9 Endo

Front 1

Question

Back 1

Answer

Front 2

50-year-old man complains of diarrhea. On physical exam, his face is plethoric and a heart murmur is detected.

Back 2

Carcinoid syndrome.

Front 3

Woman of short stature presents with shortened 4th and 5th metacarpals.

Back 3

Albright’s hereditary osteodystrophy, or pseudohypoparathyroidism.

Front 4

Surreptitious insulin injection.

Back 4

Nondiabetic patient presents with hypoglycemia but low levels of C peptide.

Front 5

Patient's MRI shows filling of sella tursica with cerebrospinal fluid. What is the most likely clinical presentation?

Back 5

Normal. Residual pituitary tissue is functional and can compensate (empty sella syndrome).

Front 6

empty sella syndrome

Back 6

sella tursica with cerebrospina fluid. Residual pituitary tissue is functional and can compensate

Front 7

Adrenal cortex and medulla derivation

Back 7

Cortex (from mesoderm) Medulla (from neural crest)

Front 8

what controls the adrenal medulla

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Preganglionic sympathetic fibers

Front 9

cell type in the adrenal medulla

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Chromaffin cells

Front 10

where are Chromaffin cells

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adrenal medulla

Front 11

Adrenal gland drainage

Back 11

Left adrenal → left adrenal vein → left renal vein → IVC. Right adrenal → right adrenal vein → IVC.

Front 12

Posterior pituitary aka

Back 12

neurohypophysis

Front 13

neurohypophysis aka

Back 13

Posterior pituitary

Front 14

Posterior pituitary products

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vasopressin and oxytocin, made in the hypothalamus and shipped to pituitary.

Front 15

Anterior pituitary products

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FLAT GiMP: FSH LH ACTH TSH GH MSH (melanotropin) Prolactin

Front 16

pituitary derivation

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Posterior pituitary (neurohypophysis) → Derived from neuroectoderm. Anterior pituitary (adenohypophysis) → Derived from oral ectoderm.

Front 17

Anterior pituitary aka

Back 17

adenohypophysis

Front 18

adenohypophysis aka

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Anterior pituitary

Front 19

staining of ant pit hormones cells

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Acidophils––GH, prolactin. B-Flat: Basophils––FSH, LH, ACTH, TSH

Front 20

Pituitary gland and different subunits of hormones

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α subunit––common subunit to TSH, LH, FSH, and hCG. β subunit––determines hormone specificity.

Front 21

Pro-opiomelanocortin

Back 21

POMC can be cleaved enzymatically into the following peptides: # adrenocorticotropic hormone (ACTH) and β-Lipotropin in the anterior pituitary gland α-MSH and β-endorphin in the intermediate lobe

Front 22

50-year-old man complains of diarrhea. On physical exam, his face is plethoric and a heart murmur is detected.

Back 22

Carcinoid syndrome.

Front 23

Woman of short stature presents with shortened 4th and 5th metacarpals.

Back 23

Albright’s hereditary osteodystrophy, or pseudohypoparathyroidism.

Front 24

Surreptitious insulin injection.

Back 24

Nondiabetic patient presents with hypoglycemia but low levels of C peptide.

Front 25

Patient's MRI shows filling of sella tursica with cerebrospinal fluid. What is the most likely clinical presentation?

Back 25

Normal. Residual pituitary tissue is functional and can compensate (empty sella syndrome).

Front 26

empty sella syndrome

Back 26

sella tursica with cerebrospina fluid. Residual pituitary tissue is functional and can compensate

Front 27

Adrenal cortex and medulla derivation

Back 27

Cortex (from mesoderm) Medulla (from neural crest)

Front 28

what controls the adrenal medulla

Back 28

Preganglionic sympathetic fibers

Front 29

cell type in the adrenal medulla

Back 29

Chromaffin cells

Front 30

where are Chromaffin cells

Back 30

adrenal medulla

Front 31

Adrenal gland drainage

Back 31

Left adrenal → left adrenal vein → left renal vein → IVC. Right adrenal → right adrenal vein → IVC.

Front 32

Posterior pituitary aka

Back 32

neurohypophysis

Front 33

neurohypophysis aka

Back 33

Posterior pituitary

Front 34

Posterior pituitary products

Back 34

vasopressin and oxytocin, made in the hypothalamus and shipped to pituitary.

Front 35

Anterior pituitary products

Back 35

FLAT GiMP: FSH LH ACTH TSH GH MSH (melanotropin) Prolactin

Front 36

pituitary derivation

Back 36

Posterior pituitary (neurohypophysis) → Derived from neuroectoderm. Anterior pituitary (adenohypophysis) → Derived from oral ectoderm.

Front 37

Anterior pituitary aka

Back 37

adenohypophysis

Front 38

adenohypophysis aka

Back 38

Anterior pituitary

Front 39

staining of ant pit hormones cells

Back 39

Acidophils––GH, prolactin. B-Flat: Basophils––FSH, LH, ACTH, TSH

Front 40

Pituitary gland and different subunits of hormones

Back 40

α subunit––common subunit to TSH, LH, FSH, and hCG. β subunit––determines hormone specificity.

