endocrine Flashcards

0
Q

aspart insulin

A

rapid acting

best for post-meal hypergylcemia

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1
Q

lispro insulin

A

rapid acting

best for post-meal hypergylcemia

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2
Q

Glulisine

A

rapid acting

best for post-meal hypergylcemia

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3
Q

regular insulin

A

short acting

best for iv use

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4
Q

NPH

A

intermediate acting

twice daily

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5
Q

Glargine

A

long-acting

once daily

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6
Q

Dtermir

A

Long-acting

once daily

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7
Q

metformin

A

biguanides: decrease gluconeo,increase glycosis, increase glu uptake
use in 1st line type 2
tos: Gi upset, lactic acidosis(CI in renal failure)

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8
Q

Tolbutamide

A

1st Generation, sulfonylureas
Close K channel in beta-cell membrane, so cell depolarizes->Ca influx–>trigger of insulin release
tox: disulfiram like side effect

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9
Q

Chlorpropamide

A

1st Generation, sulfonylureas
Close K channel in beta-cell membrane, so cell depolarizes->Ca influx–>trigger of insulin release
tox: disulfiram like side effect

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10
Q

Glyburide

A

2nd Generation, sulfonylureas
Close K channel in beta-cell membrane, so cell depolarizes->Ca influx–>trigger of insulin release
tox: hypoglycemia

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11
Q

Glimepiride

A

2nd Generation, sulfonylureas
Close K channel in beta-cell membrane, so cell depolarizes->Ca influx–>trigger of insulin release
tox: hypoglycemia

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12
Q

Glipizide

A

2nd Generation, sulfonylureas
Close K channel in beta-cell membrane, so cell depolarizes->Ca influx–>trigger of insulin release
tox: hypoglycemia

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13
Q

Pioglitazone

A

Glitazones/thiazolidinediones
increase insulin sensitivity in peripheral tissue: increase GLUT express
binds to PPAR-gamma nuclear transcription regulator: regulate release of adipokines from adipose tissue
use as monotherapy in type 2 or combined
TOX: weight gain, edema, hepatotoxicity, HF

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14
Q

Rosigilitazone

A

Glitazones/thiazolidinediones
increase insulin sensitivity in peripheral tissue: increase GLUT express
binds to PPAR-gamma nuclear transcription regulator: regulate release of adipokines from adipose tissue
use as monotherapy in type 2 or combined
TOX: weight gain, edema, hepatotoxicity, HF

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15
Q

Acarbose

A

alpha-glucosidase inhibitor: inhibit intestinal brush-boarder alpha-glucosidases, delayed sugar hydrolysis and glucose absorption–>decrease postrandial hyperglycemia
Used as monotherapy in type 2 DM or in combination with above agents
TOX: GI disturbance

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16
Q

miglitol

A

alpha-glucosidase inhibitor: inhibit intestinal brush-boarder alpha-glucosidases, delayed sugar hydrolysis and glucose absorption–>decrease postrandial hyperglycemia
Used as monotherapy in type 2 DM or in combination with above agents
TOX: GI disturbance

17
Q

pramlintide

A

amylin analogs : decrease glucagon
type1 and type2 DM
TOX:hypoglycemia, nausea, diarrhea

18
Q

exenatide

A

GLP-1 analogs: increase insulin, decrease glucagon
for type 2
TOX: N/V, pancreatitis

19
Q

liraglutide

A

GLP-1(glucagon like peptide)analogs: increase insulin, decrease glucagon
for type 2
TOX: N/V, pancreatitis

20
Q

linagliptin

A

DPP-4 inhibitor: increase insulin, decrease glucagon
Type 2 DM
TOX: mild urinary or respiratory infection

21
Q

saxaliptin

A

DPP-4 inhibitor: increase insulin, decrease glucagon
Type 2 DM
TOX: mild urinary or respiratory infection

22
Q

sitagliptin

A

DPP-4 inhibitor: increase insulin, decrease glucagon
Type 2 DM
TOX: mild urinary or respiratory infection

23
Q

Propythiouracil

A

block peroxidase, there by inhibiting organification of iodide and coupling of thyroid hormone synthesis. blocks 5’-deiodinase, increase peripheral conversion of T4 to T3
use in hyperthyoidism
TOX: skin rash, agranulocytosis(rare), aplastic anemia, hepatotoxicity

24
Q

methimazole

A

block peroxidase, there by inhibiting organification of iodide and coupling of thyroid hormone synthesis.
use in hyperthyoidism
TOX: skin rash, agranulocytosis(rare), aplastic anemia, teratogen

25
Q

betablocker

A

block T4–>T3 conversion

used before and after RAI (ratio active iodium) therapy

26
Q

potassium perchlorate

A

ion inhibitor

blocks iodide absorption by competitive inhibitor

27
Q

Levothyroxine

A

thyroxine replacement
use in hypothyroidism, myxedema
tox: tachy, heat intolerance, tremors and arrhythmias

28
Q

triiodothronine

A

thyroxine replacement
use in hypothyroidism, myxedema
tox: tachy, heat intolerance, tremors and arrhythmias

29
Q

GH

A

in GH deficiency, Turner syndrome

30
Q

Somatosatin

octreotide

A

acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices

31
Q

oxytocin

A

stimulates labor
uterine contraction,
milk let down
control uterine hemorrhage

32
Q

ADH

desmopressin

A

pituitary DI

33
Q

demeclocycline

A

ADH antagonist(tetracycline family)
used in SIADH
tox: nephrogenic DI, photosensitivity, abnormalities of bone and teeth

34
Q

hydrocortisone

A

Glucocorticoids, decrease production of leukotrienes and PG by inhibiting phospholipase A2 and expression of COX-2
use in addison’s, inflammation, immune suppression, asthma
TOX: Iatrogenic Cushing

35
Q

prednisone

A

Glucocorticoids, decrease production of leukotrienes and PG by inhibiting phospholipase A2 and expression of COX-2
use in addison’s, inflammation, immune suppression, asthma
TOX: Iatrogenic Cushing

36
Q

triamcinolone

A

Glucocorticoids, decrease production of leukotrienes and PG by inhibiting phospholipase A2 and expression of COX-2
use in addison’s, inflammation, immune suppression, asthma
TOX: Iatrogenic Cushing

37
Q

dexamethansone

A

Glucocorticoids, decrease production of leukotrienes and PG by inhibiting phospholipase A2 and expression of COX-2
use in addison’s, inflammation, immune suppression, asthma
TOX: Iatrogenic Cushing

38
Q

beclomethasone

A

Glucocorticoids, decrease production of leukotrienes and PG by inhibiting phospholipase A2 and expression of COX-2
use in addison’s, inflammation, immune suppression, asthma
TOX: Iatrogenic Cushing

39
Q

Cinacalcet

A

Calcimimetics,

suppress the secretion of parathyroid hormone by increasing the sensitivity of Ca receptor