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USLME Kiss my ass and pray > Cardio - General > Flashcards

Cardio - General Flashcards

1
Q

mitral valve prolapse =

Associated w/

A

mid systolic click

Marfan’s Syndrome

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2
Q

Cardiac output formula

A

CO=CVxHR

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3
Q

Total peripheral resistance formula

A

(MAP - R. Arterial pressure ~0)/CO

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4
Q

Resistance formula

A

R= ∆P/Q

or ∆P=QR

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5
Q

Resistance in series

A

R total = sum of Rs

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6
Q

Resistance in parallel

A

1/R total = sum of 1/R

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7
Q

1st line CHF Rx

A

ACE inhibitor - prevent cardiac remodeling
-Also beta blockers and ARBs

Loop diuretics is symptom management and HF

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8
Q

CO=

flicks equation

A

oxygen consumption/( arterial O2 content - venous O2 content)

watch units!!

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9
Q

what divides the R and L embryological atrium? (2)

A

septum primum -> osteum/foramen secundum

Septum secundom -> foramen ovale

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10
Q

How is blood shunted from the R to L atrium in embryo

A

foramen ovale (in septum secundum ) and osteum secundum (in the septum primum)

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11
Q

3 possible causes of atrial septal defect?

Common genetic abnormality associated>

A

osteum secundum overlaps foramen secundum

Absence of septum secundum

neither septum secundum nor septum primum develop

Downs syndrome

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12
Q

6 different aorticopulmonary septal(spiral septal) defects

embryological determination

A

tetralogy of fallout
persisitant truncus aretiosus
transposition of the great vessels

Dextrocardia
VSD
fenestrae

Neural crest derived

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13
Q

Ascending aorta and pulmonary trunk derived from?

A

Truncus arteriosus

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14
Q

Smooth outflow parts of L and R ventricles derived from

A

Bulbus cordis

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15
Q

trabeculated L and R ventricle derived from

A

Primitive ventricle

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16
Q

Trabeculated L and R atrium derived from

A

Primitive atrium

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17
Q

Coronary sinus derived from

A

L horn of sinus venosus

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18
Q

Smooth part of R atrium derived from

A

R horn of sinus venosus

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19
Q

Superior vena cava derived from

A

R common cardinal vein and R anterior Cardinal vein

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20
Q

1st aortic arch ->

A

maxillary artery (branch of the external carotid)

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21
Q

2nd aortic arch ->

A

stapedial artery and hyloid artery

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22
Q

3rd aortic arch ->

A

Common carotid

AND proximal part of internal carotid

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23
Q

L 4th aortic arch ->

A

aortic arch

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24
Q

R 4th aortic arch ->

A

right subclavian artery

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25
Q

6th aortic arch ->

A

proximal part of pulmonary arteries and ductus arterioles

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26
Q

ductus venosus shunt

A

shunts blood from the umbilical vein into the IVC (bypassing hepatic circulation)

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27
Q

foramen ovale shunt

A

shunts blood from the R atrium to the L

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28
Q

Ductus arteriosus shunt

A

shunts blood from the the pulmonary arteries to the descending aorta

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29
Q

What is the most oxygenated vessel in the developing fetus?

A

umbilical veins

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30
Q

What closes the foramen ovale

A

increased L Atria pressure due to decreased pulmonary vasculature and increased flow through the pulmonary system

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31
Q

What closes the ductus arteriosus

What can be given to close?

A

breathing -> increased O2 -> decreased prostaglandin E2

Indomethacin

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32
Q

What to give to keep ductus arteriosus open?

A

PGE1 or 2

KEEEEPs open

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33
Q

most common congenital anomaly

presents as?

A

VSD

Exercise intollerance

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34
Q

Most common cause of early cyanosis

A

Tetralogy of Fallot

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35
Q

L to R shunts (3)

seen as?

A

VSD - holosystolic mumor
ASD ( loud S1 and Fixed spit S2)
PDA - machine murmor

late cyanosis (blue kids

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36
Q

R -> Shunts (5)

seen as?

A 
Persistent Truncus Arteriosus
Transposition of the great vessels
Tricsupid atresia
Tetralogy of Fallot
Total anomalous pulmonary venous return
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37
Q

Tricuspid atresia is fatal unless

A

Persistant ASD and VSD to allow mixing of blood (outflow to the pulmonary circuit is impaired)

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38
Q

Persistent truncus arteriosus pathology

A

neural crest cells of aorticopulmonary septum fail to divide aorta and pumpnary trunk -> one heart

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39
Q

Total anomalous pulmonary venous return pathology

A

the pulmonary vein does not return oxygenated blood to the L Atrium but instead back to the R circuit -> closed loop

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40
Q

Eisenmenger syndrome steps (4)

A

1 - L to R shunt
2. Leads to pulmonary hypertension w/ overuse of pulmonary vasculature
3- leads to hypertrophy of vasculature and resistance
4. Resistance builds and L -> R shunt becomes a R to L shunt (Cyanotic)

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41
Q

4 defects in the tetralogy of fallout

leads to

A
  1. Pulmonary valve stenosis
  2. R ventricular hypertrophy
  3. VSD
  4. Over riding aorta over the VSD

Leads to periods of R to L Shunting and cyanosis (get spells)

Crouch down to increase Systemic press to have L to R shunt again

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42
Q

Boot shaped heart think?

A

Tetralogy of Fallot in infants

R ventricle hypertrophy in adults

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43
Q

Infantile coarctation of the heart concerns and location?

A

the stenosis is PROXIMAL to the ductous arteriosus leading to the PDA being the only way of blood getting to the lower limbs

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44
Q

Adult coarctation of the heart location

A

stenosis DISTAL to the ductous arteriosus leading to increased pressure above the stenosis and notching of the ribs

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45
Q

Ebstein animal caused by?

Presents as (3)

A

Lithium use in mothers

Descent of tricuspid valves into the R ventricle. often have patent foramen oval.

See wide S2 split and tricuspid regurgitation

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46
Q

Congenital heart defects w/ digeorge’s syndrome(2)

A

truncus arteriosus

Tetralogy of Fallot

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47
Q

Down syndrome congenital heart defects?

A

ASD, VSD or AV septal defect

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48
Q

Congenital Rubella heart defect?

A

PDA

Pulmonary arterial stenosis as well

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49
Q

Turner syndrome heart defect (2)

A 
Coarctation of the aorta
Bicuspid valve (aorta)
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50
Q

Marfans congenital heart concerns

A

Aortic regurgitation -> dissection

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51
Q

Infantile diabetic mother concerns (2)

A

Big baby and associated delivery complications

Transpositions of great vessels

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52
Q

MAP =? (2 formulas)

A

2/3 diastolic pressure + 1/3 systolic pressure

CO x TPR
~P= QR

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53
Q

SV =

A

CO/HR

EDV - ESV

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54
Q

Why does CO decrease in ventricular tachycardia?

A

The diastolic filling is incomplete - too fast of HR

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55
Q

Pulse Pressure=

A

systolic - diastolic BP

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56
Q

Stoke volume is affected by (3)

A

COntractility
Preload
afterload

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57
Q

Role of Verapamil and contractility?

