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USMLE > Cardiology > Flashcards

Cardiology Flashcards

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USMLE® Step 1 flashcards
1
Q

Truncus Arteriosus becomes…

Pathology of TA

A

Ascending Aorta and Pulmonary Trunk
Transposition of the Great Vessels (failure to spiral), Tetralogy of Fallot (skewed AP septum), Persistent TA (partial AP septum development)

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2
Q

Bulbus Cordis becomes

A

Smooth part (outflow tract) of L and R Ventricles

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3
Q

Primitive Ventricle Becomes

A

Trabeculated Ventricles

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4
Q

Primitive Atria become

A

Trabeculated Atria

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5
Q

Left Horn of Sinus Venosus becomes

A

Coronary Sinus

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6
Q

Right Horn of Sinus Venosus becomes

A

Smooth part of RA

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7
Q

Right Common Cardinal Vein and Right Anterior Cardinal Vein become

A

SVC

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8
Q

What kind of cells forms the aorticopulmonary septum

A

Neural Crest Cells. Truncal and bulbar ridges spiral and fuse to form AP septum giving rise to the Ascending Aorta and the Pulmonary Trunk

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9
Q

Interventricular Septum Development

A
  1. Muscular ventricular septum forms with interventricular foramen
  2. AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular formane
  3. Growth of endocardial cushions separate atria from ventricles and contributes to both atrial separation and membranous portion of interventricular septum
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10
Q

Membranous septal defect will lead to

A

L-R shunt which later reverses to R-L shunt due to onset of PHTN (Eisenmengers syndrome)

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11
Q

Interatrial septum development

A
  1. Foramen primum narrows as septum primum grows towards endocardial cushions
  2. Perforations in septum primum form foramen secundum and FP disappears
  3. FS maintins R-L as suptum secundum begins to grow
  4. Septum Secundum contains FO (permanent opening)
  5. Foramen secundum enlarges and upper part of septum primum degenerates
  6. Remaining portion of septum primum forms valve of FO
  7. Septum secundum and septum primum fuse to form atrial septum
  8. FO closes soon after birth because of increased LA pressure
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12
Q

PFO caused by

A

Failure of Septum Primum and Septum Secundum to fuse after birth

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13
Q

Fetal erythropoiesis occurs in?

A 
"Young Livers Synthesize Blood"
Yolk Sac: weeks 3-10
Liver: week 6 - birth
Spleen: 15-30 weeks
Bone Marrow: 22 weeks to adulthood
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14
Q

Blood in umbilical vein
PO2
O2 Sat

A

PO2 = 30mmHg

O2 Sat = 80%

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15
Q

Umbilical arteries O2 Sat?

A

Low

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16
Q

Fetal Shunts

A
  1. Umbilical vein –> ductus venosus –> IVC to bypass liver
  2. RA –> FO –> LA
  3. Pulmonary Artery –> Ductus Arteriosus –> Aorta
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17
Q

What happens to fetal circulation when the infant takes its first breath

A

Decreased resistance in pulmonary vasculature –> increased P in LA –> FO closes
Increased O2 –> decreased prostaglandins –> ductus arteriosus closes

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18
Q

Medication for PDA

A

Indomethacin closes the PDA

PGE keeps in open

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19
Q

Umbilical vein becomes

A

Ligamentum teres hepatis contained in the falciform ligament

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20
Q

Umbilical arteries become

A

Medial umbilical ligaments

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21
Q

Ductus arteriosus becomes

A

Ligamentum arteriosum

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22
Q

Ductus venosus becomes

A

Ligamentum venosum

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23
Q

Foramen Ovale becomes

A

Fossa Ovalis

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24
Q

Allantois becomes

A

Urachus - median umbilical ligament. The Urachus is part of the allantoic duct between bladder and the umbilicus
Urachal cyst or sinus is a remnant

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25
Q

Notochord becomes

A

Nucleus pulposus of IV disc

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26
Q

What vessels supplies the SA and AV nodes?

A

RCA

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27
Q

What percentage of individuals are Right Dominant? Left Dominant? Codominant?

A

PDA arises from RCA in 85% of individuals
From LCX in 8%
Both in 7%

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28
Q

Most commonly occluded coronary arteries?

A

LAD > RCA > CFX

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29
Q

Coronary arteries fill during

A

Diastole

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30
Q

Branches of RCA

A

Acute Marginal, PDA (80%)

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31
Q

Branches of LCA

A

CFX, LAD

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32
Q

If LA enlarged

How to diagnose?

