Path: Pituitary

01 Pathology of the Pituitary

02 Pathology of the Pituitary

- Panhypopituitarism: all pituitary hormones drop

ANTERIOR PITUITARY GLAND

- Pituitary Adenoma
○ Non-functional Pituitary Adenoma: presents as mass
▪ Temporal hemianopia, hypopituitarism, headache
○ Functional Pituitary Adenoma: hormonal effects
▪ "hyper-pituitarism"
- Hypopituitarism

Pituitary Adenomas
- Gsα protein mutation
- MEN1 mutation (tumor suppression)
- Soft, well-circumscribed; may push out from sella turcica
- Cellular monomorphism in sheets, cords without reticulin network
- Pituitary carcinoma: rare (<1%), functional

Prolactinoma Somatotroph Adenoma Corticotroph Adenoma Gonadotroph (LH, FSH) Adenoma

- Most common pituitary adenoma - Second most common - ↑ ACTH = hypercortisolism - ↓ libido in men
- Galactorrhea - ↑ GH = ↑ IGF 1 - Cushing Disease: ant pit makes too - Amenorrhea in women
- Amenorrhea - Anabolic effects much ACTH
• Prolactin inhibits GnRH - Gigantism: kids - Nelson Syndrome
• ↓ FSH/LH = ↓ E in ovaries • Epiphyseal plate open, bone • Cushing syndrome - tumor in
- Loss of libido grows in length adrenal glands make too much
• ↓ LH = ↓ T cortisol
- Infertility - Acromegaly: adults • Remove adrenal glands
• Epiphyseal plate closed, bone • Develop large pit adenomas
- Treat with bromocriptine grows in thickness • Basophils make POMC
• DA agonist = PIF • Enlarged facial features ○ POMC cleaves into ACTH
- Hyperglycemia, diabetes mellitus and MSH
- Hypertension ○ MSH → melanin
• = hyperpigmentation

Hypopituitarism
- ↓ pituitary hormones
- Primary hypopituitarism: pituitary dysfunction, caused by
○ Sheehan Syndrome: post-partum necrosis of anterior pituitary
▪ Anterior pituitary enlarges during pregnancy but no increase in vascularization
▪ ↓ blood supply by obstetric hemorrhage, shock → infarct
▪ Loss of prolactin = can't breastfeed
○ Craniopharyngioma
▪ From remnants of Rathke's pouch (oral ectoderm)
▪ Adamantinomas Craniopharyngioma - kids
□ Most common cause of hypopituitarism in children
□ Cords embedded in spongy reticulum
□ Palisading (left)
□ Wet keratin: compact, lamellar keratin formation (right)
□ Cysts contain cholesterol-rich, thick brown machine oil
▪ Papillary Craniopharyngioma - adults
▪ May cause central diabetes insipidus
○ Pituitary Apoplexy: sudden hemorrhage into pituitary gland
○ Empty Sella Syndrome: condition that destroys pituitary gland
- Secondary hypopituitarism: hypothalamic dysfunction

Deficient Prolactin Deficient GH Deficient ACTH Deficient FSH, LH Deficient of TSH

- Can't lactate after - Hypoglycemia in adults - Adrenal insufficiency - Delayed puberty - Secondary hypothyroidism
delivery - Pituitary dwarfism: Child growth - Secondary amenorrhea • ↓ T4, TSH

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delivery - Pituitary dwarfism: Child growth - Secondary amenorrhea • ↓ T4, TSH
delay - Male impotence - Cold intolerance, constipation,
• Normal body proportions weakness
• Normal IQ - If give TRF, TSH will NOT
• (Achondroplasia dwarf are increase
disproportionate)
- Laron Syndrome dwarfism
• Mutate GH receptor
• Low IGF

POSTERIOR PITUITARY GLAND

ADH
- Actions:
○ ↑ H2O permeability via aquaporin 2 and V2 collecting duct = [pee]
○ Constrict vascular smooth muscle (V1)
- Factors stimulate ADH secretion:
○ ↑ blood osmolarity, ↓ blood volume
- Factors inhibit ADH secretion
○ ↓ blood osmolarity, ↑ blood volume
○ Ethanol
- Diabetes Insipidus: ADH deficiency = polyuria, polydipsia
- Water deprivation test: don't drink water, urine should concentrate