Front 41

Pro-opiomelanocortin

Back 41

POMC can be cleaved enzymatically into the following peptides: # adrenocorticotropic hormone (ACTH) and β-Lipotropin in the anterior pituitary gland α-MSH and β-endorphin in the intermediate lobe

Front 42

Endocrine pancreas cell types and products and locations

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α = glucagon (peripheral); β = insulin (central); δ = somatostatin (interspersed).

Front 43

Endocrine pancreas where are the most δ endocrine cells

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in tail of pancreas

Front 44

Islets arise from

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pancreatic buds.

Front 45

regulation of Prolactin and implications

Back 45

Prolactin ↑ dopamine synthesis and secretion from the hypothalamus. Dopamine subsequently inhibits prolactin secretion. Dopamine agonists (e.g., bromocriptine therefore inhibit prolactin secretion, whereas dopamine antagonists (e.g., most antipsychotics) stimulate prolactin secretion.

Front 46

Prolactin effects in females

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prolactin inhibits GnRH synthesis and release, which inhibits ovulation. Amenorrhea is commonly seen in prolactinomas.

Front 47

Hypothalamic-pituitary hormone regulation from hypo and what they do

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TRH—→ ↑ TSH, prolactin Dopamine— → ↓ prolactin CRH— → ↑ ACTH GHRH—→ ↑ GH Somatostatin— → ↓ GH, TSH GnRH— → ↑ FSH, LH

Front 48

Congenital bilateral adrenal hyperplasias 17
α-hydroxylase deficiency labs

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↓ sex hormones, ↓ cortisol, ↑ mineralocorticoids.

Front 49

Congenital bilateral adrenal hyperplasias 21 β-hydroxylase deficiency labs

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↓ cortisol (increased ACTH), ↓ mineralocorticoids, ↑ sex hormones.

Front 50

Congenital bilateral adrenal hyperplasias 21 β-hydroxylase deficiency clinial

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Cx = masculinization, female pseudohermaphroditism, HYPOtension, hyponatremia, hyperkalemia, ↑ plasma renin activity, and volume depletion. Salt wasting can lead to hypovolemic shock in the newborn.

Front 51

Congenital bilateral adrenal hyperplasias 17
α-hydroxylase deficiency clinical

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Cx = HYPERtension, hypokalemia; phenotypically female but no maturation.

Front 52

Congenital bilateral adrenal hyperplasias 11 β-hydroxylase deficiency labs

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↓ cortisol, ↓ aldosterone and corticosterone, ↑ sex hormones.

Front 53

Congenital bilateral adrenal hyperplasias 11 β-hydroxylase deficiency clinical

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Cx = masculinization, HYPERtension (11-deoxycorticosterone acts as a weak mineralocorticoid).

Front 54

Congenital bilateral adrenal hyperplasias Most common form

Back 54

21 β-hydroxylase deficiency

Front 55

masculinization, female pseudohermaphroditism, HYPOtension, hyponatremia,

hyperkalemia, ↑ plasma renin activity, and volume depletion. Salt wasting can lead to hypovolemic shock in the newborn.

Back 55

21 β-hydroxylase deficiency

Front 56

PTH Source

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Chief cells of parathyroid.

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PTH Functions

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1. ↑ bone resorption of calcium and phosphate 2. ↑ kidney reabsorption of calcium in dct 3. ↓ kidney reabsorption of phosphate 4. ↑ 1,25-(OH)2 vitamin D (cholecalciferol) production by stimulating kidney 1 -hydroxylase

Front 58

PTH Regulation

Back 58

↓ in free serum Ca2+ ↑ PTH secretion.

Front 59

PTH effect on ions

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PTH ↑ serum Ca2+, ↓ serum (PO )3–, ↑ urine (PO )3–.

Front 60

PTH effect on bones

Back 60

PTH stimulates both osteoclasts and osteoblasts.

Front 61

If you do not get vitamin D, you get

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rickets (kids) or osteomalacia (adults).

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24,25-(OH)2 vitamin D is

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an inactive form of vitamin D.

Front 63

Vitamin D Source/process

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Vitamin D3 from sun exposure in skin. D2 from plants. Both converted to 25-OH vitamin D in liver and to 1,25-(OH)2 vitamin D (active form) in kidney.

Front 64

Vitamin D Function

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1. ↑ absorption of dietary calcium 2. ↑ absorption of dietary phosphate 3. ↑ bone resorption of Ca2+ and (PO4)3–

Front 65

Vitamin D Regulation

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--↑ PTH causes ↑ 1,25-(OH)2 production. --↓ [Ca2+] causes ↑ 1,25-(OH)2 production. --↓ phosphate causes ↑ 1,25-(OH)2 produced --1,25-(OH)2 vitamin D feedback inhibits its own production.

