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64 Cards in this Set

  • Front
  • Back
What is the underlying cause of angina pectoris?
accumulating metabolites from myocardial ischemia with an imbalance between oxygen demand and supply
What is another name for variant angina?
prinzmetal angina
What generally causes effort or classic angina?
atheromatous obstruction of large coronary vessels
What type of angina do arthromas cause?
vasospastic or variant angina
Is variant angina reversible or irreversible?
reversible coronary vasospasm
What causes episodes of unstable angina?
increased epicardial coronary tone or small platelet clots around atherosclerotic plaques
What is the best way to treat effort angina?
reduce cardiac work load, ie be lazy
What is the best way to treat variant angina?
with nitrates or Ca channel blockers to decrease arterial spasm
What does the heart favor as an energy source? In angina drugs are used to shift from this energy source to anohter. What is the other source?
1) fatty acids
2) switch to glucose because it requires less oxygen and can reduce oxygen demand in heart (fatty acid oxidation inhibitors)
What is the function and effect of increasing cGMP in smooth muscle cells?
it facilitates dephosphorylation of myosin light chains preventing myosin from interacting with actin
What enzyme does nitric oxide activate?
guanylyl cyclase which increases cGMP
What ion do beta blockers effect?
decrease intracllular Ca levels
What is the effect of minoxidil sulfate on smooth muscles?
causes relaxation of the cells by opening K+ channels increasing K+ permeability. This lower stabilizes the membrane potential near resting potential
What effect does increasing cAMP have on smooth muscle cells? What drug group increases this?
inactivation of myosin light chain kinase the enzyme needed to trigger the interaction of myosin and actin.

Beta2 agonists, though not used because they cause too much cardiac stimulation
Describe the events preceding muscle contraction in a smooth muscle cell (SMC)
Ca enters and binds calmodulin. This complex activates myosin light chain kinase which phosphorylates myosin light chains so that they interact with actin and contract
What enzyme is present in SMC and other cells that is involved in denitration of nitroglycerin? What happens to the free nitrite?
1) glutahione S-transferase
2) it gets converted to nitric oxide
Excessive nitro intake can result in what reflex?
sympathetic response
Are veins or arteries more responsive to nitro?
veins most and arterioles and capillaries least
What is the effect of nitro on preload?
decreases it by increasing the blood reserve in the veins. Note cardiac output is decreased
A person goes from sitting to standing and faints. what drug were they likely taking?
orthostatic hypotension can result from nitro
What changes in the heart are seen when someone takes nitro?
increased contractility and tachycardia
What enzyme do capillary endothelial cells have that makes nitro? What is the precursor?
endothelial nitric oxide synthase makes arginine into NO
Does phosphodiesterase inhibit or promote vasoconstriction? What drug inactivates PDE?
inhibits by degrading cGMP. PDE is inactivated by sildenafil
What type of anginal patient may not be as responsive to nitro?
people with atherosclerotic obstructive CAD
What is the effect of nitro on platelets?
guanylyl cyclase is activated in platelets producing cGMP and decreasing platelet aggregation
A patient after taking nitro for an extended period develops cyanosis what is going on?
nitrites can bind hemoglobin making methemoglobin which has a very low affinity for oxygen. it results in a pseudocyanosis
What food contains lots of nitrites?
cured meat
A patient has been exposed to high levels of cyanide. What can be given to reverse the affects?
nitrites because they form methmeglobin which has a very strong affinity for cyanide. this will reactivate the cytochromes. Vitamin B12 also has a high affinity for cyanide
what is tachyphylaxis?
'A rapid decrease in the response to a drug after repeated doses over a short period of time
What is a concern with continuous use of nitrates?
tachyphylaxis
Why would there be a paradoxically increased demand for oxygen in someone taking nitro?
because it increases heart contractility and causes tachycardia
Where are L-type Ca channels found?
cardiac, skeletal, SMC, endocrine cells, bone
Where are T-type Ca channels found?
heart and neurons
Where are N-type Ca channels found?
neurons
What are dihydropyridines?
Ca channel blockers
Why would there be a paradoxically increased demand for oxygen in someone taking nitro?
because it increases heart contractility and causes tachycardia
Where are L-type Ca channels found?
CARDIAC, SMC, skeletal, endocrine cells, bone
Where are T-type Ca channels found?
heart and neurons
Where are N-type Ca channels found?
neurons
What are dihydropyridines?
Ca channel blockers
What subunit of the L-type Ca channel do nefedipine and verapamil bind?
the alpha1 subunit
How do the L-type Ca channel blockers work? What results after binding?
they bind the intracellular part of the channel and bind more effectively to open and inactivated channels. the effect is that the frequency of opening in response to depolarization is reduced with diminished Ca flow across the membrane resulting in SMC relaxation and decreased cardiac contractility
Why would neurons or other cells not be as susceptible to dihydropyridines?
these cells have L-type channels that spend less time in the open or inactive states which are needed for dihydropyridines to act
What drugs can be given to counteract dihydropyridines?
sympathomimetics or supplemental Ca
What vessels are more sensitive to dihydropyridines? As a result what side effect is not seen with these that is seen with nitro?
1) arterioles are more sensitive than veins
2) orthostatic hypotension because the veins do not relax as much to hold more blood
Would the SA and AV nodal fibers be affected by dihydropyridines?
yes
Are dihydropyridines or verapamil better able to tachycardias?
verapamil acts more exclusively at the AV node
Why is skeletal muscle not susceptible to Ca channel blockers?
it does have the L-type Ca channel but it has a large pool of intracellular Ca that it uses to compensate for the decreased extracellular influx
What effect would Ca channel blockers have on glands?
decrease secretion in glands that require Ca for exocytosis of substances
What toxicities are noted with Ca channel blockers?
cardiac depression, bradycardia, AV block, and HF
Would the SA and AV nodal fibers be affected by dihydropyridines?
yes
Are dihydropyridines or verapamil better able to tachycardias?
verapamil acts more exclusively at the AV node
Why is skeletal muscle not susceptible to Ca channel blockers?
it does have the L-type Ca channel but it has a large pool of intracellular Ca that it uses to compensate for the decreased extracellular influx
What effect would Ca channel blockers have on glands?
decrease secretion in glands that require Ca for exocytosis of substances
What toxicities are noted with Ca channel blockers?
cardiac depression, bradycardia, AV block, and HF. Note poeple also taking beta blockers are more prone to adverse effects
What could a person with superventricular tach or atrial fib/flutter be treated with?
verapamil... remember verapamil has more effect on the SA and AV node than dihydropyridines
Which drugs will reflex tachycardia be seen less with verapamil and diltiazem or dihydropyridines?
verapamil and diltiazem because these have a prominent effect on the SA and AV node to slow them down
What are Ca channel blockers good for besides angina?
supraventricular tachyarrythmias, HTN,
What is the inotropic effect of Ca channel blockers on HF?
negative, contraindicated
Why are beta blockers good for angina?
they decrease heart rate, blood pressure and contractility
What are undesirable effects of beta blockers in angina? How can they be counteracted?
increase end diastolic volume and increase ejection time both of which can increase myocardial oxygen demand. Give nitro to counteract
When are beta blockers contraindicated?
asthma, bronchospastic conditions, severe bradycardia, AV blockade, left ventricular failure
Do nitrates, beta blockers or Ca channel blockers increase ejection fraction and end diastolic volume?
beta blockers and Ca channel blockers
In patients with unstable angina what should the focus be on?
giving aggressive antiplatelet therapy