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USMLE > Endocrine > Flashcards

Endocrine Flashcards

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USMLE® Step 1 flashcards
1
Q

insulin receptor

A

tyrosine kinase receptor that induces glucose uptake into insulin-dependent tissues via GLUT-4 receptors and affects gene transcription.

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2
Q

Regulation of insulin release

A

Glucose enters beta cell and is metabolized, increasing ATP. ATP closes K+ channels leading to depolarization. VG Ca++ channels open leading to Ca++ influx and exocytosis of insulin.

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3
Q

Effects of somatostatin

A

Decreases growth hormone and TSH release from the pitutiary. Analogues can thus be used to treat acromegaly.

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4
Q

Effects of TRH

A

increases TSH and prolactin

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5
Q

Two functions of growth hormone

A

Stimulates growth through IGF-1

Increases insulin resistance (diabetogenic)

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6
Q

Regulation of growth hormone

A

Released in pulses in response to GHRG. Secretion higher during exercise and sleep. Secretion inhibited by glucose and somatostatin.

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7
Q

Ghrelin

A

Stimulates hunger and GH release. Produced by stomach

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8
Q

Leptin

A

Satiety hormone produced by adipose tissue

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9
Q

Regulation of ADH

A

Osmoreceptors in hypothalamus

Hypovolemia

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10
Q

17-alpha-hydroxylase deficiency

A

High mineralocorticoids; low cortisol and sex steroids. High BP, low K+, low androstenedione, non-virilizing. Males have ambiguous genitalia at birth, females lack secondary sex development.

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11
Q

21-hydroxylase deficiency

A

Most common cause of CAH. high sex hormones; low mineralocorticoids and cortisol. Low BP and high K+. High 17-OH-progesterone and high renin activity.

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12
Q

11beta-hydroxylase deficiency

A

Low aldosterone and cortisol but high 11-beta-deoxycorticosterone results in increased BP. High sex hormones. Virilization and salt wasting.

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13
Q

Cortisol functions

A

BIG FIB:

  • increases BP
  • increases insulin resistance
  • increases gluconeogenesis
  • decreases fibroblast activity which is what causes striae in cushings
  • decreases inflammatory/immune response: inhibits leukotriene and PG production, inhibits WBC adhesion resulting in neutrophilia, blocks histamine release, reduces eosinophils, blocks IL-2 production
  • decreases bone formation
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14
Q

functions of vitamin D

A
  • increaes absorption of Ca++ and phosphorus in gut

- increases bone resorption, increasing Ca++ and phosphorus

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15
Q

regulation of vitamin D

A

Active levels increased by high PTH and low Ca++ and phosphorus

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16
Q

Functions of PTH

A
  • increases bone resorption of Ca++ and phosphorus by increasing production of RANK-L which binds RANK receptor on osteoclasts to stimulate them
  • increases kidney reabsorption of Ca++ in distal tubule
  • decreases reabsorption of phosphorus in distal tubule
  • increases active vitamin D production in kidney
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17
Q

Regulation of PTH

A

increased by low Ca++, high phos, low Mg++. Decreased by very low Mg++.

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18
Q

Hormones that signal through cAMP

A

FLAT ChAMP: FSH, LH, ACTH, TSH, CRH, hCG, ADH, MSH, PTH, calcitonin, GHRH

Pituitary hormones: FSH, LH, TSH, ADH (V2 receptor), ACTH, MSH (all but prolactin and oxytocin)
Hypothalamic hormones: CRH, GHRH
Others: hCG, PTH, calcitonin, glucagon

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19
Q

Hormones that signal through cGMP

A

ANP, BNP, NO

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20
Q

Hormones that signal through IP3

A

GOAT HAG: GnRH, oxytocin, ADH (V1 receptor), TRH, histamine (H1 receptor), angiotensin II, gastrin

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21
Q

Hormones that signal through intracellular receptor

A

Steroid hormones, thyroid hormone, vitamin D

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22
Q

Hormones that signal through intrinsic tyrosine kinase

A

Insulin, IGF-1, other growth factors

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23
Q

Hormones that signal through receptor-associated tyrosine kinase (JAK/STAT)

A

PIGG(L)ET: prolactin, immunomodulators, GH, G-CSF, EPO, thrombopoietin

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24
Q

Functions of T3

A

4Bs:

  • brain maturation
  • bone growth
  • beta-adrenergic effects
  • increased basal metabolic rate
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25
Q

Symptoms of adrenal insufficiency

A

Weakness, fatigue, orthostatic hypotension, muscle aches, weight loss, GI disturbance, sugar/salt cravings

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26
Q

Primary vs secondary vs tertiary adrenal insufficiency

A

Primary: Def of aldo and cortisol. Hypotension, hyperkalemia, and metabolic acidosis. ACTH high resulting in hyperpigmentation. Can be acute due to massive hemorrhage or chronic due to Addison disease

Secondary: Decreased ACTH production. No hyperpigmentation or hyperkalemia

Tertiary: Abrupt withdrawal of chronic exogenous steroid use

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27
Q

Neuroblastoma of adrenal medulla

A

Most common tumor of adrenal medulla in kids. Usually seen in those less than 4. Neural crest derivative with overexpression of N-myc. Pathology includes Homer-Wright rosettes.