Front 66

-Calcium -phosphate, -alkaline phosphatase levels Hyperparathyroidism

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↑ ↓ ↑

Front 67

-Calcium -phosphate, -alkaline phosphatase levels Paget’s disease of bone

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N/↑ N ↑↑↑

Front 68

-Calcium -phosphate, -alkaline phosphatase levels Vitamin D intoxication

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↑ ↑ N/↑

Front 69

-Calcium -phosphate, -alkaline phosphatase levels Osteoporosis

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N N N

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-Calcium -phosphate, -alkaline phosphatase levels Renal insufficiency

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↓ ↑ N

Front 71

Calcitonin Source

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Parafollicular cells (C cells) of thyroid.

Front 72

Calcitonin Function

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↓ bone resorption of calcium. Calcitonin opposes actions of PTH. It is probably not important in normal calcium homeostasis.

Front 73

Calcitonin Regulation

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↑ serum Ca causes calcitonin secretion.

Front 74

Steroid/thyroid hormones names

Back 74

PET CAT: Progesterone Estrogen Testosterone Cortisol Aldosterone Thyroxine and T3

Front 75

effects of changing levels of SHBG

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↑ levels of sex hormone–binding globulin (SHBG) lower free testosterone → gynecomastia. ↓ SHBG raises free testosterone → hirsutism.

Front 76

Steroid hormones circulation and mech

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Steroid hormones are lipophilic and relatively insoluble in plasma; therefore, they must circulatebound to specific binding globulins, which ↑ solubility and allows for ↑ delivery of steroid to the target organ

Front 77

Thyroid hormones Source

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Follicles of thyroid. Most T formed in blood.

Front 78

Thyroid hormones Function

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T3 functions––4 B’s: Brain maturation Bone growth Beta-adrenergic effects BMR ↑

Front 79

Thyroid hormones Regulation

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TRH (hypothalamus) stimulates TSH (pituitary), which stimulates follicular cells. Negative feedback by T3 to anterior pituitary ↓ sensitivity to TRH.

Front 80

Thyroxine-binding globulin role

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(TBG) binds most T3/T4 in blood;

Front 81

Thyroxine-binding globulin wrt activity

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Thyroxine-binding globulin (TBG) binds most T3/T4 in blood; only free hormone is active.

Front 82

things that affect Thyroxine-binding globulin

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↑ TBG in pregnancy OCP or hormone replacement ↓ TBG in hepatic failure, steroids or nephrotic syndrome

Front 83

TSI

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TSI, like TSH, stimulates follicular cells (Graves’ disease).

Front 84

Insulin-dependent organs and mech

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Skeletal muscle and adipose tissue depend on insulin for ↑ glucose uptake (GLUT-4).

Front 85

Insulin-independent organs and mech

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Brain and RBCs take up glucose independent of insulin levels (GLUT-1).

Front 86

Cortisol Source

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Adrenal fasciculata

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Cortisol Functions

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1. Anti-inflammatory 2. ↑ gluconeogenesis, lipolysis, proteolysis 3. ↓ immune function 4. Maintains blood pressure 5. ↓ bone formation

Front 88

Cortisol Regulation

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CRH (hypothalamus) stimulates ACTH release (pituitary) causing cortisol production in adrenal fasciculata.

Front 89

Cortisol wrt prolonged secretion

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Chronic stress induces prolonged secretion.

Front 90

Cortisol binding

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Bound to corticosteroid binding globulin (CBG).

Front 91

Cushing’s syndrome

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↑ cortisol due to a variety of causes.

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Cushing’s disease

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(1° pituitary adenoma); ↑ ACTH

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(1° pituitary adenoma); ↑ ACTH

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Cushing’s disease

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↑ cortisol due to a variety of causes.

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Cushing’s syndrome

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causes of Cushing’s syndrome

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1. Cushing’s disease (1° pituitary adenoma); ↑ ACTH 2. 1° adrenal (hyperplasia/neoplasia); ↓ ACTH (see Color Image 68) 3. Ectopic ACTH production (e.g., small cell lung cancer); ↑ ACTH 4. Iatrogenic (e.g., chronic steroids); ↓ ACTH

Front 96

Cushing’s syndrome clinical findings

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The clinical picture includes hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning, striae), osteoporosis, amenorrhea, and immune suppression

Front 97

Dexamethasone suppression test:

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Healthy––↓ cortisol after low dose. pituitary ACTH-producing tumor ↑ cortisol after low dose; ↓ cortisol after high dose. scc of lung and or Cortisone -producing tumor––↑ cortisol after low and high dose.

Front 98

Cushing’s syndrome test

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Dexamethasone suppression test:

Front 99

Hyperaldosteronism types

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Primary (Conn’s syndrome) Secondary

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Conn’s syndrome aka

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Primary Hyperaldosteronism

Front 101

Conn’s syndrome cause and effects

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Caused by an aldosterone secreting tumor, resulting in hypertension, hypokalemia, metabolic alkalosis, and low plasma renin.

Front 102

Conn’s syndrome Tx

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Treatment includes spironolactone, a K+-sparing diuretic that works by acting as an aldosterone antagonist.

Front 103

Secondary Hyperaldosteronism causes and effects

Back 103

Due to renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome. Kidney perception of low intravascular volume results in an overactive renin-angiotensin system. Therefore it is associated with high plasma renin.

