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Pharmacology > NMT200 Midterm > Flashcards

NMT200 Midterm Flashcards

1
Q

goals of therapy in obesity

A
  • overall, aim to reduce body fat for health by 5-10% for health benefits
  • stabilize and prevent further weight gain
  • prevent weight regain
  • prevent and treat obesity-related comorbidities/complications
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2
Q

drugs associated with weight gain

A
  • antidepressants (particularly tricyclic antidepressants)
  • antipsychotics - first and second generations
  • corticosteroids (ex. prednisone)
  • antihyperglycemic drugs (sulfonylureas, meglitinides, thiazolidinediones); insulin
  • lithium
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3
Q

which drugs are most likely to cause the greatest increase in weight gain

A

insulin
antipsychotics
lithium

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4
Q

T/F: lifestyle modification alone is superior to lifestyle modification and anti-obesity therapy

A

false: lifestyle modification and anti-obesity therapy together is superior

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5
Q

drugs that fall into the appetite suppressant category

A

bupropion alone
bupropion in combination with naltrexone

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6
Q

what other indications are there for bupropion?

A

antidepressant
smoking cessation aid
alcohol abuse disorder

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7
Q

indication for bupropion/naltrexone combination

A

indicated for weight management alongside diet and exercise for those with BMI of 30 or higher (27 if weight-related comorbidity present)
- mediates hormones involved in appetite and reward

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8
Q

what are the other indications for naltrexone

A

anti-opioid medication

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9
Q

adverse effects of bupropion

A

dry mouth, constipation, agitation, insomnia, anxiety

higher doses: seizures (rare)
hepatic impairment (fibrotic changes)

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10
Q

adverse effects for bupropion/naltrexone combination
contraindications

A

n/v, constipation, headache, dizziness, insomnia, dry mouth
contrindicated with concurrent opioid therapy due to precipitation of opioid withdrawal - patients must be opioid free for 7 days prior to initiation of treatment

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11
Q

avoid using bupropion with:

A

avoid concurrent use of drugs that lower seizure threshold
minimize/avoid alcohol
consuming with high-fat meal
uncontrolled hypertension, seizure disorder, severe hepatic impairment, end-stage renal failure

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12
Q

what drug for obesity falls into the class of lipase inhibitors?

A

orlistat

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13
Q

orlistat mechanism of action

A

gastric and pancreatic lipase inhibitor that reduced dietary fat absorption by 30%

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14
Q

orlistat adverse effects
contraindications

A

oily spotting, flatus with discharge, fecal urgency
decreased absorption of fat-soluble vitamins
contraindicated: chronic malabsorption syndrome or cholestasis

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15
Q

orlistat cautions

A

advise to take multivitamin daily at least 2 hrs before/after orlistat/at bedtime
high fat intake is poorly tolerated
less effective in patients on low fat diets

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16
Q

what are the major incretin hormones in humans?
what do they have in common re: metabolism?

A

GLP-1 and GIP (glucose dependent insulinotropic polypeptide)
they are responsible for most of the glucose-induced insulin secretory response following ingestion of glucose
both are metabolized by the enzyme dipeptidyl peptidase 4 (DPP4)

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17
Q

mechanism of action for incretin mimetics

A

GLP-1 - reduction of food intake and appetite, increased satiety, decreased gastric emptying, and affects reward-related systems in the brain
GIP has less effect on other organs, delays gastric emptying, plays a role where fat is depositied

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18
Q

what class of drugs does liraglutide fit into

A

incretin mimetic - a GLP-1 agonist

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19
Q

liraglutide:
administration
indications

A

administered via subcutaneous injection DAILY
indicated: type 2 diabetes, weight loss

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20
Q

liraglutide adverse effects

A

most common: n/v, constipation, diarrhea
GI side effects can be minimized in slow titration of dose
can cause pancreatitis in rare instances
severe hypoglycemia in patients with T2D

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21
Q

cautions of taking liraglutide

A
  • in patients with heart rhythm disturbances, hepatic insufficiency, severe renal impairment
  • should not be used in IBD (slows gastric emptying)
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22
Q

contraindications of liraglutide

A

pregnancy, breastfeeding
personal or family history of medullary thyroid carcinoma or multiple neoplasia syndrome type 2 (MEN2)

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23
Q

when to discontinue liraglutide in obesity

A

after 12 weeks if body weight loss is <5%

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24
Q

what class of obesity drugs does semaglutide fall into?
mechanism of action?

