Term
What type of shock is loss of blood volume?
myocardial pump failure?
impaired cardiac fillin?
abnormal distribution of blood volume due to peripheral vasodilation? |
|
Definition
hypovolemic
cardiogenic
obstructive
distributive |
|
|
Term
Which stage of shock is reversible?
Irreversible and multiple organ dysfunction? |
|
Definition
compensatory stage
refractory stage |
|
|
Term
| Which stage of shock has reduced blood flow/perfusion which leads to hypoxia and decreased mitochondrial ATP formation (switches to anaerobic respiration) |
|
Definition
|
|
Term
| In the compensatory stage, what is the prominent physiological reflex mechanism to contract the reduction in tissue perfusion that activates the SNS? |
|
Definition
|
|
Term
| In the compensatory stage, which system is stimulated during reduction in BP in the afferent arteriole that increases peripheral vasoconstriction, increase SVR, and increase salt and water reabsorption? |
|
Definition
|
|
Term
Case:
65 yo man with past medical history significant for diabetes mellitus, hypertension, and hypercholesterolemia presents to the ED complaining of crushing substernal chest pain that radiates to the jaw.
Physical Exam: Tachycardia, Diaphoretic (sweating)
EKG: Abnormal with Q-wave
Labs: Elevated troponin I and CK-MB
What is his diagnosis |
|
Definition
|
|
Term
| What is the number one complication of myocardial infarctions? |
|
Definition
|
|
Term
| What type of cardiomyopathy is when the ventricular chamber is dilated and the myocardium is modestly thickened |
|
Definition
|
|
Term
| What type of cardiomyopathy is when the myocardium is markedly thickened especially the septum |
|
Definition
|
|
Term
| what type of cardiomyopathy is when the myocardium is can be of normal thickness but it is stiff and unable to relax in diastole |
|
Definition
|
|
Term
| what is the most common toxic cause of dilate cardiomyopathy? |
|
Definition
|
|
Term
| What type of cardiomyopathy is most associated with athlete sudden death? |
|
Definition
|
|
Term
| What is right sided hypertrophy secondary to pulmonary hypertension followed by dilatation and right heart failure |
|
Definition
|
|
Term
| Which side valves are more commonly affected and produce more problems? |
|
Definition
|
|
Term
| What pattern of cardiac hypertrophy is pressure overload that causes wall thickening with a smaller chamber? |
|
Definition
|
|
Term
| What pattern of cardiac hypertrophy is volume overload that causes wall thickening with a dilated chamber? |
|
Definition
|
|
Term
| what side of the heart would you expect infectious endocarditis in an IV drug user? |
|
Definition
|
|
Term
Which bacteria is most likely to cause highly destructive infectious endocarditis?
strep viridans
staph aureus
coagulase - staph |
|
Definition
|
|
Term
| What is the only cause of simultaneous mitral and aortic stenosis? |
|
Definition
|
|
Term
| Which valve stenosis is 99% secondary to rheumatic heart disease? |
|
Definition
|
|
Term
| What is the most common cause of aortic stenosis? |
|
Definition
|
|
Term
| What is the most common valvular disease/lesion? |
|
Definition
|
|
Term
| Is mitral valve prolapse more common in young men or women? |
|
Definition
|
|
Term
| In mitral valve prolapse, which valve leaflet is stretched? |
|
Definition
|
|
Term
| Which shunt would you rather have? ASD or VSD? |
|
Definition
ASD (not a problem)
VSD (increase pressure and volume in RV) |
|
|
Term
| What type of shunt would cause cyanosis at birth due to poor oxygenation? |
|
Definition
| R to L shunt (metrology of fallot) , blood skips lungs |
|
|
Term
Case:
65 yo man with past medical history significant for diabetes mellitus, hypertension, and hypercholesterolemia and peptic ulcer disease presents to the ED complaining of crushing substernal chest pain that radiates to the jaw
Chest pain started 30 minutes ago
ECG shows ST elevation
Stat enzymes show an elevated troponin
What should you NOT do for this specific patient?