A

nondihydropyridine Ca2 channel blocker that lowers Ca intracellularly and contractility

Diltiazem also

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58
Q

Preload is the same as?(3)

A

Atrial pressure
end diastolic pressure
central venous pressure

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59
Q

hydralazine

A

decreases afterload w/ arterial dialation

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60
Q

nitrates

A

decrease preload w/ venous dialation

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61
Q

Ejection fraction =

Normally?

A

Stroke volume / End Diastolic Volume

> 55%

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62
Q

Viscosity of blood may increase in (3)

leads to?

A

polycythemia
hyperproteinemic states - multiple myeloma
hereditary spherocytosis

leads to increased resistance

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63
Q

X intercept of cardia venous function curve =

A

mean systemic filling pressure

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64
Q

normal L Atrial pressure

A

<12mmHg

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65
Q

Pulmonary wedge pressure measures?

A

L Atrial pressure

~ diastolic pressure of LV

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66
Q

BNP is released when from where?

Causes what?(2)

A

released from myocytes when they are stretched (like in CHF)

Leads to
vasodilatation
increased excretion of Na and water

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67
Q

Right sided heart signs (3)

A

Hepatomegaly (nutmeg liver
peripheral edema
JVD

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68
Q

Left sided Heart failure (5)

A

Pulmonary edema - with hemosiderin laden macrophage -> crackles and rales

  • paroxysmal nocturnal dyspnea
  • Othopnea
  • DOE -dypnea on exertion
  • Cardiac dilation
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69
Q

Renin secretion stimulated by what 3 mechanisms

A

sympathetic nervous system ( Beta 1 receptors -> CHF and compensation)

macula densa - senses low Na in glomerular filtrate

JG Apparatus - senses low BP

Leads to AT II

  • > (vasoconstriction
  • > Aldosterone secretion
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70
Q

Chronic CHF Rx (7)

First 4 improve surival and minimize heart remodeling

A
  • ACE inhibitors
  • ARBs
  • Aldosterone inhibitors - spironolactone, eplereonone,
  • beta blockers (metoprolol, carvediol, brisprolol)

Digoxin
Diuretics (loops and thalazides)
Vasodilators (Nitrate and Hydralazine)

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71
Q

Rx for Acute decompensated CHF

A

NO LIP

Nitrates 
Oxygen
Loop Diuretics
Inonotropics (stop beta, give dobutamine or phosphodiesterase)
Position - upright
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72
Q

Blurry yellow vision, confusion, bradycardia, N/V and EKG changes?

A

Think of of Digoxin toxicity

Digoxin decreases conduction through the AV node

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73
Q

3 factors predisposing to Digoxin toxicity?

A

Renal failure - decreased excretion
Hypokalemia -
Quinidine - displaces digoxin from binding sites

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74
Q

Rx for Digoxin toxicity (3)

A

normalize the [K]
Mg
anti-digoxin FAB
–Atropine or pacemaker if not available

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75
Q

Examples of increased capillary pressure

leads to ?

A

heart failure, CHF, Thrombosis, tumor clothing, cast, Na/H2O retention

Edema

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76
Q

decreased plasma proteins examples

leads to ?

A

nephrotic syndrome, liver failure, protein malnutrition, protein losing enteropathy

edema

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77
Q

Uncreased capillary permeability pathological causes (3)

permeability also known as

A

burns, sepsis and extotoxins

Kf

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78
Q

increased interstitial fluid colloid osmotic pressure due to ?

Leads to?

A

blocked lymphatics

nonpitting edema, leaked proteins have no where to go, water mixes leading to a jello like mass

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79
Q

net filtration pressure formula

A

Pnet = (Pc-Pi) - (Pi c - Pi i)

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80
Q

low cardiac output and increased systemic vascular resistance indicative of what?(2)

A

Shock

Hypovolumetric or cardiogenic

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81
Q

Rx for Cardiogenic shock

A

Dobutamine and other ionotropics

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82
Q

Sepsis is characterized by what presentation?(3)

Systemic vascular resistance?
CO?

Rx? (3)

A

Presents w/ fever and warm to the touch skin

May be lactic acidotic due to low O2 and anaerobic metabolization
DIC

high output shock w/ 1st vasodiation (leak capillaries) -> increased CO (Tachy)

Rx- Abx, NE (pressor) and fluids

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83
Q

Neurogenic shock

CO?
Systemic vascular resistance

Rx?

A

Decreased systemic vascular resistance and CO w/out sympathetic inveration

IV fluids, steroids maybe

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84
Q

Cold and clammy wet skin w/ bradycardia think of? (2)

A

Hypovolumetric Shock

Cardiogenic Shock

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85
Q

Causes of hypovolumetric shock? (2)

A

burns

blood loss - trauma

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86
Q

Causes of cardiogenic shock? (7)

A 
MI
PE
CHF
Arrythmia
Cardiac tamponode
tension pneumo
Cardiac contusion
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87
Q

femoral triangle?

Which are in the sheath?

A

NAVEL

Nerve
Artery*
Vein*
Empty
Lymph
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88
Q

Locations of central Lines (3)

How long ?

Complications?

A

Femoral

  • 5-7 days
  • can’t really move

Subclavian

  • 3-4 weeks
  • risk of pnemo
  • bad for COPD and lung tumors

Internal jugular

  • 3-4 weeks
  • may punch the carotid
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89
Q

Swan Ganz usual done through which central line

A

Right Internal jug
> left Sub clavian (easy loop)
>right sub clavian (hard angle to drop down)

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90
Q

increase of preload has what effect on SV?

A

Increased SV

NO change in pressures really seen

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91
Q

Increase in Afterload -> what change in SV and ESV

A

SV decreases while ESV increases

Heart is working harder to meet increased aortic pressure, can’t contract as much

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92
Q

increase in contractility has what change on SV and ESV

A

Increase in SV and decerease in ESV. more contraction and excretion of the blood

NO real change in pressures so aortic valve still opens fairly normal

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93
Q

Isometric contraction contraction takes place when?

A

QRS complex occurs and ventricles are contracting increasing pressure, rich before aortic valve opens

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94
Q

S3 is associated with what pathology(4)

Heard when?

A 
Dialated cardiomyopathy
CHF
Mitral regurgitation
L-> R shunt
sloshing ing

Heard right after S2 and the heart starts to fill in diastole

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95
Q

S4 is associated w/ what pathology (4)

Heard when

A

hypertrophic cardiomyopathy
aortic stenosis
chronic hypertension w/ Left ventricular hypertophy
Post MI

A stiff heart

Heard Right before S1 due to initial filling of the heart against a stiff heart wall followed by AV valve closure

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96
Q

a wave
c wave
v wave

A

Seen in JVD
a- r atrial contraction
c- r. ventricular contraction and bowing in of tricuspid
v- atrial filling against tricuspid valve

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97
Q

Normal splitting is due to?

Hear what?

A

drop in aortic pressure -> increase venous return and preload in the R ventricle -> delay in pulmonary valve closure vs aortic valve

heard on inspiration

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98
Q

wide splitting due to?

