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152 Cards in this Set

  • Front
  • Back
angina is due to
insufficient coronary blood flow to myocardium
angina =
myocardial O2 demand exceeds coronary O2 supply
stable angina is caused by
some degree of atherosclerotic occlusion in coronary vessels, so at some intensity of exercise, O2 demand exceeds O2 supply, causing pain
how do you treat stable angina?
rest and nitroglycerin
Prinzmetal (aka variant or vasospastic) angina is cause by
temporary vasospasm of coronaries; more common in women than men
tx of Prinzmetal angina
nitroglycerin
unstable angina is caused by (2 things)
1. acute plaque change --> partial trhombus
2. atherosclerotic occlusion severe enough that moment-to-moment sedentary changes in heart activity cause O2 demand to exceed O2 supply
can unstable angina be tx with NTG?
no
4 general treatments of angina
1. dilate coronary arteries
2. dilate coronaries and systemic veins
3. dilate coronaries and systemic arterioles
4. decrease cardiac contractility
to dilate coronary arteries for prompt relief of stable or Prinzmetal anginal attack
NTG
nitrolingual spray or nitrostat sublingual tabs
how does NTG relieve angina?
systemic veins dilate --> decrease in VR --> decrease in preload --> decrease in cardiac work
to dilate coronaries and systemic veins long-term to prevent anginal attacks
NTG
Nitrodur - patch
NitroBID - ointment
Isosorbide mononitrate or dinitrate - long-acting tabs
to dilate coronaries and systemic arterioles to prevent anginal attacks
dihydropyridine class of Ca-channel blocker like nifedipine (Procardia XL)
to decrease cardiac contractility to prevent anginal attacks
BB - propranolol or metoprolol
or
non-dihydropyridine class of Ca-channel blocker
- Verapamil (decreases HR and contractility)
- Diltiazem (decreases HR, contractility, dilates coronaries and arterioles - used for Prinzmetal's)
2 side effects of NTG
headache
postural hypotension
tolerance to long-acting nitrates develops rapidly -- how can you prevent this?
take the NTG patch or ointment off at night
major side effect of Ca-channel blockers
constipation
which class of drug is the only one to be used to decrease HR and contractility in a patient with a damaged heart from MI or CHF?
BBs
verapamil and diltiazem do not have the same beneficial effects as BBs
should never use Ca-channel blockers in these pts
these two things have been found to decrease risk of newly forming plaque as well as decreasing existing plaque
lifestyle changes and medication
CAD is positively correlated with
high TC, but more so with high LDL
High HDL is...
correlated with decreased risk of CAD
total cholesterol =
VLDL + LDL + HDL, where VLDL is TG/5
primary goal in cholesterol-lowering therapy is to reduce
LDL
target levels of cardiac lipids in normal person:
TC
LDL
HDL
ratio of TC to HDL
TC <200
LDL <130
HDL >60
TC:HDL ratio as low as possible
statins (HMG CoA reductase inhibitors) are used mainly to...
decrease LDL
2 statins that decrease LDL by 50%
atorvastatin (Lipitor) and rosuvastatin (Crestor)
how do statins lower LDL?
by inhibiting the rate limiting step in cholesterol synthesis
statins decrease intracellular/hepatic synthesis of cholesterol. this causes...
increased number of extracellular LDL receptors --> increased cellular uptake of LDL --> decreased plasma LDL
2 major side effects of statins
1. myopathy/muscle pain - pretty common, so need to test CPK-MM regularly
2. elevated liver enzymes, so need to test AST and ALT regularly
this drug decreases risk of CV events just as much as statins, and is cheaper
aspirin
which class of drugs is used to treat high TGs
fibrates
which fibrate can decrease TG by 50%?
another common fibrate?
fenofibrate (Lofibra)
gemfirozil (Lopid)
high TGs (>500) can cause...
pancreatitis
side effect of fibrates
myopathy
this drug causes the greatest increase in HDL (by 25%)
niacin
this drug causes the largest changes in all 3 lipids
niacin
2 side effects of niacin
1. facial flushing - can take aspirin or NSAIDs 30 minutes before taking in order to decrease this
2. gout
what can you do to prevent niacin-induced flushing?
extended release niacin
what are bile acid binding resins used for?
to lower LDL (by 30%)
3 bile acid binding resins
cholestyramine
colesevelam
colestipol
5 side effects of bile acid binding resins
1. bloating
2. flatulence
3. abdominal pain
4. decrease absorption of vitamins ADEK
5. decrease absorption of other drugs
this drug directly decreases GI tract cholesterol absorption
ezetimibe (Zetia)
do all of the anti-hyperlipidemic drugs affect both HDL and LDL?
yes
which anti-hyperlipidemic drug class decreases LDL most?
statins
which anti-hyperlipidemic drug class increases HDL most?
niacin
which anti-hyperlipidemic drug class decreases TGs most?
fibrates
the most important drug combo for cardiac lipids
fenofibrate + statin
substance that has significant cardio-protective effects and is under-utilized in practice
what is beneficial about them?