Administer tPA (tissue plasminogen activator)
Take him to the cath lab for angioplasty
Do an emergency coronary artery bypass
Have him chew some aspirin |
|
Definition
Administer tPA (tissue plasminogen activator)
because he has history of peptic ulcer |
|
|
Term
What is NOT a main artery used to bypass?
right coronary
left anterior descending
anterior interventricular
left circumflex artery |
|
Definition
| anterior interventricular |
|
|
Term
An 80 year old man with a known aortic murmur faints but recovers quickly. Physical exam reveals only the known heart murmur. An echocardiogram shows marked aortic stenosis. A CXR shows left ventricular hypertrophy and calcifications in the area of the aortic valve.
What is the diagnosis? |
|
Definition
|
|
Term
| If a person faints and when they wake up they are foggy or confused, is this a cardiac episode or neurological syncope? |
|
Definition
|
|
Term
A 24 year old woman has a 2 month history of fatigue. She reports intermittent fevers but blood cultures are normal. On auscultation she has a mitral click and a systolic murmur. An echocardiogram demonstrates a “parachute valve” and is suspicious for a mitral vegetation.
What is the diagnosis? |
|
Definition
| Mitral valve prolapse with subacute endocarditis |
|
|
Term
Case
30 year old woman presents to her family physician with severe fatigue and poor exercise tolerance. By history she was healthy until approximately 1 month prior to presentation when she had a routine upper respiratory infection. By physical exam she has poor peripheral pulses and a high jugular venous pressure and a hypodynamic apical impulse.
What do you expect this woman to have? |
|
Definition
| enlarged heart (4 chamber dilation) |
|
|
Term
Case
65 year old man status post MI complains of episodes of light headedness. Echocardiogram shows normal ejection fraction.
What will the Holter monitor most likely show? |
|
Definition
| runs of ventricular tachycardia |
|
|
Term
| What are (2) therapeutic options for ventricular tachycardia? |
|
Definition
Radiofrequency ablation
Pacemaker/cardioverter/defibrillator |
|
|
Term
Is this drug used for chronic heart failure, acute heart failure, or both?
Diuretics
Aldosterone receptor antagonists
Vasodilators
Beta agonists
Beta blockers
Angiotensin-converting enzyme inhibitors
Angiotensin receptor blockers
natriuretic peptide
Cardiac glycosides |
|
Definition
Diuretics - BOTH
Aldosterone receptor antagonists - CHRONIC
Vasodilators - BOTH
Beta agonists - ACUTE
Beta blockers - CHRONIC
Angiotensin-converting enzyme inhibitors - CHRONIC
Angiotensin receptor blockers - CHRONIC
natriuretic peptide -ACUTE
Cardiac glycosides - CHRONIC (only used for CHF) |
|
|
Term
| *What drug has the ONLY function of treating chronic heart failure? |
|
Definition
|
|
Term
| *What drug combination is used in stage C of heart disease? |
|
Definition
| ACE inhibitors + beta blockers |
|
|
Term
What is NOT a drug that decreases preload?
Diuretics
ACE inhibitor
Sodium nitroprusside |
|
Definition
| Ace inhibitor (decreases preload) |
|
|
Term
What does NOT decrease after load?
Beta blocker
Digoxin
Sodium nitroprusside
Vasodilator
ACE inhibitor/AT-1 Receptor Antagonist |
|
Definition
| Sodium nitroprusside (decreases preload) |
|
|
Term
Which is a K+ sparing diuretic?
Thiazide
Furosemide
Triamterene |
|
Definition
Triamterene (and also amiloride)
Furosemide is a loop diuretic |
|
|
Term
| Out of furosemide (loop diuretic) and thiazaide, which is given first? |
|
Definition
| thiazide ( weak, non-toxic, work on distal tubules) |
|
|
Term
If you give a pt thiazide and furosemide, will the K+ goes up, down, or stay the same?
what about thiazide and triamterene? |
|
Definition
down (both non K+ sparing)
stays the same (thiazide-non K+ sparing, triamterene-K+sparing) |
|
|
Term
Which is an aldosterone inhibitor?