Pathology associated

A

Due to delay in R ventricle contraction w/ increase fluids and pulmonic valve closes after aortic

Varies with inspiration

pulmonary stenosis or R bundle branch block

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99
Q

Fixed splitting due to ?

Pathology associated?

A

due to fixed increased blood volume in the R ventricle from a L -> R shunt that is persistent. Increased volume compared to L ventricle delays closure of pulmonic valve vs tricuspid valve

Does not vary w/ inspiration

Atrial septal defect

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100
Q

Paradoxical Splitting

Pathology associated?

A

Due to L ventricular overfilling and delay in closure of aortic valve compared to pulmonic valve - always pathological,

Aortic stenosis or L Bundle branch block

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101
Q

Benign heart sounds if no pathology(4)

A

Split S1
Split s2 on inspiration
S3 in a patient <40
Early quiet systolic murmur

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102
Q

Bounding pulses, head bobbing, diastolic murmur

A

Aortic regurgitation

Hear immediate decrescendo

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103
Q

Diastolic murmurs

A

Mitral stenosis
Tricuspid stenosis
Aortic regurgitation
Pulmonic Regurgitation

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104
Q

Systolic murmurs

A

Aortic stenosis
Pulmonic stenosis
tricuspid regurgitation
mitral regurgitation

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105
Q

Inspiration has what effect on heart sounds

A

louder tricuspid of R heart murmurs

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106
Q

Expiration has what effect on heart sounds

A

louder mitral of L heart murmurs

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107
Q

Hand grip has what effect of heart sounds

A

Increased SVR -> increased after load

makes mitral regurgitation louder

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108
Q

Valsava maneuver has what effect on heart sounds

A

increased intrathoracic pressure -> decreased preload and after load

Quieter murmurs EXCEPT - hypertrophic cardiomyopathy

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109
Q

L side of the sternum diastolic murmur with wide pulse pressure -

A

aortic regurgitation

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110
Q

Causes of aortic regurgitation (4)

A 
aortic root dilation 
-> syphilis 
->marfans
Bicuspid aortic valves - usually stenosis
rheumatic fever
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111
Q

Opening snap heard over the apex of the heart in diastole

Can lead to

A

mitral regurgitation
-enhanced w/ expiration

Left atrial dilation

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112
Q

Cause of mitral stenosis

A

rheumatic fever

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113
Q

Heart Sounds best heard in L lateral decubitus

A

mitral stenosis
mitral regurgitation
L Sided S3
L sided S4

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114
Q

Causes of mitral valve regurgitation (5)

A 
rheumatic fever
endocaritis
ischemic heart disease - ruptured chord tendineae
LV dilation 
mitral valve prolapse
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115
Q

Holosystolic blowing murmur heard loudest at the apex of the heart

made louder w?

Radiates to?

A

mitral regurgitation

expiration and hand grip/squatting

Axilla

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116
Q

Causes of tricuspid regurgitation (2)

A

infective endocarditis

rheumatic fever

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117
Q

holosystolic murmur made louder with inspiration radiating to the right sternal border?

A

Tricuspid regurgitation

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118
Q

Crescendo decrescndo systolic ejection murmur w/ Ejection Click

Radiates where?

other findings?

A

aortic stenosis

Carotids

pulsus parvus et tardes - weak pulses

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119
Q

Aortic stenosis can lead to what 3 presenting problems

A

Syncope
Angina
Dyspnea

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120
Q

Causes of aortic stenosis(5)

A 
bicuspid valve (30-40yrs old)
Age related calcification (>60)
Rheumatic valve disease
unicuspid valve
syphylis
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121
Q

Holosystolic harsh murmur that is loudest at the tricuspid?

A

tricuspid regurgitation

or VSD

Clinical picture key

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122
Q

Late systolic crescendo murmur w/ midsystolic click?

A

mitral valve prolapse

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123
Q

Phases of ventricular action potential and associated Channels of importance

What phase does myocytes contract

A

Phase 4 - I K -> polarized
Phase 0 - I Na -> depolarization w/ AP
Phase 1 - slight repolarization w/ Na channels closing and K channels opening
Phase 2 - I Ca channels open -> plateau, K channels still open (*contraction)
Phase 3 - Ca channels close and K channels open -> repolarization

Back to phase 4

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124
Q

Phases of pacemaker action potential

A

NO PHASE 1 or 2

Phase 4 - I K channels-> polarized w/ I funny channels that slowly depolarize allowing Na to leak in

Phase 0- threshold leads to I Ca channels to create AP

Skip Phase 1 and 2

Phase 3 - K channels open and Ca channels close leading to repolarization

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125
Q

Channels responsible for depolarization in Phase 0 in myocytes vs nodal cells

A

Myocytes - Na channels

Nodal cells - Ca channels

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126
Q

I funny channels are found where increasing what permeability

A

Found in nodal cells acting during phase 4 to slowly depolarize the cell by increasing Na permeability

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127
Q

4 Classes of anti arrhythmics and MOA

A

No Bad boy Keeps Clean

Na channel - phase 0 
Beta blocker - Phase IV of Nodes and rate of depolarization (Beta 1 receptive)
K channel  - phase III 
Calcium channel (Phase 0 of Nodes)
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128
Q

Class 1A anti arrhythmics

MOA

Side effect as a class?

A

double quarter pounder

Disopyramide
Procainamide
Quinidine

Na phase 0 blocker -> Increase effective refractory period
increase AP duration (time of contraction of heart)

Torsades de pointes w/ Prolonged QT

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129
Q

Class 1B anti arrhythmic

MOA

A

mayo lettuce and tomato

mexiletine
lidocatine
tocainide

Na phase 0 blocker -> increase in effective refractory period, most often used ESPECIALLY post MI arrhythmia tacky and digitalis induced

Decrease AP

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130
Q

Rx for wolf parkinson White?

A

procainamide

Amiodarone

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131
Q

class 1 C anti arrhythmic

MOA

A

fries please

flecainide
propafenone

Na phase 0 blocker -> increase in effective refractory period, not used too often- NEVER post MI

Last resort for V tachy

No effect on AP

132
Q

Cinchonism is what and a side effect of what antiarrythmic

A

HA, Tinnitus, Dizzy

Quinidine

133
Q

SLE like drug induced antiarrythmic

A

Procainamide

W/ sulfonamide
Hydralazine,
Isoniazid
Phenytoin

134
Q

Class II antiarrythmics (5)

MOA

be wary of what

A 
Metoprolol
propranolol
esmolol
atenolol
timolol

Decreases nodal (SA and AV) activity by decreasing cAMP (B1 blockade) activity and Ca currents -> slower rate of depolarization of nodal cells

I funny channels not as permeable

Worry of Beta 2 nonselective -> vasospasm in Prinzangina, or those w/ pulmonary disease

135
Q

Clinical use of beta blockers as antiarrythmics(4)

A

ventricular tachy
SVT
slowing vent rate during atrial fibrillation or flutter

136
Q

Class III anti arrhythmic (5)

MOA

Worry of?