Front 104

Hyperaldosteronism which type has high renin

Back 104

Secondary

Front 105

Addison’s disease what is it

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1° deficiency of aldosterone and cortisol due to adrenal atroph

Front 106

Addison’s disease clinical findings

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hypotension (hyponatremic volume contraction) and skin hyperpigmentation -Characterized by Adrenal Atrophy and Absence of hormone production; -involves All 3 cortical divisions.

Front 107

Addison’s disease vs secondary

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Distinguish from 2° insufficiency, which has no skin hyperpigmentation (↓ pituitary ACTH production).

Front 108

mech of hyperpigmentation in Addison's

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due to MSH, a by-product of ↑ ACTH production from POMC

Front 109

Addison’s disease what type of hypotension

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hyponatremic volume contraction

Front 110

The most common tumor of the adrenal medulla in adults.

Back 110

Pheochromocytoma

Front 111

The most common tumor of the adrenal medulla in children

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Neuroblastoma

Front 112

Neuroblastoma how common and where

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The most common tumor of the adrenal medulla in children, but it can occur anywhere along the sympathetic chain.

Front 113

Pheochromocytomas may be associated with

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neurofibromatosis, MEN types II and III.

Front 114

Pheochromocytoma vs Neuroblastoma wrt urine

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Pheochromocytoma --VMA in urine. Neuroblastoma --HVA in urine

Front 115

VMA in urine.

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Pheochromocytoma

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HVA in urine

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Neuroblastoma

Front 117

Pheochromocytoma clinical findings

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EPISODIC hyperadrenergic symptoms (5 P’s + anxiety): Pressure (elevated blood pressure) Pain (headache) Perspiration (tachycardia) Palpitations Pallor

Front 118

Neuroblastoma clinical findings

Back 118

often vague and may include fatigue, loss of appetite, and fever Less likely to develop hypertension.

Front 119

Pheochromocytoma derivation

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Derived from chromaffin cells (arise from neural crest)

Front 120

Postpartum hypopituitarism aka

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Sheehan's syndrome

Front 121

Sheehan's syndrome aka

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Postpartum hypopituitarism

Front 122

Sheehan's syndrome mech

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infarction of the pituitary gland following severe bleeding and hypoperfusion during delivery.

Front 123

Sheehan's syndrome clinical findings

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May cause fatigue, anorexia, poor lactation, and loss of pubic and axillary hair.

Front 124

Pheochromocytoma Tx

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α-antagonists, especially phenoxybenzamine, a nonselective, irreversible α-blocker.

Front 125

Pheochromocytoma mnemonic

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Rule of 10’s: 10% malignant 10% bilateral 10% extra-adrenal 10% calcify 10% kids 10% familial

Front 126

Pheochromocytoma Most of these tumors secrete

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Most of these tumors secrete epinephrine, NE, and dopamine.

Front 127

Pheochromocytoma lab findings

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Urinary VMA levels and plasma catecholamines are elevated.

Front 128

MEN type I aka

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Wermer’s syndrome

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Wermer’s syndrome aka

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MEN type I aka

Front 130

MEN type II aka

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Sipple’s syndrome

Front 131

Sipple’s syndrome aka

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MEN type II

Front 132

MEN type III aka

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formerly MEN IIb

Front 133

formerly MEN IIb

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MEN type III

Front 134

Multiple endocrine neoplasias (MEN) inheritance

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All MEN syndromes have autosomal-dominant inheritance.

Front 135

Multiple endocrine neoplasias (MEN) specific gene

Back 135

Associated with ret gene in MEN types II and III.

Front 136

MEN type I involvement

Back 136

MEN I = 3 “P” organs (Pancreas, Pituitary, and Parathyroid). (e.g., Zollinger-Ellison syndrome, insulinomas, VIPomas), parathyroid tumors, pituitary tumors (prolactinoma).

Front 137

MEN type I classic presentation

Back 137

Presents with kidney stones and stomach ulcers.

Front 138

(e.g., Zollinger-Ellison syndrome, insulinomas, VIPomas), parathyroid, and pituitary tumors (prolactinoma).

Back 138

MEN type I (Wermer’s syndrome)

Front 139

MEN type II involvement

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medullary carcinoma of the thyroid, pheochromocytoma, parathyroid tumor.

Front 140

medullary carcinoma of the thyroid, pheochromocytoma, parathyroid tumor.

Back 140

MEN type II (Sipple’s syndrome)

Front 141

MEN type III involvement

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MEN type III medullary carcinoma of the thyroid, pheochromocytoma, and oral and intestinal ganglioneuromatosis (mucosal neuromas).

Front 142

Hypothyroidism findings

Back 142

Cold intolerance, hypoactivity, weight gain, fatigue, lethargy, ↓ appetite, constipation, weakness, ↓ reflexes, myxedema (facial/periorbital), dry, cool skin, and coarse, brittle hair.

