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Pharmacology > drugs only module 12-14 > Flashcards

drugs only module 12-14 Flashcards

1
Q

what are the classes of drugs to treat elevated blood lipids?

A 
statins
bile acid sequestrants
nicotinic acid
cholesterol absorption ihibitors
fibric acid derivatives (fibrates)
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2
Q

atorvastatin

A

low oral bioavailability (14%)
large fraction of absorbed does is extracted by the liver (site of action)
distrib primarily to liver but also to spleen, adrenal glands, & skeletal muscle
metabolized by CYP3A4
elminated in feces

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3
Q

rosuvastatin

A

low oral bioavailability (20%)
large fraction of absorbed does is extracted by the liver (site of action)
distrib primarily to liver but also to skeletal muscle
not extensively metabolized
elminated in feces
*plasma concentrations approx. 2x higher in asian patients compared to caucasian - the initial dose should be 5mg and caution to be used when increasing dose

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4
Q

adverse effects of statins

A

generally well-tolerated
myopathy (muscle injury)
rhabodomyolysis rare but serious - muscle lysis with severe muscle pain & diagnosed with high levels of creatine kinase. it’s also accompanied by high levels of potassium which can lead to kidney problems
hepatotoxicity - possible but low incidence
*teratogen as cholesterol required for synth of cell membranes & many hormones

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5
Q

nicotinic acid

A

inhibits hepatic secretion of VLDL. Since, LDL is a by-product of VLDL degredation, this drug effectively reduces both
increases blood HDL levels
side effects: intense facial flushing, hepatotoxicity, hyperglycemia, skin rash, increased uric acid levels

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6
Q

bile acid sequestrants

A

large + charged molecules that attract and bind bile acids (neg charged), preventing their absorption
causes increased demand for bile acid synth in liver which uses LDL cholesterol
liver increase # of LDL receptors, increasing uptake of LDL from blood
adverse effects: limited to GI tract - constipation and bloating
also, may decrease the absorption of some drugs that are neg. charged such as thiazide diuretics, digoxin, warfarin, and certain antibiotics

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7
Q

ezetimibe (Zetia)

A

cholesterol absorption inhibitor
inhibits transport protein NPC1L1 which absorbs dietary cholesterol
lowers blood LDL cholesterol 15-20%
can produce a compensatory increase in hepatic cholesterol synth so usually an adjunct therapy used with a statin
*there is a combo pill called vytorin which contains a statin and ezetimibe (can reduce LDL cholesterol up to 60%)

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8
Q

Fibric Acid Derivatives (Fibrates)

A

most effective class for lowering plasma triglyceride levels
they also increase HDL, no effect on LDL
bind to PPARalpha in liver
effects of activating PPAR alpha:
1.increased synth of enzyme lipoprotein lipase (gets rid of triglycerides)
2.decreased apolipoprotein C-III production (which normally inhibits lipoprotein lipase)
3. increased apolipoprotein A-I and apolipoprotein A-II levels - increases HDL levels

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9
Q

adverse effects of fibrates

A

increased risk of gallstones
myopathy
hepatotoxicity
*fibrates & statins have some of the same adverse efects so pt.s on both need to be monitored for side effects

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10
Q

Loop diuretics

A

antihypertensive
most effective diuretic
block sodium and chloride ion reabsorption in the thick ascending limb of the loop of henle
reserved for situations requiring rapid loss of fluid like edma, severe hypertension not responding to other diuretics, severe renal failure

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11
Q

adverse effects of loop diuretics

A

hypokalemia (can cause fatal cardiac dysrhythmias)
hypoatremia
dehydration
hypotension

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12
Q

thiazide diuretics

A

most common drug for HTN

2 mech: 1. block sodium and chloride ion reabsorption in distal tubule 2. decreasing vascular resistance

