopathic Sporadic, familial
C
Organic neurogenic CNS tumours - craniopharyngioma R
CNS infections - TB, Post meninigitis I
CNS insult - Trauma, neuro Sx, radiation N
    O
Fig.: Congenital 11 beta hydroxylase def Malformation- Arachnoid cyst, L
hydrocephalus O
Variation in pubertal devpt G
Isolated cause Isolated premature thelarche Y
Isolated premature pubarche/
adrenarche
Isolated premature menarche

/e
Fig.: Hypokalemia in 11 beta hydroxylase def Peripheral PP in girls (Pseudo PP)
Hypothyroidism
Ovarian estrogen McCune Albright syndrome,

14
Imp. causes of ambiguous genitalia
Benign follicular cyst,
Granulosa theca cell tumours
ƒƒ In boys (46 XY )
ƒƒ Testosterone synthesis defect Adrenal estrogen Feminising adrenal neoplasia
ƒƒ Leydig cell hypoplasia/ receptor defects Exogenous estrogens Phytoestrogens, creams
S,
ƒƒ Androgen insensitivity syndrome ( AIS ) Peripheral PP in boys (Pseudo PP)
°° Complete AIS d/to receptor mutation CAH 21-hydroxylase deficiency,
°° Partial AIS (Reifenstein syndrome) 11 b -hydroxylase deficiency
AM

°° 5 a reductase def. a/w perineo-scrotal hypospadias Adrenal tumours

ƒƒ Gonadal dysgenesis Testicular tumours Leydig cell, adrenal rest tumour
ƒƒ Congenital anomalies of mullerian structures. Testotoxicosis
h -CG secreting
ƒƒ In girls (46 XX ) tumours
O

ƒƒ CAH, adrenal/ gonadal tumours Exogenous Androgen/testosterone exposure

ƒƒ Maternal androgens Heterosexual PP (True PP)
ƒƒ Placental aromatase deficiency
R

Virilisation in girls CAH, PCOS, ovarian hyperplasia

Feminisation in boys Estrogen producing adrenal tumour,
Exogenous estrogen/drugs
DELAYED PUBERTY (DP)
ƒƒ Failure of signs of sexual development by the age of 14 yrs
in a male is considered as delayed puberty in boys. 15.6 HORMONES SECRETED BY KIDNEY
ƒƒ Failure of breast budding by the age of 13 yrs in a female
is considered as delayed puberty in girls.
Renin
ƒƒ Causes:
ƒƒ Renin is an acid protease enzyme secreted from
°° Chronic systemic d/s
juxtaglomerular cells of kidney.
°° Constitutional delay ( m/c cause)
ƒƒ It converts angiotensinogen to angiotensin I.
°° Hypo- & hyper- gonadotropic gonadism
ƒƒ Tubuloglomerular feed back is a feedback from renal
tubules to regulate GFR.
ƒƒ Macula densa is the sensor for its secretion. When Na+ load
is low in Macula densa of DCT, JG cell of juxtaglomerular
apparatus are stimulated and secretes renin. 593
 E ƒƒ Factors affecting renin secretion:- GYNAECOMASTIA
N °° Renin secretion is ↑ ed by: ATP, adenosine, ACEI/
ARB's, NSAIDs [Mn: 4"A"s] ƒƒ Is enlargement of male breast tissue.
D ƒƒ It's a common, benign (non cancerous) condition that
°° Renin secretion is ↓ed by: PG's, Loop diuretics, beta
O mainly affects teenage boys.
blockers, clonidine etc.
C ƒƒ Drugs and liver disease are the most common cause in
R adults. Imp. causes:-
Erythropoietin
I °° Klinefelter syndrome
N ƒƒ Circulating glycoprotein hormone, secreted by mesangial
cells of glomeruli of JGA of kidney (85%). In fetus it is °° Malignancies: Leydig cell tumors or Sertoli cell tumors,
O choriocarcinoma, prolactinoma, SCLC.
L produced by liver /cells of monocyte/macrophage lineage.
°° Drugs- Spiranolactone, ketoconazole, cimetidine,
O ƒƒ Principal site of inactivation is liver (t½ is 5 hr. ), peritubular
anti-retroviral drugs
G capillary interstitium.
ƒƒ Blood level is ↑ed in hypoxia (physiological stimulus) °° Newborn may develop temporary gynecomastia due to
Y the influence of maternal hormones.
and anemia. Secretion of E~ is ↑ed by cobalt, androgens,
ƒƒ T/t
high altitude, alkalosis, adenosine, catechol amines and
↓ed by adenosine antagonist theophylline. °° 75% of pubertal gynecomastia cases resolve within two
years of onset without treatment.

