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Endocrine II DF > Diabetes Drugs DSA > Flashcards

Diabetes Drugs DSA Flashcards

1
Q

which pathway has direct effect on increased glut-4 expression

A

CBL

PI3K/AKT

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2
Q

insulin effects on MEK/ERK–> increased ___ and effects

A

ELK1

cell growth and differentiation
cell proliferation and increased survival

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3
Q

insulin and increased AP-1

A

cell growth and differntiation

cell proliferation and apoptosis

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4
Q

insulin and FOX01

A

decreased FOX1–> increased PPAR-y =lipogenesis

decreased glycogenolysis

decreased gluconeogenesis

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5
Q

inhibition of gluconeogenesis

A

PI3K/AKT—-> ^PDE —>decrease cAMP which
reduced expression glucose-6 phosphatase
decreased fructose 1,6 bisphosphatse
reduced PEPCK

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6
Q

clinical use of aspart, lispro, glulisine

duration

A

postprandial hyperglycemia
-take before meal
1-3 hrs

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7
Q

clinical use of regular insulin

duration

A

basal insulin maintenance
overnight coverage
if for postprandial hyperglycemia, inject 45 min before the meal
10 hrs

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8
Q

NPH, protamine has to what before what

A

be digested by tissue proteolytic enzymes before insulin can be absorbed

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9
Q

clinical use of NPH

A

basal insulin maintenance and or overnight coverage

duration is 10-12 hrs

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10
Q

loop diuretics on K+

A

K+ wasting

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11
Q

AE of insulin

A

hypoglycemia

lipodistrophy (hypertroph/atrophy of subcut fat at site of injection, change site to prevent)

resistance: IgG Abs can develop to neutralize exogenous insulin

allergic reactions

hypokalemia

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12
Q

common causes of hypoglycemia

A

delay of meal or missed meal
exercise
overdose of insulin

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13
Q

treatment for hypoglycemia

A

glucose: juice, candy, IV glucose

diazoxide-> K+ channel opener, inhibits insulin release

glucagon

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14
Q

MOA of glucagon

A

Gs coupled GPCR
activates AC–>PKA–>glycogen phosphorylase = glycogenolysis

increased PEPCK and Glu-6-phosphatase = gluconeogenesis

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15
Q

glucagon effects

A

hepatocytes: increased glucose output, glycogen depletion (no depletion in skeletel muscle)

potent inotropic and chronotropic effect on heart

GI smooth muslce relaxation

increase insulin release by beta cells

increase release of catecholamines by chromaffin cells

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16
Q

what pts is glucagon contraindicated in

A

pts with pheochromocytomas

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17
Q

clinical uses of glucagon

A

mod to severe hypoglycemia
beta blocker overdose
radiology of the bowel

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18
Q

clinical use of pramlintide

A

type 1 diabetes

type 2 diabetes as adjunt to insulin therapy before meal

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19
Q

onset
duration
pramlintide

A

rapid

3 hr

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20
Q

AE pramlintide

A

nausea, vomiting, diarrhea, anorexia

severe hypoglycemia

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21
Q

drug interactions of pramlintide

A

enhances effects of anticholinergic drugs in GI tract (constipation)

22
Q

long acting GLP-1 receptor agonists and half life

A

exenatide =2.4hrs

liraglutide = 11-15 hrs

23
Q

clinical use of long acting GLP-1 receptor agonists

A

GLP-1 inhibits glucagon secretion and excesive hepatic glucose output postprandially

  • this is diminished in type 2 diabetic pts
  • approved for these pts who can’t control diabetes with metformin/sulfonylureas/thiazolidineodiones
24
Q

GLP receptor against and weight

A

can induce some weight loss

25
Q

AE long actinv GLP-1 receptor agonists

A

GI disturbance
acute pancreatitis and pancreatic cancer
possible link to thyroid cancer

26
Q

DDP-4 inhibitor clinical use

alone or in combo?