A 
Amiodarone*
Ibutilide
Dofetilide
Sotalol*
Bretylium

Blocks K channels in myocytes in phase III -> increased effective refractory period

Worry of QT prolongation and torsades

137
Q

Toxicity w/ Amiodarone - 3 key, are others

A

pulmonary fibrosis/ cough
hepatoxicity
hyper/hypothryoidsm
- 40% iodine

Check LFTs, PFTs, TFTs

Also skin (blue/grey), corneal deposits, photodermatitis, constipation, bradycardia

138
Q

Class IV antiarrythmics (2)

MOA

Worry about?

A

Verapamil and Diltiazem
- nondihydropyridine CCB vs dihydropyridine CCBs(nifedipine, felodipine, Amlodipine)

Affects phase 0 through Ca channel blocking in the nodes lowering the slope and thus increasing effective refractory period

also lowers conduction velocity

Worry about CHF, take off beta blockers if giving

139
Q

Side effects of adenosine and uses?

Blocked by?

A

flushing, hypotension, chest pain

used for diagnosing/abolishing SVT

Theophylline (COPD Rx)

140
Q

Role of K and Mg in arrythmias?

A

want to keep above 4 for K and >2 in Mg to prevent, especially in a peri MI setting

K depresses ectopic pace maker in hypokalemia

give Mg for torsades

141
Q

Irregular irregular rhythym?

also characteristic?

A

atrial fibrilation

No P waves

142
Q

Biggest Atrial fibrillation concerns?

Guides Rx how?

A

Risk of stasis -> clots

< 48 hrs you can have synchronized cardioversion before clot forms

> 48 hrs or unknown need to coat first due to risk of thromboemboli

143
Q

Rx goals in atrial fibrilation - 3

A

Anticoag

  • heparin of enoxaparin (LMWH) 1st
  • Warfarin later

Rate control - especially older
- Beta blockers, digoxin, CCb

Rhythm control - especially younger
- K channel blockers

144
Q

Risk factors for atrial fibrillation (3)

A

HTN
CVD
Heart failure

all lead to dilated L atrium and odd conduction patterns

145
Q

Atrial flutter characterized by what ECG line?

P waves?

A

sawtooth appearance

a lot of P waves that are regular - > increased HR

146
Q

1st degree HB characterized by?

infectious cause?

A

PR interval greater than 200mse (5 little boxes)

Borrelia burgorferi (may cause 3rd degree as well)

147
Q

2 types of 2nd degree HB and difference?

Rx?

A

Mobitz type 1/ Wenckebach - progressive lengthening of the PR interval leading to a dropped beat
- none mentioned

Mobitz type II - dropped beats w/out warning usually at regular intervals
- pacemaker,

148
Q

3rd degree HB characteristic

A

P waves and RS complexes bear no relation to another,

Bradycardia

maybe narrow QRS but (1/3 are wide)

149
Q

Wolf parkinson white characteristic ECG tracing?

Due to?

A

delta wave

due to premature stimulation of the ventricles from an accessory pathway most likely the bundle of Kent

150
Q

Wolf parkinson white leads to risk of?

RX w?(2)

A

Risk of SVT w/ re-entry

Amiodarone or procainamide

151
Q

Paroxysmal SVT tracing?

A

narrow QRS w. rapid rate

above the node? Re-entry mechanism?

152
Q

failure of the AV or SA node to generate a beat leads to ?

characterized by? (3)

A

ventricular escape rhythm

Characterized by

  • wide QRS
  • no P wave
  • bradycardia
153
Q

Junctional escape rhythm has signal generated by?

Characteristic Tracing? (3)

A

AV node, SA node is not working

  • Narrow QRS
  • Bradycardia
  • p wave most likely absent
154
Q

Wide QRS complexes seen w/out P wave at random on a tracing

whys are they called cannon alpha waves?

A

Preventricular contraction
Usually >0.16s (4 little boxes)

maybe bigeminal or trigeminal in relation to p waves (1:1 or 2:1)
3 or > is potentially ventricular tachycardia

R Atria are contracting against closed tricuspid valve seen in the JVD

155
Q

Ventricular tachycardia

HR?

Biggest concern?

A

3 or more successive ventricular complexes w/ widths > 0.16s (4 little boxes), QRS shifted to the left

HR greater than 100 BPM usually

Progression to V fib; defibrilate to prevent before hem dynamic collapse

156
Q

Shockable rhythms? (2)

A

V tach

VFib

157
Q

Drugs at risk for Torsades by prolonging the QT interval?(5)

A 
Abx - Macrolides and choroquine
Antipsycholics - Haloperidol and rispiridone
Methadone
Antiarrythmics - Class IA and III
Protease inhibitors
158
Q

Rx for Torsades de Point?

A

Push of Magnesium sulfate

159
Q

Concern w/ torsades de points?

A

V fib

-essentially it is ventricual tachycardia w/ shifting amplitude

160
Q

Normal BP in
R ventricle
L Ventricle

A

25/5

130/12

161
Q

Barocreptors are located where and what are their respective signals out

A

Aortic barroreceptor responds to HTN only
-> sends increase signal with high pressure to the medulla via the vagus nerve

Carotid barroreceptor responds to HTN and hypotension. ∆stretch leads to change in firing in the glossopharyngeal nerve to the solitary nucleus of the medulla

162
Q

Chemoreceptors are located where and respond to what

A

Chemoreceptors in the aortic arch and carotid artery respond to decrease PaO2, hypercapneia and acidosis

Central chemoreceptors in the brain respond to acidosis and increase CO2 in the CSF (responds to the arterial hypercapneia)

163
Q

Patient presents w/ hypertension, bradycardia and depressed respiration, what is going on

A

Cushing reflex. Increased BP to overcome intracranial pressure from a lesion. Bradycardia is a reflex to the HTN

164
Q

Carotid massage does what

A

stimulates the glossopharyngeal nerve to increase firing to the solitary nucleus of the medulla to make it perceive HTN an slow down the HR

165
Q

Organ that receives the most of the systemic blood

A

Liver

166
Q

Organ that receives the most systemic blood by weight

A

kidney

167
Q

Which organ receives 100% of the CO

A

Lungs from the R ventricle

168
Q

Local metabolites that result in vasodilatation of the heart(3)

A

CO2 - hypoxia

NO - from constituiatve NOS and all its associated factors

adenosine - ATP w/o any phosphates indicates low energy

169
Q

ANP is released from where ?

What are its actions (2)

A

From the atrium of the myocytes in response to increase pressure

Results in vascular relaxation and decreased Na absorption (by increasing GFR through efferent arteriole constriction and afferent arteriole dilation) ~counteract aldosterone

170
Q

How does dihydropyradine CCBs block vasoconstriction?

A

Drugs like nefedipine block the Ca-Calmodulin complex from forming which normally would: increase myosin light chain kinase activity, phosphrylating myosin and leads to contraction.

The presence of the drug inhibits this

171
Q

What does does epinephrine on B2 (not alpha1 for this example) and prostaglandin E2 do to result increase vasorelaxation?

A

B2 and PGE2 act to increase cAMP which blocks myosin light chain kinase from phosphorylating myosin which leads to contration

172
Q

How does LPS from gram (-) lead to shock and vasodialtion

A

LPS stimulates inducible NOS chich converts L arginine to NO which activates Guanylyl cyclase which increases cGMP and ultimately activets myosin phosphatase which takes the phosphate off any activated myosin leading to relax ion of the vessel

173
Q

Sildenafil acts to vasodialate how?

