March 12 - Endocrine Flashcards Preview

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

Flashcards in March 12 - Endocrine Deck (43):
1

Glargine

Long acting insulin

2

Detemir

Long acting insulin

3

Lispro

Short acting insulin

4

Aspart

Short acting insulin

5

Glulisine

Short acting insulin

6

SGLT2 inhibitors: Names, MOA, Side effects, Contraindications

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

7

Flutamide: MOA, Use

MOA: competitive inhibitor of testosterone receptor

Use: Prostate cancer

8

Finasteride: MOA, Use

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

Use: BPH, male pattern baldness

9

Ketoconazole: endocrine MOA and use, toxicity

MOA: inhibits steroid hormone synthesis

UsE: hirsutism in PCOS

Toxicity: gynecomastia, amenorrhea

10

Spironolactone: endocrine MOA and use, toxicity

MOA: inhibits steroid hormone binding

Use: Hirsutism of PCOS

Toxicity: gynecomastia, amenorrhea

11

Hashimoto's vs subacute granulomatous thyroiditis: presentation and pathology

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

12

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

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

13

Familial chylomicronemia: defect and presentation

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

Presentation: increased chylomicrons, acute pancreatitis

14

Familial hypercholesterolemia: defect, presentation, and inheritance

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

Presentation: increased LDL, premature atherosclerosis, tendon xanthomas

15

Familial dysbetalipoproteinemia: defect, presentation, inheritance

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

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

16

Familial hypertriglyceridemia: defect and presentation

Defect: polygenic

Presentation: increased VLDL, pancreatitis, coronary disease, diabetes

17

Niacin: MOA and side effects

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

18

Cholestyramine: MOA and side effects

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

Ezetimibe: MOA and side effects

MOA: inhibits cholesterol absorption resulting in decreased LDL

Side effects: hepatotoxicity

20

Gaucher disease: genetic defect and presentation

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

Fanconi anemia: presentation

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

22

Hypoglycemia threatment

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

Effect of pituitary resection of catecholamine synthesis

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

Medullary thyroid carcinoma: pathology

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

25

Thiazolidinediones: Name, MOA, side effects

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

Glucagonoma presentation

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

Diabetes

GI symptoms

27

Corticosteroids and neutrophils

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

28

Drainage of R vs L adrenal

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

29

Pineal mass

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

HLA associations for diabets

HLA-DR3 and HLA-DR4

31

MOA of beta blockers in hyperthyroidism

1. decrease HR, agitation, anxiety
2. decrease peripheral T4 to T3 conversion

32

PTH regulation: Ca++ sensing receptor

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

33

Familial hypocalciuric hypercalcemia

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

34

Causes of central DI

Damage to posterior pituitary results in temporary DI
Damage to hypothalamus results in permanent DI

35

Pathophys of cataracts in diabetes

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

Long vs short acting sulfonylureas

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

37

Silagliptin

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

38

Bone findings in hyperparathyroidism

-subperiosteal erosions
-salt and pepper skull
-osteolytic cysts in long bones

39

Fructose detection in urine

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

SIADH and volume status

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

Neglitinides: names, MOA, use, side effect

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

Metabolic side effect of HAART

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

43

Major side effect of antithyroid drugs

Agranulocytosis