• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/183

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

183 Cards in this Set

  • Front
  • Back
blood vessels
ACE inhibitors have what 2 effects
↓ BP
ACE inhibitors are CI in pt with
bilateral renal artery stenosis
what is the perfusion of the kidney with ACE
ACE → efferent arteriole constriction → ↑ perfusion
what is the perfusion of the kidney with an ACE inhibitor
ACE inhibitor → ↓ perfusion → possible renal failure if the renal artery is stenotic
niacin is a tx for
hyperlipidemia
what are the SE of niacin
flushing, warmth, itching
niacin, the flushing SE is mediated by
prostaglandins
how would you prevent the flushing SE with niacin
aspirin pre-treatment
the body synthesizes histamine from the amino acid
histamine
histamine is released from _____ cells
mast cells (H1)
the body synthesizes serotonin from the amino acid
tryptophan
where is serotonin stored in the body
GI tract 90%
what is substance P
pain neurotransmitter in both PNS and CNS
what is the function of “capsaicin”
decreases pain by ↓ level of substance P in the PNS
what is the most recognized SE of ACE inhibitors?
cough
what is the mechanism behind ACE inhibitor induced cough?
accumulation of:
what is the effect of low dose dopamine?
D1: kidney perfusion ↑
what is the effect of high dose dopamine?
A1: peripheral vasoconstriction (inc renal vasoconstriction)
what drug characteristics would trap a drug in the plasma compartment
↑ MW fat, water loving, protein-hugging and charged!
would the volume of distribution of the above drug be?
low
Equation for distribution
Vd = amount of drug given/ plasma [drug]
how is bioavailibility related to drug distribution?
they are not related
bioavailability is a measure of _____
absorption
in a pt with diabetes, what kind of antihypertensive will you prescribe?
ACE-I and ARB
what are the effects of ACE-I and ARB in addition to anti-HTN action
↓ ESRD (end stage renal disease)
what antihypertensives should be selected for a pt with BPH (benign prostatic hyperplasia)?
alpha-1 blockers:
what antihypertensives should be selected for a pt with CAD and CHF
cardioselective beta blockers:
what antihypertensive should be selected for a pt with osteoporosis?
hydrochlorothiazide
what is the first line medication for tx of essentiao HTN in the general population
hydrochlorothiazides
what antihypertensive should be selected for a pt with a state of hyperaldosteronism (aldosterone-secreting tumor)
spironolactone
which one affects the vasculature and which one affects the heart?
nifedipine: vascular sm. M. (slit your wrists with a knife)
how would you alter the systolic blood pressure?
alpha 1 agonist → ↑ systolic bp
how would you alter the diastolic blood pressure?
beta 2 agonist → ↓ diastolic bp
SE of
cardiology
litium is linked to what anomaly in utero
Ebsteins anomaly
what is Ebsteins anomaly
apical displacement of the tricuspid valve leaflets, ↑ volume of the RV, and atrialization of the RV
what drugs can cause drug-induced lupus syndrome?
procainamide
what drug causes blue/grey skin discoloration
amiodarone
what are the other side effects of amiodarone
thyroid disease, lung fibrosis and liver toxicity
what is the most common SE of beta blockers
negative inotropy
SE of lidocaine
nonfocal neurologic signs:
SE of adenosine
chest burning
SE quinidine
weakness, GI effects
isosorbide dinitrate: what load does it affect
↓ cardiac work ← ↓ preload ← venodilation
digoxin: effect on K
digoxin toxicity → hyperkalemia
hepatobiliary system
↓ warfarmin conc
phenytoin and other P450 inducers
↑ warfarin conc
trimethroprim
↑ warfarin conc
cimetidine
hypercholesterolemia = ↑ _____
↑ LDL
what is the TOC for hypercholestrolemia
statins
SE of statins
myopathy
statins + _____ → ↑ risk of myopathy
statins + fibrates
why is the risk of myopathy increased in the above scenario
because fibrates increase the concentration of statins
what is the most likely statin to cause myopathy
simvastatin
GI
what stimulates gastric acid secretion from parietal cells?
