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168 Cards in this Set
- Front
- Back
Fast Response Fibers:
Na channel blocker ____ slope of phase ___. K channel blocker ____ duration of phase ___. (affect QT) |
Decrease; 0
Increase; 3 |
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Fast Response Fibers:
Antiarrhythmics have no significant effect on phase _____ & ____. |
1; 2 (Na channels inactivated)
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What are the slow response fibers?
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SA/AV node
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What type of arrythmia is slow response fibers responsible for?
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SVT
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Which phase is missing from slow compared to fast response fiber?
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Phase 1 & 2
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What channel does phase 0 of slow response fiber depend on?
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Ca
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**Summary of location of action:
Fast fibers: Na blocker K blocker Slow fiber: CCB BB |
Phase 0
Phase 3 Phase 0 Phase 4 |
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What is phase 4 in both fast and slow response fibers?
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Depolarization
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What is the general function of Na channel blockers?
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Increase refractory period
(Na+ channel spends most of its time in this state, right after phase 0) |
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What is the general function of K channel blocker?
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Increase AP duration
Prolong refractory period |
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Why is conduction slower in ischemic heart tissue?
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Refractory period is longer
(cells are partly depolarized, and this reduces the number of channels able to participate in next depolarization) |
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What channel does Class 1A block?
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Na & K
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**What is the class SE of class 1A?
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Torsades (K+ channel blocker)
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How is Class 1A different from other class 1 agents?
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Prefers open/activated state (state dependent blockade) rather than inactive state preferred by all other Class 1 agents
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What is the problem w/ quinidine in an antiarrhythmic context?
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It is proarrhythmic
atropine like effect --> M blockade --> increase HR & AV conduction -zosin like effect --> Alpha 1 blockade --> Reflex tachycardia |
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What do you need to give to patients taking quinidine to make it safer?
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Digitalis (reduce reflex tachycardia)
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**What are the SE of quinidine?
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Cinchonism
-GI -Tinnitis -Ocular dysfunction -CNS excitation Increase QT (block K+) Displace Dig |
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Why is procainamide a bit safer than quinidine?
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Less M & Alpha1 blockade
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**What is a main SE of procainamide?
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SLE (in slow acetylators)
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What active metabolite of procainamide is responsible for the K+ blocking effect?
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NAPA (N-acetyl procainamide)
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What channels does class 1B affect?
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Na
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What type of tissue does Class 1B drug prefer?
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Partially depolarized (ischemic) tissue
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What is the effect of class 1B?
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Decrease HR (decrease AP duration slightly, but increase diastole)
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What is the uses for lidocaine?
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#1 Ventricular Arrhythmia drug
(Post MI, dig toxicity) |
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What is the SE of lidocaine?
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CNS toxicity (seizures)
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Why is lidocaine given IV?
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Extensive first pass metabolism
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What are other class 1B drugs?
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Mexiletine/Tocainide (same use as lidocaine, oral)
Phenytoin (used as antiseizure) |
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What does class 1 c drugs block?
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Fast Na Channels
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Why is class 1c drug Flecainide not used much?
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Proarrhythmogenic in post-MI & prophylatic VT pts --> Death!!!
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1A _____ AP (___ shift)
1B _____ AP (___ shift) 1C _____ AP (___ shift) |
Lengthen; R
Shorten; L DN affect; No |
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Which of the following is non-selective, while others are cardioselective BB?
Propranolol Acebutolol Esmolol |
Non-Selective: Propranolol
Cardioselective: Acebutolol, Esmolol |
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What are the uses of BB?
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SVT
Prophylaxis post-MI |
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**Why is esmolol used only in acute SVT?
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It only last ~10 min
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What are the class 3?
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Amiodarone
Sotalol |
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What makes amiodarone so special?
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It has all class activity, tx almost anything, and extensive activit --> Low chance of torsades
("Ami"=Friend who always help you) |
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How do you distinguish amiodarone from amiloride?
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"Lo-ride"=Kidney=K+ sparing
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**What are the SE of amiodarone?
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Pulmonary Fibrosis (also bleomycin)
Iodine effect -"Smurf skin" -Thryoid dysfunction -Phototoxicity |
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What additional SE does sotolol have besides torsades?
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B1 blockade effect
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What are the cardioselective CCB?
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Verapamil & Diltiazem
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What are the CCB used for?
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SVT
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What is a prominent GI SE of verapamil?
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Constipation
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What does Class 3 Antiarrhythmic do to AP & Refractory?