/e
ƒƒ It does not cross placenta therefore stimulation of maternal
EPO does not result in stimulation of fetal RBC production. °° Aromatase inhibitors are effective in aromatase excess
syndrome or Peutz–Jeghers syndrome,but surgical

14
Vasopressin (ADH) removal of the excess is usually required.
ƒƒ Circulated as free form in plasma.
ƒƒ Greatest stimulus for its secretion is hyperosmolarity.
ƒƒ Secreted from supra-optic nucleus posterior pituitary
(and hypothalamus)
S,
ƒƒ Osmolality of urine depends on the action of vasopressin
on the collecting ducts.
ƒƒ There are 3 type of vasopressin receptors:
AM

Type Site Action

Image: Gynaecomastia in an adolescent male
V1A Vascular SM Vasoconstriction
Brain ↓ cardiac output
Liver, platelet ↑ glycogenesis NImportant negative points: Endocrinology
ŽŽ Hirsuitism is NOT caused by → Hyperthyroidism
O

V1B or V3 Anterior pituitary ↑ ACTH

ŽŽ Gynecomastia is NOT seen with
V2 CD of kidney, ↑ water diffusion through °° SCLC (Seen with large cell adeno Ca. of lung)
R

blood vessels aquaporin-2 °° Sarcoidosis.

Site of Action of Some Imp. Hormones HIRSUITISM

Hormone Stimulus Secreted Site and action ƒƒ Hair grows in unusual areas of a woman's face and body,
from such as the face or back. [Cf. hypertrichosis, which is
Angiotensin ↓ BP P cells of Constriction of excessive hair growth anywhere on the body].
II Cortical CD afferent arteriole. ƒƒ Usually d/to hormonal imbalance.
and DT ↓ GFR
ƒƒ The amount and location of the hair is measured by a
Aldosterone Zona Retention of Na+ Ferriman-Gallwey score.
glomerulosa Excretion of K+ → M/s
ƒƒ The Ferriman–Gallwey score is a method of evaluating
of the fatigue, expansion of
adrenal ECF volume and quantifying hirsutism ( amount & location of hairs)
cortex in women.
ADH Low Posterior Medullary CD and DT ƒƒ Imp. causes:-
(Vasopres- pressure pituitary → Water retention °° PCOS (MC cause in women).
594 sin) in atria °° Hyper or hypo -insulinemia
ANP RA of heart Promotes natriuresis

[CD = collecting ducts, DT = Distal tubules]

 °° Androgen producing ovarian tumors e.g. granulosa -- Metformin: In patient with obesity and type 2 DM E
cell tumors, thecomas, Sertoli–Leydig cell tumors -- Orlistat N
(androblastomas). D
°° Adrenal tumours. O
°° 21-hydroxylase deficiency C
°° Cause of hirsuitism not related to hyperandrogenism R
are: Minoxidil, porphyria cutanea tarda.
I
ŽŽ N Hirsutism is NOT caused by → Hyperthyroidism
N
ƒƒ T/t: Antiandrogens e.g.
O
°° Spironolactone L
°° Cyproterone acetate O
°° Eflornithine etc. G
Y
OBESITY
ƒƒ Is a state of excess adipose tissue.