Presents with abdominal distension and firm, irregular mass (vs smooth Wilms tumor). May see dancing eyes-dancing feet.

Labs: elevated HVA, VMA in urine due to breakdown or dopamine and NE. Bombesin and neuron-specific enolase pos.

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28
Q

Genetic syndromes associated with pheo

A

NF1, VHL, MEN2A, MEN2B

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29
Q

treatment of pheo

A

1) irreversible alpha antag (before beta blocker to prevent hypertensive crisis)
2) beta blocker
3) surgery

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30
Q

Reflexes in hypoand hyperthyroidism

A

decreased in hypo, increased in hyper

31
Q

Autoantibodies and HLA type in hashimoto thyroiditis

A

anti-thyroid peroxidase, antimicrosomal, antithyroglobulin

HLA-DR5 associated

32
Q

Tender vs non-tender thyroid in hypothyroidism

A

Nontender: hashimoto, Riedel thyroiditis
Tender: subacute thyroiditis

33
Q

Congenital hypothyroidism presentation

A 
pot-belly
pale
puffy face
protruding umbilicus
protuberant tongue
poor brain development
34
Q

subacute thyroiditis

A

self-limited
hyperthyroid progressing to hypothyroid
granulomatous inflammation
very tender thyroid

35
Q

Riedel thyroiditis

A

thryoid replaced by fibrous tissue
IgG4-related systemic disease
fixed, hard, painless goiter

36
Q

Presentation of Graves disease

A

hyperthyroidism, exophtalmos, pretibial myxedema

37
Q

toxic multinodular goiter

A

focal patches of hyperfunctioning follicular cells due to TSH receptor mutation. Hot nodules rarely malignant

38
Q

Thyroid storm

A

Stress induced catecholamine surge due to thyrotoxicosis. Agitation, delirium, fever, diarrhea, coma, tachyarrhythmia.

Treatment: beta blocker, propylthiouracil, corticosteroids

39
Q

Thyroid cancers: papillary, follicular, medullary, anaplastic, lymphoma

A

Papillary carcinoma: Most common and excellent prognosis. Empty-appearing nuclei with central clearing. Psammoma bodies with nuclear grooves.

Follicular carcinoma: Good prognosis. Distinguished from follicular adenoma by invasion of the capsule.

Medullary carcinoma: C-cell drived. Produces calcitonin. Associated with MEN2A and 2B

Anaplastic carcinoma: seen in older patients. Very poor prognosis

Lymphoma: associated with hashimoto

40
Q

Symptoms of hypoparathyroidism

A

Hypocalcemia and tetany.

Chvostek sign: tap facial nerve and see contraction of facial muscles

Trousseau sign: occlude brachial artery with BP cuff and see carpal spasm

41
Q

Pseudohypoparathyroidism

A

AD condition in which kidney unresponsive to PTH. Causes hypocalcemia, shortened 4th/5th digits, short stature

42
Q

Familial hypocalciuric hypercalcemia

A

Defective Ca++ receptor on parathyroid cells so PTH not suppressed. High calcium with normal to high PTH.

43
Q

Presentation of acromegaly

A 
Large tongue with deep furrows
Deep voice
Large hands and feet
Coarse facial features
Insulin resistance
Risk of colorectal polyps and cancer
44
Q

Sheehan syndrome

A

Ischemic infarct of pituitary following postpartum bleeding leading to hypopituitarism. Presents with failure to lactate, absent menstruation, cold intolerance.

45
Q

Empty sella syndrome

A

Atrophy or compression of pituitary leading to hypopit. Common in obese women

46
Q

Pituiary apoplexy

A

Sudden hemorrhage of pituitary leading to hypopit

47
Q

Diabetic complications of osmotic damage

A

Sorbitol accumulates in organs with aldolase reductase is what causes the damage. Neuropathy and cataracts.

48
Q

Diabetic complications due to small vessel disease

A

Diffuse thickening of BM. Retinopathy, glaucoma, neuropathy, nephropathy.