thiazide
furosemide
spironolactone
amiloride |
|
Definition
|
|
Term
| When people are put on diuretics or an aldosterone receptor blocker, what is often added? |
|
Definition
ACE inhibitor (prevents formation of angiotensin II)
or angiotensin receptor blocker (blocks binding of angiotensin II to its receptors) |
|
|
Term
| What is the main side effect of ACE inhibitors and why does it cause that? |
|
Definition
severe cough
elevated bradykinin |
|
|
Term
| If someone with high BP on an ACE inhibitor has a hacking cough, what would you switch them to? |
|
Definition
| AT1 receptor antagonist (more expensive) |
|
|
Term
What is NOT an effect of ACE inhibitors?
increase systemic vascular resistance and BP
increase cardiac output
decrease heart rate
increase exercise tolerance
increase renal blood flow |
|
Definition
decrease heart
NO CHANGE in HR/contractility (doesn't directly affect heart) |
|
|
Term
| What drug inhibis the Na/K ATPase to increase intracellular Ca2+ = increase cardiac contractility and cardiac output? |
|
Definition
| cardiac glycosides (digoxin) |
|
|
Term
| *If a patient has yellow-green vision, what drug is this a side effect of? |
|
Definition
|
|
Term
Which drug, when taken with digoxin, elevates serum digoxin level (and vice versa)?
Quinidine
Verapamil
Diuretics
Catecholamines |
|
Definition
|
|
Term
Which drug should you NEVER give with Digoxin because of the additive effects on the heart?
Quinidine
Verapamil
Diuretics
Catecholamines |
|
Definition
|
|
Term
| Should you use nonspecific or K+ sparing diuretics with digoxin? |
|
Definition
K+ sparing
(digoxin blocks K+, so if there's less K+ then the digoxin is more toxic) |
|
|
Term
| What should you give someone experiencing a heart block due to verapamil and digoxin toxicity? |
|
Definition
|
|
Term
| What should you give someone who is experiencing digoxin toxicity due to taking thiazide? |
|
Definition
give K+
thiazide is a nonspecific diuretic = hypokalemia |
|
|
Term
| What is the only antibody we have to a drug? |
|
Definition
| digibind (antibody to digoxin) |
|
|
Term
What is NOT a drug you would give someone that has acute heart failure (MI, lost a leg and bleeding, etc)
Beta agonists
Bipyridines
ACE inhibitor
Natriuretic peptide |
|
Definition
| ACE inhibitor (chronic heart failure drug) |
|
|
Term
| In phase 0, what ion rushes into the cell? |
|
Definition
|
|
Term
What is the Na concentration inside the cell at resting state?
What is NA concentration in your bloodstream? |
|
Definition
|
|
Term
| All arrhthmias result from disturbance in what 2 things? |
|
Definition
| impulse formation and/or impulse conduction |
|
|
Term
Which class of anti-arrhythmic drugs are fast Na+ channel blockers?
What phase is this? |
|
Definition
|
|
Term
What class of anti-arrhythmic drugs are beta blockers
What phase is this? |
|
Definition
|
|
Term
What class of anti-arrhythmic drugs are K+ channel blockers?
What phase is this? |
|
Definition
|
|
Term
Class of anti-arrhythmic drugs are Ca2+ channel blockers?
What phase is this? |
|
Definition
|
|
Term
| What subclass action prolong the APD and dissociate from the channel with intermediate kinetics? |
|
Definition
|
|
Term
| what subclass action shorten the APD in some tissues of the heart and dissociate from the channel with rapid kinetics; |
|
Definition
|
|
Term
| What subclass action have minimal effects on the APD and dissociate from the channel with slow kinetics |
|
Definition
|
|
Term
| Is procainamide and quinidine better at suppressing abnormal ectopic pacemaker activity? |
|
Definition
|
|
Term
| Is procainamide or quinidine more effective in blocking sodium channels in depolarized cells? |
|
Definition
|
|
Term
| *What is the major adverse effect in long-term use of procainamide? |
|
Definition
| syndrome resembling lupus erythematosus |
|
|
Term
| What is the drug of second or third choice (after lidocaine or amiodarone) in most coronary care units for the treatment of sustained ventricular arrhythmias associated with acute myocardial infarction. |
|
Definition
|
|
Term
| *What is the major adverse effect of quinidine? |
|
Definition
|
|
Term
| What is the orally active congener of lidocain? |
|
Definition
|
|
Term
What drug would you NOT want to use on a patient with an ischemic heart condition or previous myocardial infarction?