/e
ƒƒ Pathological features and complications a/w obesity:
°° Glucose intolerance
°° Insulin resistance. Image: Obesity with hypogonadism

14
°° HTN, ↑ed risk of CVS d/s, gout, OA.
°° Hypothyroidism High-yield Points
°° ↓ GH 44 Surgery (bariatric surgery) is required for morbid obesity (BMI >
°° Cortisol production and urinary metabolites (17- 40) or BMI > 35 with comorbidity.
OH steroids) ↑ed.
S,
44 Dual energy x-ray absorptiometry (DEXA) provides the best
°° Menstrual irregularities in females esp. oligomenorrhea assessment of total body fat.
and PCOS
°° Obstructive sleep apnea and obesity hypoventilation
AM

syndrome. Obesity Hypoventilation Syndrome (OHS)

°° Gallstones ƒƒ Also k/as Pickwickian syndrome.
°° Cancers of colon, rectum and prostate in male ƒƒ Abnormal central ventilatory drive and obesity contribute
and cancers of gall bladder, endometrium, cervix, to the development of OHS.
ovaries and breast in female. ƒƒ Approximately 90% of patients with OHS also have
O

°° ↑ed risk of osteoarthritis and gout. obstructive sleep apnea (OSA). OSA is worse during REM
ƒƒ Conditions a/w obesity — Cushing, Hypothyroidism, sleep.
Insulinoma ƒƒ Diagnostic criteria includes:
R

ƒƒ Syndromes a/w obesity °° BMI >30 kg/m2

°° Pradder -Willi °° PaCO2 >45 mm Hg
°° Laurance Moon Biedl (LMB) °° PaO2 < 70 mm Hg
°° Cohen ƒƒ T/t: Breathing support, weight loss, and medicines.
°° Carpenter
ƒƒ W:H ratio if >1 in men or > 0.85 in women it is
METABOLIC SYNDROME
considered obesity.
ƒƒ T/t: ƒƒ Also called Dysmetabolic syndrome/Syndrome-X or
°° Reduced caloric intake is the cornerstone of obesity t/t Insulin resistance Syndrome.
°° Exercise, lifestyle modifications ƒƒ Components are:-
°° Drugs °° Obesity
-- Phentermine: amphetamine like drug which acts °° High fasting triglycerides
centrally by reducing appetite °° Low levels of HDL- C
-- Fenfluramine: SRI °° Elevated fasting plasma insulin
-- Fen-Phen: (Phentermine + Fenfluramine) °° Impaired GT (Hyperglycemia) and
-- Sibutramine: NSRI °° Hypertension 595
 E ƒƒ Comorbidities: MULTIPLE ENDOCRINE NEOPLASIA (MEN)
N °° Obesity related
-- Diabetes (new onset T2DM) Tumour Type MEN 1 MEN 2a MEN 2b
D (Werner’s) (Sipple’s) (Waggen
-- Hypertension
O Pollock
-- Dyslipidemia
C Vicks
-- Sleep apnea (OSA) synd)
R
-- Gall bladder d/s
I Chr. 11q13 Chr. 10q11 Chr. 10q11,
°° Joint pain RET gene
N
O °° NAFLD, NAHS, PCOS Parathyroid >80% 50% Rare
L Pancreatic 75% – –
O Pituitary adenoma 60% – –
G 15.7 PGA & MEN MTC (Medullary) – >50% 80%
Y Pheochromocy- – 20% 60%
POLYGLANDULAR AUTOIMMUNE toma
SYNDROMES (PGA) Mucosal and GI – Rare >90%

/e
ganglioneuromas
ƒƒ PGA1:
Other features Occasional Hirschsprung
°° Autosomal recessive, mutations in APECED gene Lipoma, d/s
°° Mucocutaneous candidiasis, hypothyroidism, hypo-

14
parathyroidism, adrenal insufficiency, dental enamel Adrenocorti- Cutaneous Mucosal
hypoplasia, malabsorption, vitiligo, pernicious anemia, cal adenoma amyloidosis neuroma
hypogonadism, alopecia etc. Carcinoid, Familial MTC Marfanoid
ƒƒ PGA II: Thyroid ad- habitus
enoma
°° Polygenic inheritance, a/w HLA- DR3 and DR4, adult
S,
onset, more in female Gene MEN 1 Chr RET gene RET gene
11q13 Chr 10q11
°° A/w hypothyroidism, Grave's d/s, MG, celiac d/s, type1
DM, adrenal insufficiency, hypophysitis, vitiligo,
AM

pernicious anemia, hypogonadism, alopecia etc. High-yield Points

44 When medullary thyroid carcinoma and pheochromocytoma
High-yield Points are a/w hyperparathyroidism then it is called MEN 2a or Sipple
44 Autoimmune hypothyroidism is a/w → PGA. syndrome and if they are a/w mucosal neuromas and marfanoid
habitus it is MEN 2b.
O