Central Diabetes Insipidus Nephrogenic Diabetes Insipidus SIADH

Description - ADH deficiency - Kidney resistant to ADH - Too much ADH secretion
Etiology - Hypothalamic, posterior pit pathology - Chronic lithium use (bipolar) - Ectopic production: Small cell carcinoma of lung
• Tumor, trauma, infection - Demeclocycline - CNS disorders, head trauma
- Hypercalcemia - Pulmonary disease
- Hereditary (ADH receptor mutation) - Drugs: cyclophosphamide
Lab - ↓ ADH - Normal, ↑ ADH - ↑ ADH
- High Na - High Na - Low Na
- Osmolality serum > urine - Osmolality serum > urine - Osmolality serum > urine
Notes - Loss of free water: Polyuria, polydipsia, - Loss of free water: Polyuria, polydipsia, - Keep free water
dehydration dehydration - Concentrated pee
- Can't produce concentrated pee - Can't produce concentrated pee - Body responds to water retention with ↓
• Fail water deprivation test • Fail water deprivation test aldosterone, ↑ ANP, BNP
- No response to desmopressin ○ ↑ Na secretion = normal ECF volume =
euvolemic hyponatremia
○ (no edema)
- Low Na levels = mental status change, seizures
○ Neuronal swelling, cerebral edema
Treatment - Desmopressin - HCTZ - Fluid restriction
- Demeclocycline

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Path: Thyroid
May 21, 2018 11:33 AM

03 Pathology of the Thyroid

04 Pathology of the Thyroid

TSH Levels
- Total serum T4 = T4 bound to TBG + floating T4
- Radioactive 123I: thyroid uptakes for T4 synthesis

Graves Patient on Primary Secondary

Excess Hormone Hypothyroidism Hypothyroidism
Serum TSH low low
Inactive gland: large follicles, flat 123I Uptake high low high low
lining, big colloid
Serum T4 high high low low
Free T4 high high low Low

- Euthryoid Sick Syndrome: T3, T4 levels abnormal but gland function is normal
○ Associated with malignancy, heart failure, anorexia, renal failure, sepsis

Active gland: large lining

CONGENITAL ANOMOLIES
- Thyroglossal Duct Cyst: remnant in anterior neck mass, moves with swallowing
- Lingual Thyroid: thyroid no descend from base of tongue

HYPOTHYROIDISM
Cretinism Myxedema Common Symptoms of Hypothyroidism
- Underdrive
- ↓ metabolic rate
- Positive nitrogen balance
- Overweight
- ↓ heat = cold intolerance
- Bradycardia
- Hypoventilation
- Lethargy, mental slowness, delayed DTR
Description - Hypothyroidism in infants - Hypothyroidism in children, adults - Droopy eyelids
- Mental retardation, short stature, coarse facial - Myxedema: accumulation of GAGs in skin, soft tissue
features, macroglossia, umbilical hernia ○ Deep voice, large tongue
Caused by - Maternal hypothyroidism - Iodine deficiency ○ "puffy"
- Thyroid agenesis - Hashimoto thyroiditis - Goiter
- Dyshormonogenetic goiter: congenital defect
in thyroid hormone production

HYPERTHYROIDISM
- Thyrotoxicosis: "toxic" = has effects
○ ↑ circulating thyroid hormone
○ = ↑ synthesis of NaK ATPase = ↑ basal metabolic rate
○ = ↑ β 1 receptors = ↑ sympathetic nervous system
○ Body goes into overdrive
- Factitious hyperthyroidism: high thyroid hormone levels from taking too much thyroid hormone medicine
- Struma Ovarri: teratoma in ovary with thyroid tissue; RAI uptake in pelvis

Graves Disease Diffuse, Simple Goiter Multinodular Goiter

Descript - Auto-antibody stimulates TSH receptor - Enlarged thyroid without nodules - Enlarged thyroid with multiple nodules
ion • Type II hypersensitivity - Due to iodine deficiency
• No I = no thyroid hormones
• Feedback = ↑ TSH to thyroid
• Thyroid can only make thyroglobulin
• = enlarged thyroid, goiter
Present - Hyperthyroidism, diffuse goiter - Size ≠ functional status - Size ≠ functional status
- Exophthalmos, pretibial myxedema • May be hypo, hyper (toxic), • May be hypo, hyper (toxic), euthyroid
• Auto-antibodies bind to TSH euthyroid
receptors on fibroblasts behind eye, - Cabbage diet

