Endocrine

Question 1

Potassium perchlorate/Petechenate

Answer 1

MOA: competitively inhibits NA/I symporter into thyroid gland

Inhibits release of T3/T4 further down the line

Question 2

Growth hormone

Answer 2

Clinical: GH deficiency, turner syndrome

Question 3

Regular Insulin

Answer 3

Short acting

Starts working in 30 mins, peaks at 2-4 hours
Lasts 5-8 hours

Subcutaneous

Clinical: DM1, DM2, GDM, DKA (IV), hyperkaleia, stress hyperglycemia
TREATMENT OF CHOICE FOR GESTATIONAL DIABETES

Question 4

Demeclocycline

Answer 4

MOA: ADH antagonist

Clinical: SIADH

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

Question 6

Glitazones, thiazolidinediones

Answer 6

-azones
MOA: increase insulin sensitivity in peripheral tissue
Binds PPAR nuclear transcription regulator
Decreases insulin resistance
Increases adiponectin
Increase fatty acid transport protein leading to decreased circulating free fatty acids
Increases GLUT4 translocation

Clinical: DM2

Toxicity: weight gain, edema, hepatotoxicity, heart failure
NO hypoglycemia

takes days to weeks to observe effects

Question 7

Acarbose, miglitol

Answer 7

MOA:inhbit intestinal brush border a-glucosidases
Delaying carb absorption

Clinical: DM2 with meals

Toxicity: flatulence, GI bloating, abdominal pain, rash

Not used in inflammatory bowel disease

Question 8

Canagliflozin

Answer 8

all -flozins
MOA: SGLT2 cotransproter inhibitor leading to glucose lost in urine
SGLT2 reabsorbs glucose in proximal tubule

toxicity: urinary tract infections, genital mycotic infectins, increased osmotic diuresis leading to symptomatic hypotension (elderly)

Avoid in renal impairment patients

Question 9

NPH

Answer 9

Insulin intermediate acting

Clinical: DM1, DM2 GDM

Protamine sulfate increases half life

Question 10

Sulfonylureas

Answer 10

-mides, -rides, -zides

MOA: close K+ channel in B cell membrane so cell depolarizes triggering insulin release via Ca influx
increased release of C peptide and proinsulin
Increase production and secretion of insulin

Clinical: DM2, requires some islet function

Toxicity: hypoglycemia increased in renal failure,
-mides: disulfiram reaction

Question 11

Linagliptin, Saxagliptin, Sitagliptin

Answer 11

MOA: DPP-4 Inibitors
Increase Insulin, decrease glucagon

Clinical: Type 2 DM

Toxicity: Mild urinary or respiratory infections

Question 12

Desmopressin

Answer 12

central diabetic insipidus

also induces endothelial procoagulatory protein (vWF) release

Question 13

Propylthiouracil, methimazole

Answer 13

MOA: block thyroid peroxidase, inhibiting oxidation of iodide and organification of iodine leading to inhibition of thyroid hormones
Propylthiouracil blocks 5’-deiodinase which inhibits peripheral conversion of T4 to T3

Clinical: hyperthyroidism,
Propylthioruracil used in pregnancy and thyroid storm

Toxicity: skin rash, agranulocytosis (sore throat, oral ulcerations), aplastic anemia,
Hepatotoxicty and ANCA vasculitis-propyl
Methimazole: cholestasis and possible teratogen

Question 14

Glargine, Determir

Answer 14

Long acting Insulin

Clinical: DM1, DM2, GDM
Basal glucose control

Question 15

Pegvisomant

Answer 15

GH receptor antagonist used in acromegaly

Question 16

Lispro, Apart, Glulisine

Answer 16

Rapid acting insulin analogs
MOA: bind insulin receptor (tyrosine Kinase activity)
Liver: increase glucose stored as glycogen
Muscle: increase glycogen, protein synthesis, increase K uptake
Fat: increase TG storage

Clinical: DM1, DM2, GDM
Postprandial glucose control
Treatment of choice in pregnancy

Toxicity: hypoglycemia, rare hypersensitivity reactions

onset less than 15 mins peak at 45-75 mins

Question 17

Pramlintide

Answer 17

MOA: amylin analog
decrease gastric emptying, decrease glucagon

Clinical: DM1 and DM2

Toxicity: hypoglycemia, nausea, diarrhea

Question 19

Oxytocin

Answer 19

Clinical: stimulates labor, uterine contractions, milk let down, controls uterine hemorrhage

Question 20

Metformin

Answer 20

Decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake, increses insulin sensitivity, decrease GI glucose absorption

Clinical: oral
First line treatment for DM2
Can be used without islet functin

Toxicity: GI upset, lactic acidosis (CI in renal failure, hepatic failure, alcoholics and CHF)
NO HYPOGLYCEMIA

Question 20

Levothyroxine, triiodothryronine

Answer 20

MOA: thyroxine replacement

Clinical: hypothyroidism, myxedema

Toxicity: tachycardia, heat intolerance, tremors, arrhythmias

Interactions
Decreased absorption: cholestyramine, iron, calcium, aluminum hydroxide, proton pump inhibitors, divulge ate

Increased Thyroglobulin: estrogen, tamoxifen, raloxifene, heroin, methadone

Decreased thyroglobulin: androgens, glucocorticoids, anabolic steroids, nicotinic acid

Increased thyroid hormone metabolism: rifampicin, phenytoin, carbamazepine

Question 20

Ocretreotide

Answer 20

MOA: somatostatin analog

Clinical: Acromegaly, carcinoid, gastrinoma, glucogonoma, esophageal varices

Question 21

Exenatide, liraglutide

Answer 21

MOA: GLP-1 analog
Increase insulin, decresae glucagon release
coupled to G protein AC

Clinical: Type 2 DM

toxicity: nausea, vomiting, pancreatitis

Question 22

Glucocorticoids

Answer 22

-sone
MOA: metabolic, catabolic, anti-inflammatory and immunosuppressive effects (but increase the number of neutrophils)
inhibition of NF-kB

Clinical: addison disease, inlfammation, immune suppression, asthma

Toxicity: iatrogenic Cushing syndrome-buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy brusing, oteoporosis, adrenocortical atrophy, peptic ulcer disease, diabetes
Adrenal insuffieciency when drug stopped abruptly