A

Dysphagia (compression of esophagus) + Hoarseness (compression recurrent laryngeal nerve)
Transesophageal Echocardiography

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33
Q

What can transesophageal echocardiography be used to diagnose?

A

LA Enlargement, Aortic Dissection, Thoracic Aortic Aneurysm

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34
Q

What does LAD supply?

A

Ant 2/3 of IV septum, anterior papillary muscles, anterior surface of LV

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35
Q

What does LCX supply?

A

Lateral and Posterior walls of LV

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36
Q

What does PDA supply?

A

Posterior 1/3 of IV septum and posterior walls of ventricles

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37
Q

Cardiac Output Equation (2)?

A

CO = SV x HR
Fick Principle
CO = (Rate of O2 consumption)/(arterial O2 - venous O2)

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38
Q

Mean Arterial Pressure Equation? (2)

A 
MAP = CO x TPR
MAP = 2/3 Diastole + 1/3 Systole
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39
Q

Pulse Pressure Equation?

What is PP proportional to?

A

PP = Systolic - Diastolic

PP α SV

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40
Q

Stroke Volume Equation?

A

EDV - ESV

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41
Q

During exercise, how is CO maintained?
Early?
Late

A

Early: Increases in HR and SV
Late: HR only, SV plateaus

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42
Q

What happens if HR is too high?

A

Diastolic filling is incomplete and CO decreases resulting in ventricular tachycardia

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43
Q

What variables affect SV?

A

SV CAP

Contractility, Afterload, Preload

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44
Q

What decreases Contractility?

A

BACH
β Blockers (decreased cAMP), Acidosis, Ca Channel Blockers (non-dihydropyridine), Hypoxia/Hypercapnea, Systolic Heart Failure

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45
Q

What Chemicals Increase Contractility?

A

Catecholamines (increase activity of Ca pump in SR). Digitalis (Increased intracellular Na –> increased intracellular Ca)

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46
Q

SV increases in what states?

A

Pregnancy, Exercise, Anxiety

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47
Q

Myocardial O2 demands increase with

A

CARS

Increased Contractility, Afterload, Rate, Size (wall tension)

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48
Q

Preload is equal to?

A

EDV

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49
Q

Afterload is equal to?

A

MAP

Proportional to peripheral resistance

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50
Q

What kind of drugs reduce preload?

A

Venodilators like Nitroglycerin

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51
Q

What kind of drug reduce afterload?

A

Vasodilators like Hydralazine

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52
Q

Preload increases with

A

Exercise, Volume, Excitement

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53
Q

Force of contraction proportional to?

A

Preload

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54
Q 
Ejection Fraction
Formula
Index for?
Normal value
Decreases in?
A

EF = SV/EDV
Index for ventricular contractility
Normally ≥ 55%
Decreases in Systolic HF

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55
Q

Pressure formula

A

P = Q x R

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56
Q

Resistance formula (2)

A

R = P/Q = (8 x viscosity x length)/π(r^4)

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57
Q

Viscosity depends on…

Increases with…

A

Hct

Increases with Polycythemia, Hyperproteinemic state (multiple myeloma), Hereditary spherocytosis

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58
Q

Viscosity decreases with

A

Anemia

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59
Q

Most of the total peripheral resistance due to

A

Arterioles

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60
Q

S1

Loudest at

A

Mitral and Tricuspid valves close

Loudest in Mitral area

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61
Q

S2

Loudest at

A

Aortic and Pulmonary valves close

Loudest at L sternal border

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62
Q 
S3
When
Associated with 
Sign of 
Normal in
A 
In early diastole
Associated with increased filling pressures
MR, CHF
Sign of dilated ventricles
Normal in Pregnants and Children
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63
Q

S4
When
Caused by
Associated with

A

Atrial Kick in late diastole
Caused by high atrial pressure
Associated with ventricular hypertrophy

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64
Q

JVP wave

A

a: atrial contraction
c: RV contraction (tricuspid valve bulges into atrium)
x: atrial relaxation
v: RA filling
y: blood flow from RA to RV

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65
Q

Normal Splitting Physiology

A

S1 - A2-P2
Inspiration –> drop in intrathoracic pressure –> increased venous return to RV –> increased RV SV –> increased RV ejection time –> delayed closure of pulmonic valve
Inspiration also leads to increased capacity of pulmonary circulation which also delays P closing

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66
Q

Wide Splitting
Pathology
Seen in conditions with

A

Due to delayed RV emptying

Pulmonic stenosis, R bundle branch block

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67
Q

Fixed Splitting
Seen in
Pathophysiology

A

ASD. L-R shunt –> ⇑ RA and RV volumes –> ⇑ flow through pulmonic valves such that regardless of breath, valve closure greatly delayed

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68
Q

Paradoxical Splitting
PathoPhys
Seen in what conditions

A

Seen in conditions that delay LV emptying (Aortic Stenosis, Left Bundle Branch Block).
Reversal of A2 and P2

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69
Q

What can be heard in aortic area?