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Lengthen
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MOA of adenosine
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+ adenosine receptor --> +Gi --> Increase K efflux--> Hyperpolarize SA &AV node
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Use of Adenosine
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DOC paroxysmal SVT
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Use of Mg
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Torsades (if low Mg)
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SVT use:
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Class II, IV, Adenosine, Dig
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VT use:
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Class I, III
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A. fib use:
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SVT drugs + Warfarin
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Causes of Torsades
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K Channel Blocker (Class 1A & 3)
Antypsychotic (Thioridazine) TCA |
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MOA of alpha2 agonist in anti-HTN
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Decrease sympathetic outflow
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Y is alpha2 agonist 2nd line in HTN?
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Powerful drop in BP --> Rebound HTN & Fatigue/Depression
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Which alpha2 agonist is used for opiate w/drawal?
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Clonidine
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**DOC of HTN in pregnancy?
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Methyldopa
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**What test should u run b4 administering methyldopa in pregnant women?
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Coomb's Test (+=AIHA)
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**MOA reserpine in HTN
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Destroy vesicle --> Amine depletion (NE/DA/Serotonin)
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What is main SE of reserpine?
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Depression (this forms our theory of depression)
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MOA alpha1 blocker in HTN
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Dilate aa AND vv
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SE of Alpha1 blocker
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First dose syncope
Orthostatic HypoTN |
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**What is the cause of orthostatic hypoTN?
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VEIN dilation
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What is a common cause for pt going off BB?
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Sexual dysf (leads to rebound tachycardia)
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Caution in BB use in pts w/:
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Asthma
DM (reduce insulin release & mask hypoglycemic tachy) Vasospastic Dz |
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What are primary uses of direct acting vasodilators?
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Severe HTN
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Which 3/4 DA vasodilators are arteriolar selective?
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Hydralazine, Minoxidil,Diazoxide
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Which 1/4 DA vasodilator act on both aa & vv?
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Nitroprusside
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What is MOA of hydralazine?
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Increase NO
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Hydralazine SE?
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SLE in slow acetylator
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Nitroprusside use?
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HTN emergency
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SE nitroprusside?
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CN toxicity
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How do u tx CN poisoning in nitroprusside?
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Coadminister:
-Nitrite: Form MetHb which bind CN --> CyanoMetHb--> resist CN inhibition of complex IV of ETC -Thiosulfate: Reconvert cyanometHb--> MetHb by forming less toxic thiocyanate ion (SCN) |
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How do u tx metHb as a SE of nitrite tx?
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Methylene Blue
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Which drugs directly open K channel --> Hyperpolarization?
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Minoxidil
Diazoxide |
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SE minoxidil
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Hypertrichosis (tx baldness)
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SE diazoxide
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Hyperglycemia (decrease insulin release)
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Vasodilator that are arteriolar selective
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CCB/Hydralazine/K channel opener
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Vasodilator that are venoselective
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Nitrate
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CCB use for HTN
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Diltiazem (jack of all trade, cover cardio & vessels)
-dipines (vascular selective) |
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**-dipine SE
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Gingival hyperplasia (also phenytoin/cyclosporin)
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**DOC primary HTN
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Thiazide
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Aliskiren?
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Renin blocker
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ACE function?
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AT1 --> AT2
Bradykinin-->inactivate |
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Where does ATII bind?
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AT1 receptor (AT II type 1 receptor)
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AT1 receptor function?
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Increase aldosterone release (adrenal cx)
Vasoconstriction |
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ACE & ARB suffix
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-pril
-sartan |
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Use of ACE/ARB
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HTN
DM nephropathy (Renal protective) CHF (Cardioprotective) |
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SE ACEI
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Cough/Angioedema (Bradykinin)
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SE both ACE/ARB
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Hyperkalemia (decrease Ald)
Acute RF in renal aa stenosis pt (dilate efferent arteriole --> RF) |
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How does NSAID cause RF?
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Decrease PG (which dilates aff aa)
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**Tx of pulmonary HTN
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Bosentan
Sidenafil |
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MOA Bosentan
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Endothelin (ET-A) receptor antagonist (endothelin is a powerful vasoconstrictor released by stretched vessels)
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What are the body's rxn to HF (Decreased CO)?
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Remodelling (fibrosis & lose myocyte)
Intrinsic compensation (eg: hypertrophy) |
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**How do we prevent cardiac remodelling?
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Decrease SANS (metoprolol/carvedilol)
Decrease Ald -ACE/ARB: Decrease production -Spironolactone: Block receptor |
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What are ionotropes used for primarily?
