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Autonomic Drugs N Stuff > Things to Remember > Flashcards

Things to Remember Flashcards

1
Q

Pulsus Paradoxus

A

Cardiac tamponade sign where you have an accentuation/exaggeration of the normal drop in BP during inspiration to >10 mm Hg bc less blood to heart and less filling from inspiration and also tamponade pushing in on atria/ventricles

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2
Q

Pulse Deficit

A

Atrial Fibrillation
count heart beats and peripheral pulse rate doesn’t match bc not every heart beat generates a strong peripheral beat bc not long enough time for diastolic filling in Afib

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3
Q

Pulsus Parvus et Tardus

A

Slow and Late Pulse associated with Aortic Stenosis bc harder to get aortic pressures up

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4
Q

Pulsus bisference

A

HOCM and AR !!! Double beating arterial pulse bc squeeze a lot out initially and rapid rise in aortic pressure but then blood quickly bounces back and re-raises pressure again a little - returning waves from periphery

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5
Q

In Dilated Cardiomyopathy, how can you tell difference between Cardiogenic etiology and Volume overload etiology?

A

Poor pump = low EF

Volume overload = good EF

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6
Q

What EKG leads do you check to see if sinus rhythm?

A

P axis on Limb Lead I and avF p waves need to be upright from SA node

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7
Q

How do you count HR in EKG?

A

take 300 and divide by number of big boxes

normal is 3 (100 bpm) to 5 (60 bpm)

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8
Q

How would you see an LAD infarct on EKG?

A

Precordial leads V1-V5 and shows anterior wall infarct

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9
Q

How would you see a RCA infarct on EKG?

A

Leads 2, 3, avF and means Inferior wall infarct

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10
Q

How would you see a Left Circumflex infarct on EKG?

A

Leads I, avL and V6 and shows lateral wall infarct

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11
Q

What is a normal PR interval?

A

3-5 small blockes = 120-200 msec

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12
Q

What is First degree AV block?

A

PR interval longer than 5 blocks >.2 sec and slow conduction

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13
Q

What are the 2 types of Second degree AV block and how can you distinguish them?

A

Mobitz 1 - Weinkeback = PR widens prior to dropping a QRS

Mobitz 2 - PR unchanging and suddenly missing QRS ( worse)

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14
Q

What is 3rd degree AV block?

A

complete heart block where P wave completely divorced from QRS

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15
Q

Symptoms/Exam findings for Mitral Stenosis

cause? treatment

A

Caused from Rhuematic Heart Disease and see Fish mouth fused commissures and hockey stick appearance to valves on Echo

Symptoms arise from increased pressure gradient from LA and LV - like CHF and increased Atrial pressure is the cause! Can get RHF and pulmonary edema

Signs are mitral facies, Loud P2 as mitral slams shut, RV heave from dilatoin, Large A wave in JVP

Auscultation - opening snap!!! Diastolic low pitched rumble murmur with presystolic accentuation and Loud S1 when it shuts

Radiology LAE - see double density, upliting L main bronchus, and enlarged posterior area on lateral

Tx - control HR - allow more diastolic filling, Diureses (less volume) manage Atrial Fibrillation

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16
Q

Symptoms, cause, clinical findings treatment etc for Mitral Regurgitation

A

Cause - valve pathology (ex papillary rupture or myxomatous) or LV dilation

Acute - BAD - rupture, endocarditis, trauma and no time to dilate so pulmonary edema!

Patho- LA dilation, reduced outflow, LV dilation (both get big) leading to LHF and see good EF

Auscultation -

1) Holosystolic murmur high intensity
2) S3 “Slushing In” extra volume reverberating
3) Hyperdynamic apex with thrill to back and axilla

Tx- AFterload reduction!!!

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17
Q

Mitral Prolapse

A

usually asymptomatic but can see palpitations, chest pain, fatigue syncope - REgurgitation!

posterior valve leaflestts enalred, change collagen, myomatous material, Marfans

Mid to late systolic click and late systolic murmur and changes with manuver

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18
Q

Aortic Stenosis

A

Bicuspid, Senile, Rheumatic

thicker hypertrophic ventricle with increased pressure - like systemic HTN = Concentric LV hypertrophy = CHF and Angina

CHF bc high diastolic pressure

Get HF, Syncope and angina!!!! (cant increase CO with exercise - syncope on exertion) can get arrhythmias

1) Crescendo-decrescendo systolic flow murmur
2) Ejection Click - bicuspid valve after S1 opening of aortic
3) Pulsus Parvus et Tardus harder to raise aortic pressure
4) S4 gallop = “A stiff wall” bc atrial kick onto stiff wall

Bicuspid valve - accellerated degeneration process and likely to see aoric dilation, aneurism and disssection

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19
Q

Aortic Regurgitation

A

Valve leaky from congenital, rhumatic, endoc OR Root dilation from dissection or syphilis or marphans

Chronic AR - Wide Pulse Pressure!!!!! eccentric LVH changes in caivty side and wall stress – results in CHF and angina

1) wide PP - head bob, uvula etc
2) cardiomegaly
3) early diastolic high pitched blowing decrescendo murmur
3) Pulsus Bisferience (like HOCM) 2 beats in periphery

Acute - emergency and massive pulmonary edema, no wide PP - same volume overload but no dilation

Treatment - Diuretics - decrase diastolic in ventricle to stop flooding lungs and AFterload decreasing to encourage forward flow

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20
Q

AS vs AR

A

AS - pressure overload and systolic problem - LV hypertrophy

AR - volume overload and diastolic problem - LV dilation

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21
Q

Drugs to use for HTN in pregnancy

A

MethylDopa!!!! (central A2 agonist that doesnt change CO to placenta)

Hydralazine - for preecclampsia

Only 1 beta blocker - lobatolol?