A

Systolic murmors: AS, Flow Murmur, Aortic Valve Sclerosis.

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70
Q

What can be heard over Left Sternal Border

A

Diastolic murmurs: AR, PR

Systolic murmurs: HOCM

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71
Q

What can be heard in Pulmonic Area?

A

Systolic ejection murmur: Pulmonic stenosis, Flow murmur from ASD or PDA.

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72
Q

What can be heard in the tricuspid area?

A

Pansystolic murmurs: Tricuspid Regurg, VSD

Diastolic murmurs: Tricuspid stenosis, ASD

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73
Q

What can be heard over Mitral area?

A

Systolic: MR
Diastolic: MS

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74
Q

ASD
Early presentation
PathoPhys
Later presentation

A

“Drs press forward”
Diastolic rumble and pulmonary flow murmur
Blood flow across ASD does not cause the murmur because there is no pressure gradient
The murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilation of pulmonary artery

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75
Q

Where is the best place to hear a PDA?
What does it sound like?
Due to

A

Left infraclavicular region. Continuous machine like murmur. Loudest at S2
Often due to congenital rubella or prematurity

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76
Q

Bedside Maneuver: Inspiration

A

Increased intensity of R heart sounds

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77
Q

Bedside Maneuver: Expiration

A

Increased intensity of L heart sounds

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78
Q

Bedside Maneuver: Hand Grip

What does it do physiologically

A

⇑systemic vascualr resistance.
⇑ intensity of MR, AR, VSD, MVP
⇓ intensity of AS, HOCM

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79
Q

Bedside Maneuver: Valsala

What does it do physiologically

A

⇓ venous return
Bedside Maneuver: Valsala
⇑ MVP and HOCM

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80
Q

Bedside Maneuver: Rapid Squatting

What does it do physiologically?

A

⇑ venous return, ⇑ preload, ⇑ afterload (if prolonged)

⇓ MVP and HOCM

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81
Q 
Sound of MR
Loudest at?
Radiates?
Enhanced by?
Often due to?
A

Holosystolic high pitched blowing murmur.
Loudest at apex and radiates towards axilla
Enhanced by maneuvers that ↑ TPR (squatting, hand grip) and ↑ LA return (expiration)
Most often due to Ischemic heart disease, MVP, LV dilation, RF, infective endocarditis

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82
Q 
Sound of TR
Loudest at?
Radiates?
Enhanced by?
Often due to?
A

Holosystolic high pitched blowing murmur.
Loudest at tricuspid area and radiates to R sternal border
Enhanced by maneuvers ↑ RA return (inspiration)
Most often due to RV dilation, RF, infective endocarditis

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83
Q 
Aortic Stenosis 
Sound and Radiation
Pressures
Presentation 
Caused by
A

Crescendo-decrescendo systolic ejection murmur following ejection click (due to abrupt halting of valve leaflets) that radiates towards carotids and loudest at heart base
P in LV > P in Aorta
“SAD” –> Syncope, Angina, Dyspnea
Pulsus Parvus et Tardus
Age related calcification or bicuspid valve

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84
Q

VSD
Sound
Location
Maneuvers

A

Holosystolic, harsh sounding murmur loudest at tricuspid area and ↑ by handgrip (increased afterload)

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85
Q 
MVP
Sound
Location? When?
Predisposes pts to
Caused by
Enhanced by
A

Late systolic crescendo murmur with midsystolic click (from sudden tensing of chordae tendineae)
Best heard over apex during S2
Predisposes to infective endocarditis
Caused by myxomatous degeneration, RF, chordae rupture.
Enhanced by maneuvers that ↓ venous return (standing, valsala)

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86
Q

Most frequent valvular lesion

A

MVP

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87
Q 
Aortic Regurgitation
Sound
Presentation
Due to
Affected by
A

Immediate high pitched blowing diastolic decrescendo murmur.
Wide pulse pressure, bounding pulse, head bobbing.
Due to aortic root dilation, bicuspid endocarditis, RF.
↓ by vasodilators
↑ by hand grip

