Martin pharm DM part II Flashcards

1
Q

what are adverse effects to insulin therapy

A

hypoglycemia
insuline allergy and resistance
lipoatrophy and lipohypertrophy

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2
Q

biggest risk factor hypoglycemia

A

the more rigorous attempt to achieve euglycemia

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3
Q

causes of hypoglycemia with Tx

A

inappropriate dose
mismatch of time of injection vs food intake
exercise induced increase glucose utilization

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4
Q

what is the dominant counter regulatory hormone for hypoglycemia in DM I patients and why

A

epinephrine because glucagon secretion becomres deficient

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5
Q

most frequent allergic reaction to insulin

A

IgE mediated local cutaneous reactions

occasionally anaphylactic reaction or insulin R due to circulating IgG Ab

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6
Q

what causes the lipohypertrophy/atrophy from insulin

A

site of constant injection

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7
Q

what are conditions that require IV insulin

A

ketoacidosis

perioperative control and childbirth

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8
Q

msot common drug induced ypoglycemic states are those caused by

A

ethanol, beta-adrenergic antagonists and salicylates

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9
Q

why can beta antagonists cause hypoglycemia

A

inhibit the effects of catecholamines on gluconeogensis and glycogenolysis
also mask the sympathetically mediated Sx assoc with fall in blood glucose (tremors and palpiataions)

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10
Q

what drugs either have direct hyperglycemic effect ot indirect

A

epi, glucocorticoids, oral contraceptions (direct)
phenytoin, clonidine, Ca Ch blockers (inhibit insulin secretion
some diuretics deplete K and indirectly inhibit insulin secretion

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11
Q

Initial monotherapy for DM II

A

metformin

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12
Q

effects of metformin

A

reduce haptic glucose output by inhibiting gluconeogenesis
increase insulin action in peripheral tissues
increase glucose uptake dna utilization by muscle
reduce intestinal absorption of glucose

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13
Q

why is metformin preferred over sulfonylureas

A

does not cause weight gain or provoke hypoglycemia

has lipid lowering effect

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14
Q

side effects metformin

A

abdominal discomfort, anorexia, nausea, metallic taste, diarrhea

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15
Q

CI to metformin

A

lactic acidosis, hepatic disease, renal impairment, cardiac failure, chronic hypoxic lung disease

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16
Q

what clears metformin

A

kidneys

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17
Q

what type of sulfonylureas are used now

A

the second generations
glipizide
glyburide
glimepiride

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18
Q

glyburide should be used cautiously in what patients

A

elderly with renal failure and otheres predisposed to hypoglycemia

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19
Q

how do sulfonylureas work

A

lower blood glucose by stimulating insulin release from pancreatic beta cells
bind to and bloc ATP sensitive K channel
extrapancreatic effects like increased # receprtors for insulin and LGUT transporters

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20
Q

what metabolizes sulfonylureas

A

liver

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21
Q

patients most likley to respond to sulfonlyureas

A

older than 30 recently Dx
not overtly obese
some beta cell function
<300 fasting level glucose

22
Q

drug of choice if CI for sulfonlyureas

A

insulin

23
Q

adverse reactions sulfonlyureas

A

hypoglycemic reactions like a coma

nausea, vomiting, cholestatic jaundice, hypoNa, agranulocytosis, aplastic anemia, HS reactions

24
Q

drug drug interactions with sulfonylureas

A

many transiently increase hypoglycemic effects

25
Q

CI to sulfonlyureas

A

type I DM, sulfa allergies, pregnant or nursing mothers and significant hepatic or renal insufficiency

26
Q

what are the non sulfonylure secretagogues

A

repaglinide and natedlinide

27
Q

what type of patient adheres better to repaglinide and nateflinide

A

those whoe are erratic eaters because rapid action if taken right before a meal

28
Q

can repaglinide and nateflinide be combined with metformin

A

yes

29
Q

how do acarbose and miglitol work

A

alpha glucosidase inhibitors

competitive inhibition of sugar digestion delaying absorption of carbs and limits postprandial rise in glucose

30
Q

drugs most useful in newly diagnosed DM II patients with mild hyperglycemia

A

alpha glucosidase inhibitors

31
Q

if combined with what drugs will the alpha glucosidase inhibitors cause hypoglycemia

A

insulin or sulfonlyureas

32
Q

side effects alpha glucosidase inhibitors

A

flatulence, diarrhea and GI upset from undigested carbohydrate

33
Q

CI for alpha glucosidase inhibitors

A

diabetic ketoacidosis, cirrhosis, IBD, colonic ulcers, partial intestinal obstruction

34
Q

what are TZDs used for (thiazolidinediones)

A

poorly controlled DM II

35
Q

what must you do if Tx patient with TZD

A

liver function tests every 3 mo

36
Q

how do TZDs work

A

bind nuclear transcription factors PPAR-gamma site that resensitize target tissue to insulin

37
Q

effects of pioglitazone TZD

A

reduce insulin R
improve peripheral action insulin
reduce hyperglycemia by inc glucose uptake
reduce hepatic glucose production
take several weeks to produce a clinical effect

38
Q

pioglitazone is approved for regimen with what

A

monotherapy
insulin
sulfonylureas or metformin

39
Q

side effects pioglitazone

A

moderate weight gain, edema, mild anemia

fluid retention

40
Q

risk with rosiglitazone

A

MI

41
Q

What is pramlintide

A

maylin analog

42
Q

how is pramlinitide administered

A

SQ injection before meals

43
Q

advserse effects pramlinitide

A

increased risk hypoglycemia, nausea

decreased appetite, comiting, stomach pain, tiredness, dizziness or indigestion

44
Q

what secretes glucagon like peptide

A

intestinal L cells

45
Q

what is the GLP analog

A

exenatide

46
Q

effects of GLP-1 agonists

A

glucose dependent enhancement of endogenous insulin secretion
inhbition of endogenous glucagon secretion
appetite suppression
reduction in speed of gastric emptying
stimualte islet growth

47
Q

most common adverse effects GLP-1 agonists

A

nausea, vomiting, diarrhea and upper resp Sx

48
Q

biggest drawback to GLP-1 agonists

A

need 2x SQ injection

49
Q

adverse effects of the Na glucose co transporter 2 inhibitors

A

genital mycotic infections and UTIs
diuretic effects sometimes
bladder cancer

50
Q

which drug class in DM causes increased risk for acute pancreatitis and severe HS reactions

A

DPP-4 inhibitors