omega-3 fatty acids (from fish oil or dietary supplements)
they decrease TGs
this potentiates the toxicity of digoxin
hypoK
how do thiazides tx HTN?
dump some fluid volume
long-term they cause arteriolar vasodilation*
how do thiazides tx diabetes insipidus?
polydipsia and polyuria paradoxically respond because of the decrease in plasma volume
first, aldosterone causes increased Na and water retention which decreases polydipsia; second, there is less volume being filtered which decreases polyuria
ceiling diuretics
thiazides; ceiling b/c they are no better at higher doses
2 most commonly used thiazides
hydrochlorothiazide
Chlorthalidone
what do thiazide diuretics decrease? how about loop diuretics?
thiazides - Na reabsorption in distal convoluted tubule
loops - Na reabsorption in ascending limb of loop of Henle
when do thiazides become ineffective?
GFR <30
Ccr < 50
2 common uses for thiazides
tx of CHF and HTN
first choice of drug for mild HTN
thiazide diuretic
thiazides do what to Ca and K? so what can they treat?
loops do what to Ca and K? so what can they treat?
thiazides increase Ca reabsorption and K excretion; tx osteoporosis and prevent Ca stones
loops increase excretion; tx hyperCa and hyperK
3 side effects of thiazides
increase K excretion --> hypoK
increase H+ excretion --> alkalemia
decrease uric acid excretion --> gout
3 things that can be used to compensate for thiazide-induced hypoK
1. K-sparing diuretic
2. K supplement
3. bananas
3 loop diuretics
1. furosemide (Lasix)
2. bumetanide
3. ethacrynic acid
which kind of diuretic still works in a patient with renal insufficiency? why?
loops
decrease renal vascular resistance and increase renal blood flow
drug of choice for reducing/mobilizing pulmonary edema of heart failure
loop diuretics
these diuretics work quickly and so are useful in emergencies
loops
2 side effects of loops
1. ototoxicity (esp. when given with aminoglycoside)
2. shock (b/c of severe rapid reduction in blood volume and hypovolemia)
loop most likely to cause ototoxic deafness
ethacrynic acid
3 K-sparing drugs
TAS
triamterene
amiloride
spironolactone
possible side effect of K-sparing drugs
hyperK
aldosterone receptor antagonist and therefore not useful in normoaldosteronism; can't treat Addison's
spironolactone
2 side effects of spironolactone
1. gynecomastia
2. menstrual abnormalities

b/c it resembles sex steroids
most common osmotic diuretic
mannitol
how does mannitol work? how must it be given?
it increases water excretion
must be given IV
used to maintain tubular fluid after toxic ingestion, prevents ARF due to circulatory shock, lowers increased ICP
mannitol
what must be given with mannitol
PO or IV fluid to prevent dehydration
most common cause of heart failure
left systolic dysfunction due to CAD
3 compensatory mechanisms in HF to increase CO and maintain GF pressure
1. sympathetic tone - increases HR and contractility, increases renin secretion, and vasoconstriction
2. RAS system to increase volume
3. cardiac hypertrophy (dilated and globular)
increased salt intake, increased exertion, illness/fever, emotion, not taking meds, and AMI can cause this in chronic HF patient
decompensation, exacerbation, or acute HF
DOC for all stages of heart failure b/c limit cardiac remodeling and decrease M&M
ACEIs
2 ACEIs
Lisinopril, Captopril
3 side effects of ACEIs
1. dry cough
2. pharyngeal angioedema and airway closure
3. ARF in pt with RAS b/c it vasoconstricts the dilated efferent arterioles causing no pressure
2 ARBs
Losartan, Candesartan
why do ACEIs and ARBs decrease cardiac remodeling?
they decrease aldosterone, so no volume overload and decreased filling pressures
this drug is used in advanced HF for the same reason ACEIs and ARBs are used
spironolactone
negative inotropes that improve systolic function in HF and decrease remodeling b/c they block renin
beta blockers
2 beta blockers for heart failure
Carvedilol
Metoprolol
beta blocker that is also an alpha blocker
Carvedilol
which class of drugs have no use in HF
Ca-channel blockers
positive inotrope reserved for pts not responding to combo therapy of ACEI, BB, and diuretic
digoxin
which kind of HF is digoxin used for
only left-sided systolic HF
sx of digoxin toxicity
1. severe dysrhythmias
2. N/V
3. headache and confusion
4. blurred vision, halos, etc.