44 In t/t of hypothyroidism the efficacy of drug t/t is assessed by

testing TSH. 44 Pheochromocytoma should be operated first then medullary
44 Drugs that have profound effect on the thyroid function → carcinoma of thyroid in MEN - II.
44 In MEN - 1 hyperparathyroidism is treated 1st and when Ca ++
R

Amiodarone, PAS, Li.

44 Hypothyroidism is a/w ↑ed level of → Cholesterol. levels are controlled, treat ZES or pancreatic islet tumours.
44 Weight gain is seen in → hypothyroidism, insulinoma, 44 M/c tumour a/w MEN 1 is parathyroid adenoma. (Overall in
craniopharyngioma, PCOD, cushing's d/s. MEN1 Hyperplasia > adenoma).
44 Gastrinomas are m/c enteropancreatic tumours in MEN-1.
44 Insulinomas are m/c pancreatic tumour in MEN-I.

ƒƒ MEN 4 syndrome (CDNK1B) mutations (chromosome 12)

→ Parathyroid adenoma, Pituitary adenoma, Reproduction
organ tumors (e.g. testicular cancer, neuroendocrine
cervical carcinoma), Adrenal + renal tumors.

 
Fig.: PGA-II, DM-1 with Coelic with hyperpigmentation
596
PHEOCHROMOCYTOMA ƒƒ Adrenal diabetes is cortisol induced diabetes as seen in E
Cushing syndrome. N
ƒƒ Arises from paraganglionic cells of ANS in adrenal ƒƒ Bronze diabetes is seen in hemochromatosis.
medulla. D
ƒƒ NIFTY gene is related to type 2 DM.
ƒƒ M/c extraadrenal site is → paravertebral sympathetic O
ƒƒ IN DM HLA implicated is HLA DQ8, DR4,3,2.
ganglia in organ of Zuckerkandl (near aortic bifurcation) C
ƒƒ Impaired glucose tolerance is said when Fasting blood
ƒƒ IOC is MRI (for adrenal p~) R
sugar is normal and PP blood is 140-200 mg%
ƒƒ IOC for locally recurrent, metastatic, ectopic and I
ƒƒ Glycemic index :
extraadrenal p~ is MIBG scan (MIBG > MRI) N
White bread: 100
ƒƒ Rule of 10: 10% are extra-adrenal, 10% of sporadic O
White rice: 89
adrenal p~ are bilateral, 10% are malignant, 10% are not L
Milk, full cream: 41
a/w hypertension. O
ƒƒ Diabetes dyslipidemia consists of increase TGs & decrease
ƒƒ Loco-regional spread is seen. G
HDL.
ƒƒ Presenting symptoms include episodes of palpitations Y
+ headaches (MC symptom) + profuse sweating and Type-I Vs. Type-II Diabetes Mellitus
constitute a classic triad.
ƒƒ DOPA - PET has 100% sensitivity in diagnosing Features DM-I (IDDM/JOD) DM-II (NIDDM,

/e
pheochromocytoma. MODY)
ƒƒ Clonidine suppression test is done in pheochromocytoma. Occurrence 10-20% 80-90%

14
Dose of clonidine is 0.3 mg. Concordance in 50% 95%
ƒƒ Hormone secreted in pheochromocytoma: twins
NE (maxm), E, DA, VME (in urine).
Onset Early (juvenile Late onset (>40
ƒƒ Adrenal pheochromocytoma → Mainly epinephrine (Adr) onset) year) (maturity
is ↑ed. onset)
S,
ƒƒ Extra-adrenal pheochromocytoma → Mainly Nor Normal weight Yes No (Obese)
epinephrine (NE) is ↑ed.
HLA association Yes (HLA DR3, DR4) No
AM