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 receptors on fibroblasts behind eye, - Cabbage diet
shin - Pemberton sign: raise hands over head
• GAG build up to compressed jugular vein = neck
- Thyroid Storm: fatal complication congestion, face turns red
• High catecholamines, hormones due
to stress
• Arrhythmia, hyperthermia, vomiting,
shock
Morph - Irregular follicles with scalloped colloid + - Colloid rich follicles with flat, inactive epithelium
chronic inflammation - No capsule! (differentiate from neoplasm)

THYROIDITIS
Hashimoto Subacute Lymphocytic Painless Thyroiditis Granulomatous De Quervain Thyroiditis Riedel Fibrosing Thyroiditis

Descript - Auto immune destroy thyroid gland - Postpartum thyroiditis - Granulomatous thyroiditis after virus - Chronic inflammation with
ion • Anti-microsomal, antiglobulin antibodies infection fibrosis thyroid gland
• Associated with HLA-DR5, Pernicious - IgG4 related systemic disease
Anemia
Present - Painless enlarged thyroid with hypothyroidism, - Painless - Tender, painful thyroid - Hypothyroidism
yellowish color middle-age woman - Transient hyperthyroidism - Hard, non-tender thyroid gland
- Transient hyperthyroidism, then hypothyroidism - Young patient
• Damage follicles thyroid hormones leak out - May extend to local structures
→ transient hyperthyroidism
• Negative feedback
- ↑ risk marginal zone B-cell lymphoma
Morph - Plasma, lymphocytes + germinal centers Multinucleate giant cells enclose naked
- Hurthle cells: thyroid oncocytes, eosinophilic pools/fragments of colloid
cells that line follicles

NEOPLASMS
- May be hyper or hypothyroid
Follicular Adenoma Papillary Carcinoma Follicular Carcinoma Medullary Carcinoma Anaplastic Carcinoma

Descript - Benign proliferation of follicles - Papillae, Psammoma bodies - Malignant proliferation of follicles - Malignant proliferation of parafollicular C cells - Undifferentiated malignant
ion surrounded by fibrous capsule - Orphan Annie Eye and nuclear groove surrounded by fibrous capsule + • Secrete calcitonin: ↑ renal calcium tumor of thyroid
invasion excretion = ↓ serum Ca - Large, pleomorphic giant cells
• = Hypocalcaemia
- Amyloids: Ca deposits in tumor
Epidem - Most common - Older patients - MEN 2A, 2B Elderly
- Exposure to ionizing radiation in - Iodine deficiency • mutated RET oncogene
childhood • MEN 2A: medullary carcinoma,
- Mutate RET, BRAF pheochromocytoma, hyperparathyroidism
• MEN 2B: medullary carcinoma,
pheochromocytoma, mucosal neuromas,
paragangliomas in GIT
Present - Cold adenoma: clinically silent - Spreads to cervical LN - FNA cannot differentiate from - Invades local structures →
- Hot adenoma: functional - Slow growing follicular adenoma dysphagia, respiratory
- Toxic adenoma: hyperthyroidism - Good prognosis - Spreads hematogenous problems
- Poor prognosis

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Path: Parathyroid
May 28, 2018 9:13 AM

05 Pathology of the Parathyroid

- PTH ↑ Ca
• Bone: stimulate osteoclasts = ↑ Ca, P
• Kidney DCT: ↑ Ca reabsorption , ↓ P
• Kidney: ↑ Vit D activation

Primary Hyperparathyroidism Secondary Hyperparathyroidism Tertiary Hyperparathyroidism Hypoparathyroidism Pseudo hypoparathyroidism

Descripti - Parathyroid makes too much PTH - ↑ PTH in response to low Ca - High PTH despite - Low PTH levels - Multihormone resistance
on • Vit D deficiency hypercalcemia corrected
• ↓ Ca intake (renal transplant)
• Chronic renal failure
Caused - Parathyroid Adenoma - Chronic renal disease - Surgery - End-organ resist PTH
by • MEN1 mutate • No excrete P = ↑ blood P - Autoimmune • Kidney doesn't respond
• Right, inferior gland • P bind to free Ca = ↓ Ca - Autosomal dominant to PTH
- Parathyroid hyperplasia • Parathyroid detects - Familial isolated • = hypocalcaemia
• MEN1 hypocalcaemia, compensates hypoparathyroidism FIH - Autosomal dominant disease
• Asymmetric - Di George Syndrome • Defect Gs α-unit
- Parathyroid Carcinoma - Hypomagnesia • Inherit from mom,
imprint
Presentat - "painful bones, renal stones, abdominal - Diffuse bone disease - Tetany, neuromuscular - Short 4th, 5th metacarpals,
ion groans, psychic moans" - Metastatic calcification excitability metatarsals
- Osteoporosis • ↓ serum Ca = nerve • Knuckle, knuckle,
- Brown tumor: Bone loss leads to excitability dimple, dimple
microfractures, secondary hemorrhages - Chvostek's sign: tap side of - Short stature
→ fibrous tissue face, get facial muscle spasm - Skeletal abnormalities
- Osteitis Fibrosa Cystica, Von - Trousseau's sign: block
Recklinghausen Disease brachial artery with BP cuff =
• ↑ osteoclast activity erosion + carpopedal spasm
cystic brown tumors - Circumoral numbness
- Kidney Ca stones, renal calculi
- Metastatic calcification in many tissues
- Short QT interval
Lab - ↑ PTH - ↑ PTH - ↑ ↑ PTH - ↓ PTH - Normal, high PTH
- High Ca - Normal, low calcium - Normal, high Ca - Low Ca - Low Ca
- Low P - High P - High P - High P
- ↑ urinary cAMP
- ↑ alkaline phosphatase