Lidocaine
Quinidine
Flecainide
Procainamide |
|
Definition
| Flecainide (toxic, not used much) |
|
|
Term
Which drug is the agent of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia?
Lidocaine
Quinidine
Flecainide
Procainamide |
|
Definition
|
|
Term
Which drug has a low incidence of toxicity and a high degree of effectiveness in treating arrhythmias associated with acute myocardial infarction?
Lidocaine
Quinidine
Flecainide
Procainamide |
|
Definition
|
|
Term
Where do you find beta 1s? contraction or relaxation?
Where do you find beta 2s? contraction or relaxation? |
|
Definition
beta 1s- In the heart. It causes contractions.
beta 2s- In the lungs. It causes relaxation. |
|
|
Term
*If a pt is having a heart attack and also has asthma, which drug would you NOT give him?
Metopolol
Propanolol
Atenolol |
|
Definition
| Propanolol (beta 1 and beta 2 blocker) |
|
|
Term
Which drug is a beta 1, beta 2, and alpha 1 blocker?
metopolol
sotalol
esmolol
carvedilol |
|
Definition
| carvedilol (use for people with MI that does NOT have asthma) |
|
|
Term
Which of these drugs would you use in the cardiac intensive care to treat arrhythmia?
sotalol
acebutolol
esmolol
carvedilol |
|
Definition
| esmolol (fast-acting Beta 1 selective blocker) |
|
|
Term
Amiodarone belongs in what class?
What does it block? |
|
Definition
III
blocks K, Na, Ca, and beta receptors |
|
|
Term
What K+ blocker drug can cause fatal pulmonary fibrosis and contains iodine atoms that may disrupt the thyroid gland?
Amiodarone
Sotalol
Procainamide
Verapamil |
|
Definition
|
|
Term
*Which one of these is a Ca2+ channel blocker is not used to treat an arrhythmia?
Verapamil
Diltiazem
Nifedipine |
|
Definition
|
|
Term
| What is the major underlying cause of angina? |
|
Definition
|
|
Term
What type of angina is reduced blood flow to heart muscle due to atherosclerosis, especially prominent during exertion
Classic
Variant
Unstable |
|
Definition
| Classic Angina (Stable Angina) |
|
|
Term
What type of angina is reduced blood flow to heart muscle due to spasm of coronary vessels at specific loci?
Classic
Variant
Unstable |
|
Definition
|
|
Term
What type of angina is episodic reduced blood flow to heart muscle due to increase in vascular resistance or formation of small platelet clot, not caused by exertion?
Classic
Variant
Unstable |
|
Definition
|
|
Term
| What 2 coronary vasodilators are used together to prevent vasospasms in variant angina? |
|
Definition
| nitrates + calcium channel blockers |
|
|
Term
| Is Glyceryl trinitrate (Nitroglycerin) or Isosorbide Dinitrate (Isorbid) orally effective? |
|
Definition
Isosorbide Dinitrate (Isorbid)
Glyceryl trinitrate (Nitroglycerin) is sublingual or patch (causes flushing) |
|
|
Term
You would NOT want to prescribe this drug to someone on Viagra. Why?
Glyceryl trinitrate
Verapamil
Diltiazem
Amiodarone |
|
Definition
| Glyceryl trinitrate (build up of cGMP leads to heart failure) |
|
|
Term
*Which of the following does NOT happen when you give some nitroglycerin? (2 answers)
-produce nitric oxide
-form active form of guanylate cyclase
-binds myosin with actin
-increase leave of cGMP
-inhibition of phosphodiesterase |
|
Definition
binds myosin with actin (actually dephosphorylates myosin light chain so doesn't bind)
inhibits phosphodiesterase (Sildenafil inhibits phosphodiesterase to change cGMP to GMP, nitroglycerin synthesizes GTP to cGMP) |
|
|
Term
| What is the prostaglandin synthesized from arachidonic acid within platelets and is a platelet activator and potent vasoconstrictor. |
|
Definition
|
|
Term
Which product of platelet granules is a powerful inducer of platelet aggregation?
Which stimulates both platelet aggregation and vasoconstriction? |
|
Definition
|
|
Term
Would you give Heparin or Warfarin in the hospital setting (after a surgery)?