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88
Q 
Mitral Stenosis
Sound
Pressures 
Due to 
Can lead to
Enhanced by
A

Delayed rumble in late diastole with opening snap (abrupt halting of leaflets due to fusion)
P in LA (measured by PCWP) > P in LV
Due to RF and can lead to LA dilation
Enhanced by maneuvers that ↑ LA return (expiration)

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89
Q

Ventricular AP also occurs in

A

Bundles of His and Purkinje fibers

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90
Q

Phases of Ventricular AP

A

0: INa
1: Na channels inactivated, K channels open
2: Plateau. Ca channels open
3: Repolarization. K channels open. Ca channels close
4: Resting Potential. High K permeability

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91
Q

Ca enters cardiac myocytes by

A

Ca induced Ca release

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92
Q

Pacemaker AP Phases

A

0: Ca mediated upstroke
2: no plateau
3: Inactivation of Ca channels, Opening of K
4: Slow diastolic depolarization because of Na funny channels

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93
Q

What affects Slope of Phase 4 in pacemaker cells?

A

ACh and Adenosine –> ↓ Slope –> ↓ HR

Catecholamines –> ↑ Slope –> ↑ HR

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94
Q

P wave on EKG

A

Atrial depolarization

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95
Q

Speed of conduction of parts of heart

A

Purkinje > atra > ventricles > AV node

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96
Q

Speed of conduction of pacemaker cells

A

SA > AV > Bundle of His/Purkinje/Ventricles

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97
Q

PR interval represents

Normal value

A

Conduction delay through AV node

Normally < 200 msec

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98
Q

QRS Complex represents

Normally

A

Ventricular depolarization

Normally < 120 msec

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99
Q

QT interval represents

A

Mechanical contraction of the ventricles

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100
Q

T wave represents

Inversion may indicate

A

Ventricular repolarization

T wave inversion may indicate recent MI

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101
Q

ST segment

A

Isoelectric

Ventricles Depolarize

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102
Q

U Wave causes

A

HypoK, Bradycardia

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103
Q

Conduction pathway in heart

A

SA –> Atria –> AV –> Common Bundle –> Bundle Branches –> Purkinje Fibers –> Ventricles

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104
Q

Atrioventricular delay?

Allows for?

A

100 msec delay allows for ventricular filling

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105
Q

V Tach
Can progress to
What predisposes towards it
Treatment

A

Can progress to Vfib
Long QT interval predisposes towards it
Treatment is Magnesium Sulfate

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106
Q

Congenital Long QT syndrome
Defect in
Can present as

A

Defect in cardiac Na or K channels

Can present with congenitcal sensorineural deafness (Jervell and Lang Nielsen Syndrome)

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107
Q

Afib
ECG
Can lead to
Treatment

A

Irregularly irregular with no discrete P wave between irregularly spaced QRS
Can result in atrial stasis which leads to stroke
Treatment: anticoagulants, β Blockers, cardioversion, Ca Channel Blockers, Digoxin

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108
Q

Atrial Flutter
EKG
Treatment

A

Back to back P waves (sawtooth)

IA, IC, II, III, IV

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109
Q

V fib
EKG
Treatment

A

Erratic rhythm with no identifiable waves

Fatal without CPR and Defib

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110
Q

1st Degree AV Block

A

PR interval prolonged (>200 msec)

Asymptomatic

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111
Q

2nd Degree AV Block

Mobitz Type I

A

Wenckenbach
Progressive lengthening of PR interval until a beat is dropped
Usually asymptomatic

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112
Q

2nd Degree AV Block
Mobitz Type II
Treatment
Risk

A

Extra P waves
Treat with pacemaker
Can progress to 3rd degree black

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113
Q

3rd Degree AV Block
Treat with
Can be caused by

A

A and V beat independently
Treat with pacemaker
Can be caused by Lyme Disease

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114
Q

ANP
Released by
In response to
Leads to

A

Released by atrial myocytes in response to ↑ vol and atrial pressure.
Leads to vascular relaxation and ↓ Na reabsorption in medullary collecting tubule.
Constricts EA and dilates AA (via cGMP)

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115
Q

Aortic arch receptors

Transmit via … to … responds to …

A

Transmit via Vagus nerve to NTS in medulla and respond to ↑ BP only

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116
Q

Carotid Sinus

Transmits via … to … and responds to …

A

Transmits via glossopharyngeal nerve to NTS and responds to any change in BP

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117
Q

Baroreceptors

Course of signals

A

↓ BP –> ↓ stretch –> ↓ afferent baroreceptor firing –> ↑ efferent sympathetic firing and ↓ efferent parasympathetic firing –> vasoconstriction, ↑ HR, ↑ contractility, ↑ BP