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13
Q

adverse effects of thiazide diuretics

A

hypokalemia (can cause fatal cardiac dysrhythmias)
dehydration
hyponatremia

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14
Q

potassium sparing diuretics/aldosterone atnagonists

A

minimal lowering of BP
inhibit aldosterone receptors in collecting duct
blocking these receptors causes increased sodium excretion and potassium retention
main use is in combo with loop or thiazide diuretics to counteract potential hypokalemia side effect
NOT to be used with ACE inhibitors or renin inhibitors as these drugs conserve potassium

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15
Q

adverse effects of potassium sparing diuretics/aldosterone atnagonists

A

hyperkalemia (can cause fatal cardiac dysrhythmias)

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16
Q

beta blockers

A

tx HTN
“olol”
antagonist
2 mech: 1.block cardiac beta 1 receptors - as blocks binding of catecholamines therefore decreasing CO 2.blocks beta 1 receptors juxtaglomerular cells -blocks renin release which decreases RAAS mediated vasoconstriction therefore decreasing peripheral resistance

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17
Q

what is the difference between 1st and 2nd generation beta blockers?

A

1st gen - inhibit both beta 1 and beta 2 - beta 2 found in lung and can be problematic for those with lung issues
2nd gen- selective for beta 1 receptors

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18
Q

adverse effects of beta blockers

A

selective beta 1: bradycardia, decreased CO, heart failure (rare), rebound hypertension if withdrawn abruptly
non-selective: bronchoconstriction, inhibition of hepatic and muscle glycogenolysis

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19
Q

Angiotensin Converting Enzyme (ACE) inhibitors

A

tx HTN
“pril”
2 mech: 1.decreased production of angiotensin II therefore causing vasodilation and decreased blood vol therefore decrease CO and peripheral resistance 2.inhibit the breakdown of bradykinin - having more bradykinin causes vasodilation

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20
Q

adverse effects of ACE inhibitors

A

generally well tolerated
side effects from decreased angiotensin II - first dose hypotension, hyperkalemia
side effects from increased bradykinin: persistent cough, angioedema
*use with certain NSAIDs may decrease effect of ACE inhibitors

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21
Q

Angiotensin Receptor Blockers (ARBs)

A

tx HTN
“sartan”
block binding of angiotensin II to recptor AT1
cause vasodilation as blocking effect of angiotensin II
also decrease aldosterone release from adrenal cortex causing increase water and sodium excretion

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22
Q

adverse effects of ARBs

A

not really any significant adverse effects

low risk of angioedema

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23
Q

Direct Renin Inhibitors (DRIs)

A

bind to renin and block the conversion of angiotensinogen to angiotensin I
influences entire RAAS pathway
BP lowering effect similar to other HTN drugs

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24
Q

adverse effects of DRIs

A

hyperkalemia - should not be taken with other drugs that may cause hyperkalemia and no potassium supplements
very low incidence of persisten cough and angioedema
diarrhea

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25
Q

calcium channel blockers

A

tx HTN
calcium essential for contraction
blocks calcium from entering heart and smooth muscle cells, decreasing contraction
2 categories: dihydropyridine calcium channel blockers and non-dihydropyridine calcium channel blockers

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26
Q

dihydropyridine calcium channel blockers

A

“dipine”
significantly decrease calcium influx into cmooth muscle of arteries leads to relaxation of muscles = vasodilation
-therapeutic doses don’t act on heart

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27
Q

adverse effects of dihydropyridine calcium channel blockers

A

flushing, dizziness, headache, peripheral edema, reflex tachycardia, rash

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28
Q

non-dihydropyridine calcium channel blockers

A

block calcium influx in heart and smooth muscles of arteries

decrease peripheral resistance and CO

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29
Q

adverse effects of non-dihydropyridine calcium channel blockers

A 
constipation
dizziness
flushing
headache
edema
may compromise cardiac function
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30
Q

Centrally Acting Alpha 2 agonists

A

bind to and activate alpha 2 receptors in the brainstem
decreases sympathetic outflow to heart and blood vessels
inhibiting sympathetic outflow decreases peripheral resistance and CO