- Most common cause of hypercalcemia is malignancy

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Path: Adrenal Gland
May 21, 2018 11:34 AM

06 Pathology of the Adrenal

07 Pathology of the Adrenal

- Aldosterone: Na reabsorption, K+ and H+ excretion

- Cortisol: mobilize energy stores, anti-inflammatory, vasoconstriction
- Androgens:

HYPOADRENALISM
- Adrenal glands don't make enough glucocorticoids ± mineralocorticoids
- Weakness, fatigue, orthostatic HTN, muscle ache, GI, sugar/salt craving
- Metyrapone stimulation test
○ Metyrapone: blocks last step of cortisol synthesis (11-deoxycortisol → cortisol)
○ Normal response: ↓ cortisol
▪ Compensatory ↑ ACTH, ↑ 11-deoxycortisol

Primary Acute Primary Chronic Secondary

Adrenal Crisis Addison Disease
Description - Weakness and shock - Progressive destruction of adrenal - Hypothalamic, pituitary disorder
- Caused by cortex - ALL Zones doesn't secrete enough ACTH
• Abrupt withdrawal of - Caused by
glucocorticoids • Autoimmune adrenalitis
• Treatment of Cushing Syndrome • TB Granulomatous adrenalitis (if
• Waterhouse Friedrich endemic area)
Syndrome: Neisseria Meningitis • Metastatic carcinoma of lungs
→ sepsis → DIC, hemorrhagic ○ Bilateral adrenal mass
adrenal glands
Presentation - Purpuric rash - Skin + mucosal hyperpigmentation - NO pigmentation
• POMC → ACTH, MSH - Normal aldosterone levels
- High K+
- Low Na+
- HTN
Metyrapone - ↑ ACTH - ↑ ACTH - ↓ ACTH
Test - ↓ 11-deoxycortisol - ↓ 11-deoxycortisol - ↓ 11-deoxycortisol

HYPERADRENALISM
Hyperaldosteronism Hypercortisolism Congenital Adrenal Hyperplasia
Conn Syndrome Cushing's Syndrome Androgenital Syndrome
Description - Excess aldosterone - Excess cortisol - Enzyme defect in glucocorticoid, mineralocorticoid
- Primary: ○ Exogenous cortisol: ↓ ACTH, bilateral adrenal and androgen production
• Bilateral adrenal hyperplasia atrophy - ↓ aldosterone, cortisol, androgen biosynthesis =
• Conn Syndrome: adrenocortical neoplasm ○ Primary adrenal neoplasm: ↓ ACTH, atrophy of compensatory ↑ ACTH = hyperplasia + steroid
- Secondary: due to ↑ renin via activated renin- uninvolved gland buildup
angiotensin system ○ Pituitary Adenoma secrete ACTH: Cushing
• Patient with renovascular HTN Disease - 21 hydroxylase deficiency
• JXG active tumors ○ Paraneoplastic ACTH: - 11 hydroxylase deficiency
○ Small-cell carcinoma of lung - 17 hydroxylase deficiency
Presentation - ↑ aldosterone - Moon face, buffalo hump, truncal obesity - High ACTH levels negative feedback = bilateral
- Hypokalemia: excrete K+ • High blood glucose = high insulin adrenal hyperplasia
• Tired, weak, nocturia • Hyperglycemia - CAH 21: no aldosterone, no cortisol
- Metabolic alkalosis (↑ pH, ↑ HCO3-) - Loss of collagen → weak skin, abdominal striae • = salt wasting adrenogenitalsim
- HTN (↓ renin, angiotensin II) - HTN with hypokalemia, metabolic alkalosis • Females - virilization
• Left ventricle hypertrophy • ↑ α1 receptors, vasoconstrict • Males - salt losing crisis
- Normal, high Na: Na reabsorb - Muscle weakness - CAH 11: no aldosterone, no cortisol
• Sodium Escape: No sodium • Cortisol break down muscle to release amino • ↑ DOC = HTN
retention/edema due to compensatory acids for gluconeogenesis • ↑ androgen = androgen effects
changes to restore Na+ excretion - Amenorrhea - CAH 17: no cortisol, no androgen
○ ↑ arterial pressure - Osteoporosis • ↑ aldosterone = HTN
○ ↑ ANP - Immune suppression • No sex development
○ ↓ angiotensin II