Front 143

Hyperthyroidism findings

Back 143

Heat intolerance, hyperactivity, weight loss, chest pain/palpitations, arrhythmias, diarrhea, ↑ reflexes, warm, moist skin, and fine hair.

Front 144

Riedel’s thyroiditis

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thyroid replaced by fibrous tissue (hypothyroid).

Front 145

thyroid replaced by fibrous tissue (hypothyroid).

Back 145

Riedel’s thyroiditis

Front 146

Graves’ disease findings

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Hyperthyroid Ophthalmopathy (proptosis, EOM swelling), pretibial myxedema, diffuse goiter.

Front 147

Thyroid storm findings

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Underlying Graves' disease with a stress-induced catecholamine surge leading to death by arrhythmia.

Front 148

Underlying Graves' disease with a stress-induced catecholamine surge leading to death by arrhythmia.

Back 148

Thyroid storm

Front 149

Graves’ disease Often presents during

Back 149

stress (e.g., childbirth)

Front 150

Hashimoto’s thyroiditis

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Autoimmune disorder resulting in hypothyroidism (can have thyrotoxicosis during follicular rupture).

Front 151

Autoimmune disorder resulting in hypothyroidism (can have thyrotoxicosis during follicular rupture).

Back 151

Hashimoto’s thyroiditis

Front 152

Hashimoto’s thyroiditis course and findings

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Slow course; moderately enlarged, nontender thyroid.

Front 153

Hashimoto’s thyroiditis lab findings

Back 153

Lymphocytic infiltrate with germinal centers. Antimicrosomal and antithyroglobulin antibodies. Hurthle cells.

Front 154

Lymphocytic infiltrate with germinal centers. Antimicrosomal Ab's

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Hashimoto’s thyroiditis

Front 155

Hurthle cells.

Back 155

Hashimoto’s thyroiditis

Front 156

Subacute thyroiditis aka

Back 156

de Quervain’s)

Front 157

de Quervain’s aka

Back 157

Subacute thyroiditis

Front 158

Subacute thyroiditis (de Quervain’s) description

Back 158

Self-limited hypothyroidism often following a flulike illness. May be hyperthyroid early in course.

Front 159

Self-limited hypothyroidism often following a flulike illness

Back 159

Subacute thyroiditis (de Quervain’s)

Front 160

Subacute thyroiditis (de Quervain’s) labs

Back 160

Elevated ESR

Front 161

Subacute thyroiditis (de Quervain’s) clinical findings

Back 161

hypothyroidism jaw pain, early inflammation, and very tender thyroid gland.

Front 162

Toxic multinodular goiter mechanism

Back 162

Iodine deprivation followed by iodine restoration. Causes release of T3 and T4.

Front 163

Toxic multinodular goiter wrt cancer

Back 163

Nodules are not malignant.

Front 164

Iodine deprivation followed by iodine restoration. Causes release of T3 and T4.

Back 164

Toxic multinodular goiter

Front 165

Jod-Basedow phenomenon

Back 165

thyrotoxicosis if a patient with endemic goiter moves to iodine-replete area.

Front 166

thyrotoxicosis if a patient with endemic goiter moves to iodine-replete area.

Back 166

Jod-Basedow phenomenon

Front 167

Wolff-Chaikoff effect

Back 167

hypothyroidism caused by ingestion of a large amount of iodine.[1]

Front 168

hypothyroidism caused by ingestion of a large amount of iodine

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Wolff-Chaikoff effect

Front 169

Thyroid cancer most common

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Papillary carcinoma

Front 170

Thyroid cancer describe Papillary carcinoma

Back 170

most common, excellent prognosis, “ground-glass” nuclei Orphan Annie), psammoma bodies. Increased risk with childhood irradiation.

Front 171

Thyroid cancer Orphan Annie

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Papillary carcinoma

Front 172

Thyroid cancer psammoma bodies

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Papillary carcinoma

Front 173

Thyroid cancer Follicular carcinoma

Back 173

good prognosis, uniform follicles.

Front 174

Thyroid cancer good prognosis, uniform follicles.

Back 174

Follicular carcinoma

Front 175

Thyroid cancer Medullary carcinoma

Back 175

from parafollicular “C cells”; produces calcitonin, sheets of cells in amyloid stroma. MEN types II and III.

Front 176

Thyroid cancer from parafollicular “C cells”

Back 176

Medullary carcinoma

Front 177

Thyroid cancer produces calcitonin

Back 177

Medullary carcinoma

Front 178

Thyroid cancer sheets of cells in amyloid stroma

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Medullary carcinoma

Front 179

Thyroid cancer MEN types II and III.

Back 179

Medullary carcinoma

Front 180

Thyroid cancer Undifferentiated/anaplastic

Back 180

––older patients, very poor prognosis.

Front 181

Thyroid cancer older patients, very poor prognosis.

Back 181

Undifferentiated/anaplastic

Front 182

Thyroid cancer Lymphoma

Back 182

associated with Hashimoto's thyroiditis.

Front 183

Thyroid cancer associated with Hashimoto's thyroiditis.