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31
Q

adverse effects of Centrally Acting Alpha 2 agonists

A

drowsiness
dry mouth
rebound HTN if withdrawn abruptly

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32
Q

Levodopa (L-Dopa)

A

tx of parkinson’s disease
dopamine replacement
most effective drug for PD
crosses BBB
inactive until converted to dopamin in dopaminergic nerve terminals mediated by decarboxylase enzymes
cofactor pyridoxine (vit B6) speeds up reaction
*usually given with carbidopa which inhibits peripheral metabolism mediated by decarboxylase enzymes so more L-Dopa reaches the brain (10%)

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33
Q

adverse effects of L-Dopa

A 
nausea and vomiting
dyskinesias
cardiac dysrhythmias
orthostatic hypotension
psychosis

may experience 2 types of loss of effect:
1 - wearing off - gradual loss of effect
2. on-off - abrupt loss of effect

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34
Q

dopamine agonist

A

tx PD
directly activate dopamine receptors on post-synaptic cell membrane
not as effective as L-Dopa but usually first line of tx for people with milder symptoms

35
Q

adverse effects of dopamine agonists

A

hallucinations
daytime drowsiness
orthostatic hypotension

36
Q

dopamine releaser

A

tx PD
stim release of dopamine from neurons, blocks dopamine reuptake, blocks NMDA receptors (blockade of these decreases dyskinesia side effect of L-Dopa)
*used in combo with L-Dopa or alone

37
Q

adverse effects of dopamine releaser

A

dizziness, nausea, vomiting, lethargy, and anticholinergic side effects

38
Q

Catecholamine-O-Methyltransferase Inhibitor (COMT inhibitor)

A

Tx PD
COMT is exnyme that adds methyl group to dopamine and L-Dopa which inactivates them
by inhibiting COMT, greater fraction of L-Dopa avail
*often combined with L-Dopa

39
Q

adverse effects COMT inhibitor

A

nausea
orthostatic hypotension
vivid dreams
hallucinations

40
Q

Monoamine oxidase-B (MAO-B) inhibitors

A

tx PD
MAO-B is an enzyme that metabolizes dopamine and L-Dopa through oxidation, causing inactivation
therefore, inhibiting MAO-B allows more L-Dopa to be converted and more dopamine to remain in nerve terminals
*often combined with L-Dopa

41
Q

adverse effects of MAO-B inhibitors

A

insomnia, orthostatic hypotension, dizziness
*at therapeutic doese MAO-B inhibitors used to tx PD don’t inhibit MAO-A in the liver and so they don’t cause hypertensive crisis when pt.s eat tyrosine containing foods

42
Q

aticholinergic drugs

A

tx PD
block binding of acetylcholine to receptor
may increase effectiveness of L-Dopa
decrease incidence of diaphoresis, salivation, and incontinence (symptoms of relative excess of acetylcholine)

43
Q

adverse effects of aticholinergic drugs

A

dry mouth, blurred vision, urinary retention, constipation, tachycardia
*elderly people may experience severe CNS effects such as hallucination, confusion, and delirium so usually these drugs not given to elderly

44
Q

cholinesterase inhibitors

A

tx AD
inhibit metabolism of acteylcholine by enzyme acetylcholinesterase
allows more acetylcholine to remain in synaptic cleft
only able to enhance cholinergic transmission is remaining healthy neurons
only effective in approx 25% of pt.s

45
Q

adverse effects of cholinesterase inhibitors

A

nausea and vomiting
diarrhea
insomnia

46
Q

NMDA receptor antagonists

A

tx AD
in AD there is excess glutamate release so the NMDA receptor remains open allowing excess calcium into cells (excess calcium detrimental to learning/memory & causes degredation of neurons)
NMDA receptor antagonists blocks calcium influx into the post-synaptic neuron

47
Q

adverse effects of NMDA receptor antagonists

A

well tolerated

side effects same incidence as placebo group in trials

48
Q

what are the two classes of drugs to treat schizophrenia?