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Acute CHF
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**How does ionotorpe work generally w/ HF?
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Incease Ca(cytoplasmic) --> Increase Ca release from SR --> Increase contraction
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**MOA dig in CHF & Arrhythmia
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CHF: Block Na/K ATPase --> Decrease Na gradient --> Decrease Na/Ca pump activity --> Increase IC Ca
Arr: Block Na/K ATPase in neuron --> Increase Vagal activity --> M2 --> Slow AV/SA |
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**Dig is DOC for:
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Pt w/ CHF AND SVT (both HF & Arrhythmia)
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Dig SE
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Visual (halo/blurry yellow)=CNS
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Dig DI
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Diuretics: Hypokalemia (thiazides)
Quinidine & Verapamil (displace dig) |
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How does Inam/mil-rinon work as ionotrope?
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PDE III I --> Increase cAMP --> Open Ca channel on memebrane
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Hw does dobutamine & DA work?
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Sympathomimetic --> + B1 receptor --> increase cAMP --> Open Ca channel on memebrane
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Dobutamine is a B agonist w/ > activty on B1/B2?
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B1
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What is nesiritide?
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rhBNP
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What are drugs for acute HF?
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Dobutamine/DA
PDE III I Nesiritide |
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Drug for chronic CHF?
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ACE/ARB (hydralazine (dilate aa) +
Isosorbide dinitrate (dilate vv) if intolerant to ACE) BB Diuretic Poss. Dig |
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2 Types of angina
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Classic/Stable=Atherosclerosis (effort)
Prinzmetal=Vasospastic (decrease BF) |
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What's special about M3 in vessels?
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No innervation/circulating Ach, rely only on NO (endothelium derived relaxation factor)
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What endogenous cpd + receptors that activate NOS?
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Bradykinin
Histamine 5HT |
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What does NO do?
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+ Guanylyl cyclase --> relax
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What is main SE of nitroglycerin?
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H/A
|
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Y can't u wear nitro patch all day?
|
Tachyphylaxis (wear patch 1/2 day only)
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U can use ____ CCB for angina, but ____ is especially impo for vasospastic angina.
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ALL; Nifedipine (DOC for Raynauds)
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**BB are used in ______ angina, but CI in _______ angina.
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Classic; Prinzmetal
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POST MI Tx= MONA then ___, ____, ___.
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Morphine, O2, Nitroglycerin, Aspirin
BB;ACE;Statin |
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cGMP cause myosine LC ______.
cAMP cause myosine LC kinase ______. |
Dephosphorylation (inactivation)
Phosphorylation (inactivatoin) |
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Loops and thiazides are _____ biochemically --> Will compete w/ ____ for excretion.
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acids; UA
|
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*******************************************Why will loops & thiazides cause hypokalemia?
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They block proximal resorption of Na --> increase resorption of Na downstream w/ corresponding loss of K
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***********************************Why will loops and thiazides cause alkalosis?
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K secretion is coupled to H secretion
(reason K good for u?) |
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What is the use of Carbonic Anhydrase in PCT?
|
Convert CO2 and H2O to:
-H: Power resorption of Na from lumen via antiporter -HCO3: Absorbed into bloodstream |
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What are CA suffix?
|
-zolamide
|
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What are uses of CA?
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Glaucoma
Acute mountain sickness (>10k ft) |
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**Where does CAI primarily affect?
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PCT (85% of HCO3 resorption)
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SE of CAI:
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Bicarbonaturia/acidosis
Sulfonamide HS Hypokalemia (K secretion increased b/c Na resorption decreased upstream) |
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**How does loop work?
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Block Na/K/2Cl symporter in Thick Ascending LOH
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**What is the importance of K in Thick Ascending LOH?
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Backleak of K into lumen--> Mg/C1 entry through paracellular space
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What are the uses for loops?
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Acute pulmonary edema (DOC: fast)
HTN (but require frequent dosing) Hypercalcemia |
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What are the loops?
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Furosemide/torsemide/bumetanide
Ethacrynic acid |
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**When is the only time you use ethacrynic acid?
|
When u want to use a loop but pt have sulfonamide allergy
|
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What is the main unpredicted SE for loops?
|
Ototoxicity (esp w/ Ethacrynic acid)
|
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MOA thiazide
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Block lumenal NaCl symporter (lose Na & Cl)--> increase basolateral Na/Ca antiporter (increase Ca)
|
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Uses of thiazides
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HTN
Nephrolithiasis (decrease Ca in urine) Nephrogenic DI (force Na loss--> increase Na resorption in PCT --> H2O resorption) |
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What is the physiological problem in nephrogenic DI?
|
Uncoupled V2 (vasopressin 2) receptor in CD
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What are the SE of thiazide?
|
Sulfonamide HS
Hyperglycemia (makes B-cell harder to release insulin b/c K lost) Hyperlipidemia |
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What are the thiazides
|
HCT
Indapamide |
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**Loops & Thiazides are the MCC of hypo_____ & metabolic ______.