Islet cell Yes No

antibodies,
15.8 DIABETES MELLITUS (DM) insulitis
ƒƒ Criteria for diagnosis of DM:- 4 options (Autoimmune
phenomena)
°° Diabetes symptoms (e.g. polyuria, polydipsia and
unexplained weight loss for Type 1) + Insulin sensitivity Yes No (insulin
O

(response) resistance +nt) [But

°° A random venous plasma glucose ≥ 11.1 mmol/l
respond to SU]
(200mg%) in individuals with symptoms of
hyperglycemia or hyperglycemic crisis or Frequent DKA Nonketotic
R

complication Hyperosmolar Coma

°° A fasting plasma glucose ≥ 7.0 mmol/l (126 mg%) or
whole blood ≥ 6.1 mmol/l) or Glucagon High, suppressible High, Not
°° A 2-hr PG ≥200 mg/dL (11.1 mmol/L) during OGTT suppressible
(75-g) using a glucose load containing the equivalent of Blood insulin ↓ Normal or ↑
75g anhydrous glucose dissolved in water. or
Pathophysiology Severe lack of Insufficient insulin
°° HbA1C ≥6.5% (48 mmol/mol) performed in a lab using insulin caused by secretion relative to
NGSP-certified method and standardized to DCCT reduction in B-cell glucose load.
assay mass
ƒƒ WHO 2011: An HbA1c of 48 mmol/mol (6.5%) is [Remember that most of the points in type-II DM are— no, non and
recommended as the cut point for diagnosing diabetes. not]
HbA1c reflects average plasma glucose over the prev
ious eight to 12 weeks ƒƒ MODY (Maturity onset diabetes of the young)
°° HbA1c <5.7 °° Refers to any of several hereditary forms of DM
caused by mutations in an AD gene disrupting insulin
°° HbA1c 5.7- 6.5 = Pre diabetes
production.
°° HbA1c > 6.5 = Diabetes
°° MODY-2 and MODY-3 are MC forms. 597
 E ƒƒ LADA (Latent Autoimmune diabetes of adults) ƒƒ There is overnight GH secretion (predwan surge of GH
N °° Refers to a form of type 1 DM, with slower progression in IDDM) and increased insulin clearance and, hence the
D to insulin dependence than child-onset type 1 DM night dose of insulin has to be ↑ed.
O °° Occurs later in life.
Complications in DM
C High-yield Points
R ƒƒ Complications of DKA: cerebral edema (most dangerous),
I 44 Type-I DM, malnutrition related DM and pregnancy related DM venous thrombosis, ARDS, MI, acute gastric dilatation, .
N is associated with HLA. ƒƒ Life threatening infections a/w DM are ---Rhinocerebral
44 Adrenal diabetes is cortisol induced diabetes as seen in Cushing mucormycosis, emphysematous pyelonephritis. malignant
O
syndrome. otitis externa.
L 44 Bronze diabetes term is used for hemochromatosis.
O ƒƒ Silent MI may occur.
G ƒƒ Most common cause of peripheral neuropathy → DM
Y Malnutrition related DM (MRDM) ƒƒ Most common neuropathy in diabetes → DSPN
ƒƒ Most common cause of small fibre neuropathy - idiopathic/
ƒƒ M/c type of diabetes in India a/w PEM (Kwashiorkor).In
if known cause then DM.
tropical countries onset < 30 yr
ƒƒ Bruns-Garland syndrome is seen in → diabetes amyotrophy
ƒƒ hallmark is non dependence on exogenous insulin to

/e
also known as diabetes radiculoplexus neuropathy.
prevent ketosis.
ƒƒ Ketosis is absent because of subnormal β-cell function and
Microvascular complications in DM are
absence of hyperglucagonemia

14
ƒƒ a/w environmental toxin cassava (tapioca), fibrocalceous ƒƒ Diabetic nephropathy
pancreatic diabetes ƒƒ Diabetic retinopathy (NPDR/PDR, macular edema)
ƒƒ Protein deficiency is responsible for CBH intolerance in ƒƒ Diabetic neuropathy (Sensory, autonomic)
Kwashiorkor and also fasting normo-or hypoglycemia is
Macrovascular complications in DM are
S,
present in Kwashiorkor.
ƒƒ CAD (Coronary artery d/s)
Honeymoon phase ƒƒ CVD (Cerebrovascular d/s)
ƒƒ PAD (Peripheral vascular d/s)
AM

