March 12 - Endocrine Flashcards
Glargine
Long acting insulin
Detemir
Long acting insulin
Lispro
Short acting insulin
Aspart
Short acting insulin
Glulisine
Short acting insulin
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
Flutamide: MOA, Use
MOA: competitive inhibitor of testosterone receptor
Use: Prostate cancer
Finasteride: MOA, Use
MOA: 5 alpha reductase inhibitor, decreases peripheral conversion of testosterone to DHT
Use: BPH, male pattern baldness
Ketoconazole: endocrine MOA and use, toxicity
MOA: inhibits steroid hormone synthesis
UsE: hirsutism in PCOS
Toxicity: gynecomastia, amenorrhea
Spironolactone: endocrine MOA and use, toxicity
MOA: inhibits steroid hormone binding
Use: Hirsutism of PCOS
Toxicity: gynecomastia, amenorrhea
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
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
Familial chylomicronemia: defect and presentation
Defect: LPL (can’t cleave TGs from chylomicrons and VLDL)
Presentation: increased chylomicrons, acute pancreatitis
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
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
Familial hypertriglyceridemia: defect and presentation
Defect: polygenic
Presentation: increased VLDL, pancreatitis, coronary disease, diabetes
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
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
Ezetimibe: MOA and side effects
MOA: inhibits cholesterol absorption resulting in decreased LDL
Side effects: hepatotoxicity
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
Fanconi anemia: presentation
Inherited aplastic anemia. Also has risk of malignancy, hypo/hyperpigmented patches, short stature, hypoplastic thumbs
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
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.
Medullary thyroid carcinoma: pathology
Nests of polygonal cells with extracellular amyoid deposits that stain with congo red. Arises from parafollicular C cells
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
Glucagonoma presentation
Necrolytic migratory erythema: plaques that enlarge and coalesce, leaving bronze-colored, central indurated area
Diabetes
GI symptoms
Corticosteroids and neutrophils
Cause neutrophil demargination leading to neutrophilia. Decreases neutrophil recruitment to fight tissue infection.
Drainage of R vs L adrenal
R drains into IVC directly. L drains into L renal vein.
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.
HLA associations for diabets
HLA-DR3 and HLA-DR4
MOA of beta blockers in hyperthyroidism
- decrease HR, agitation, anxiety
2. decrease peripheral T4 to T3 conversion
PTH regulation: Ca++ sensing receptor
transmembrane GPCR. Binding of Ca++ to feceptr inhibits PTH release
Familial hypocalciuric hypercalcemia
AD defect in Ca++ sensing receptor. Results in lack ot PTH suppression of Ca++. High Ca++ and high PTH
Causes of central DI
Damage to posterior pituitary results in temporary DI
Damage to hypothalamus results in permanent DI
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
Long vs short acting sulfonylureas
Long acting: glyburide and glimepiride, high hypoglycemia risk
Short acting: glipizide, lower hypoglycemia risk
Silagliptin
DDP-4 inhibitor. Causes glucose-dependent increase in insulin release.
Bone findings in hyperparathyroidism
- subperiosteal erosions
- salt and pepper skull
- osteolytic cysts in long bones
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
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)
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.
Metabolic side effect of HAART
Can cause fat redistribution from extremities to trunk. This can lead to insulin resistance and lipid abnormalities
Major side effect of antithyroid drugs
Agranulocytosis