A

approved as adjunctive therapy in DM2

monotherapy and in combo with metformin/sulfonylureas/TZDs

27
Q

AE of DDP-4 inhibitor

A

URI
nasopharyngitis
acute pancreatitis
hypoglycemia

28
Q

adverse effects of sulfonylureas

A

hypoglycemia
weight gain
secondary failure- respond initially then later cease to respond = hyperglycemia again
disulfiram-like effect of alcohol induced flushing
dermatological and gen hypersens rxns

29
Q

clinical use of sulfonylureas

A

type 2 diabetes as monotherapy or in combo with insulin or other anti-diabetic drugs

30
Q

drug interactions of sulfonylureas

enhancing hypoglycemic effect

A

displace from binding with plasma proteins: sulfonamides, clofibrate, salicylates

enhance effect on KATP channel: ethanol

inhibiting CYP enzymes: azoles, gemfibrozil, cimetidine

31
Q

drug interactions of sulfonylureas decreaseing glucose lowering effect

A

inhibiting insulin secretion: beta blocker, CCB

antagonizing effect on Katp channel: diazoxide

inducing hepatic CYP enzymes: phenyotoin, griseofulvin, rifampin

32
Q

side effects of meglitinides

A

hypoglycemia
secdonary failure
weight gain

33
Q

clinical use of meglitinides
take how
combo or alone?

A

control postprandial hyperglycemia in pts with DM2
take orally before meal
use alone or in combo with other antidiabetic drugs

34
Q

MOA biguanides (metformin)

A

activation of AMP-dep protein kinase

inhibit respiratory complex I in mitochondria

35
Q

clinical use of metformin

-advantages

A

most common oral agent for DM2, first line
advantages:
-taken orally, no hypoglycemia, no weight gain, decreased risk of micro and macro vascular complications, superior glucose lowering efficacy

36
Q

AE and contraindications of metformin

A

GI complications
decreased B12 absorption
lactic acidosis, especailly with hypoxia, renal and hepatic insufficiency

contraindicatied in pts with HF and copd, renal fialure, alcholism and cirrhosis

37
Q

MOA thiazolidinediones

effects of MOA

A

ligand of PPAR-y nuclear receptor which dimerizes with RXR binds to PPRE

effects of PPARy activation

increased GLUT4 in skeletal muscle and adipocytes

increased IRS1,2, PI3K = increased insulin sensitivity

increased adiponectin = increased insulin sensitivity

decreased: NFK-B, AP-1, PEPCK (RL step gluconeogensis)

38
Q

pk of thiazolidinediones
-taken how
effects when and persist how long

A

orally
takes 1-3 months for full effect
effects persist after drugs elminated for weeks-months

39
Q

metabolization of thiazolidinediones

  • pioglitazone
  • rosiglitazone
A

metabolized by liver

pioglitazone by CYP2C8 and CYP34A

rosiglitazone by CYP2C8 and CYP2C9
(rosie from lake was a 2 from neck up and 8-9 from neck down)

40
Q

clincial use TZDs

A 
type 2 diabetes alone or in combo
delay progression of prediabetes to DM2
euglycemi drugs (no hypoglycemia when used alone)
41
Q

AE TZDs

A

exacerbation heart failure
link to increased risk bladder cancer
osteoporisis
increased TC and LDL-C

42
Q

other effects of SGLT2 inhibitors

A 
osmotic diuresis
weight loss
reduced BP
reduced plasma uric acid
no hypoglycemia when used alone
43
Q

how should flozins (SGLT2 inhibitors) be taken

and clinical use

A

orally before first meal once a day

adjunct to diet and exerceise in adults with DM2

44
Q

AE SGLT2 inhibitors

A

hypotension
hypoveolemia (orthostatic HTN, dizziness, syncope)
UTI (can lead to urosepsis and pyelonephritis)
increased LDL-C
renal function impairment
ketoacidosis
hyperkalemia

45
Q

hyperkalemia can form in which pts taking SGLT2 inhibitors

A

pts with impaired renal fnct

htose taking ACEIs, ARBs, and K+ sparing diuretics

46
Q

MOA of miglitol and acarbose

A

competivie inhibtion of a-glycosidases

47
Q

clinical use of miglitol and acarbose

does not cause

A

DM2 monotherapy or in combo
take orally at mealtime
no hypoglycemia or weight gain

48
Q

AE of miglitol and acarbose

A

malabsorption, flautulence, diarrhea, abdominal bloating

49
Q

drug interactions of miglitol

A

decrease absorption of propranolol and ranitidine

Miggy ran the game proper

50
Q

drug interaction of acarbose

A

decrease absorption of digoxin

dont dial phone digits in ACAR(bose)

Endocrine II DF (7 decks)

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