Endocrinology Flashcards

1
Q

What is the function of LH

A

Testis: Releases T
Ovary: Androgens and Progesterone

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2
Q

What is the function of FSH

A

Male: Sperm, MIF Inhibin B
Female: Estradiol (E2)

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3
Q

What is Central DI?

A

Brain doesn’t produce enough ADH

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4
Q

What is nephrogenic DI?

A

ADH receptor (Aqp V2) broken
Li and Demeclocycline

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5
Q

What does the water deprivation test tell you?

A

Failing to concentrate urine means pathology (not primary DI / drinking too much water)

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6
Q

What does DDAVP during the water deprivation test tell you?

A

More than 50% increase: Central complete DI
10-50%: Central partial DI
Less than 10%: psychogenic polydipsia
No change: Nephrogenic DI

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7
Q

What does ANP do?

A

Inhibits aldosterone
Dilates Afferent Arteriole

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8
Q

Presentation of Neuroblastoma

A

Dancing eyes and feet
Adrenal medulla tumor in kids that secretes catecholamines

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9
Q

Conn’s Syndrome

A

High Aldosterone from primary tumor
Captopril test makes it worse (increases secretin)

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10
Q

MEN 1

A

Parathyroid (Hyper-Ca++)
Pancreas (Z-E)
Pituitary (Prolactinoma)

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11
Q

MEN 2a

A

Parathyroid
Pheochromocytoma
Medullary Thyroid CA (RET)

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12
Q

MEN 2b

A

Pheochromocytoma
Medullary Thread CA (RET)
Mucosal Neuromas
Marfanoid body

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13
Q

What does CCK do?

A

Contracts gallbladder to release bile
Inhibits gastric motility
Made by I-Cells of Duodenum

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14
Q

What is Cushings?

A

High ACTH causing high cortisol
Primary pituitary tumor or Small Cell Lunch CA

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15
Q

What does a Low-Dose Dexamethasone test tell you?

A

Depresses ACTH and therefore cortisol? Not Pathology
No suppression? Cushing’s syndrome. Do High dose.

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16
Q

What does a High-Dose Dexamethasone test tell you?

A

Depresses ACTH and therefore cortisol? Pituitary (ACTH) Tumor / Cushing’s Disease
Still high cortisol but ACTH lowered? Adrenal Tumor secreting cortisol
Still high cortisol and ACTH high? Ectopic ACTH

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17
Q

What does Gastrin do?

A

Stimulates Parietal cells to release Intrinsic factor and H+

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18
Q

Achondroplasia

A

Abnormal FGF receptors in extremities (FGF3)

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19
Q

Pathology of “midgets”

A

Decreased Somatomedin receptor sensitivity

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20
Q

What does GIP do?

A

Gastric Inhibitory Peptide
Increases insulin action
Responsible for post-prandial hypoglycemia

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21
Q

Abs responsible for DM1

A

Anti-islet cell / GAD (Glutamic Acid Decarboxylase)

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22
Q

Dawn phenomenon

A

Morning hyperglycemia secondary to Growth hormone

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23
Q

Somogyi Effect

A

Morning hyperglycemia from evening hypoglycemia

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24
Q

Erythrasma

A

Rash in the skin folds, coral red under Wood’s lamp

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25
Q

What does Motilin do?

A

Stimulates segmentation, primary peristalsis, migrating motor complexes

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26
Q

What does PTH do?

A

Stimulates osteoblasts to activate osteoclasts
Stimulates reabsorption of Ca+ and exertion of phosphate from kidneys
Activates Vit D

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27
Q

What do stomach chief cells secrete?

A

Pepsin

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28
Q

Disease: Serum Ca+ and Serum PO4 are decreased

A

Vitamin D deficiency

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29
Q

Pseudo-Hypoparathyroidism

A

Bad kidney, PTH receptor, decreased urinary cAMP

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30
Q

Pseudo-Pseudo-Hypoparathyroidism

A

G-Protein defect, no calcium problem

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31
Q

Hungry bone syndrome

A

Removal of PTH causes bones to suck up calcium

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32
Q

What does secretin do?

A

Secretion of HCO3-
Inhibits Gastrin
Tightens Pyloric sphincter
Secreted by S-Cells of Duodenum

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33
Q

What does somatostatin do?

A

Inhibits secretin, motilin, CCK

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34
Q

Hyperthyroid diseases

A

Graves, DeQuervians, Silent, Plummer’s, Jod-Basedow

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35
Q

What do you see in Grave’s?

A

Exophthalmos, pre-tibial myxedema, anti-TSH Abs

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36
Q

DeQuervian’s disease

A

Viral origin, painful jaw, hypothyroid

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37
Q

Jod-Basedow

A

Transient hyperthyroidism from increased Iodine

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38
Q

Euthyroid Sick

A

Low T3, decreased conversion from T4
From decreased Deiodinase activity
Normally from acute or chronic conditions

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39
Q

Wolff-Chaikoff

A

Transient Hypothyroidism

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40
Q

Plummer’s Syndrome

A

Hyperthyroid Adenoma
+ Esophageal webs = Vinson

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41
Q

Sub-clinical thyroiditis

A

Decreased thyroid function
Increased TSH, NORMAL T4
Mild Sx like increased LDL

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42
Q

What does TPO and Thymosin do?