Would you give heparin or warfarin orally after the hospital? |
|
Definition
|
|
Term
If someone is having a cerebral bleed, what drug would you give them?
t-PA
urokinase
aminocaproic acid
streptokinase |
|
Definition
| aminocaproic acid (block plasmin formation and encourage fibrin clot formation) |
|
|
Term
| Antithrombin, in the presence of _______, is accelerated 1000-fold. |
|
Definition
| heparin (in absence of heparin reactions are slow) |
|
|
Term
| What is the major adverse effect of heparin? |
|
Definition
|
|
Term
| *What is given to treat an overdose of heparin? |
|
Definition
|
|
Term
| *What is given to reverse warfarin? |
|
Definition
| vitamin K1 (phytonadione) |
|
|
Term
What drug is used in combination with warfarin to inhibit formation of thromboemboli from prosthetic heart valves?
Aspirin
Dipyridamole
glycoprotein inhibitor
clopidogral |
|
Definition
|
|
Term
Which drug reduces serum LDL and should NOT be used in pregnancy?
HMG-CoA reductase inhibitor (statin)
Niacin (vitamin B3)
Fibric Acid Derivative
Bile acid binding resin
Inhibitors of sterol absorption (ezetimibe) |
|
Definition
| HMG-CoA Reductase Inhibitor |
|
|
Term
Which drug reduces plasma levels of LDL, VLDL, cholesterol, and triglycerides and increases HDL levels but may cause flushing?
HMG-CoA reductase inhibitor (statin)
Niacin (vitamin B3)
Fibric Acid Derivative
Bile acid binding resin
Inhibitors of sterol absorption (ezetimibe) |
|
Definition
|
|
Term
Which drug reduces serum level of VLDL and triglycerides but NOT LDL and a modest increase in HDL?
HMG-CoA reductase inhibitor (statin)
Niacin (vitamin B3)
Fibric Acid Derivative
Bile acid binding resin
Inhibitors of sterol absorption (ezetimibe) |
|
Definition
|
|
Term
Which drug binds to bile acids in the lumen of the gut and regents it's reabsorption which causes plasma LDL concentration to decrease when cholesterol precursors in the liver is used to synthesize new bile acids rather than new cholesterol?
HMG-CoA reductase inhibitor (statin)
Niacin (vitamin B3)
Fibric Acid Derivative
Bile acid binding resin
Inhibitors of sterol absorption (ezetimibe) |
|
Definition
|
|
Term
Which drug inhibits cholesterol absorption from the gut?
HMG-CoA reductase inhibitor (statin)
Niacin (vitamin B3)
Fibric Acid Derivative
Bile acid binding resin
Inhibitors of sterol absorption (ezetimibe) |
|
Definition
|
|
Term
Where will you see foam cells first?
coronary
cerebral vessels
aorta |
|
Definition
aorta
then coronary, then cerebral vessels |
|
|
Term
| During normal (laminar) flow, what 2 things are produced that prevents platelet aggregation/anti-inflammator and protects against reactive O2 species? |
|
Definition
|
|
Term
| What type of aneurysm involves the intima, media, and adventitia that pockets on 1 side of the vessel wall? |
|
Definition
|
|
Term
| What type of aneurysm involves the intima, media, and adventitia that pockets/bulges in the entire vessel? |
|
Definition
|
|
Term
| What type of aneurysm results from a wall defect that leads to the formation of an extravascular hematoma that communicates with intravascular space |
|
Definition
|
|
Term
| What type of aneurysm occurs when blood splays apart the laminar planes of the media to form a blood-filled channel with the vessel wall |
|
Definition
|
|
Term
| What is the abnormal, direct connections between arteries and veins, bypassing intervening capillaries that occur as developmental defects and as result of trauma or necrosis |
|
Definition
| Arteriovenous Malformations |
|
|
Term
| What is the irregular thickening of walls of medium & large arteries due to medial and intimal hyperplasia and fibrosis |
|
Definition
|
|
Term
| What vessels does fibromuscular dysplasia typically affect? |
|
Definition
|
|
Term
| Hypertension usually affects small or larger aa? |
|
Definition
|
|
Term
| Vasculitis usually affects small or larger aa? |
|
Definition
|
|
Term
| How do you treat Giant Cell arteritis? |
|
Definition
| anti-TNF therapy and corticosteroids |
|
|
Term
Increase or decrease peripheral resistance?