Histamine
what stimulates the acetylcholine → gastric acid secretion
vagal stimulation
atropine blocks the gastric parietal cell _____ receptor
M3 acetylcholine receptor
cimetidine blocks the gastric parietal cell _____ receptor
histamine H2 receptor
sucralfate – action?
binds to base of mucosal ulcers, providing physical protection against acid
musculoskeletal
chronic use of corticosteroids like prednisone has what effect on bones
osteoporosis
TOC for rheumatoid arthritis (moderate to severe)
methothrexate
TOC for mild, early seronegative rheumatoid arthritis
sulfasalazine
is raloxifene an estrogen-agonist or antanist?
both
alendronate belongs to what class of drugs
bisphosphonate
alendronate: action on bones
bone resorption inhibitor; prevents and treats osteoporosis
leuprolide: it’s effects on bones if given in a pusatile fashion
[estrogen antagonism]
leuprolide: it’s effects on bones if given in a continous fashion
[estrogen antagonism]
prolonged use of parenteral medroxyprogesterone is associated with _____ bone mineral density in women of all ages
decreased
finasteride: effect on bone
none
finasteride: MOA
inhibits 5alpha reductase
TNF-alpha inhibitor: clinical use
tx for rheumatoid arthritis
name the TNF-alpha inhibitors
vowels: AEI
TNF-alpha inhibitor: SE
infections ← ↓ macrophage function
name the RA txs that inhibit purine and pyrmidine synthesis
go to the mall, you will see a lot of RA
name the RA tx that inhibits phospholipid degradation?
corticosteroids
name the RA tx that inhibits prostaglandin synthesis
NSAIDS
neurology
reserpine used for _____ in disadvantaged countries
as an antihypertensive that ↓ BP through sympatholytic effects
reserpine MOA
binds irreversibly to presynaptic vesicles and blocks the tranpsort of neuropeptides like NE, dopamine, and serotoinin INTO these vesicles
what happens to the neurotransmitters if they can’t be packaged into vesicles?
they are degraded by MOAs within the cytoplasm
what are the SE of reserpine
depression
what is reserpine used for in our country?
guanethidine MOA
prevents NE release into the synaptic cleft by
cocaine MOA
prevents NE reuptake from the synaptic cleft by presynaptic neuron
what other drugs act like cocaine at the synaptic cleft?
older TCAs
pulmonology
theophylline MOA
inhibits phosphodiesterase
what does the blockage of phosphodiesterase do?
prevents cAMP → AMP
SE of theophylline … the most dangerous
seizures and arrhythmias
what is tx for theophylline-induzed arrhythmia
beta blockers
what is the tx for theophylline-induced seizures
benzodiazepines
why?
hematemesis and melena
when would you see bradycardia, hypotension, and cardiovascular collapse
beta blocker toxicity
why?
glucagon → ↑ [cAMP] intracellular and cardiac contractility
when would you see severe sedation, respiratory depression, and constricted pupils
opioid intoxication
who would you treat opioid intoxication?
naloxone
renal
thiazide diuretics: location of action
DCT
thiazide diuretic: SE regarding K, Na, Mg
hypokalemia
thiazide diuretics vs. loop diuretics regarding Ca
thiazide → ↑ Ca 2+ = hypercalcemia
what is the mechanism of hypercalcemia in with the use of thiazide diuretics
unknown;
when do you use thiazide diuretics?
tx for edema secondary to:
carbonic anhydrase inhibitors: location of action
PCT
what are the most potent diuretics?
loop diuretics
loop diuretics: location of action
ascending limb
why are thiazide diuretics more potent than loop diuretics?