Why is adding a nitrate a bad idea on top of this?

A

Sildenafil blocks the enzyme cGMP phosphodiesterase that degrades cGMP. Thus there is more cGMP around to encourage myosin phosphatase to be active and take off the phosphate on myosin and relax

Nitrate induces guanylyl cyclase to make more cGMP and thus have even more cGMP around

174
Q

bradykinin, ACh, alpha 1 agonists, histamine, serotonin an dshear stress all act to vasodialate vessels how

A

Act on endothelial cells to increase intracellular Ca. This works on constitutive NOS system to convert L arginine to NO and citrulline. The NO diffuses to nearby smooth muscle to induce guanylyl cyclase to creaste more cGMP -> increases myosin phosphatase which takes the phosphate off activated myosin -> relaxation

175
Q

Values describing hypertension and prehypertension

A

HTN >140/90

Pre HTN >120/80

176
Q

Most common cause of HTN

A

Essential HTN

177
Q

Most common cause of 2ry HTN

Other causes?(6)

A

Renal disease and Renal artery stenosis
-Hypokalemia, ab bruits, increase creatinine/BUN

Pheochromo
Cushing
Drugs
Hyperthyroid
Sleep Apnea
hyperaldosereone (Conns)
178
Q

Complications of HTN (6)

A 
Arteriosclerosis
L Ventrical hypertrophy
CHF
Stroke
-hemorragic and ischemic
retinopathy
aortic dissection
179
Q

Risk factors for HTN

A 
Age
Obesity
Race Back>white>asian
DM
Smokine
180
Q

Hypertensive urgency?

A

BP > 180/120 w/o signs of end organ damage

Becomes an emergency w/ end organ damage

181
Q

L ventriculae hypertrophy complications

A

A stiff heart (S4)
lack of myocardial perfusion w/ thickening (MI risk)
Decreased CO with less room for filling

182
Q

Risks for aortic dissection(3)

A

HTN
Cystic medial necrosis (Marfans)
bicuspid valve

183
Q

CXR of aortic dissection

A

mediastinal widening

CT shows false lumen between tunica intima and media

184
Q

Differnece between type A and type B atherscerosis and management techniques

A

Type A involves the arch and the ascending aorta
-medical emergency w/ surgical intervention

Type B involves the aorta distal to the branches- often use a beta blocker to Rx

185
Q

antihypertensive that causes 1st dose orthostatic hypertension

A

Alpha 1 antagonists

186
Q

ototoxic anti HTN - especially w/ aminoglycosides

A

Loop dieuretics

187
Q

Hypertrichosis as a SFx for anti -HTN

A

minoxidil

Hair gain

188
Q

Cynaide toxicity concern w/ this anti-HTN

A

Nitroprusside, used in malignant HTN

189
Q

Bradycardia an asthma exacerbation concern w/ this anti-HTN

A

beta blockers

190
Q

Reflex tachycardia ant -HTN

A

Any thing that vasodialates

- ACE, Hydralazine, Nitro, CCBs

191
Q

Cough is seen as a side effect w. this anti-HTN due to?

A

Ace inhibitors

Due to increase in bradikinin(not broken down)

192
Q

Anti HTN drug to avoid with sulfa allergy

A

Thiazides and Loop dieuretics

193
Q

Possible concern w/ angioedema w this anti-HTN (2)

A

ACE inhibitors

ARBs

194
Q

Hypercalcemia as a concernw/ hypocalemia if used as a dieuretic

A

Thiazide

Loops lose Ca

195
Q

What antihypertensives benefit heart failure patients (4)

A

ARBs
ACE inhibitors
Aldosterone antagonists
Beta blockers - carvediol, metoprolol, bisoprolol

Loops are only symptomatic

196
Q

Which antihypertenisves are safe in pregnancy (4)

A

HTN mothers love Nifedipine

Hydralazine*
Methyldopa
Lobetelol
Nifedipine

NO ACE

197
Q

Avoid this Anti HTN in gout

A

Thiazide -> hyperuricemia

198
Q

Anti HTN to avoid in renal artery stenosis-

Why?

A

ACE inhibitors/ARBs

due to renal insufficiency from dilation of the efferent arterial leading to a drop in GFR

199
Q

Drug of choice in lowering HTN w/ DM

A

Ace inhibitors/ARBs

200
Q

First line Rx for essential HTN

A

Thiazide dieuretics

Maybe anACE

201
Q

Drug of choice for malignant HTN

Risk?

A

Nitroprusside, short acting, titrated IV

Risk of cyanide poisoning

202
Q

Why does creatine increase and serum potassium level increase w/ an ACE inhibitor

A

Less angiotension II means less constriction of the efferent arteriole of the glomeruli and as a result there will be less GFR and filtration of creatinine

K increases due to the blocking of angiotension II increasing aldosterone secretion from the adrenal cortex

DO NOT GIVE W/ BILATERAL RENAL STENOSIS

203
Q

ARBS and ACE inhibitors share what big concern of S FX

A

Angioedema

204
Q

Most common locations of athersclerotic plaque and associated complications (4)

A

Abdominal aorta; AAA
Coronary Arteries; CAD and MI
Popliteal Artery; PAD and Claudication
Carotids; Stroke and TIA

205
Q

ST segment elevation only during brief episodes of chest pain

A

prinzmetal angina

206
Q

CAD risk factors (5)

A 
>45
family history 
high LDL
Smoking
HTN
207
Q

Patient is able to point to their chest pain with one finger is most likely due to

A

muscularskeletal

208
Q

Chestwall tenderness on palpation

A

muscular skeletal

209
Q

Rapid onset of sharp chest pain in a 20 something and SOB

A

Spontaneous pneumo

210
Q

Chest pain that occurs after heavy meals and improved by antiacis

A

GERD or could be esophageal spasm

211
Q

Deadly causes of chest pain (5)

A

MI
aortic dissection
Unstable angina

tension pneumothorax
PE

212
Q

Arteriosclerosis

vs atherosclerosis

A

Arteriosclerosis is general term for hardening of the arteries

Athersclerosis is fibrous plaques and atheromas in the intima of the arteries
-it is a type of arteriosclerosis

213
Q

Monckeberg

A

Type of athersclerosis where the tunica media calcifies and hardens

especially the radial and ulnar nerve in the elderly

benign

Does NOT obstruct blood flow

214
Q

Arteriolosclerosis

A

hyaline thickening go the small arteries

-seen in HTN and DM

215
Q

Atherosclerosis pathophysiology(8)

A

Risk factors of smoking, HTN, DM and dyslipidemia -> inflammation

Endothelia dysfunction

  • > macrophage and LDL accumulation
  • > foam cell formation
  • > fatty streaks
  • > smooth cell migration (PDGF and FGF)
  • > proliferation and EC matrix depostion
  • > fibrous plaques
  • > complex atheromas in the intima
216
Q

Abdominal aneurism complications(4)

Pathophys?