Hypercortisolism - Cushing's Syndrome

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 Exogenous Cortisol Primary adrenal Cushing Disease Paraneoplastic ACTH Tumor
neoplasia Pituitary Adenoma Small Cell Lung Carcinoma
Cortisol ↑ ↑ ↑ ↑
ACTH ↓ ↓ ↑ ↑
Dexamethasone NA N/A Suppress No respond
test - ACTH level
Notes Bilateral adrenal Mass in kidney Mass in brain
atrophy

- Dexamethasone: cortisol analog

○ When administer, negative feedback to ant pit = ↓ ACTH
○ Pituitary adenoma should stop releasing ACTH
○ Ectopic ACTH won't respond

Congenital Adrenal Hyperplasia

21 hydroxylase defect 11 hydroxylase defect 17 hydroxylase defect
Descriptio - No aldosterone - No aldosterone - ↑ aldosterone
n - No cortisol - No cortisol - No cortisol
- ↑ androgen - ↑ androgen - No androgen
- ↑ DOC = weak
mineralocorticoid
Presentati - Salt-wasting - HTN - HTN
on adrenogenitalsim - Mild hypokalemia - Mild hypokalemia
- Hyponatremia - Low renin, aldosterone - Low renin, aldosterone
- Hyperkalemia - Clitoral enlargement in - Primary amenorrhea
- Life-threatening HTN females - No pubic hair
- Genital ambiguity - Undescended testes in
males

TUMORS
- Associated with
○ Li-Fraumeni syndrome
○ Beckwith-Wiedemann syndrome (epigenetic imprinting)
- Adrenocortical Adenoma: silent, but functional have atrophy
○ Well-defined
○ Yellow, homogenous appearance
- Adrenocortical Carcinoma: functional

ADRENAL MEDULLA
Pheochromocytoma Neuroblastoma

Description - Tumor of chromaffin cell (neural crest) - Tumor of sympathetic ganglia and adrenal medulla
• secrete E, NE, DA - Common tumor in kids
- Episodic hyperadrenergic HTN - Abdominal distention, firm irregular mass that crosses midline
• Pressure, pain, perspiration, - Less-likely to develop HTN
palpitations - Present with opsoclonus-myoclonus syndrome
• Sense of apprehension • "dancing eyes, dancing feet"
- Rule of 10
• 10% malignant
• 10% bilateral (more if familial)
• 10% extra-adrenal
• 10% calcify
• 10% kids

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 • 10% kids
Morph - Zellballen appearance: nests of chromaffin - Homer-Wright rosettes
cells around sustentacular cells
Mutate - NF1, VHL - N-MYC
- RET - MEN 2A, 2B

Multiple Endocrine Neoplasia Syndrome

- Autosomal dominant
- MEN 1: chromosome 11

MEN Type 1 MEN Type 2A Type 2B

Wermer Syndrome Sipple Sydrome
Tumors - Pituitary tumor - Parathyroid hyperplasia - Pheochromocytoma
- Pancreatic tumor - Pheochromocytoma - Medullary thyroid cancer
- Parathyroid adenoma - Medullary thyroid carcinoma - Mucosal neuromas
Genes MEN 1 RET RET
Presenta - Pituitary tumor: - Parathyroid: - Pheochromocytoma: hyper E, NE
tion • Prolactinoma → galactorrhea • PTH hypercalcemia → - Medullary carcinoma of thyroid: calcitonin
- Pancreatic tumor: kidney stones - Marfanoid Habitus
• Insulinoma → recurrent - Pheochromocytoma: hyper E, NE - Mucosal neuroma:
hypoglycemia - Medullary carcinoma of thyroid:
• Zollinger-Ellison: peptic ulcers calcitonin
- Parathyroid adenoma
• PTH induced hypercalcemia
stones