A

Helps T cells mature

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43
Q

What does VIP do?

A

Opens sphincters
Inhibits secretin, motilin, CCK

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44
Q

Hashimoto’s thyroiditis Ab

A

Anti-Microsomal and Anti-TPO

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45
Q

Indications for Insulin

A

DM, Hyperkalemia, Stress-induced hyperglycemia, gestational DM

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46
Q

Rapid acting insulins

A

Aspart, Lispro, Glulisine

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47
Q

Long-Acting insulins

A

Detemir, Glargine (also Ultralente, Zinc, Protamine)

48
Q

Sulfonylurea MOA

A

Closes K+Channels in b-Cells so K can’t get out making Ca+ come in. This depolarizes it for the release of more endogenous insulin

49
Q

First gen sulfonylureas

A

Chlorpropramide and Tolbutamide
AE: Disulfiram-like rxn

50
Q

Second gen sulfonylureas

A

Glyburide
Glimepiride
Glipizide

51
Q

MOA of Biguanides

A

Decreased Gluconeogenesis
Increased Glycolysis
Increased peripheral glucose uptake (insulin sensitivity)

52
Q

AE of biguanides

A

Lactic Acidosis (C/I in RF pts, stop when using contrast)

53
Q

MOA of Thiazolidinediones

A

PPAR-y increased, more insulin influx from more channels

54
Q

a-Glucosidase inhibitors

A

Inhibits it on intestinal brush border
Delays sugar hydrolysis and glucose absorption
Decreases post-prandial hyperglycemia
Acarbose and Miglitol

55
Q

KPP-4 Inhibitors

A

This is the enzyme that deactivates GLP-1, so therefore GLP-1 gets increased
-Gliptins

56
Q

Mimetics

A

Decreases glucagon
Pramlintide

57
Q

GLP-1 Analogs

A

-tides (exanetide, liraglutide)
WEIGHT LOSS, pancreatitis

58
Q

Octreotide

A

Somatostatin analogue
Decreases release of GH, Gastrin, CCK, Carcinoid, VIP, Glucagon, Insulin

59
Q

Indications for octreotide

A

Acromegaly, Carcinoid syndrome, glucagonoma, insulinoma

60
Q

Oxytocin

A

Induces labor
Controls Uterine hemorrhage

61
Q

Desmopressin

A

aka DDAVP aka ADH
Recruits water channels to luminal membrane in collecting duct
Anti-diuresis, Central (pituitary) DI

62
Q

PTU, Methimazole

A

Inhibits peroxidase enzyme in Thyroid and decreases thyroid hormone synthesis
Agranulocytosis

63
Q

Demeclocycline

A

ADH antagonist
Used for SIADH
AE: Nephrogenic DI, photosensitivity, bone abnormalities

64
Q

Cinacalcet

A

Sensitize Ca+ receptor in Parathyroid
Used for Primary hyperparathyroidism or RF

65
Q

Sevelamer

A

Phosphate binder: prevents PO4 absorption in gut
Used for CKD

66
Q

Steroids and the Cortisol pathway

A

Double negative: Inihibits cortisol’s inhibition on precursors
+CRH, +ACTH

67
Q

Cushing’s syndrome vs disease

A

Syndrome: many organs (primary Increased cortisol)
Disease: 1 organ (Increased ACTH)

68
Q

Labs of Cushing’s

A

Hyperglycemia
Hypokalemia
Glucosuria
Dexamethasone doesn’t suppress

69
Q

Treat Cushing’s

A

Hydrocortisone (replacement)
Ketoconazole (decreases cortisol synthesis)
Mitotane (tx adrenal CA)
Bisphosphonates
Surgery (Transsphenoidal resection of pit. adenoma)

70
Q

Bilateral Adrenalectomy

A

Causes Nelson’s: Cortisol withdrawal
HTN, DM

71
Q

Pheochromocytoma

A

Episodic ER visits for NE/Epi
Palpitations, HTN, diaphoresis, HA
Dx w/ Urinary VMA, metanephrines, Phentolamine
Tx w/ Phenoxybenzamine to stabilize until surgery

72
Q

Dancing feet, dancing eyes

A

Neuroblastoma
Like Pheo, Dx w/ urinary VMA, Metanephrines, Phentolamine
Tx w Phenoxybenzamine until surgery

73
Q

Dx Pheochromocytoma

A

VMA, metanephrines. Elevated? CT
CT(-)? MIGB Scitntigraphy with MRI

74
Q

What does Vit D do?