A

nutrient and waste diffusion compromised due to thickened vessel -> necrosis and weakness

Pulsating mass

rupture
embolize
obstruct branch vessel
impinge on adjacent structure

217
Q

AAA are more common in (2)

A

due to athersclerosis

seen in smokers and men >50

218
Q

When do you repair a AAA

A

athersclerotic plaque -> problems w/ diffusion of waste and nutrients -> wall necrosis and weakness

US serially q 6 months until > 5cm then repair

219
Q

3 types of Angina and causes

A

Stable - predictable in onset, usually due to atherscerosis. may see ST depression w/ exertion

Unstable -rupture of thrombosis w/ incomplete artery occlusion, ∆ in pattern and maybe increasing severity in pain

Prinzmetal - more often younger patients w/ coronary vasospasm, transient pain at REST w/ ST elevations seen

220
Q

Rx for prinzmetal angina

A

Give dihydropradine CCBs like

  • Verapamil
  • Diltiazem
221
Q

Chronic ischemic heart disease is/?

A

progressive onset of CHF over yrs due to chronic ischemic myocardial damage; patchy fibrosis replacing cardiac muscle -> decreaes contractility

222
Q

Right dominant circulation means what?

A

the SA nodal branch feeding the SA node is coming off the posterior descding /interventricular artery (PDA) which is coming off the R coronary artery

223
Q

Coronary arteries fill when?

A

during diastole,

the aortic valve closes and the blood falls back into the sinuses right above the valve

224
Q

Left atrial heart enlargement can have what 2 extra cardiomanifestations?

A

Dysphagia - impinging the esophagus

Hoarseness- impinging the R recurrent laryngeal nerve

225
Q

Branches off the Right and Left Coronary artery

2 and 2

A

Right coronary artery (RCA)

  • Right marginal artery (R atrium)
  • Posterior descending/interventricular artery (PDA)

Left coronary artery (LCA)

  • Left anterior descending artery (LAD)
  • Left Circumflex coronary artery (LCX)
  • —may sometimes have the PAD off it (20%)
226
Q

coronary artery most commonly affected in an MI

A

LAD - left anterior descending

supplies anterioe 2/3 of the inter ventricular septum

227
Q

What part of the heart is most posterior?

Anterior?

A

Posterior is the L atrium
- sitting on the posterior wall

Anterior is the R Ventricle

228
Q

2 cholesterol lowering drugs that may cause RUQ pain?

A

Cholesterol Gallstones

Fibrates (gemfibrizil, clofibrate, bezafibrate, fenofibrate)

Bile acid resins (cholestryramine, colestipol, colesevelam)

229
Q

drugs good for lowering tryglycerides (2)

preventing what complication?

A

Omega 3

Fibrates (gemfibrozil and clofibrate

pancreatitis

230
Q

Prevent the most adverse complication of niacin by doing what>

A

giving ASA or NSAIDs 30 min prior

also have skin rashes and itching

hyperuricemi and hyperglycemia

231
Q

Combination of drugs given to help w/ CAD?(2)

goal of treatment

A 
Beta blockers  (lowers after load)
-NOT pindolol, acebutolol - (partial beta agonist)

Nitrates(lowers preload)

Maybe throw in an ACE

Goal of treatment is to reduce myocardial oxygen demand

232
Q

Factors looked at when trying to lower oxygen demand of heart in angina pectoris(5)

A

preload, contractility, BP (afterload), ejection time, HR

Thus the beta blockers and nitrates

Also CCBs, ACE inhibiters

233
Q

Myocardial infarction ECG changes in

Acute
Hours
Day 1-2
Days
Weeks
A

Acute - ST elevation

Hrs - ST elevation w/ R decreasing and Q appearing

Days 1-2 - T wave inverts and Q deepens

Days - ST normal; T inverted

Weeks: ST normal, T normal Q wave persists

234
Q

Indication on ECG of an MI weeks later

A

persisitent Q wave

one block wide or 1/3 the height of the qrs

235
Q

ECG changes w/ MI (4)

A

ST segment elevation at least 1mm in 2 contiguous leads

T wave inversion

New LBBB

New Q waves that are > 1 block wide or 1/3 the height of the QRS

236
Q

most common lethal complication post MI

A

Arrhythmia

237
Q

0-4 hrs after a MI see what?

A

a lot of nothing.

Only have an increase risk of arrhythmia and changes on the ECG

238
Q

4-12 hrs later in an MI see

Grossly

Microscopically (2)

Risks(1)

A

gross- dark mottling

Micro

  • coagulative necrosis
  • hemorrhage, edema, NO inflam yet

Risk of Arrhythmia

239
Q

12-24 hrs later in an MI see

Grossly

Microscopically(3)

Risks?(1)

A

goss- dark mottling (still)

Micro

  • coag necrosis -> release of necrotic cell content into the blood (cardiac enzymes)
  • Contraction bands from reprofusion injury
  • PMN infiltration begins

arrhythmia

240
Q

1 day 3 days later in an MI see?

Grossly

Microscopically (3)

Risks (2)

A

gross - hyperemia* (redness of the infarct) on top of the dark mottling

Micro

  • extensive coag necrosis
  • Acute inflammation
  • PMN migration
Arrhythmia
fibrinous pericarditis (especially transmural)
241
Q

3-14 days after an MI see?

Grossly

Microscopically(2)

Risks?(3)

A

gross- yellow tan w/ hyperemic border (softens) ~ bruise

micro

  • macrophage** infiltration
  • Granulation tissue w/ remodeing

Risk of Free wall rupture -> cardiac tamponade
papillary muscle rupture -> murmur
ventral wall aneurism

242
Q

Weeks after an MI see?

Grossly

Microscopically(3)

Risks?(3)

A

Grey scar tissue seen

microscopically

  • contracted scar complete
  • hypocellularity
  • increased collagen

Risk of
Dresslers syndrome - autoimmune pericarditis
Ventricular aneurism
CHF

Both of the last 2 have to due w/ lack of myocytes and inefficient pumping

243
Q

3 Cardiac enzymes and timeline of them being seen in serum

A

Cardiac troponin I seen w/in 4 hrs - stays elevated for 7-10 days

CK-MB - in cardiac and skeleton muscle, stays elevated only for 48 hrs (good for MI on top of another) -

CPK is another, any muscle damage

May also see myoglobin

244
Q

What cardiac enzyme would be good to check to see if a patient had 2 MIs w/in a week of each other

A

CK-MB stays elevated for only 48 hrs

CK-MB may also be helpful in blunt trauma to the chest to asses cardiac contusion
ratio CK-MB : total creatine Kinase

245
Q

2 types of MIs and how do they differ

A

Transmural MI

  • ST elevation and Q waves
  • Affects the entire wall

Subendocardial MI

  • ST depression
  • only the subendocardial wall, <50% of the wall
  • -times of hypoperfusion
246
Q

What sort of ECG changes would you see with an anterior wall MI

Artery affected?

A

Leads V1-V3, maybe V4 and V5 - ST changes

LAD

247
Q

What sort of ECG changes would you see with a lateral anterior wall MI

Artery Affected?

