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Endocrine Flashcards

1
Q

cAMP

A

FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2 receptor), MSH, PTH, calcitonin, GHRH, glucagon

“FLAT CHAMP”

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2
Q

cGMP

A

ANP, NO “think vasodilators”

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3
Q

IP3

A

GnRH, Oxytocin, ADH (V1 receptor), TRH “GOAT”

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4
Q

Steroid receptor (cytosolic)

A

Vitamin D, Estrogen, Testosterone, Cortisol, Aldosterone, Progesterone
“VET CAP”

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5
Q

Steroid receptor (nuclear)

A

T3/T4

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6
Q

Intrinsic tyrosine kinase (MAP kinase pathway)

A

Insulin, IGF-1, FGF, PDGF (think growth factors)

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7
Q

Receptor-associated tyrosine kinase (JAK/STAT pathway)

A

GH, prolactin (also cytokine Il-2)

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8
Q

For the pituitary gland, what hormones is the alpha subunit common to?

A

TSH, LH, FSH, hCG

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9
Q

What are the four functions of T3?

A

4B’s: brain maturation, bone growth, increased basal metabolic rate, beta-adrenergic

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10
Q

Conn’s syndrome

A

primary hyperaldosteronism; caused by an aldosterone-secreting tumor –> hypertension, hypokalemia, metabolic alkalosis, and LOW plasma renin

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11
Q

What is secondary hyperaldosteronism?

A

Kidney perception of low intravascular volume –> overactive renin-angiotensin system (HIGH plasma renin); due to renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome

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12
Q

What is Waterhouse-Friderichsen syndrome?

A

acute primary adrenal insufficiency due to adrenal hemorrhage associated with N. meningitis septicemia, DIC, endotoxin shock

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13
Q

phenoxygbenzamine

A

nonselective, irreversible alpha-blocker; used for treatment of pheochromocytoma

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14
Q

What are the five episodic hyperadrenergic symptoms of pheochromocytoma?

A

5 P’s: pressure (elevated), pain (headache), perspiration, palpitations (tachycardia), pallor

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15
Q

What is the rule of 10’s for pheochromocytoma?

A

10%: malignant, bilateral, extra-adrenal, calcify, kids, familial

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16
Q

Neuroblastoma

A

most common tumor of the adrenal medulla in children; HVA (breakdown of dopamine) is elevated in urine; overexpression of N-myc associated with rapid tumor progression

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17
Q

What are the features of cretinism?

A

pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue (due to severe fetal hypothyroidism, lack of dietary iodine)

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18
Q

What is the action of insulin?

A

Binds insulin receptor (tyrosine kinase activity

Liver: increases glucose stored as glycogen

Muscle: increases glycogen and protein synthesis, K uptake

Fat: aids TG storage

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19
Q

What is the clinical use and toxicities of insulin?

A

Type 1 and 2 DM, gestational diabetes, life-threatening hyperkalemia, stress-induced hyperglycemia

Toxicities: hypoglycemia, hypersensitivity reaction (very rare)

20
Q

What is the action of sulfonylureas?

A

Close K channel in the B-cell –> depolarizes –> triggering of insulin release via increased calcium influx

“Kicking the pancreas” to increase insulin output

21
Q

What are the clinical use and toxicities of sulfonylureas?

A

Clinical use: stimulate release of endogenous insulin in type 2 DM; requires some islet fxn, so useless in DM type 1.

Toxicities; first generation: disulfiram-like effects, second generation: hypoglycemia

22
Q

What is the action of biguanides (metformin)?

A

Decrease gluconeogenesis, increase glycolysis and increase peripheral insulin sensitivity

23
Q

What are the clinical use and toxicities of biguanides?

A

Clinical use: oral, can be used with pts w/out islet fxn

Toxicities: most grave adverse effect is lactic acidosis (contraindicated for those with renal failure)

24
Q

What is the action of glitazones/thiazolidinediones?

A

increase insulin sensitivity in peripheral tissue; binds to PPAR-gamma nuclear transcription regulator

25
Q

What are the clinical use and toxicities of glitazones/TZDs?

A

Clinical use: used as monotherapy in type 2 DM or combined with other agents

Toxicity: weight gain, edema, hepatotoxicity, CV toxicity

26
Q

What is the action of alpha-glucosidase inhibitors?

A

inhibit intestinal brush border alpha-glucosides; delayed sugar hydrolysis and glucose absorption lead to decreased postprandial hyperglycemia

27
Q

What are the clinical use and toxicities of alpha-glucosidase inhibitors?

A

Clinical use: monotherapy in type 2 DM or in combination with other agents

Toxicities: GI disturbance

28
Q

How are mimetics (pramlintide) used?

A

Action: decrease glucagon
Clinical use: Type 2 DM
Toxicities: hypoglycemia, nausea, diarrhea

29
Q

How are GLP-1 analogs (exenatide) used?

A

Action: increased insulin, decreased glucagon release
Clinical use: Type 2 DM
Toxicities: nausea, vomiting, pancreatitis

30
Q

Lispro

A

rapid acting insulin

31
Q

Aspart

A

rapid acting insulin

32
Q

NPH

A

intermediate acting insulin

33
Q

Glargine

A

long acting insulin

34
Q

Detemir

A

long acting insulin

35
Q

Tolbutamide

A

first generation sulfonylurea

36
Q

Chlorpropamide

A

first generation sulfonylurea

37
Q

Glyburide

A

second generation sulfonylurea

38
Q

Glimepiride

A

second generation sulfonylurea

39
Q

Glipizide

A

second generation sulfonylurea

40
Q

Pioglitazone

A

Glitazone/ TZD

41
Q

Rosiglitazone

A

Glitazone/ TZD

42
Q

Acarbose

A

alpha-glucosidase inhibitor

43
Q

Miglitol

A

alpha-glucosidase inhibitor

44
Q

Propylthiouracil, methimazole

A

Mechanism: inhibit organification of iodide and coupling of thyroid hormone synthesis. Propylthiouracil also decreases conversion of T4 to T3.

Clinical use: hyperthyroidism

Toxicity: skin rase, agranulocytosis (rare), aplastic anemia, methimazole (possible teratogen), hepatotoxicity (propylthiouracil)

45
Q

Levothyroxine, trioodothyronine

A

Mechanism: thyroxine replacement

Clinical use: hypothyroidism, myxedema

Toxicity: tachycardia, heat intolerance, tremors, arrhythmias

46
Q

demeclocycline

A

Mechanism: ADH antagonist (member of tetracycline)

Clinical use: SIADH

Toxicity: nephrogenic DI, photosensitivity, abnormalities of bone and teeth

47
Q

glucocorticoids

A

Mechanism: decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of cox-2

Clinical use: Addison’s, inflammation, immune suppression, asthma

Toxicities: Cushings syndrome, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcer disease, diabetes, adrenal insufficiency when drug stopped after chronic use

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