angiotensin II
catecholamine
alpha receptor
beta receptor
H+ and adenosine
O2
NO |
|
Definition
angiotensin II - increase
catecholamine - increase
alpha receptor - increase (vasoconstrictor)
beta receptor - decrease (vasodilate)
H+ and adenosine - decrease
O2-increase
NO-decrease |
|
|
Term
| What causes renin release in the afferent arterioles? |
|
Definition
| stretch and baroreceptor- decreased pressure and volume |
|
|
Term
| What causes renin release in the macula densa |
|
Definition
|
|
Term
| What cause renin release in the juxtaglomerular cells? |
|
Definition
| Beta adrenergic receptor activation |
|
|
Term
| What is the negative feedback of renin release? |
|
Definition
| Ang II binds to JG cells to inhibit renin release |
|
|
Term
| What enzyme converts ANGI to ANGII and cleaves bradykinin |
|
Definition
| peptidyldipeptide hydrolase (vasoconstrictor) |
|
|
Term
What does aminopeptidase turn ANGII into?
What does prolyendopeptidase turn ANGII into? |
|
Definition
ANG III (less potent)
ANG1-7 (CNS actions, lacks vasoconstrictor activity) |
|
|
Term
What is NOT true about ANGII cardiovascular effects?
increase blood pressure
decrease heart rate
increase myocardial contractility
increase cardiac output |
|
Definition
does NOT change cardiac output due to reflex bradycardia
(decreases HR because of reflex bradycardia) |
|
|
Term
| What was the peptide ACE inhibitors that was the experimental agent isolated from snake venom and is effective in renin-dependent hypertension? |
|
Definition
|
|
Term
Which non-peptide ACE inhibitor is a sulfhydryl group that facilitate binding of the drug to the active site of the enzyme?
enalapril
captopril
enaloprilat |
|
Definition
| captopril (as well as lisinopril) |
|
|
Term
Which non-peptide ACE inhibitor is administered for treatment of hypertension when oral therapy is not practical (eg. post surgery)?
captopril
lisinopril
benazepril
enalaprilat |
|
Definition
| enalaprilat (active metabolite of enalapril) |
|
|
Term
Which is the mechanism of action for captopril
-blocks the active site of ACE and prevents the formation of Ang II
-Inhibition of the Ca2+ current during phase 2 of the action potential
-activates VSMC K+ channels resulting in hyperpolarization and relaxation
-acts as an NO donor and thus induces cGMP
phosphorylation |
|
Definition
| blocks the active site of ACE and prevents the formation of Ang II |
|
|
Term
What drug is a peptide ANGII receptor blocker (ARBs) that must given intravenously?
Losartan
Saralasin
Verapamil |
|
Definition
|
|
Term
What drug is a non peptide ANGII receptor blocker that can be given orally and is specific for ATI receptors to stimulate renin release?
Losartan
Saralasin
Verapamil |
|
Definition
|
|
Term
| Are all calcium channel blockers given orally or intravenously? |
|
Definition
|
|
Term
| Are large or small aa more sensitive to calcium channel blockers? |
|
Definition
|
|
Term
The hypotensive effect of CCBs may be limited by the reflex tachycardia and increased CO more often when which drug is used?
dihydropyridines
verapamil
diltiazem |
|
Definition
|
|
Term
What is NOT a common adverse effect of direct vasodilators?
-reflex tachycardia
-decrease cardiac contractility
-increase plasma renin
-increase salt retention |
|
Definition
| decrease cardiac contractility |
|
|
Term
| What direct vasodilator drug may have lupus like syndrome? |
|
Definition
|
|
Term
| What is hydrazine and minoxidil usually administered with? |
|
Definition
| diuretic and beta blocker |
|
|
Term
What is the mechanism of action for minoxidil?
-blocks the active site of ACE and prevents the formation of Ang II
-Inhibition of the Ca2+ current during phase 2 of the action potential
-activates VSMC K+ channels resulting in hyperpolarization and relaxation
-acts as an NO donor and thus induces cGMP
phosphorylation |
|
Definition
| activates VSMC K+ channels resulting in hyperpolarization and relaxation |
|
|
Term
Which direct vasodilator drug(s) would you NOT want to give to a patient with renal failure?