A

Leads aVL, V5 and V6 - ST changes

LCX

248
Q

What sort of ECG changes would you with an inferior wall MI; Posterior wall MI

A

Leads II, III and aVF; ST Changes
- Change in r precordial EKG and V4 if posterior wall

-RCA infarct

249
Q

Cardiac complications post MI (7)

A

Arrhythmia- V tach most common cause of mortality

LV failure and pulmonary edema

Cardiogenic shock

Structural integrity compompromised

  • Papillary muscle -> mitral regurg
  • Free ventral wall rupture -> cardiac tampanode
  • interventicualr wall rupture -> VSD

Ventricular anuerism -> mural thrombosis
-> stasis -> emboli risk and stroke

Post infarct pericarditis (1-3 after)

Dressler’s syndrome - Autoimmune rxn weeks after

250
Q

Patient a couple days after an MI has a murmur. What can be the cause? (2)

A

Papilalry muscle tear-> mitral regurb

Interventricular rupture -> VSD

251
Q

Muffeled heart sounds w/ hypotension and a JVD right after an MI

A

be concerned of cardiac tamponode where the free wall ruptured

252
Q

Rx for every acute MI (10)

A 
ABCs
MONA
-Morphine
-O2 if hyperemic
-Nitrates
-ASA
Beta blockers (if no HF or asthma)
Statins
Antiplatelet- Clopidogril or ticagrelor
Anticoag - Heparin or enoxaparin
K > 4 and Mg >2
253
Q

If having a STEMI what are your reprofusion options after initial management

A

Cath lab

or if less than 2 hrs fibrinolytics

254
Q

If having a NSTEMI what are your reprofusion options after initial management?

A

Just the Cath lab, no fibrinolytics

255
Q

Patient is having symptoms of CAD, hap acceded is is arteries

A

75%

256
Q

Fibrinolytic therapy timeline for
Stroke?
MI?

A

Stroke - 3Hrs

MI - 2hrs

257
Q

Drugs for post MI patient(6)

A 
ASA +/or clopidogril
Beta blocker*
ACE*
ARBs
K sparing diuretics
Statins*

Stars reduce mortality

258
Q

Most common cardiomyopathy?

Causes?

A

Dialated

Chronic alcoholism
chronic myocardial ischemia
wet beriberi
Cox B myocarditis
Chagas
Doxorubacin
Cocain use
hemachormaosis (also restricted but less)
259
Q

Symptoms of dilated cardiomyopathy (3)

A

Systolic dysfunction due to large heart

S3
Enlarged heart on CXR
Apical impulse displaced laterally

260
Q

Most common cause of hypertrophic cardiomyopathy

General pathophys

A

hereditary in a Auto Dom (b mysoin heavy chain mutation)

Intraventricular thickening due to disorganized tangled hypertrophied myocardium being made leads to an outlet obstruction with the mitral valves being closer to the heart wall

Systolic murmur heard as a result

261
Q

Most common cause of sudden death in young athletes

A

Hypertophied cardiomyopathy

Auto dom inheritied. Thick inter ventricular heart wall leads to outlet obstruction. Hypovolumia in a game leads to decrease pre lead which is necessary to keep the valve open.

262
Q

Findings in asymmetric conncentric hypertrophy of the the heart (4)

A

S4
increased ejection fraction (less filling, easier to empty)
Systolic murmur
Increased apical impulse

263
Q

Rx for hypertrophy of the heart(2)

A

Want to slow the heart down and allow it to fill

Beta blockers
Ca channel blockers - Verapamil

264
Q

What sort of murmur is hear in hypertrophy of the heart and what maneuvers can change the quality of the murmur

A

Systolic murmur

  • valvsava makes it quieter due to decreased preload and less LV outflow (opposite of others)
  • squating reduces after load and thus makes the murmur quieter
265
Q

Major causes of restrictive heart disease(5)

A

LEASH

Lofflers syndome - eosinophilic infiltrate and endocardial fibrosis

Encocardial fibroelastosis-thick fibroelastic tissue in endocardium of kids

Amyloidosis - MOST common

Sarcoidois

Hemochromatosis(more dilated)

266
Q

Lowfflers syndrome

A

Form of restrictive endocarditis

w/ eosinophilic infiltrate and endocardial fibrosis

267
Q

Culture negative endocarditis causes (5)

A

HACEK

Hamopholis
Actinobacillus
Cardiobacertum
Eikenella
Kingella
268
Q

Myocarditis is most commonly due to

A

Coxsackie B

-generalized inflammation of the myocardium

269
Q

See diffuse interstitial infiltrate w/ myocyte necrosis on histology

Causal agent

A

myocarditis w/ Coxsackie B most likely

270
Q

Diagnosis of infective endocarditis

A

Dukes criteria

New murmur
Echo - transesophageal
positive blood cultures (2/3)

Also
-fever, emboli, immune problems

271
Q

Oslers nodes vs Janeway lesions

A

Osler nodes are painful emboli found on the tips of the fingers

Janeway lesions are more on the plans and soles and painless

Also have roth spots

272
Q

4 most common causes of infectious endocarditis

A

Staph aureus - acute
viridans step - sub acute
Enteroccci - Rx resistant
Staph epidermidis - prosthetic valves

273
Q

2 forms of non infectious endocarditis

A

Liedman sacks
-SLE
Both sides to the valve affected

Marantic endocarditis

  • METS
  • platelet fibrin aggregates in pts w/ hypercoagable states
274
Q

Complications of endocarditis - long term(4)

A

chordae rupture
glomerulonephritis
supperlative pericaditis
emboli - brain, spleen, kidneys

275
Q

Most common cause of constrictive pericarditis in the US

A

Lepus

TB worldwide

276
Q

Kassmaul Sign

What is it?

MOA
Diseases

A

It is presence of JVD on inspiration

Due to Decreased capacity of R ventricle to fill

Primary due to constrictive pericarditis

277
Q

Pulsus paradox

What is it?
MOA
Diseases associated

A

it is decreased systemic BP by at least 10mmHg upon inspiration

Due to insufficient L ventricile filling due to over expansion of the R ventricle w decreased intrathoracic pressure

Associated w/ cardiac tampanode and disease requiring increased straining of breath -asthma, etc…

278
Q

major criteria for rheumatic fever

A

JONES

J- Joints - polymigratory
heart - pancarditis
N - nodules - Sub Q, painless
E -erythema margininatum 
S - Sydnea Chorea
279
Q

4 non superlative diseases associated w/ Strep Pyrongenes

A

Scarlet Fever - toxin mediated

Rheumatic fever - Type II Hypersens

post strep glumerulolnephritis - Type III hypersens

Strep Toxic shock syndrome - post skin infection mainly, can be sore throat too

280
Q

Aschoff bodies

A

granulomas w/ giant cells seen in rheumatic fever

281
Q

Anischkows bodies

A

activated histiocytes seen in rheumatic fever (owl eye appearance)

282
Q

Specialty cells seen in rheumatic fever (2)

A

Aschoff bodies - granulomas w/ giant cells

Anischkow bodies - activated histiocytes

283
Q

Which valve is affected most in rheumatic fever and what is the presentation early and late

A

Mitral valve

Early you have regurgitation

Late- stenosis

284
Q

Presentation of pericarditis(3)

A

sharp peuritic pain that is more painful with inspiration, less leaning forward

Friction rub

ECG changes DIFFUSE ST elevation

285
Q

Categories of pericarditis etiology (4)

A

Fibrinous

  • Dresslers
  • uremia
  • radiation
  • RA

Serous

  • viral
  • SLE
  • Rheumatic fever

Superlative
-Pneumococcus and strep, TB

Cancer METs

286
Q

Kassmaul sign and sharp peurtic chest pain w/ a creatinine of 5

A

Fibrinous pericarditis

287
Q

Pathophys of cardiac tampanode

What are the findings in a cardiac tampanode(5)

A

compression of the heart by fluid -> lower CO and equilibrium of diastolic pressure in all 4 chambers

hypotension
increase in JVD
distant heart sounds
increase HR
pulsless paridoxis
288
Q

ECG shows electrical alternans

Dx?