ƒƒ When insulin requirement is decreased to < 50%. This is

f/b overt diabetes. D/to residual β-cell function. ƒƒ Complications which may be reversed with t/t in DM are
early diabetic nephropathy (microalbuminuria stage) and
Somogyi phenomenon diabetic neuropathy.
ƒƒ Complications which may not be reversed with t/t in DM
ƒƒ Refers to wide swings in insulin levels (hypoglycemia
are early diabetic retinopathy and peripheral vascular d/s.
O

begetting hyperglycemia). Rebound nocturnal

hypoglycemia with sweating, headache is followed by
Diabetic Nephropathy
early morning hyperglycemia d/to release of counter
R

regulatory hormones. Usually seen in patient given excess ƒƒ Microalbuminuria is the most sensitive for early diagnosis
insulin. of diabetic nephropathy.
ƒƒ If suspected, insulin dose adjustment is required (dose ƒƒ Urine microalbumin to creatinine ratio (MAU: UCr) is
should be ↓ ed). important for early diagnosis.
ƒƒ M/c renal lesion in DM is diffuse glomerulosclerosis but
Dawn phenomena nodular glomerulosclerosis with Kimmeisteil Wilson
wire lesions are most pathognomonic.
ƒƒ Is early morning hyperglycemia (5-9 a.m.) without a
ƒƒ Renal amyloidosis may develop.
preceding nocturnal hypoglycemia d/to exhaustion of
ƒƒ Glycosylated Hb reflects the mean blood glucose level of
biologically available insulin. Both midnight and early
previous 3 months.
morning RBS is high.
[Mn: Don does not have hypoglycemia]
Diabetic Neuropathy
ƒƒ Hypoglycemia unawareness may occur.
ƒƒ Glove and stockings type of peripheral neuropathy.
ƒƒ ANS dysfunction.
598
ƒƒ M/c form of diabetic neuropathy is distal symmetric Factors Affecting Insulin Requirement E
sensorimotor polyneuropathy (DSPN). ƒƒ Insulin sensitivity is ↑ed with progress of renal N
ƒƒ Mononeuropathy is less common. Involvement of 3rd CN insufficiency. As a rule, insulin requirement declines in D
(oculomotor) nerve is m/c and is heralded by diplopia. cases with renal failure, exercise. O
Ptosis + diplopia + ophthalmoplegia with pupillary sparing. ƒƒ Insulin requirement is ↑ed in high calorie intake, C
hyperadrenalism (d/to high EpiN, NE, glucocorticoid), R
Skin manifestations of DM Drugs (Diazoxide, thiazide, phenytoin propanolol), I
ƒƒ Necrobiosis lipoidica diabeticorum: Front of leg Somatostatin, K+ depletion. N
ƒƒ Acanthosis nigricans: Nape area ƒƒ Insulin stimulators (which ↓e the requirement) are amino O
Diabetic dyslipidemia acids, Drugs (theophylline, Sulfonylureas, β-agonist), L
ƒƒ M/c pattern of diabetic dyslipidemia is ↑TGs and ↓HDL. Intestinal hormones (GIP, gastrin, secretin, CCK), Ach, O
cAMP etc. G
T/t Goals for adults with diabetes Y
High-yield Points
Index Goal
44 In animals with experimental diabetes, adrenalectomy markedly
Glycemic control HbA1C < 7.0%
ameliorates the diabetes.

/e
PreP Glucose 70-130 mg% 44 If a patient with hyperglycemia is given insulin, it results in →
PostP Glucose <180 mg% Hypokalemia.
BP <130/80 mm Hg

14
ƒƒ Bariatric Sx should be considered in individuals with
Lipids LDL < 100 mg/dL type2 DM and BMI >35kg/m2.
HDL >40 mg/dL (for men),
>50 mg/dL (for women)
TGs <150 mg/dL
S,
ƒƒ Overdose of insulin is managed by → oral glucose
supplementation.
AM