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118
Q

Carotid Massage

A

↑ pressure on carotid artery –> increase stretch –> ↑ afferent firing –> ↓ HR

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119
Q

Cushings Rxn
Presentation
PathoPhys

A

HTN, Bradycardia, Respiratory Depression
↑ ICP constricts arterioles –> cerebral ischemia –> reflex HTN –> ↑ stretch –> Reflex baroreceptor induced bradycardia

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120
Q

Peripheral Chemoreceptors

A

Carotid and Aortic bodies stimulated by ↓ PO2 (< 60mmHg), ↑ PCO2, and ↓ pH

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121
Q

Central Chemoreceptors

A

Stimulated by change in pH and PCO2 of brain interstitial fluid
Do not directly respond to PO2

122
Q

Organ with largest share of systemic CO

A

Liver

123
Q

Organ with highest blood flow per gram of tissue

A

Kidney

124
Q

Organ with largest O2 extraction

A

Heart

~80%. ↑ O2 demand must be met with ↑ blood flow

125
Q

Pressures in the Heart

A 
RA: less than 5
RV: 5-25
PA: 25-10
LA: less than 12
LV: 130-10
Aorta: 130-90
126
Q

Approximation of P in LA

Measured with…

A

PCWP measured with Swan-Ganz catheter

127
Q

Autoregulation of blood flow to heat mediated by

A

Local metabolites - CO2, Adenosine, NO

128
Q

Autoregulation of blood flow to Brain mediated by

A

Local metabolites - CO2, pH

129
Q

Autoregulation of blood flow to Kidneys mediated by

A

Myogenic and tubuloglomerular feedback

130
Q

Autoregulation of blood flow to Lungs mediated by

A

Hypoxia vasoconstriction

131
Q

Autoregulation of blood flow to Skeletal Muscle mediated by

A

Local metabolites - lactate, adenosine, K

132
Q

Autoregulation of blood flow to Skin mediated by

A

Sympathetic stimulation for temperature control

133
Q

Starling Equation

A

J = K[(Pc-Pi)-(πc-πi)]

134
Q

Edema from Heart Failure in terms of Starling Equation

A

↑ Pc pushes fluid out of capillaries

135
Q

Edema from ↓ plasma proteins in terms of Starling Equation

A

↓ πc

136
Q

Edema from ↑ capillary permeability in terms of Starling Equation
What causes a change in capillary permeability?

A

↑ K

Toxins, Infections, Burns

137
Q

Edema from ↑ interstitial fluid colloid osmotic pressure in terms of Starling Equation
Caused by

A

πi

Caused by lymphatic blockage

138
Q

Blue Baby
PathoPhys
Causes

A 
R-L shunt
Tetralogy of Fallot (most common)
Transposition of the great vessels
Persistent Truncus arteriosus (with PDA)
Tricuspid atresia 
Total Anomalous Pulmonary Venous Return
139
Q

What usually accompanies a persistent truncus arteriosus?

A

PDA

140
Q

What accompanies TAPVR?

A

ASD and sometimes PDA to allow for R-L shunt to maintain CO

141
Q

Blue Kids
PathoPhys
Causes
Frequency of causes

A

L-R shunt

VSD > ASD > PDA

142
Q

Eisenmengers Syndrome
PathyPhys
Presents as

A

Uncorrected VSD, ASD, PDA causes compensatory pulmonary vascular hypertrophy –> PHTN
As pulmonary resistance ↑, the shunt reverses and becomes R-L
Presents as Cyanosis, Clubbing, Polycythemia

143
Q 
Tetralogy of Fallot
Caused by
Characteristics
Shunting?
XR
Treatment
A

Caused by anterosuperior displacement of infundibular septum
PROV
Pul stenosis, RVH, Overriding Aorta (overrides VSD), VSD
R-L shunting –> cyanosis
Boot-shaped heart on XR
Surgery

144
Q

What do pts with ToF do to relieve symptoms

A

Squatting –> ↓ blood flow to legs –> ↑ Resistance –> ↓ R-L shunt across VSD

145
Q

Transposition of the Great Vessels
Only compatible with life if there is a
Due to
Treatment

A

Only compatible with life if there is a VSD, PDA, or PFO
Due to failure of the aorticopulmonary septum to spiral
Surgery