A

Cardiac tamponade

The QRS complex alternates in intensity of size

289
Q

most common primary cardiac tumor in adults?

in kids?

A

Left atrium myxoma

Rhabdomyoma
associated w/ tuberous sclerosis -> astrocytoma and angiomyolipoma

290
Q

Most common tumor of the heart

A

METS

291
Q

4 disorders associated w/ Reynolds phenomenon

A

Mixed connective tissue disease
Bruegers
CREST scleroderma
SLE

292
Q

Most common childhood systemic vascultis?

Presentation(4)

A

Henoch schonelin Purpura

Palpable purpura on the butt/legs
Arthralgia (knee)
GI - ab pain, melan
Renal Disease -> Bergers/IgA glomerulonephritis

293
Q

Vascultitis associated w/ IgA deposition in many areas in =cluding the kidney

A

Hencoh Schonlein

Most common in kids

294
Q

History of asthma and has necrotizing vasculitis w/ eosinophilia

Lab marker?

A

Churg Strauss

maybe a pANCA

295
Q

Vasculitis associated w/ cANCA

A

Granulomatosis w/ polyangitis

- Wegeners

296
Q

Vasculitis associated w/ pANCA

A

microscopic polyangiitis

Churg Straus sometimes

297
Q

Churg Strauss presentation(3)

A

asthma/sinusitus
palable puprua
peripheral neuropathy (foot drop)

also can involve the heart, GI and kidneys -> pauci-immune glomerulonephritis

pANCA

298
Q

Triad of Wegeners?

A

Focal necrotising vasculitis
necrotizing granulomas in the lung and upper airway
necrotizing glomerulonephritis

299
Q

small vessel vasculitis commonly involving the lung, kidneys and skin w/ paucu glomerulonephritis and papable purport

lab test?

A

Microscopic polyangiitis

pANCA

300
Q

Microscopic polyangiitis presentation(3)

A

small vessel vasculitis commonly involving the
lung,
kidneys
skin w/ pauci glomerulonephritis and papable purport

pANCA

301
Q

3 symptoms of unilateral HA, jaw claudication and irreversible blindness risk

Disease affects branches of what artery?

A lab you could run ?

A

Giant cell/temporal arteritis

Affects branches of the carotid artery

ESR to r/o if NOT the case

302
Q

vasculitis associated w/ polymylagia rheumatica

A
  • dosas of pain and joint stiffness (proximally)

Giant cell/temporal arteritis

303
Q

Vasculitis is found in a young asian female?

Also known as?

A

Takayasu

pulses disease

304
Q

granulomatous thickening of the aortic arch and proximal great vessels

Affects which population mainly?

A

takayasu’s pulseless disease

asian females <40yrs

also have fever, night sweats, arthritis, myalgias and skin nodules

305
Q

Patient w/ HBV is at increased risk of this vasculitis

Preferentially attacks which vessels (2)

A

Polyarteritis nodosa (PAN_

attacks renal and visceral vessels(sparing the lung)

306
Q

Polyarteritis nodosa presentation

A

Young adult that is HBV positive(30%0

transmural inflammation of the medium arteries sparing the lungs preferring the renal and visceral arteries

307
Q

PAN lab test?

A

no ANCA

308
Q

Kawasacki vaculitis symptoms

A

CRASH

Conjunctivitis
Rash - diffuse 
Adenopathy 
Strawberry tounge
Hands and soles - desquamitating

Also fever

309
Q

Kawasakis most concering complication

A

coronary artery spasm -> MI or thrombosis

310
Q

Rx for Kawasacki disease(2)

Age group affected?

A

< 4 yrs, usually asian

IV immunoglobin to have negative feedback on the deranged immune system

Aspirin - thrombosis risk

311
Q

Intermittent claudication that may lead to gangrene and autoamputation of the digits?

also superficial nodular phlebitis

A

Buergers Syndrome
-associated w/ Reynalds

Due to smoking
Rx - stop smoking

312
Q

Strawberry hemangioma

A

benign capillary tumor found in infants,

regresses spontaneously around 5-8yrs

313
Q

cherry hemangioma

A

benign capillary hemangioma in the elderly, red, around the size of a mole

Do not regress

314
Q

Pyogenic granuloma

associated w?(2)
Found

A

Polypoid capillary hemangioma

Associated w/ trauma and pregnancy

Found on luis and gums and can ulcerate and bleed

315
Q

Cystic hyproma

Associated w?

A

cavernous lymphangioma of the neck

associated w/ Turners Syndrome

316
Q

Red vascular tumors(3)

A

Strawberry hemangioma
Cherry hemangioma
Pyogenic hemangioma

317
Q

Glomus Tumor

location?

A

Benign painful red/blue tumor under the fingernails

Arises from smooth muscle cells

318
Q

Bacillary angiomatosis

A

benign capillary papule due to Bartonella henselae infection

Mistaken for karposi’s often

319
Q

Karposi’s sarcoma is often mistaken w/

A

Bacilliary angiomatosis
-Bartonella henslae infection

also higher prevalence in HIV

320
Q

Angiosarcoma

Due to?

Location?

A

rare blood vessel malignancy
- due to radiation exposure

Usually in the head, neck and breast

321
Q

Lymphangiosarcoma

Due to?

Location

A

lymphatic malignancy associated w/ persistent lymphedema

arms can be affected post radical mysectomy and nicking the lymph ducts

322
Q

Karposi sarcoma

3 etiologies

A

Indolent - Older men and mediterranian descent

Endemic - Sub saharra

HHV8 - HIV

323
Q

Karposi sarcoma

Location

A

endothelial malignant most commonly on the skin but also the mouth, GI and respiratory tract

324
Q

Sturge Weber disease

Sign

Path

A

Congenital vascualr disorder that affects capillaries

Port wine stain w/ ophthalmic distribution on the face indicates an ipsilateral lelomeningeal angiomatosis (intracranial Arterial-ventrical malformation)

also siezures and glaucoma

325
Q

Nevus flames seen over a patients eye

be concerned of what congenital disease and ultimately what complication

A

Sturge Weber disease

worry of leptomeningeal angiomatosis - and intracerebral AVM

also have seizures and early glaucoma

USLME Kiss my ass and pray (33 decks)

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