A

conventional antipsychotics
atypical antipsychotics
*differ in mech of action and side effect profile

49
Q

conventional antipsychotics

A

block dopamine 2 (D2) receptors in the medolimbic area of the brain
also block (to a lesser extent) acetylcholine, histamine, and norepinephrine
more effective at treating + symptoms
initial effects 1 or 2 days but improvement 2 to 4 weeks

50
Q

adverse effects of conventional antipsychotics and atypical

A

shared: anticholinergic effects, orthostatic hypotension, sedation

Uniqe to conventional: extrapyramidal symptoms, sudden high fever, skin reactions

Unique to atypical: weight gain, risk of devel type II diabetes

51
Q

what are extra pyramidal symptoms?

A

a.k.a. EPS
movement disorders that resemble symptoms of PD
d/t blockade of D2 & 4 types
1. acute dystonia - involuntary spasm face, tongue, neck, or back. occurs early in therapy
2. parkinsonism - same as symptoms of PD. may treat with anticholinergic to help relieve. L-Dopa must be avoided>
3. Akathesia - pacing, squirming, and a desire to continually be in motion. early in tx.
4. tardive dyskinesia - irreversible so early detection is important. includes involuntary twisting and writhing of face and tongue along with lipsmacking. should be switched to atypical antipsychotic

52
Q

atypical antipsychotics

A

block D2 and 5-HT1A and 5-HT2A receptors
affinity for D2 is very low
therapeutic action attributed to blocking of the 5-HT receptors

53
Q

compare and contrast conventional with atypical antipsychotics

A

comapred with conventional, atypical antipsychotics…

  1. Same efficacy vs. + symptoms
  2. greater efficacy vs. - symptoms
  3. much lower risk of devel. extrapyramidal symptoms, esp. tardive dyskinesia. attributable to decreased D2 blocking
54
Q

what are the 4 mech of action that antiepileptic drugs (AEDs) work by?

A

blocking sodium channels
blocking voltage-dependent calcium channels
glutamate antagonists
potentiating the actions of GABA

55
Q

Phenytoin

A

antiepileptic drug
blocking sodium channels - prolong the inactivation state of the sodium channel and therefore don’t allow neurons to fire at a high freq
all seizures except absence
metabolic capacity by liver limited, so easy to spike blood levels
narrow therapeutic range

56
Q

adverse effects of phenytoin

A

sedation, gingival hyperplasia, skin rash

*teratogenic

57
Q

blocking voltage-gated calcium channels

A

inhibition of voltage-gated calcium channels suppresses neurotransmitter release

58
Q

glutamate antagonists

A

blocking glutamate decreases CNS excitation

-glutamate binds to NMDA and AMPA receptirs so the antagonists bind to these

59
Q

potentiating the actions of GAVA

A

increase inhibitory stimuli in the CNS and therefor suppress seizure activity

  • these drugs mediate their effects in 4 different ways:
    1. enhancing binding of GABA to its receptor
    2. stimulating GABA release
    3. inhibiting GABA reuptake
    4. inhibiting GABA metabolism
60
Q

talk about traditional vs. newer antiepileptic drugs

A

traditional - phenytoin, valproic acid
newer - lamotigrine
*newer = decreased side effects, decreased propensity to induce hepatic drug metabolizing enzymes

61
Q

classes of antidepressants

A

tricyclic antidepressents
selective serotonin reuptake inhibitors (SSRIs)
selective serotonin/norepinephrine reuptake inhibitors (SNRIs)
monoamine oxidase inhibitors (MAOIs)

62
Q

tricyclic antidepressents (TCAs)