Back 183

Lymphoma

Front 184

Cretinism endemic

Back 184

Endemic cretinism occurs wherever endemic goiter is prevalent (lack of dietary iodine)

Front 185

Cretinism sporadic

Back 185

defect in T4 formation or developmental failure in thyroid formation.

Front 186

Cretinism findings

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Findings: pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue.

Front 187

pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue.

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Cretinism

Front 188

Cretinism where still common

Back 188

china

Front 189

Acromegaly clinical and labfindings

Back 189

Excess GH in adults. Findings: large tongue with deep furrows, deep voice, large hands and feet, coarse facial features, impaired glucose tolerance (insulin resistance).

Front 190

↑ GH is normal in

Back 190

stress, exercise, and hypoglycemia.

Front 191

↑ GH in children → and Tx

Back 191

gigantism. Treat medically with octreotide.

Front 192

Acromegaly test

Back 192

Test with oral glucose tolerance test. GH levels not suppressed below 1 μg/L means acromegaly.

Front 193

Primary Hyperparathyroidism cause

Back 193

Usually an adenoma

Front 194

Primary Hyperparathyroidism clinical and lab findings

Back 194

“Stones, bones, and groans.” Hypercalcemia, hypercalciuria (renal stones), hypophosphatemia, ↑ PTH, ↑ cAMP in urine. Often asymptomatic, or may present with weakness and constipation (“groans”).

Front 195

secondary Hyperparathyroidism mech

Back 195

2° hyperplasia due to ↓ serum Ca2+, most often in chronic renal disease.

Front 196

secondary Hyperparathyroidism findings

Back 196

Renal osteodystrophy Hypocalcemia, hyperphosphatemia, ↑ PTH.

Front 197

Renal osteodystrophy

Back 197

bone lesions due to 2˚ hyperparathyroidism due in turn to renal disease.

Front 198

bone lesions due to 2˚ hyperparathyroidism due in turn to renal disease.

Back 198

Renal osteodystrophy

Front 199

Hypoparathyroidism causes

Back 199

Due to accidental surgical excision (thyroid surgery) or DiGeorge syndrome.

Front 200

Due to accidental surgical excision or DiGeorge syndrome.

Back 200

Hypoparathyroidism

Front 201

Hypoparathyroidism findings

Back 201

Hypocalcemia, tetany Chvostek’s sign– Trousseau sign of latent tetany-

Front 202

Chvostek’s sign

Back 202

tap facial nerve → contraction of facial muscles.

Front 203

tap facial nerve → contraction of facial muscles.

Back 203

Chvostek’s sign

Front 204

Trousseau’s sign (not of malignancy)

Back 204

––occlusion of brachial artery with BP cuff → carpal spasm.

Front 205

––occlusion of brachial artery with BP cuff → carpal spasm.

Back 205

The Trousseau sign of latent tetany

Front 206

The Trousseau sign (not of latent tetany)

Back 206

a medical sign found in certain cancers that is associated with hypercoagulability. esp specially adenocarcinomas of the pancreas and lung,

Front 207

sign found in certain cancers associated with hpercoagulability.

Back 207

Trousseau sign of malignancy

Front 208

Pseudohypoparathyroidism genetics, mech, lab, clinical

Back 208

autosomal-dominant kidney unresponsiveness to PTH. Hypocalcemia, shortened 4th/5th digits, short stature.

Front 209

Pseudohypoparathyroidism inheritance

Back 209

autosomal-dominant

Front 210

autosomal-dominant kidney unresponsiveness to PTH.

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Pseudohypoparathyroidism

Front 211

Hypocalcemia, shortened 4th/5th digits, short stature.

Back 211

Pseudohypoparathyroidism

Front 212

Hypercalcemia causes

Back 212

CHIMPANZEES. Calcium ingestion (milk-alkali syndrome),Hyperparathyroid/thyroid, Iatrogenic (thiazides), Multiple myeloma, Paget’s, Addison’s, Neoplasms, Zollinger-Ellison, Excess vitamin D, Excess vitamin A, Sarcoidosis.

Front 213

Pituitary adenoma most common type

Back 213

prolactinoma

Front 214

Pituitary adenoma most common type and findings

Back 214

prolactinoma ammenorrhea, galactorrhea, low libido, infertility.

Front 215

Pituitary adenoma Tx

Back 215

Bromocriptine (dopamine agonist) causes shrinkage.

Front 216

Bromocriptine (dopamine agonist) causes shrinkage.

Back 216

prolactinoma

Front 217

Diabetes mellitus Acute manifestations (8)

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Polydipsia, polyuria, polyphagia, weight loss, DKA (type 1), hyperosmolar coma (type 2), unopposed secretion of GH and epinephrine (exacerbating hyperglycemia).

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Diabetes mellitus chronic manifestations due to Nonenzymatic glycosylation:

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1. Small vessel disease (diffuse thickening of basement membrane) → retinopathy, glaucoma, nephropathy 2. Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease and gangrene, cerebrovascular disease

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Diabetes mellitus chronic manifestations due to Osmotic damage:

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1. Neuropathy (motor, sensory, and autonomic degeneration) 2. Cataracts (sorbitol accumulation)

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Tests for DM

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Fasting serum glucose, glucose tolerance test, HbA1c (measures long-term diabetic control).