INSULIN CHART
Rapid Acting Short-Acting Intermediate Long Acting
Acting
Type of Insulin, Insulin Insulin lispro Insulin Insulin Insulin IV Isophane Insulin glargine Insululin
Brands available glulisine (HumALOG) aspart injection (regular insulin insulin (Lantus) detemir
O

(NovOLOG) S/c only) suspension (Levemir)

(Novolin R. (Novolin NPH,
Humulin R Humulin N)
RU.
R

500, Hurn
ULIN R)

Onset < 15 < 15 min 10-20 min 30 min - 1 h 10-30 min 1-2 h 3-4 h 3-4 h
min

Peak effect 1h 1-1.5 h 1-3 h 2-4 h 15-30 min 4-12 h Plateau/ Peakless

Duration (h) 2-4 h 6-8 h 3-5 h 5-7 h 30 min - 1 h 18-24 h 24 h 24 h

Appearance Clear Clear Clear Clear Clear Cloudy Clear Clear

Compatibility NPH NPH NPH NPH Regular, Hum None

ALOG, Novo LG, (Can't be mixed with other
Apidra Insulins)

Remark ƒƒ Take immediately before eating / ƒƒ Take 30 minutes prior to Given 1-2 time ƒƒ Once daily
meals. Timing of meal should match eating. per day ƒƒ Injection site pain becoz of
peak effect of insulin. ƒƒ Regular (concentrated) insulin s/q collection.
ƒƒ Best mimics the body's release of U-500 should not be given
pre-meal insulin when given at right
time.
ƒƒ Hypoglycemia is less likely
599
ƒƒ Overdose of insulin is managed by → oral glucose supplementation.
 E Newer Drugs
High-yield Points
N ƒƒ DPA IV inhibitor: Vidagliptin, Sidagliptin
D ƒƒ Glucagon like peptides (GLP): Exenatide, Liraglutide 44 Androgen receptor is encoded by the gene located on → Xq
(Long arm of X-chromosome).
O ƒƒ Amylin anologue: Premalinitide.
44 Penis at 12 syndrome is seen in → Congenital 5 a reductase
C ƒƒ Therapy which can results in β cell preservation: Incretins.
deficiency.
R ƒƒ Inhaled insulin: Afrezza
I ƒƒ Oral sodium glucose cotransporter type 2 (SGCT II)
N inhibitors: Dapagliflozin, Canagliflozins,Empagliflozins. Inhibin
O ƒƒ Mainly produced by Sertoli cells in males. In females it is
L Important negative points: DM produced by granulosa cells of graaffian follicles of ovary
O ŽŽ Uncontrolled hypertension is NOT a/w increased risk of during follicular phase.
G → DM. ƒƒ Strong inhibitor of FSH secretion, hence called inhibin.
Y ŽŽ Insulin resistance is not seen in → Addison's disease ƒƒ Non steroidal water soluble protein. ↑ed in PCOD.
ŽŽ NOT true of DM → Patient with type 2 DM never requires
insulin Testosterone
ŽŽ NOT a test for DM → D- xylose ƒƒ Testosterone is synthesized from interstitial cells of

/e
ŽŽ Dextroamphetamine is NOT useful in diabetic neuropathy. Leydig under influence of LH.
ŽŽ Fasting hypoglycemia is NOT seen in → glucagon excess. ƒƒ Testosterone in male embryo is synthesized from hCG.
ƒƒ Cholesterol is staring material for its synthesis.

14
ƒƒ C-terminal end of androgen receptor is concern with ligand
binding.
15.9 MALE SEX HORMONES ƒƒ Rate limiting enzyme in testosterone biosynthesis is
→ Cholesterol desmolase (which catalyze cholesterol
S,
pregnenolone).
ANDROGENS ƒƒ Testosterone is converted into more active form DHT
ƒƒ The male sex hormones are collectively k/as androgens. (dihydrotestosterone) in extra-glandular tissue with the
help of enzyme 5a-reductase.
AM

ƒƒ The most abundant of these hormones is testosterone and

it is therefore considered as the major male sex hormone.
Hormones involved in spermatogenesis:-
ƒƒ They are secreted by testes in males and adrenal glands in
males and females. 1. Testosterone → principal hormone in spermatogenesis.
ƒƒ Types:- 2. LH → stimulate release of testosterone from Leydig
cells.
O