only a small amount of filtered Na reaches DT; loop has access to it first
potassium sparing diuretics: location of action
collecting duct
oncology
folinic acid (leucovorin): clinical use
can reverse the toxicity of methotraxate in non-cancerous cells in the GI mucosa and bone marrow (if given at the appropriate time)
allopurinol: clinical use
tx of gout and prevention of tumor lysis syndrome
allopurinol: MOA
inhibit xanthine oxidase
filgrastim: clinical use
tx of neutropenia
filgrastim: MOA
analog of G-CSF (granulocyte colony-stimulating factor), used to simulate the proliferation and differentiation of granulocytes in pt with neutropenia
mesna: clinical use
prevents hemorrhagic cystitis in pt receiving cyclophosphamide or ifosfamide
mesna: MOA
binds acreolin , the toxic metabolite that is formed by cyclophosphamide and ofosfamide
dexrazoxane: clinical use
prevents anthracycline-induced cardiotoxicity
dexrazoxane: MOA
iron-chelating agent
amifostine: clinical use
↓ cumulative nephrotoxicity associated with platinum-containing and alkylating chemotherapeutic agents
amifostine: MOA
free-radical scavenger
vinca alkaloids: name an example
vincristine
vinca alkaloids: MOA
inhibit micrtubule formation
vinca alkaloids: SE
neurotoxicity
what are the four main stages of the cell cycle?
G1 → S → G2 → M
when would the cell be in G0?
G1 → S → G2 → M → G0 → G1
genitourinary
what are the absolute contraindications to OCP use
1.
2.
hx of estrogen-dependent tumor
3.
smokers > 35 y/o
4.
hypertriglyceridemia
5.
liver problems (would impair steroid metab)
6.
pregnancy
hematology
t-PA (tissue plasminogen activator): clinical use
mgmnt of:
t-PA: MOA
plaminogen → plasmin = thrombi breaks down
clopedigrel: clinical use
tx of CAD, peripheral vascular disease, cerebrovascular disease
would you use clopedigrel for a DVT?
no
in pregnancy, what anti-coagulant should you use?
heparin
can warfarin be used in pregnancy?
no
heparin: MOA
↑ antithrombin III activity
what is the DOC for DVT?
warfarin
microbiology
tx for N. gonorrhoeae
ceftriaxone
tx for C. trachomatis
doxycycline or azithromycin
metronidazle: clinical use
infx caused by anaerobic bacteria or protozoa
fluconazole: clincial use
antifungal to tx:
what are NNRTIs
nonnucleoside reverse transcriptase inhibitors
do NNRTIs require activation via intracelllar phosphorylation
no
name the common NNRTIs
nevirapine
what are NRTIs
nucleoside reverse transcriptase inhibitors
do NRTIs require activation via intracelllar phosphorylation
yes; must be converted by thymidine kinase from current form → monophosphate form before it can be converted into a pharmacologically active triphosphate form
ritonavir: MOA
HIV protease inhibitor; prevents assembly and maturation fo the virus
enfuvirtide: MOA
HIV fusion inhibitor; prevents HIV genome from entering uninfected CD4+ T cells
indinavir: belongs to what drug class?
protease inhibitor class of antiretroviral drugs
what are the important SE of ALL protease inhibitors
1.
2.
lipodystrophy
3.
P450 inhibition
what rx is used in HIV pt for prevention and tx of pneumonia caused by Pneumocystis jiroveci?
TMP-SMX
TMP-SFX: SE
1.
2.
Steven-Johnson syndrome
3.
toxic epidermal necrolysis
zidovudine: what group does it belong to?
NRTI
zidovudine: SE
bone marrow toxicity → anemia
acyclovir is an anti-viral rx against _____
HSV-1 and HSV-2
acyclovir: SE
renal toxicity
what rx is used in HIV pt for prevention and tx of Mycobacterium avium intracellulare (MAC) infections?
azithromycin
what rx is used for tx of CMV in HIV pt?
foscarnet
foscarnet SE
nephrotoxicity
protease inhibitors are anti-HIV medications that _____ inot mature viral proteins
inhibit cleavage of polypeptide precursor
define:odynophagia