A

incretin mimetics - is a GLP-1 agonist like liraglutide

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25
Q

how is semaglutide different from liraglutide?

A

both GLP-1 agonists, subcutaneous
semaglutide has a longer half life so only needs to be administered once/week

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25
Q

adverse effects of semaglutide

A

n/v diarrhea, abdominal pain, constipation, digestive upset, fatigue, dizziness
increase in amylase and lipase - suggests possible pancreatitis

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25
Q

what is the general advice for weight loss during pregnancy?

A

despite increased risks to mother and infant, weight loss during pregnancy is not recommended
consensus is to counsel regarding weight gain targets during pregnancy
none of these drugs have evidence for safe use during pregnancy

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25
Q

which weight loss drugs are not recommended during pregnancy specifically?
which drug has conflicting evidence?

A

orlistat is not recommended because of reduced fat soluble vitamin absorption

evidence for bupropion is conflicting - it should not necessarily be discontinued if patient is already taking it pre-conception and if the therapy is needed

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26
Q

what is important to remember about the STEP 5 trial?

A
  • compared semaglutide to placebo for obesity, but the placebo wasn’t a true placebo because it included lifestyle interventions
  • the papers discuss the absolute weight change in the drug group (15%) but the actual MEAN change in weight in the drug group was 12%
  • adverse effects: pancreatitis not present but lab values increasing towards pancreatitis
  • subjects were mostly white women, middle aged
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27
Q

what classes of drugs can cause dyslipidema

A
  • beta blockers (ending in -olol)
  • corticosteroids (prednisone)
  • HMG CoA Reductase Inhibitors (statins)
  • thiazide or loop diuretics: hydrochlorothiazide, furosemide
  • protease antiviral medications
  • second generation antipsychotics: olanzapine, quetiapine
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28
Q

goals of therapy in drugs for diabetes

A

control symptoms
maintain glycemic control, avoid hypoglycemia
prevent/minimize risk of complications
achieve optimal control of risk factors (hypertension, obesity, dyslipidemia)

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29
Q

where is insulin sourced from when used as a therapy for diabetes? why

A
  • most options are lab derived insulin, or human insulin analogues since they cause less antibody generation and adverse effects
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30
Q

what is meant by onset of action and duration of action of insulin in terms of diabetes management

A

rapid onset insulin preparation: useful for postprandial insulin injections or use with an insulin pump (continuous infusion)

long acting insulin preparations: useful for basal insulin infusion

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31
Q

adverse effects of insulin medication in diabetes

A

hypoglycemia - most common due due missed meals or increase in exercise
localized fat hypertrophy
allergic reactions - usually animal insulin

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32
Q

what drug class does metforin fall into?

A

biguanides
it is the only drug in this class

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33
Q

metformin mechanism of action

A

decreases hepatic glucose production
not associated with weight gain

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34
Q

adverse effects of taking metformin

A

nausea, diarrhea, abdominal discomfort, anorexia, metallic taste
lactic acidosis in cases of existing hepatic or renal disease (contraindicated)
vitamin B12 deficiency with long-term use
risk of hypoglycemia is low when used as monotherapy

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35
Q

what is an example of a drug in the alpha-glucosidase inhibitor group?

A

acarbose

36
Q

acarbose mechanism of action

A

inhibits INTESTINAL (not systemic) alpha-glucosidases - results in delayed digestion of starches and disacchardies which reduces postprandial glucose levels

37
Q

how does acarbose have an effect on intestinal lactase?

A

it doesn’t really - is does not significantly inhibit lactose metabolism

38
Q

important things to know about taking acarbose

A

requires TID dosing
only effective if taken with a meal
hypoglycemic patients taking acarbose should be treated with GLUCOSE rather than sucrose (bc it inhibits the absorption of sucrose)
does not cause weight gain

39
Q

adverse effects of taking acarbose

A

flatulence, diarrhea, abdominal pain, cramps, nausea
may reduce metformin bioavailability
contraindicated in IBS, IBD

40
Q

what group of diabetic drugs ends in -gliptin?
what is an example of one of these drugs?

A

dipeptidyl peptidase 4 inhibitors
ex. sitagliptin

41
Q

mechanism of action of sitagliptin

A

indirectly acts as an incretin mimetic
- inhibits the enzyme responsible for the degradation of GLP-1 and other active peptides involved in glucose homeostasis (increases its biological half life)

42
Q

how effective are dipeptidyl peptidase 4 inhibitors in diabetes?