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K; Alkalosis
|
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**Hypokalemia _____ insulin secretion
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Decrease
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Where does K-sparing agents work?
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CD's Na channel
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How does Na channel (lumenal) in CD work?
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Allow Na to enter, this entry is driven by Na/K pump at basolateral side
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How does aldosterone receptor antagonist work?
|
Decrease Tc of Na channels on the lumenal side
|
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What are Ald receptor antagonist?
|
Spironolactone/Eplerenone
|
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What can spironolactone also be used for?
|
Hirsuitism (antiandrogenic effect)
Epleronone is SELECTIVE at ald, so no antiandrogenic effect (Newer drug w/ more specificity) |
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What are the Na channel blocker that are K-sparing?
|
Amiloride
Triamterene |
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What are the use for K-sparing Na channel blockers?
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Adjunct to K+ wasting diuretic
Li induced nephrogenic DI |
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What is MOA of Li induced Nephrogenic DI?
|
Li goes through Na channel in the CD, then damage the V2 receptors.
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AcCoA-->--> ______ --> ______ -->--> Cholesterol
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HMG CoA; Mevalonic Acid
|
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What are statins?
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HMG-CoA Reductase inhibitor
|
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What does statins help w/?
|
Everything
|
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**SE of statins:
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Myalgia (Check CK)
Rhabdomyolysis Hepatotoxicity (Check LFT) |
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DI of statin:
|
Gemfibrozil (increase rhabdomyolysis)
P450 inhibitors (eg: grapefruit juice) increase toxicity |
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MOA of Bile Sequestrants
|
Prevent recycling of Bile Salt (Bile salt 95% recycled)
|
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SE of Bile Sequestrant:
|
Increase VLDL& TG (liver forced to make stuff)
B.S. CI: HyperTG pt |
|
What are the B.S. drugs?
|
Cholestyramine
Colestipol |
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What is the main use of Nicotinic acid (niacin, aka vitamin B3)?
|
Increase HDL (by inhibiting VLDL syn)
|
|
**SE niacin:
|
Pruritis (pretx w/ aspirin)
|
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MOA of fibrates:
|
PPAR-alpha agonist (Peroxisome Proliferator Activated Receptor) & regulate Tc--> Activate lipoprotein lipase
SN: -glitazones are PPAR-gamma (g=glucose) activators that are used for DM type II |
|
**Primary use of fibrates:
|
Lower TG
|
|
MOA ezetimibe?
|
Prevent GI absorption of cholesterol --> Decrease LDL
|
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What is orlistat and its use?
|
Pancreatic lipase inhibitor; weight loss
(rem: to bring a change of black pants) |
|
PDE III inhibitors increase cAMP, causing:
______ in heart contractility. ______ in sm mm contractility. |
Increase (ionotrope)
Decrease |
|
Progression of sedative/hypnotic/anxiolytics:
|
Paradoxical disinhibition --> anxiolysis --> hypnosis --> anesthesia --> Medullary depression --> coma
|
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Why is BZD safer than barbiturates/EtOH?
|
BZD effect ceiling at around medullary depression, while Barb/EtOH can go all the way to coma
|
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CNS excitatory NT:
|
Glutamine
|
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CNS inhibitory NT:
|
GABA, DA, Opioid
|
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CNS exc&inhibitory NT:
|
ACh, NE, 5HT
|
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BZD/Barb/EtOH all bind to ____ parts of the GABA binding site.
|
Different
|
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MOA of:
GABA-A (ionotropic=ion channel) GABA-B (metabotropic=G-protein) |
Increase Cl influx (hyperpolarize)
Increase K efflux (hyperpolarize) |
|
**Sedative Hypnotics works PRIMARILY on which GABA receptors?
|
GABA-A
|
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**MOA BZD VS Barb:
|
BZD: Potentiate GABA
Barb: Prolong GABA duration "Ben like frequency, Barb like duration" |
|
What addn'l activity does barb have at high doses?
|
GABA mimetic
|
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**What non-specific BZD receptor antagonist is used to tx BZD OD, but dn work on Barb/EtOH OD?
|
Flumazenil
|