A

inhibit reuptake of serotonin and norepinephrine

tx major depression

63
Q

adverse effects of tricyclic antidepressents

A 
anticholinergic effects
sedation
orthostatic hypotension
decreased seizure threshold
cardiac toxicity (rare but serious)
weight gain
sexual dysfunction
64
Q

selective serotonin reuptake inhibitors (SSRIs)

A

block serotonin reuptake
less incidence of side effects than TCAs
*most common tx and most commonly used in major depression

65
Q

adverse effects of selective serotonin reuptake inhibitors (SSRIs)

A

weight gain
sexual dysfunction
insomnia
serotonin syndrome - increased serotonin can cause agitation, confusion, anxiety, hallucinations, incoordination
*may appear within 3 days of therapy & stop when drug is stopped

66
Q

selective serotonin/norepinephrine reuptake inhibitors (SNRIs)

A

block reuptake of norepinephrine and serotonin
tx major depression
faster onset of action (than TCAs)

67
Q

adverse effects of selective serotonin/norepinephrine reuptake inhibitors (SNRIs)

A

nausea
diastolic hypertension
sexual dysfunction

68
Q

monoamine oxidase inhibitors (MAOIs)

A

MAO-A enzymes metabolize serotonin and norepinephrine
MAO-B enzymes metabolize dopamine
MAOIs inhibit both types of MAO enzymes
tx atypical depression and dysrhythmia

69
Q

adverse effects of MAOIs

A

CNS excitation - anxiety, insomnia, agitation
orthostatic hypotension
**hypertensive crisis if taken with tyrosine containing foods

70
Q

three major groups of drugs to treat bipolar disorder

A

mood stabilizers
antipsychotics
antidepressants

71
Q

mood stabilizers

A

1.relieve symptoms during manic/depressive episodes
2.prevent recurrence of episodes
3. don’t worsen the manic or depressive symptoms
primary drugs: lithium and valproic acid

72
Q

lithium

A

mood stabilizer
thought to alter release and uptake of glutamate and block the binding of serotonin
narrow therapeutic range and plasma concentrations may be altered by sodium
sodium loss from body may increase the plasma concentrations and cause toxicity

73
Q

antipsychotics for bipolar

A

used acutely for manic symptoms and long term to stabilize mood
atypical antipsychotics are preferred over conventional antipsychotics d/t less risk of extrapyramidal sympoms

74
Q

antidepressants for bipolar

A

tx depressive episodes

always combined with mood stabilizer

75
Q

drugs treat anxiety

A

benzodiazepines (BDZs)
buspirone
antidepressants

76
Q

benzodiazepines (BDZs)

A

first line therapy
potentiaing action of GABA
they are not agonists - they bind to a different site on the receptor and cause increased binding of endogenous GABA
causes CNS depression
tx generalized anxiety disorder and social anxiety disorder

77
Q

adverse effects of benzodiazepines (BDZs)

A 
CNS depression
anterograde amneisa
respiratory depression
teratogenic
tolerance
withdrawal
78
Q

Buspirone

A

acts on serotonergic and/or dopaminergic neurons
useful in tx clts who use alcohol (no CNS depression)
tx generalized anxiety disorder
its effect on anxiety if slow going so not good for immediate relief

79
Q

adverse effects of Buspirone

A

generally well-tolerated and non-sedating

dizziness
lightheadedness
excitement

80
Q

which antidepressants are good for treating generalized anxiety disorder?

A

SSRIs and SNRIs

81
Q

which antidepressants are good for treating panic disorder/agoraphobia?

A

SSRIs, TCAs and MAO inhibitors

*SSRIs preferred as better tolerated

82
Q

which antidepressants are good for treating OCD?

A

SSRIs first line therapy

*also require behavioural therapy

83
Q

which antidepressants are good for treating social anxiety disorder?

A

SSRIs first line therapy although BDZs may also be used

*BDZs provide immediate relief while SSRIs take a while to kick in

84
Q

PTSD

A

no good evidence that any drug is effective in treating PTSD

Pharmacology (7 decks)

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