Nagelhout Pharm 2 Exam 3 |82
Accurate Q’s and A’s
Class I antiarrhythmics - -Sodium channel blockers (procainamide, lidocaine)
- Class II antiarrhythmics - -Beta blockers (propranolol)
- Class III antiarrhythmics - -K channel blockers (prolongs depolarization)
(amiodarone)
- Class IV antiarrhythmic - -Calcium channel blocker (verapamil, diltiazem)
- adenosine works on what kind of receptor? - -purinergic receptors
- 3 populations to be cautious of beta blockers in - -asthmatics (cause
bronchoconstriction), diabetics (cause hypoglycemia), this with claudication
- drug of choice for A-fib/flutter - -CCB-diltiazem
alternate: beta blocker
- drug of choice for ventricular arrhythmias - -amiodarone (K-blocker);
alternate: lido
- drug of choice for torsades - -magnesium
- drug of choice for bradycardia - -atropine
- drug of choice for tachycardia - -beta-blocker
- how to you treat dig toxicity - -treat however it presents- like a normal
arrhythmia (atrial vs ventricular etc)
- BP Category: Normal - -SBP <120 and DBP <80
- BP Category: Elevated - -SBP: 120-129 and DBP <80
- BP Category: HTN Stage 1 - -SBP:130-139 or DBP: 80-89
- BP Category: HTN Stage 2 - -SBP: >140 or DBP:>90
- Hypertensive crisis - -SBP>180 or DBP>120
- Definition: Hypertensive urgency - -hypertensive urgency- the a patient
comes to medical attention with severe hypertension (SBP>180 or DBP
, >120) but does not have associated acute end organ damage of the CNS, CV
system or kidneys
reduce BP over hours to days
- Definition: Hypertensive Emergency - -hallmark: presence of acute end
organ damage and high degree of BP elevation. End-organ damage is the
result of acute rise in BP
treatment in Minutes- hours to prevent morbidity/mortality
- Definition: Hypertensive crisis - -more reflective of the high degree of BP
elevation
- 3 primary systems in the body to maintain BP - -autonomic nervous
system (catecholamines--> increased B in kidneys which increases renin-->
RAAS)
RAAS
vasopressin
- when you stimulate one, you stimulate them all
- How do ACE-I work? - -preventing the conversion of angiotensin I to
angiotensin II
- how do ACE-I cause cough - -bradykinin is broken down by ACE; ACE-I
increases bradykinin--> cough
- how do ARBs work? - -ARBs work by blocking the angiotensin receptor
blocker
- Esmolol vs Labetalol - -Labetalol:
-is a B and a blocker--> vasodilation
-not cardioselective
-preferred for HTN
Esmolol
-just a B blocker--> vasoconstriction
-shorter acting (broken down by RBC esterase in the plasma)
- "cardioselective" (not really)
-preferred for tachycardia
- how does nitroprusside work? - -its part of the nitro group so it vasodilates
- how is nitroprusside metabolized? - -by hemoglobin
- how is nitroprusside eliminated? - -It goes to the liver. Rhodanese causes
cyanide to act with vitamin B 12 to become thiocyanate which you pee out
Accurate Q’s and A’s
Class I antiarrhythmics - -Sodium channel blockers (procainamide, lidocaine)
- Class II antiarrhythmics - -Beta blockers (propranolol)
- Class III antiarrhythmics - -K channel blockers (prolongs depolarization)
(amiodarone)
- Class IV antiarrhythmic - -Calcium channel blocker (verapamil, diltiazem)
- adenosine works on what kind of receptor? - -purinergic receptors
- 3 populations to be cautious of beta blockers in - -asthmatics (cause
bronchoconstriction), diabetics (cause hypoglycemia), this with claudication
- drug of choice for A-fib/flutter - -CCB-diltiazem
alternate: beta blocker
- drug of choice for ventricular arrhythmias - -amiodarone (K-blocker);
alternate: lido
- drug of choice for torsades - -magnesium
- drug of choice for bradycardia - -atropine
- drug of choice for tachycardia - -beta-blocker
- how to you treat dig toxicity - -treat however it presents- like a normal
arrhythmia (atrial vs ventricular etc)
- BP Category: Normal - -SBP <120 and DBP <80
- BP Category: Elevated - -SBP: 120-129 and DBP <80
- BP Category: HTN Stage 1 - -SBP:130-139 or DBP: 80-89
- BP Category: HTN Stage 2 - -SBP: >140 or DBP:>90
- Hypertensive crisis - -SBP>180 or DBP>120
- Definition: Hypertensive urgency - -hypertensive urgency- the a patient
comes to medical attention with severe hypertension (SBP>180 or DBP
, >120) but does not have associated acute end organ damage of the CNS, CV
system or kidneys
reduce BP over hours to days
- Definition: Hypertensive Emergency - -hallmark: presence of acute end
organ damage and high degree of BP elevation. End-organ damage is the
result of acute rise in BP
treatment in Minutes- hours to prevent morbidity/mortality
- Definition: Hypertensive crisis - -more reflective of the high degree of BP
elevation
- 3 primary systems in the body to maintain BP - -autonomic nervous
system (catecholamines--> increased B in kidneys which increases renin-->
RAAS)
RAAS
vasopressin
- when you stimulate one, you stimulate them all
- How do ACE-I work? - -preventing the conversion of angiotensin I to
angiotensin II
- how do ACE-I cause cough - -bradykinin is broken down by ACE; ACE-I
increases bradykinin--> cough
- how do ARBs work? - -ARBs work by blocking the angiotensin receptor
blocker
- Esmolol vs Labetalol - -Labetalol:
-is a B and a blocker--> vasodilation
-not cardioselective
-preferred for HTN
Esmolol
-just a B blocker--> vasoconstriction
-shorter acting (broken down by RBC esterase in the plasma)
- "cardioselective" (not really)
-preferred for tachycardia
- how does nitroprusside work? - -its part of the nitro group so it vasodilates
- how is nitroprusside metabolized? - -by hemoglobin
- how is nitroprusside eliminated? - -It goes to the liver. Rhodanese causes
cyanide to act with vitamin B 12 to become thiocyanate which you pee out