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22
Q

when do you hear S3?

A

vibration of a distended ventrile during filling “from volume overload in CHF or MR”

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23
Q

whats the first step and subsequent steps in atheroma formation?

A

LDL OXIDATION!!! then endothelial dysfunction then monocyte activation and VCAM1 to recruit them to eat the LDL and create foam cells that then cause SM proliferation and creation of plaqe

24
Q

What drugs cause INCREASED mortality after MI?

A

Class Ic propafenone and flecanide - only used for VTACh or SVT

25
Q

Digoxin

A

positive inotrope that has high toxicity but when used at lower levels increases parasympathatic responses and slows HR but can lead to AV block if already have bradycardia

26
Q

How do Fibrates work? what are tey?

A

Gemfibrozol??

act tio DECREASE TG by increasing LPL through PPAR

27
Q

What do you do to treat salycylate OD?

A

Urine Trap with Bicarbonate!

28
Q

How do you treat Iron overload?

A

Deferoxamine

29
Q

what is reverse use dependence?

A

K+ channel blockers (Class 3) bind better and Prolong QT more in bradycardia and slower rhythms so pace people to keep HR up

30
Q

how do you treat torsade?

A

Magnesium

31
Q

Aflutter treatment

A

regular - irregular 300 bpm with 2-4 conduction
GIVE BB/CCB/Dig for rate control
no heart disease can use 1c or 3

Use Rhythm control when rate control doesnt work OR on bypass tracts (class 3 or class 1c if no heart damage)

32
Q

BRUGADAS!!

A

SE Asian men (sleep like women at night)

Na channel deficit LONG QT3 bc they die in their sleep

33
Q

What should you DEFINITELY use CCB for?

A

Prinzmetals!!! coronary spasm use DHP long term

34
Q

What is Ritrodine?

A

Beta 2 agonist used for tocolysis to relax sm

35
Q

What should you not give in WPW?

A

BB, CCB, Dig - nothing to slow AV node!

36
Q

Long QT 2?

A

Herg Channel - die in emotional or startle OR drug induced

37
Q

Long QT1

A

Die in exercise - pool

Inward rectifier

38
Q

Long QT3

A

Die in sleep
Sodium channel
Like Brugadas

39
Q

2 drugs taht can give lupus?

A

Hydralazine

Procainamide

40
Q

A2 and insulin and clonidine

A

Clonidine is an A2 agonist and so will decrease insulin release

41
Q

Statins - Discuss

A

Decrease LDL and cholesterol - INCREASE LDLR and decrease Isoprenylation of proteins and inflammation
GIVE WITH CoQ10 for Ubiquinone

Side Effects = Hepatitis, Rhadmyalisis/Myositis, Teratogenic, Polyneuropathy

CYPS reaction so don’t give with Warfairin or CCBs or Clopidogrel

42
Q

Bile Resins - discuss

A

Cholestyramine and they block reuptrake of bile acids and so then get activation of FXR which acts to increase Bile Acid PRoduction

43
Q

Eezetimibe

A

Stop cholesterol uptake!
NPC1L - take up plant sterol and cholesterol

sitosterolemia blocks ABCG5/8 so hyperabsorption

44
Q

NIACIN

A

INCREASE HDL

receptor on fat cells to stop lypolysis and decrase FFA and TG syntehstsis and decrease LDL/VLDL and increase ApoA thereofre less THa nd increase HDL

BUT causes GI distress, liver problems, flush – beta arrestin pathway

45
Q

Fibrates

A

LOWER TG!
Gemfibrozil and Fenofibrate
Decrese TG and Increase HDL with PPAR to decrease LPL and ApoC to increase lipolysis

46
Q

Dypradimole

A

Persantine

Stopes PDE and stops platelets

47
Q

When do you not use prasugrel?

A

Prior stroke, >75 or low weight

48
Q

what GP2a3b agents are there and when do you use them?

A

Abciximab, Tirofiban and Eptifiatide

use for PCI so like UA and NSETMI

49
Q

Familial Hypercholesterolemia

A

increased LDL
LDL receptor defect or polygenic

Xanthomas and corneal arcus

50
Q

Familial Combined Hyperlipidemia

A

Increased ApoB

51
Q

RRD Remnant Removal Disease = Type 3 Hyperlipidemia

A

ApoE 2 cant take up IDL from liver and lots of remantns - YELLOW PALMAR STREAKS and xanthomas

52
Q

Hypertrygliceridria

A

lots of VLDL and increased TG
CeTP makes it so when more FFA and TG then added to decraese HDL and excreted and increase LDL so smaller and denser and can oxidze easier/greater affinity for monocytes

NO LPL!!! so increase VLDL and TG

53
Q

Hypoalphalipoproteinemia

A

Tangeers = no ABCA1 so increased cholesterol in macrophages bc not going to APOa1 and yellow throwat

or bad LCAT and so CE in HDL free and goes to eyes and kidneys - EYES AND KINDEYS

54
Q

Calculate LDL

A

= TC - HDL - TG/5

55
Q

what do saturated FA do?

A

down regulate LDLR

Autonomic Drugs N Stuff (19 decks)

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