A

they do not seem to affect CVD risk
they lower HbA1c by 1% or less (not awesome)
do not cause weight gain/are considered weight neutral

43
Q

adverse effects of sitagliptin

A

nasopharyngitis, hypersensitivity reactions
rare events: pancreatitis, severe joint pain
low potential for drug interactions because does not inhibit cytochrome P450 enzymes
low risk of hypoglycemia

44
Q

what drugs are considered GLP-1 receptor agonists? used for diabetes

A

semaglutide
liraglutide

45
Q

how do semaglutide and liraglutide work in diabetes?

A

as direct incretin mimetics, they act on GLP-1 receptors
increase insulin secretion, suppress postprandial glucagon secretion, slow gastric emptying, increases satiety

46
Q

how does semaglutide and liraglutide prescription differ in diabetes vs weight loss?

A

in lower doses, used as antidiabetics
higher doses cause weight loss

47
Q

what effect do semaglutide and liraglutide have on CVD risk?

A

serve as primary and secondary prevention in patients

48
Q

adverse effects of semaglutide and liraglutide

A

GI adverse effects are common and nausea upon initiation
injection site reactions
rare: acute pancreatitis

49
Q

semaglutide and liraglutide contraindications

A

caution in patients with heart rhythm disturbances and severe renal impairment

contraindicated: in pregnancy, those with personal/family history of MENS2

50
Q

what class of drugs does glyburide belong to?

A

sulfonylureas
a diabetic drug

51
Q

what drug class often begins with “gly” or “gli”?
what is an example?

A

sulfonylureas
ex. glyburide

52
Q

glyburide mechanism of action

A

an insulin secretagogue which stimulates both basal and meal-stimulated insulin release
generally considered add-on therapies to metformin rather than used as monotherapy

53
Q

glyburide risks in general?
does it help reduce CVD risk?

A

higher risk of hypoglycemia and more weight gain
ability to reduce CV events is uncertain due to lack of evidence

54
Q

adverse effects of glyburide

A
  • weight gain, prolonged hypoglycemia
  • risk of hypoglycemia may be greater in elderly or patients with renal imapirment
55
Q

what is the concern with beta-blockers and glyburide?

A

beta blockers may mask hypoglycemic symptoms - patient blood sugar may be low and they won’t fully know

56
Q

what drug class does repaglinide belong to?

A

meglitinides

57
Q

repaglinide mechanism of action

A

is another class of insulin secretagogues - sitmulates insulin release but the activity is much shorter

58
Q

adverse effects of repaglinide

A

metabolic drug interactions (because of its effect on the liver)
side effects similar to sulfonylureas: weight gain, prolonged hypoglycemia
lower risk of hypoglycemia in the context of skipped meals

59
Q

what class of drugs does canagliflozin belong to? what does it treat?

A

sodium-glucose cotransporter 2 inhibitors
treats daibetes

60
Q

mechanism of action for canagliflozin
does it cause weight gain

A

works by preventing glucose reabsorption in the kidneys which leads to enhanced glucose absorption
does not cause weight gain

61
Q

how effective if canagliflozin?

A

reduced CV mortality and reduced CV events
slightly decreases BP
requires sufficient kidney function so, provided the kidneys are working it is effective
slows progression of neuropathy

62
Q

adverse effects of canagliflozin

A

increased risk of genitourinary infections
reduced intravascular volume -> hypotension
hyperkalemia
risk of diabetic ketoacidosis
use with look diuretics increases risk of hypotension

63
Q

what class of drugs does pioglitazone belong to? what is it used to treat?

A

thiazolidinediones
treats diabetes

64
Q

pioglitazone mechanism of action

A

agonists at PPAR-gamma receptors located on the cell nucleus, especially in adipose tissue:
- this influences gene expression -> upregulates GLUT4 transporters and lipoprotein lipase -> enhanced glucose reabsorption and hydrolysis of circulating TGs

65
Q

clinical effects of taking pioglitazone

A
  • increased peripheral glucose uptake
  • enhanced fat cell sensitivity to insulin
  • decreased hepatic glucose output
  • reduced HbA1c by 1-1.5%
    associated with weight gain
66
Q

adverse effects of taking pioglitazone

A

increased incidence of heart failure (due to increased fluid retention and edema)
increase risk of hip and wrist fracture
worsen macular edema

67
Q

which antidiabetic medication requires physicians to expressly perform informed consent and obtain written consent?

