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Designated study period: daily cards > March 12 - Endocrine > Flashcards

March 12 - Endocrine Flashcards

1
Q

Glargine

A

Long acting insulin

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2
Q

Detemir

A

Long acting insulin

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3
Q

Lispro

A

Short acting insulin

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4
Q

Aspart

A

Short acting insulin

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5
Q

Glulisine

A

Short acting insulin

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6
Q

SGLT2 inhibitors: Names, MOA, Side effects, Contraindications

A

Names: canagliflozin, dapagliflozin

MOA: Oral agents for type 2 diabetes that inhibit sodium glucose co-transporter in proximal tubule, decreasing glucose reabsoprtion and increasing urinary glucose loss

Side effects: UTIs due to glucosuria, hypotension due to osmotic diuresis

CIs: renal insufficiency

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7
Q

Flutamide: MOA, Use

A

MOA: competitive inhibitor of testosterone receptor

Use: Prostate cancer

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8
Q

Finasteride: MOA, Use

A

MOA: 5 alpha reductase inhibitor, decreases peripheral conversion of testosterone to DHT

Use: BPH, male pattern baldness

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9
Q

Ketoconazole: endocrine MOA and use, toxicity

A

MOA: inhibits steroid hormone synthesis

UsE: hirsutism in PCOS

Toxicity: gynecomastia, amenorrhea

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10
Q

Spironolactone: endocrine MOA and use, toxicity

A

MOA: inhibits steroid hormone binding

Use: Hirsutism of PCOS

Toxicity: gynecomastia, amenorrhea

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11
Q

Hashimoto’s vs subacute granulomatous thyroiditis: presentation and pathology

A

Hashimoto’s: presents as painless goiter with well developed germinal centers on pathology

Subacute granulomatous: presents as painful goiter following viral illness, inflammatory infiltrate with macropahges and giant cells on path

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12
Q

CAH: side chain cleavage enzyme, 17alpha reductase, 21-hydroxylase, and 11beta hydroxylase deficiency.

A

Side chain cleavage enzyme def

  • can’t convert cholesterol to pregnenolone
  • low in all three adrenal hormones

17alpha reductase def

  • can’t convert progesterone to 17-OH progesterone
  • increased aldo, decreased cortisol, decreased androgens

21-hydroxylase def
-decreased aldo, decreased cortisol, increased androgens

11beta hydroxylase def

  • can’t convert weak mineralocorticoid to aldo, can’t make cortisol
  • increased mineralocorticoids, decreased cortisol, increased androgens
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13
Q

Familial chylomicronemia: defect and presentation

A

Defect: LPL (can’t cleave TGs from chylomicrons and VLDL)

Presentation: increased chylomicrons, acute pancreatitis

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14
Q

Familial hypercholesterolemia: defect, presentation, and inheritance

A

Defect: AD defect in LDL receptor, ApoB100 which binds the LDL receptor

Presentation: increased LDL, premature atherosclerosis, tendon xanthomas

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15
Q

Familial dysbetalipoproteinemia: defect, presentation, inheritance

A

Defect: AR defect in ApoE which is responsible for reuptake of lipoproteins by liver

Presentation: increased chylomicrons, increased VLDL remnants, premature atherosclerosis, palmar xanthomas

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16
Q

Familial hypertriglyceridemia: defect and presentation

A

Defect: polygenic

Presentation: increased VLDL, pancreatitis, coronary disease, diabetes

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17
Q

Niacin: MOA and side effects

A

MOA: decreases hepatic triglyceride and VLDL synthesis; decreases HDL clearance resulting in increased HDL levels

Side effects: flushing, hyperglycemia, hepatotoxic, increased uric acid which can precipitate gout

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18
Q

Cholestyramine: MOA and side effects

A

MOA: binds bile acids in GI tract, decreasing enterohepatic circulation. Decreases LDL.

Side effects: GI upset, impaired absorption, increased hepatic TG production resulting in high TGs

19
Q

Ezetimibe: MOA and side effects

A

MOA: inhibits cholesterol absorption resulting in decreased LDL

Side effects: hepatotoxicity

20
Q

Gaucher disease: genetic defect and presentation

A

Genetic defect: AR beta-glucocerebrosidase deficiency. Results in high glucocerebroside.