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DM and HLA

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Type 1 (HLA-DR3 and 4)

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IDDM aka

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Type 1––juvenile onset

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Type 1––juvenile onset aka

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IDDM

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NIDDM aka

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Type 2––adult onset

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Type 1 vs. type 2 diabetes mellitus wrt Ketoacidosis

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Type 1––Common Type 2––Rare

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Type 1 vs. type 2 diabetes mellitus wrt β-cell numbers in the islets

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Type 1––↓ Type 2––Variable

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Type 1 vs. type 2 diabetes mellitus wrt Serum insulin level

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Type 1––↓ Type 2––Variable

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Type 1 vs. type 2 diabetes mellitus wrt Classic symptoms of polyuria, polydipsia, thirst, weight loss

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Type 1–– Common Type 2––Sometimes

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Type 1 vs. type 2 diabetes mellitus wrt 1° defect

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Type 1––Viral or immune destruction of β cells Type 2––↑ resistance to insulin

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Diabetic ketoacidosis mech

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Usually due to ↑ insulin requirements from an ↑ in stress (e.g., infection). Excess fat breakdown and ↑ ketogenesis from the ↑ in free fatty acids, which are then made into ketone bodies.

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Diabetic ketoacidosis Signs/symptoms

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Kussmaul respirations, hyperthermia, nausea/vomiting, abdominal pain, psychosis/dementia, dehydration. Fruity breath odor (due to exhaled acetone).

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Diabetic ketoacidosis Labs

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Hyperglycemia, ↑ H , ↓ HCO3 (anion gap metabolic acidosis), ↑ blood ketone levels, leukocytosis. Hyperkalemia, but depleted intracellular K+.

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Diabetic ketoacidosis Complications

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Life-threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythmias, heart failure.

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Diabetic ketoacidosis Treatment

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Fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia.

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Kussmaul respirations what and cause

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(rapid/deep breathing) The cause of Kussmaul breathing is respiratory compensation for a metabolic acidosis, most commonly occurring in diabetics in diabetic ketoacidosis.

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Diabetes insipidus clinical findings

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intensive thirst and polyuria together

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Diabetes insipidus Diagnosis

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Water deprivation test––urine osmolality doesn’t ↑.

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Diabetes insipidus lab Findings

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Urine specific gravity < 1.006; serum osmolality > 290 mOsm/L.

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Central Diabetes insipidus Treatment

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Adequate fluid intake. –intranasal desmopressin (ADH analog).

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Central Diabetes insipidus mech

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lack of ADH (pituitary tumor, trauma, surgery, histiocytosis X)

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Nephrogenic Diabetes insipidus mech

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lack of renal response to ADH (hereditary or 2° to hypercalcemia, lithium, demeclocycline)

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Nephrogenic Diabetes insipidus Tx

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fluid intake -hydrochlorothiazide, indomethacin, or amiloride.

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SIADH causes

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1. Ectopic ADH (small cell lung cancer) 2. CNS disorders/head trauma 3. Pulmonary disease 4. Drugs (e.g., cyclophosphamide)

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SIADH labs

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1. Excessive water retention 2. Hyponatremia 3. Urine osmolarity > serum osmolarity

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SIADH complications

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Very low serum sodium levels can lead to seizures (correct slowly).

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SIADH Tx

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Treat with demeclocycline or H2O restriction.

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Carcinoid syndrome causes

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carcinoid tumors especially metastatic small bowel tumors, which secrete high levels of serotonin (5-HT).

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Carcinoid syndrome wrt location and why

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Not seen if tumor is limited to GI tract (5-HT undergoes first-pass metabolism in liver).

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Carcinoid syndrome symptoms

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Results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease.

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Most common tumor of appendix.

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carcinoid tumors

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carcinoid tumor derivation

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neuroendocrine cells (usually of the GI tract)

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Carcinoid syndrome Dx

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↑ 5-HIAA in urine.

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↑ 5-HIAA in urine.

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Carcinoid syndrome

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Carcinoid syndrome Tx

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octreotide.

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carcinoid tumor mnemonic

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Rule of 1/3s: 1/3 metastasize 1/3 present with 2nd malignancy 1/3 multiple

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Zollinger-Ellison syndrome what, where, complications, associations

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Gastrin-secreting tumor of pancreas or duodenum. Causes recurrent ulcers. May be associated with MEN type I.

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Gastrin-secreting tumor of pancreas or duodenum

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Zollinger-Ellison syndrome

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Treatment strategy for type 1 DM–

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low-sugar diet, insulin replacement.

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Treatment strategy for type 2 DM

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dietary modification and exercise for weight loss; oral hypoglycemics.

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Sulfonylureas: Names

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-ide First generation: Tolbutamide Chlorpropamide Second generation: Glyburide Glimepiride Glipizide

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Sulfonylureas: Mech

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Close K+ channel in β-cell membrane, so cell depolarizes → triggering of insulin release via ↑ Ca2+ influx.