A

piaglitzaone

68
Q

thyrotoxicosis definition

A

any condition of excessive thyroid hormone and its effects

69
Q

hyperthyroidism definition

A

is due to excess thyroid hormone production

70
Q

thyroid storm definition

A

a life threatening medical emergency, caused by severe thyrotoxicosis

71
Q

what is a toxic nodule (re: thyroid)

A

a functional nodule that is secreting thyroid hormone

72
Q

what is a nonpharmacological choice used in managing hyperthyroidism? what is a common and likely adverse effect of this treatment?

A

surgery
adverse effect: hypothyroidism

73
Q

indications for radioactive iodine prescription?
how does it work?

A

used to ablate thyroid tissue in patients with Graves disease and toxic nodules

since the thyroid rapidly concentrates iodine, an oral dose has minimal effect on the rest of the body. Also, uses beta waves which only destroys the tissue within a very small range

74
Q

adverse effects of radioactive iodine therapy

A

high risk of hypothyroidism
possible worsening of Graves orbitopathy
risk of radiation thyroiditis

75
Q

what is methimazole used to treat? what it its mechanism of action?

A

treats: hyperthyroidism
decreases production of thyroid hormone by interfering with iodination of tyrosine as well as coupling
does not affect stored thyroid hormone or thyroid hormone in circulation, so it takes a bit for the drug to have an overall effect

76
Q

adverse effects of methimazole

A

risk of skin rash, allergic reaction, agranulocytosis
rare: hepatotoxicity

77
Q

contraindications of methimazole

A

first trimester of pregnancy - can cause aplasia cutis

78
Q

what is propylthiouracil used to treat? what is its mechanism of action? how is this different from methimazole?

A

decreases production of thyroid hormone

different from methimazole: additionally, inhibits conversion of T4 to T3 in periphery;
affects production of thyroid hormone and existing thyroid hormone (so it actually can be used to treat thyroid storm)

79
Q

adverse effects of propylthiouracil

A

risk of skin rash, allergic reaction, agranulocytosis
rare: severe hepatotoxicity
does NOT cause aplasia cutis

80
Q

when are beta blockers used to treat thyroid conditions? what is the mechanism?
example of a beta blocker?

A

hyperthyroidism
used to ameliorate the symptoms of adrenergic excess caused by excess thyroid hormones (elevated HR, hypertension)
ex. propranolol can decrease conversion of T4-> T3 in periphery

81
Q

adverse effects of beta blockers in hyperthyroidism

A

bradycardia
dizziness
fatigue
headache
hypotension

82
Q

when are beta blockers contraindicated/avoided when addressing hyperthyroidism?

A

avoid in patients with asthma or conditions associated with bradycardia

83
Q

how long does it take to attain a new steady state after dosage adjustments of levothyroxine? why is this? why is this important?

A

6 weeks - half life is fairly long
don’t adjust the dose earlier than 6 weeks because any sooner may result in too large of dosing

84
Q

what factors are levothyroxine dosage based on?

A

lean body mass - for BMI <25 we don’t need to figure out LBM
elderly patients may need less
those at risk of angina start with less
initial dose depends on endogenous thyroid function

85
Q

interactions with levothyroxine

A

absorption may be reduced by:
- antacids
- mineral supplements
- PPIs
- estrogens
variable effects with anticoagulant drugs

86
Q

how far apart from other drugs should levothyroxine be taken?

A

6 hours before any other meds

87
Q

adverse effects of levothyroxine treatment

A

symptoms of hyperthyroidism if over treated
possible exacerbation of angina
glycemic control may decline when first starting the dose - may need to adjust antihyperglycemic drugs

88
Q

what to know about desiccated thyroid

A

it can be used based on patient preference
good for those who are not converting T4-> T3 very well
tablets come in fixed amounts (30, 60, 125 mg) so may have to split tablets to get the right dose

89
Q

what is the threshold dose of desiccated thyroid where there is increased risk of having cardiovascular effects?

A

> 100mg

90
Q

adverse effects of desiccated thyroid

A

similar to levothyroxine: symptoms of hyperthyroidism if over treated, possible exacerbation of angina

risk of CV and neurological effects with larger doses due to T3: palpitation, tachycardia, arrhythmias, angina, nervousness, tremors, headache, insomnia, sweating, heat intolerance, fever, weight loss

91
Q
A

Pharmacology (1 decks)

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