49
Q

Type I diabetes: HLA association

A

HLA-DR3 and HLA-DR4

50
Q

Zollinger-Ellison syndrome

A

Gastrin-secreting tumor in pancreas or duodenum. Acid hypersecreting reulting in ulcers.

presentation: abdominal pain and diarrhea

Diagnosis: Pos secretin stim tes (gastrin stays high after giving secretin which should suppress it

Associated with MEN 1

51
Q

MEN1

A

Parathyroid tumors, pituitary tumors, pancreatic endocrine tumors (zollinger-ellison syndrome, insulinomas, VIPomas, glucagonomas)

52
Q

MEN2A

A

Parathyroid hyperplasia, pheochromocytoma, medullary carcinoma, marfanoid habitus, RET mutation

53
Q

MEN2B

A

Pheochromocytoma, Medullar thyroid carcinoma, oral/intestinal ganglioneuromatosis, marfanoid habitus, RET mutation

54
Q

Names of insulins

A

Rapid acting: aspart, glulisine, lispro

Short acting: regular insulin

Intermediate acting: NPO

Long acting: glargine, detemir

55
Q

Metformin

A

MOA: unkown, decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitizer)

Use: Oral for type 2 DM. Modest weight loss.

ADRs: lactic acidosis (contraindicated in renal insufficiency)

56
Q

Sulfonylureas

A

Names: chlorpropramide and tolutamide (first gen); glimepiride, glipizide, glyburide (second gen)

MOA; Close K+ channel in beta cell membane resulting in depolarization and insulin release

Use: Type 2 DM only

ADRs: risk of hypoglycemia; disulfiram-like effects for first gen only

DDIs: non-specific beta blockers can mask symptoms of hypoglycemia

57
Q

Thiazolidinediones

A

Names: pioglitazone, rosiglitazone

MOA: increase insulin sensitivity by binding PPAR-gamma

Use: Type 2 DM

ADRs: weight gain, hepatotoxicity, risk of fracture

58
Q

GLP-1 agonists

A

Names: exenatide, liraglutide

MOA: increase insulin, decrease glucagon release

Use: Type 2 DM

ADRS: pancreatitis, N/V

59
Q

DPP-4 inhibitors

A

Names: linagliptin, saxagliptin, sitagliptin

MOA: increase insulin, decrease glucagon release

Use: Type 2 DM

ADRs: urinary or resp infections

60
Q

Amylin analogs (pramlintide)

A

MOA: decreases gastric emptying and decreases glucagon

Use: Type 1 and type 2 DM

ADRs: hypoglycemia

61
Q

SGLT-2 inhibitors (canagliflozin)

A

MOA: blocks reabsorption of glucose in prox collecting tubule

Use: Type 2 DM

ADRs: UTIs and yeast infections due to glucosuria

62
Q

alpha-glucosidase inhibitors

A

Names: acarbose, miglitol

MOA: inhibits intesinal brush border alpha glucosidases, delaying glucose absorption and decreasing postprandial hyperglycemia

Use: type 2 DM

63
Q

Propylthiouracil and methimazole

A

MOA: block thyroid peroxidase, inhibiting oxidation and organification of iodine and thus inhibiting thryoid hormone synthesis. PTU also blocks peripheral conversion of T4 to T3

Use: Hyperthyroidism. PTU used in pregnancy because methimazole is possible teratogen

ADRs: agranulocytosis, aplasatic anemia

64
Q

ADH antagonists

A

Names: Conivaptan, tolvaptan, demeclocycline

MOA: block ADH receptor

Use: SIADH

ADR: demeclocycline is of tetracycline family and so can cause bone and teeth abnormalities

65
Q

Octreotide

A

MOA: somatostatin analogue

Use: acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices

66
Q

Cinacalcet

A

MOA: sensitizes parathyroid gland to calcium, decreasing PTH

Use: primary or secondary hyperparathyroidism

67
Q

Bromocriptine

A

MOA: dopamine agonist

Use: hyperprolactinemia

68
Q

Central DI: damage to pituitary vs hypothalamus

A

Damage to pituitary or infundibulum causes only transient DI because hypothalamic axons regenerate and hypertrophy. Damage to hypothalamic neurons results in permanent DI

69
Q

Acetyl coA carboxylase

A

Fatty acid metabolism enzyme: converts acetyl coA to malonyl coA

70
Q

Glycerol kinase

A

Part of gluconeogenesis from triglycerides

71
Q

Parathyroid Ca++ sensing receptors

A

Transmembrane G protein coupled receptors

72
Q

Neurophysins

A

Carrier proteins for oxytocin and vasopressin

73
Q

glucagon receptor activates

A

Acts through Gs coupled receptor. Binds to receptor, alpha subunit releases GDP and binds GTP so can dissociate. Gs activates adenylate cyclase, which converts ATP to cAMP. cAMP activates PKA which phosphorylates serine/threonine residues in enzymes to activate or deactivate the,

USMLE (17 decks)

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