Hormone Secreted from Remark

3. FSH → stimulate release of ABP (androgen binding
Testosterone Interstitial cells Most abundant protein) from Sertoli (tubular) cells and promotes
R

of Leydig in spermatogenesis.
testes 4. GnRH → ↑se LH and FSH.
DHT Testes Most active form 5. ABPs.
(Dihydro testosterone) of androgens
Androstenedione Testes, adrenal MIS
cortex and a
ƒƒ Also k/as Mullerian inhibiting substance or Mullerian
small amount by
the ovaries regression factor.
ƒƒ Secreted by Sertoli cells in males and by granulosa cells of
Dehydroepi- ZR of adrenal 17-ketosteroid,
androsterone (DHEA) cortex Major adrenal ovary in females.
androgen ƒƒ Probably role in germs cell maturation (in both males and
ƒƒ Weak androgens: DHEA (dehydroepiandrosterone) and females) and in testicular descent (in male).
androstenidione. These are produced in small quantity ƒƒ New marker of ovarian reserve.
from adrenal cortex.
ƒƒ Androgen receptor is encoded by AR gene located on long
Anti-Mullerian hormone (AMH)
arm of X-chromosome. ƒƒ AMH, a dimeric glycoprotein and member of the TGFb
600 (transforming growth factor-beta) family, is produced by
 ovarian follicular granulosa cells in late pre-antral and ƒƒ Estrogen synthesis from endometrial stromal cells is E
small antral follicles. upregulated by: aromatase
N
ƒƒ Role in folliculogenesis at the two extremes of this ƒƒ M/c cause of ambiguous genitalia in female is →
D
process: (a) by restricting the progression of development Congenital adrenal hyperplasia (CAH).
O
of primordial follicles; and (b) by an inhibition of the
C
sensitivity of antral follicles to FSH and inhibition of N Important negative points: Hormones
R
aromatase activity during an ovulatory cycle. ŽŽ Hormone NOT decreased in sectioning of pituitary stalk I
→ Prolactin.
N
Relaxin ŽŽ Pituitary gland does NOT have sodium iodine symporter
O
ƒƒ Secreted in females by Corpus luteum of ovary and ŽŽ NOT an effect of hyperaldosteronism → Metabolic
L
placenta acidosis and High Na+ in plasma.
O
ƒƒ Relaxes pubic symphysis during labour (augments labour). ŽŽ NOT produced by ovary → Gonadotropins.
G
ƒƒ Structural similarity with insulin and IGF. ŽŽ NOT acts through cAMP → NO (Nitric oxide).
Y
ŽŽ Hyperkalemia is NOT a feature of glucocorticoid
High-yield Points deficiency.
44 Estrogen is mainly responsible for → skeletal maturation. ŽŽ NOT involved in calcium homeostasis → lungs and spleen.

/e
44 Insulin receptor has 4 parts → 2 a (outside cells) and 2 b(inside ŽŽ Weight loss is NOT seen in Insulinoma.
cells). ŽŽ Weight gain is NOT seen in → Pheochromocytoma and
44 Fetus starts insulin production at → 5 months of IUL. during 1st week of IV hyperalimentation.

14
S,
AM
O
R

601
 Exam Oriented Prototype IBQs (Including PGMEE 2016-17 IBQs)
E
N 1. A 16 year old boy with 88 kg weight presents 3. A patient inward deviation of hand at wrist joint
D with pathology depicted in the image. Most likely with tightening while physician started taking his
O diagnosis is ? BP. Most likely cause for this condition is ?
C
R
I
N
O
L
O
G
Y

/e
a. Urticaria a. Hyperparathyroidism
b. Acanthosis nigricans b. Hyperthyroidism
c. Contact dermatitis c. Hypocalcemia

14
d. Eczema herpetiformis d. Hypercalcemia

2. Clinical condition shown in the photograph is most

likely due to ?
S,
AM
O

Ans.
1. b
2. b
R

3. c

a. Deficiency of Iron
b. Deficiency of Iodine
c. Hypofunctioning thyroid
d. Auto antibodies against thyroid tissue

602