Hydralazine
Minoxidil
Diazoxide
Sodium nitroprusside |
|
Definition
hydralazine (renal elimination only)
Sodium nitroprusside (converted in liver but excreted in kidney)
minoxidil-hepatic metabolism
diazoxide-liver and kidney |
|
|
Term
What is the mechanism of action for diazoxide?
-blocks the active site of ACE and prevents the formation of Ang II
-Inhibition of the Ca2+ current during phase 2 of the action potential
-activates VSMC K+ channels resulting in hyperpolarization and relaxation
-acts as an NO donor and thus induces cGMP
phosphorylation |
|
Definition
| -activates VSMC K+ channels resulting in hyperpolarization and relaxation (same as minoxidil) |
|
|
Term
Oral or intravenous?
Hydralazine
Diazoxide
Sodium nitoprusside
Minoxidil |
|
Definition
Hydralazine-oral
Diazoxide-IV
Sodium nitoprusside-IV
Minoxidil-oral |
|
|
Term
What is the mechanism of action for sodium nitroprusside?
-blocks the active site of ACE and prevents the formation of Ang II
-Inhibition of the Ca2+ current during phase 2 of the action potential
-activates VSMC K+ channels resulting in hyperpolarization and relaxation
-acts as an NO donor and thus induces cGMP
phosphorylation |
|
Definition
-acts as an NO donor and thus induces cGMP
phosphorylation |
|
|
Term
Which drug is most likely to cause postural hypotension (venous dilator)
minoxidil
hydralazine
sodium nitroprusside |
|
Definition
| sodium nitroprusside (vasodilates arterioles and venules) |
|
|
Term
Which drug would you want to use to treat hypertensive emergencies associated with myocardial infarct and LVF?
Hydralazine
Minoxidil
Diazoxide
Sodium nitroprusside |
|
Definition
|
|
Term
Ambulance delivers a 21-year-old male to the ER. Patient was involved in motorcycle crash. He was wearing a helmet and had no loss of consciousness. He is conscious, alert, and oriented, but complaining of abdominal pain. Heart rate 110 bpm with BP 120/90.
Several moments later, the patient is taken to an examination room. He appears anxious and complains of severe abdominal pain, which he rates at 8 on a 0-to-10 pain intensity scale. His skin is pale. Breathing is 22 breaths per minute and the radial pulse is fast.
The ER physician examines the patient who is becoming increasingly confused. His abdomen is distended and tender to light palpation. Despite receiving 100% oxygen, he remains tachypneic. After placing him on a cardiac monitor, you see sinus tachycardia at 120 bpm. An indwelling urinary catheter is inserted with minimal initial output. His BP is now 90/70.”
What does he have? |
|
Definition
|
|
Term
| hypovolemic shock will cause a reduction in preload or after load? |
|
Definition
| Reduced venous pressure and return causes a reduction in preload. |
|
|
Term
What is NOT a treatment for hypvolemic shock?
blood transfusion
infusion of crystalloid or colloidal electrolyte solutions
vasoconstrictor therapy |
|
Definition
| Vasoconstrictor therapy is ineffective as an early intervention since these drugs are ineffective in the context of acidosis. |
|
|
Term
| *A patient has pulses paradoxus (Heart beat is detected but the radial pulse is weak or absent), what type of shock do you expect? |
|
Definition
|
|
Term
| What are 2 causes for obstructive shock? |
|
Definition
1) Cardiac tamponade
2) Pulmonary embolism (obstruction to outflow) |
|
|
Term
What type of distributive shock causes airway narrowing due to swelling may impair respiration, facial edema
Anaphylactic shock
Neurogenic shock
Septic shock |
|
Definition
|
|
Term
What type of distributive shock causes skin remains warm due to lack of SNS-mediated vasoconstriction
Anaphylactic shock
Neurogenic shock
Septic shock |
|
Definition
|
|
Term
What type of distributive shock causes fever is common in early stages and is related to severe bacterial infection
Anaphylactic shock
Neurogenic shock
Septic shock |
|
Definition
|
|