A

Produces Ca binding proteins
Produces CaATPase
Stimulates Osteoblasts (reduces serum Ca, good for bone)

75
Q

Paget’s Disease

A

Increased All Phos
Tx w/ Bisphosphonates (inhibit osteoclasts)

76
Q

Labs of Primary Hypo-Parathyroidism

A

Decreased PTH
Decreased Ca++
Increased PO4-

77
Q

Labs of Primary Hyper-parathyroidism

A

Increased PTH
Increased Ca++
Decreased PO4-

78
Q

Labs of Secondary Hyper-Parathyroidism

A

Renal Failure: Decreased Ca++, Increased PTH, PO4-
X 1a-Hydrox: Decreased Ca++, PO4-, Increased PTH

79
Q

Labs of Secondary Hypo-Parathyroidism

A

From increased Vitamin D
Increased Ca++ and PO4-
Decreased PO4-

80
Q

Causes of secondary, tertiary hyper-parathyroidism

A

Chronic RF
Renal osteodystrophy
MEN

81
Q

DEXA lab interpretation

A

Normal: Below 1
1-2.5: Osteopenia
2.5+: Oestoporosis

82
Q

Cinacalcet

A

Fake / decoy Ca, binds to and decreases PTH

83
Q

PTU, propranolol MOA

A

Inhibits 5’ deiodonase, the thing that converts T4 to T3

84
Q

DeQuervian (subacute) Thyroiditis

A

Viral, painful, Self-Limiting
Reassurance, propranolol, Ipodate sodium

85
Q

Anti-TPO Abs

A

Hashimoto

86
Q

TSH receptor antibodies

A

Grave’s

87
Q

Tx amiodarone-induced thyroiditis

A

Propranolol, methimazole, prednisone, ipodate

88
Q

Agranulocytosis

A

Methimazole, PTU
Clozapine, carbamazepine

89
Q

Cretinism

A

Maternal child cognitive impairment

90
Q

myxedema coma

A

Decompensated hypothyroidism
Give IV T3, Warm, O2, Abx

91
Q

Papillary thyroid cancer

A

Young people
Psammoma bodies, Orphan Annie eye nuclear inclusions

92
Q

Follicular Carcinoma

A

Old people
Mutations in RAS

93
Q

Medullary carcinoma

A

From the parafollicular cells (C cells) produce Calcitonin
Inhibited by GLP-1
RET mutation

94
Q

Anaplastic carcinoma

A

Old people
Lymphovascular invasion
Death within 1 year

95
Q

Radioactive iodine uptake

A

Graves is uniform
Vinson is heterogenous

96
Q

Nesidioblastosis

A

Infants w/ high insulin
tx w/ diazoxide

97
Q

Criteria for DM

A

Fasting over 126
2 hour test over 200
A1c over 6.5

98
Q

Somogyi

A

Too much PM insulin
Hyperglycemic AM, becomes hypoglycemic

99
Q

Waning (DAWN)

A

From too little insulin
Hyperglycemic AM, remains hyperglycemic

100
Q

Meglitinide analogs

A

Repaglinide, Mitiglinide
Block K+, like sulfonylureas

101
Q

Theca Cells

A

Ovary
Stimulated by LH
Secretes Androgens

102
Q

Granulosa Cells

A

Ovary
Stimulated by FSH
Secretes inhibin (negative feedback) and aromatase
Dies in menopause

103
Q

Leydig Cells

A

Testicular
Stimulated by LH
Secretes T

104
Q

Sertoli Cells

A

Testicular
Stimulated by FSH
Secretes Inhibin B, Sperm, Mullein Inhibin Factor

105
Q

Central DI

A

Low ADH secretion
Head trauma, tumor, surgery
DDAVP concentrates urine
Get an MRI

106
Q

Nephrogenic DI

A

ADH receptor broken
DDAVP doesn’t help
Give Amiloride to get rid of Li
Give HCTZ to replace Aquaporins
Switch to Valproic Acid

107
Q

Null-Cell adenoma

A

Non-functional pituitary adenoma

108
Q

Acidophilic Adenoma

A

Pituitary tumor that stains pale pink
Secretes growth hormone

109
Q

Basophilic Adenoma

A

Pituitary tumor stains pale blue with basic dyes
Secretes adrenocorticotrophic hormone

110
Q

Cosyntropin

A

Synthetic ADH, tests adrenal function

111
Q

Treat adrenal insufficiency

A

Hydrocortisone and D50W now
Test for ACTH, cortisol

112
Q

Captopril challenge

A

Increase in HTN means hyperaldosteronism, CONN’s

113
Q

Labs of Conn’s

A

HTN
Hypokalemia
Increased Aldo, low renin

114
Q

17 a-hydroxylase deficiency

A

HTN (high aldosterone)
Hypokalemia
Low cortisol, sex steroids

115
Q

21 a-hydroxylase deficiency

A

High Androgens
Hypotension (low aldosterone)
Low cortisol
Buildup of 17 a-hydroxylase

116
Q

11 b-hydroxylase deficiency

A

High androgens
HTN
Low renin / aldosterone, cortisol
Buildup of 11-deoxycortisone

117
Q

Weight changes with DM medications

A

GLP-1 Analogues: Weight Loss
Thiazolinadiones: Weight Gain