3 electrolyte disturbances that predispose to dig toxicity
1. hypoK
2. hypoMg
3. hyperCa
digoxin Ab
Digiband
DOC for mild asthma and also for rescue in all severities of asthma
short-acting B2 agonists
2 short-acting B2 agonists
albuterol
terbutaline
salmeterol
formoterol
2 long-acting B2 agonists
do short-acting B2 agonists have anti-inflammatory action? how about inhaled glucocorticoids?
no
yes
DOC for moderate or severe asthma
inhaled glucocorticoids
fluticasone (Flovent)
triamcinolone (Azmacort)
inhaled glucocorticoids
best combination therapy for controlling moderate and severe asthma
inhaled steroid + long-acting B2 agonist
tx of status asthmaticus
sometimes PO steroid like prednisone
or IV steroid like methylprednisolone
side effect of inhaled steroids
oral candidiasis
po anti-leukotrienes
inhaled anticholinergics
po theophylline
inhaled cromolyn and nedocromil
subq monoclonal Ab to IgE
alternatives to inhaled steroid + long-acting B2 agonist
only remaining anti-leukotriene (leukotriene receptor blocker)
montelukast (Singulair)
anti-inflammatory
inhaled anticholinergic that causes bronchodilation and decreased mucus secretion
ipratropium (Atrovent)
bronchodilator with slight anti-inflammatory effect
theophylline
cromolyn and nedocromil
mast cell stabilizers used to block allergen and exercise induced asthma
Xolair
monoclonal Ab that binds IgE and prevents it from binding to mast cells
expensive and not first-line
long-acting anticholinergic for COPD
tiotropium (Spiriva)
what drugs other than Spiriva can be used for COPD
B2 agonists
combo of long-acting anticholinergic (Spiriva) + long-acting B2 agonist (salmeterol)
used for COPD
do inhaled steroids aid in COPD?
no, except in exacerbation
propranolol or verapamil
A-flutter
SVTs (AV nodal re-entry)
propranolol or amiodarone + Coumadin
A-fib
lidocaine or amiodarone
acute V-tach (in AMI)
V-fib not responding to defibrillation
3 classes of antiplatelets and examples of each
1. COX-1 inhibitor (aspirin)
2. ADP receptor blocker (Plavix)
3. GP IIb/IIIa receptor blocker (ReoPro and Aggrastat)
Disalcid
non-acetylated salicyclic acid, so has no anti-platelet effect
Celebrex, APAP, Vioxx
COX-2 inhibitors (no anti-platelet effect)
when taken alone, believed to cause CV events b/c of increased production of thromboxane A2
claudication, visible arterial insufficiency, ankle-brachial index <0.9
PAD - should be taking ASA
side effects of ASA
prolonged bleeding time --> increased risk of hemorrhagic stroke, GI bleed
what is used if ASA cannot be tolerated
Plavix
side effect of Plavix and other ADP blockers
neutropenia
inhibits action of thrombin by binding anti-thrombin and activating it to inhibit thrombin
heparin and lepirudin
inhibits synthesis of thrombin
warfarin
anticoag of choice in pregnancy b/c doesn't cross placenta
LMWH
aPPT used to monitor effect of...
IV heparin
1.5-2.5x NL
enoxaparin (Lovenox)
dalteparin (Fragmin)
LMWH - given subq and don't need aTTP (replacing IV heparins)
antidote for heparin-induced hemorrhage
lower dose, D/C, or Protamine sulfate (doesn't work as well for antidote to LMWH)
4 side effects of heparin
hemorrhage
hypersensitivity
thrombocytopenia
DIC
tx of DIC
stop heparin, may use lepirudin
direct thrombin antagonist
lepirudin
vitamin K antagonist
coumadin
b/c during synthesis of clotting factors, vit K is deactivated and coumadin doesn't allow reactivation
monitored by PT
coumadin
1.5-2.5x normal
antidote for coumadin-induced bleeding
vitamin K oral
if very severe, IV or FFP
teratogenic anti-coag
warfarin
alteplase and streptokinase
thrombolytics
convert plasminogen to plasmin
thrombolytics
"fibrin-selective" thrombolytic b/c it has greater affinity for plasminogen already bound to fibrin
alteplase
induces a systemic fibrinolytic state b/c it binds to free plasminogen in the plasma
streptokinase
side effect of streptokinase
increases risk of hemorrhage
antidote for fibrinolytic state of streptokinase
aminocaproic acid (Amicar)
pts with healing wounds, pregnancy, recent CVA, or metz CA should no take these
thrombolytics
what is the window for use of thrombolytics?
2-6 hours (acute)
most successful delivery of thrombolytics for AMI
intra-coronary (cardiac cath) but usually have to give IV b/c of the window
tx for Fe-deficiency anemia
oral ferrous sulfate
Fe supplements 3-6 months
side effects include constipation and black stools
Fe supplements
in pt who can't take or absorb oral Fe, such as inflammatory bowel disease, what should they take?
parenteral Fe therapy - Iron Dextran
3 causes of folate-deficiency anemia
pregnancy
alcoholism
folate-antagonistic drugs like trimethoprim
tx of folate-deficiency anemia
folic acid
2 causes of B12-deficiency anemia
lack of intrinsic factor: pernicious anemia or gastric resection
dietary deficiency
tx of dietary B12 deficiency anemia
tx of pernicious anemia or B12 malabsorption
oral B12
IM B12 to normalize and Nascobal nasal gel to maintain
neurologic sx of B12 deficiency
1. parasthesias
2. tinnitus
3. decreased vibration sense
4. decreased proprioception and balance problems
tx of severe anemia from ESRD, HIV, CA
erythropoietin and Fe supplement