Presentation: bone pain, HSM, pancytopenia. Gaucher cells are lipid laden macrophages with a wrinkled tissue paper appearance that can be seen in bone marrow, liver, lymphatic tissue

21
Q

Fanconi anemia: presentation

A

Inherited aplastic anemia. Also has risk of malignancy, hypo/hyperpigmented patches, short stature, hypoplastic thumbs

22
Q

Hypoglycemia threatment

A

Mild to moderate: glucose tablets or fruit juice

Severe, patient unconscious:

  • in medical setting: IV glucose
  • outside medcial setting: IM or SC glucagon
  • no glucagon available: sublingual/subbuccal glucose or sucrose
23
Q

Effect of pituitary resection of catecholamine synthesis

A

While dopamine and norepinephrine made both centrally and peripherally, epinephrine made in adrenal medulla. Pituitary resection results in low ACTH and thus decreased cortisol synthesis. Cortisol normally increases PNMT, the enzyme that converts norepinephrine to epinephrine.

24
Q

Medullary thyroid carcinoma: pathology

A

Nests of polygonal cells with extracellular amyoid deposits that stain with congo red. Arises from parafollicular C cells

25
Q

Thiazolidinediones: Name, MOA, side effects

A

Name: pioglitazone

MOA: decrease insulin resistance by binding PPAR gamma causing alteration in gene expression. Takes weeks to see effect

Side effects: fluid retention, weight gain

26
Q

Glucagonoma presentation

A

Necrolytic migratory erythema: plaques that enlarge and coalesce, leaving bronze-colored, central indurated area

Diabetes

GI symptoms

27
Q

Corticosteroids and neutrophils

A

Cause neutrophil demargination leading to neutrophilia. Decreases neutrophil recruitment to fight tissue infection.

28
Q

Drainage of R vs L adrenal

A

R drains into IVC directly. L drains into L renal vein.

29
Q

Pineal mass

A

Rare brain tumor. Presents with symptoms of increased ICP and CSF obstruction. Can also cause vertical gaze and pupil abnormalities. Located between the thalamic bodies.

30
Q

HLA associations for diabets

A

HLA-DR3 and HLA-DR4

31
Q

MOA of beta blockers in hyperthyroidism

A
  1. decrease HR, agitation, anxiety

2. decrease peripheral T4 to T3 conversion

32
Q

PTH regulation: Ca++ sensing receptor

A

transmembrane GPCR. Binding of Ca++ to feceptr inhibits PTH release

33
Q

Familial hypocalciuric hypercalcemia

A

AD defect in Ca++ sensing receptor. Results in lack ot PTH suppression of Ca++. High Ca++ and high PTH

34
Q

Causes of central DI

A

Damage to posterior pituitary results in temporary DI

Damage to hypothalamus results in permanent DI

35
Q

Pathophys of cataracts in diabetes

A

Aldose reductase converts glucose to sorbitol at high rate
Sorbitol dehydrogenase converts sorbitol to fructose with lower Vmax that is overwhelmed in diabetes
Leads to build up of sorbitol which is toxic and causes cataract formation

36
Q

Long vs short acting sulfonylureas

A

Long acting: glyburide and glimepiride, high hypoglycemia risk
Short acting: glipizide, lower hypoglycemia risk

37
Q

Silagliptin

A

DDP-4 inhibitor. Causes glucose-dependent increase in insulin release.

38
Q

Bone findings in hyperparathyroidism

A
  • subperiosteal erosions
  • salt and pepper skull
  • osteolytic cysts in long bones
39
Q

Fructose detection in urine

A

Fructose a reducing sugar and can be detected by copper reduction test, which is non-specific. Negative glucose oxidase test which specifically looks for glucose in urine

40
Q

SIADH and volume status

A

Transient subclinical hypervolemia. RAAS gets suppressed leading to natriuresis and correction of TBW so have normal fluid volume with low serum sodium (euvolemic hyponatremia)

41
Q

Neglitinides: names, MOA, use, side effect

A

Repaglinidine and nateglinidine. Short acting glucose lowering meds that act similarly to sulfonylruias. Good for patients with high post-prandial glucose. Side effect is weight gain.

42
Q

Metabolic side effect of HAART

A

Can cause fat redistribution from extremities to trunk. This can lead to insulin resistance and lipid abnormalities

43
Q

Major side effect of antithyroid drugs

A

Agranulocytosis

Designated study period: daily cards (32 decks)

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