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Sulfonylureas: Clinical use

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Stimulate release of endogenous insulin in type 2 DM. useless in type 1

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Sulfonylureas: Toxicity

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First generation: disulfiram-like effects. Second generation: hypoglycemia.

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Close K+ channel in β-cell membrane, so cell depolarizes → triggering of insulin release via ↑ Ca2+ influx.

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Sulfonylureas:

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Insulin: names and time frames

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Lispro (short-acting) Insulin (short-acting) NPH (intermediate) Lente (long-acting) Ultralente (long-acting)

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Insulin: mech and action in different tissues

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Binds insulin receptor (tyrosine kinase activity). Liver: ↑ glucose stored as glycogen. Muscle: ↑ glycogen and protein synthesis, K+ uptake. Fat: aids TG storage.

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Insulin: Clinical Use

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Type 1 DM. uncontrolable type 2 Also life-threatening hyperkalemia and stress-induced hyperglycemia.

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Insulin: Toxicity

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Hypoglycemia, hypersensitivity reaction (very rare).

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Biguanides names

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Metformin

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Biguanides mech

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Exact mechanism is unknown. Possibly ↓gluconeogenesis, ↑ glycolysis, ↓ serum glucose levels.

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Biguanides clinical use

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type 1 and 2 Used as oral hypoglycemic. Can be used in patients without islet function.

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Biguanides Toxicity

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lactic acidosis.

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DM drugs lactic acidosis.

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Biguanides: (Metformin)

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Used as oral hypoglycemic. Can be used in patients without islet function.

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Biguanides: (Metformin)

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Glitazones names

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Pioglitazone Rosiglitazone

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Glitazones mech

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↑ target cell response to insulin.

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Glitazones clinical use

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monotherapy in type 2 DM or combined with other agents.

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Glitazones toxicity

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Weight gain, edema. Hepatotoxicity (troglitazone— no longer used).

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Weight gain, edema. Hepatotoxicity (troglitazone— no longer used).

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Glitazones

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α-glucosidase inhibitors: names

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Acarbose Miglitol

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α-glucosidase inhibitors: mech

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Inhibit intestinal brush border α-glucosidases. Delayed sugar hydrolysis and glucose absorption lead to ↓ postprandial hyperglycemia.

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α-glucosidase inhibitors: clinical use

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Used as monotherapy in type 2 DM in combination with other agents.

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α-glucosidase inhibitors: Toxicity

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GI disturbances.

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Inhibit intestinal brush border α-glucosidases. Delayed sugar hydrolysis and glucose absorption lead to ↓ postprandial hyperglycemia.

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α-glucosidase inhibitors: Acarbose Miglitol

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Orlistat Mechanism

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Alters fat metabolism by inhibiting pancreatic lipases.

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Orlistat Clinical use

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ong-term obesity management (in conjunction with modified diet).

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Orlistat Toxicity

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Steatorrhea, GI discomfort, reduced absorption of fat-soluble vitamins, headache.

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Sibutramine Mechanism

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Sympathomimetic serotonin and norepinephrine reuptake inhibitor.

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Sibutramine Clinical use

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Short-term and long-term obesity management.

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Sibutramine Toxicity

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Hypertension and tachycardia.

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Sympathomimetic serotonin and norepinephrine reuptake inhibitor. for weight loss

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Sibutramine

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Alters fat metabolism by inhibiting pancreatic lipases.

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Orlistat

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Propylthiouracil, methimazole Mechanism

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Inhibit organification and coupling of thyroid hormone synthesis. Propylthiouracil also ↓ peripheral conversion of T to T .

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Propylthiouracil, methimazole Clinical use

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Hyperthyroidism.

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Propylthiouracil, methimazole Toxicity

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Skin rash, agranulocytosis (rare), aplastic anemia.

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Inhibit organification and coupling of thyroid hormone synthesis. ???????also ↓ peripheral conversion of T to T .

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Propylthiouracil, methimazole Propylthiouracil

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GH Clinical use

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GH deficiency, Turner’s syndrome

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octreotide Clinical use

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Acromegaly, carcinoid, gastrinoma, glucagonoma

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Oxytocin Clinical use

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Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage

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desmopressin Clinical use

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Pituitary (central, not nephrogenic) DI

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octreotide aka

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Somatostatin

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Somatostatin drug

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octreotide

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ADH aka

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desmopressin

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desmopressin aka

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ADH

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Levothyroxine, triiodothyronine Mechanism

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Thyroxine replacement.

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Levothyroxine, triiodothyronine Clinical use

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Hypothyroidism, myxedema.

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Levothyroxine, triiodothyronine Toxicity

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Tachycardia, heat intolerance, tremors.

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myxedema describe it

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the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesional and normal skin

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the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesional and normal skin

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myxedema

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Glucocorticoids names

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Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone.

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Glucocorticoids Mechanism

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↓ the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2.

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Glucocorticoids Clinical use

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Addison’s disease, inflammation, immune suppression, asthma.