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Path: Diabetes Mellitis
May 21, 2018 11:35 AM

08 Pathology of Diabetes Mellitus

DIABETES
- Metabolic Syndrome: characterized by hyperinsulinemia, obesity, fasting glucose >110 mg/DL
○ Associated with PCOS, acanthosis nigricans
- Mature Onset Diabetes of Young MODY: mutated glucokinase gene
- Latent Autoimmune Diabetes of Young
- Gestational Diabetes: pregnant women develop impaired glucose tolerance
○ Glucose cross placenta
○ Fetal liver makes extra insulin
• Macrosomia: hyperglycemia in fetus = insulin stores fat in adipose tissue, amino acid in muscle
• Respiratory Distress Syndrome: insulin inhibit fetal surfactant production
• Risk neural tube defect
• Neonatal hypoglycemia

Type 1: Insulin Dependent Type 2: Insulin Independent

Descriptio - Auto-immune: T cells destroy β cell - Peripheral resistance to insulin leading to metabolic
n • HLA D43, HLA-DR4 disorder characterized by hyperglycemia
• Inflamed islet cells • Genetics, obesity, sedentary lifestyle
- No insulin levels • Obesity leads to less insulin receptors
- Normal, high insulin levels
Morph - Islet leukocyte infiltrate - Islet amyloid polypeptide IAPP deposits (pink)
Presentati - Polyuria, polydipsia, glycosuria - Polyuria, polydipsia, hyperglycemia
on - Weight loss, low muscle mass, polyphagia - Acanthosis nigricans: brown velvety patch in skin folds
• Unopposed gluconeogenesis,
glycogenolysis, lipolysis
Complicat - Ketoacidosis - Hyperosmolar coma: hyperglycemia-induced
ions • No insulin = high glucagon dehydration and ↑ serum osmolality
○ Enhanced by stress, E • Elderly diabetics, limited ability to drink
• High lipolysis = high FA in plasma • Hyperglycemia leads to excessive osmotic diuresis
• Liver absorbs FA → Acetyl CoA → dehydration, coma
• Acetyl CoA → ketogenesis,
ketoacidosis, coma
Treatmen - Insulin - Exercise
t - Metformin, sulfonylureas

Long-Term Complications of Diabetes

- Advanced Glycosylation End products (AGE): non-enzymatic glycosylation of vascular basement membranes
○ Microvascular: small vessels
• Retinopathy, glaucoma
• Nephropathy
□ Microalbuminuria
□ Nodular glomerulosclerosis: renal arterioles
□ Kimmelstiel-Wilson nodules in glomeruli
○ Macrovascular: large vessels
• Atherosclerosis → Cardiovascular disease, stroke
• Hyaline arteriosclerosis Kimmelstiel-Wilson nodules in
• Peripheral vascular disease → neuropathy → amputations kidney glomerulus
- Osmotic damage
○ Enter Schwann cells → peripheral neuropathy
○ Sorbitol in eye → cataracts, blindness
- Necrobiosis lipoidica diabeticorum: skin lesion
- Charcot arthropathy: neuropathic joint lack sensation, repeated trauma deform joints

NEOPLASIA - Pancreatic Neuroendocrine Tumors

Insulinoma Glucagonoma Somatostatinoma Zollinger-Ellison Syndrome VIPoma

Descript - Tumor of β cell - Tumor of α cell - Tumor of δ cells - Gastrin-secreting tumor - - Verner Morrison, Pancreatic cholera
ion - MEN1 - ↓ secretion of secretin, gastrinoma - VIP:
cholecystokinin, glucagon, insulin, • Pancreas • ↑ intestinal water and electrolyte
gastrin, gastric inhibitory protein • Duodenum secretion

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 gastrin, gastric inhibitory protein • Duodenum secretion
- MEN1 • relax intestinal smooth muscle and
sphincters

Present - Whipple Triad - Necrolytic migratory erythema - Diabetes, glucose intolerance - Acid hypersecretion = peptic - WDHA
ation • Hypoglycemia - Weight loss - Steatorrhea ulcers - Watery diarrhea
• CNS dysfunction - Diabetes (hyperglycemia) - Gallstones - Diarrhea - Hypokalemia
(diplopia, syncope) - Depression - Achlorhydria - Achlorhydria
• Reversible with glucose - DVT
administration
Notes - Secretin test:
• Secretin normally inhibit gastric
release

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