146
Q

Coarctation of the aorta

Results in

A

Aortic Regurgitation

147
Q

Coarctation of the aorta: Infantile Type
Location of stenosis?
Associated with?
On physical exam remember to check…

A

Stenosis proximal to ductus arteriosus
Associated with Turners Syndrome
Check femoral pulses

148
Q

Coarctation of the aorta: Adult Type
Location of stenosis?
Associated with?
On physical exam remember to check…

A

Stenosis distal to ligamentum arteriosum
Associated with bicuspid aortic valve
On Physical Exam: Notching of the ribs due to collateral circulation, HTN in upper extremities, Weak pulses in lower extremities

149
Q

Presentation of uncorrected PDA

A

Cyanosis in the lower extremities (differential cyanosis)

150
Q

Consequences of PDA on the heart?

A

L-R shunt –> RVH and/or LVH and failure

151
Q

Cardiac defect associated with 22q11 syndrome (DiGeorge syndrome)

A

Truncus arteriosus and ToF

152
Q

Cardiac defect associated with Down Syndrome

A

ASD, VSD, AVSD (endocardial cushion defect)

153
Q

Cardiac defect associated with Congenital Rubella?

A

Septal defects, PDA, Pulmonary artery stenosis

154
Q

Cardiac defect associated with Turners Syndrome

A

Preductal coarctation of the aorta

155
Q

Cardiac defect associated with Marfan’s Syndrome

A

Aortic insufficiency and dissection (late)

156
Q

Cardiac defect associated with diabetic mother

A

Transposition of the great vessels

157
Q

TAPVR pathophys?

A

Pulmonary veins drain into R heart

158
Q

Definition of HTN?

A

> 140/90

159
Q

Risk factors for HTN

A

Age, diabetes, obesity, smoking, genetics

160
Q

Risk of HTN in different races?

A

Black > White > Asian

161
Q

Primary vs Secondary HTN

A

90% primary. 10% Secondary

162
Q

Primary HTN

A

Related to ↑ CO and TPR

163
Q

Secondary HTN usually caused by

A

Renal disease

164
Q

Malignant HTN definition and prognosis

A

> 180/120 and rapidly progressing

165
Q

HTN predisposes pts to

A

Aterosclerosis, LVH, Stroke, CHF, Renal Failure, Retinopathy, Aortic Dissection

166
Q

Atheroma definition

A

Lipid plaques in blood vessel walls

167
Q

Xanthomas definition. Where are they found?

A

Plaques or nodules composed of lipid laden histiocytes in the skin. Found on eyelids (xanthelasma), tendons (Tendinous Xanthomas) (esp Achilles tendon)

168
Q

Corneal arcus definition.

Sign of?

A

Lipid deposits in cornea.

Nonspecific (arcus senilis)

169
Q 
Monckeberg 
PathoPhys
Usually affects
Problem?
Layers involved?
A

Calcification of media of arteries. Especially radial or ulnar. Usually benign and does not obstruct blood flow. Only involves media, not intima

170
Q

Arteriolosclerosis
Types
Where is each type present?

A

Hyaline: Thickening of small arteries seen in essential HTN and DM
Hyperplastic: “onion skinning” seen in MHTN

171
Q

Atherosclerosis
Definition
What kind of arteries
Where in the artery?

A

Fibrous plaques and atheromas for in the intima of elastic arteries and large/medium muscular arteries.

172
Q

Modifiable risk factors of Atherosclerosis

A

Smoking, HTN, Hyperlipidemia, Diabetes

173
Q

Non-modifiable risk factors for Atherosclerosis

A

Age, Male, Postmenopausal women, family history

174
Q

Progression of Atherosclerosis

A

Endothelial cell dysfunction –> macs and LDL accumulation –> Foam cells –> Fatty streaks –> SM migration (PDGF and FGF), proliferation, and ECM deposition –> Fibrous plaque

175
Q

Complications of Atherosclerosis

A

Aneurysm, ischemia, infarcts, peripheral vascular disease, thrombus, emboli

176
Q

Common locations of Atherosclerosis

A

Abdominal Aorta > coronary arteries > Popliteal arteries > carotid arteries

177
Q

Atherosclerosis presentation

A

angina, claudication, but may be asymptomatic

178
Q

Abdominal Aortic Aneurysm

Classic pt?

A

Atherosclerosis in Male smoker >50 with HTN

179
Q

Thoracic Aortic Aneurysm associations

A

HTN, Marfan’s (Cystic Medial Necrosis), and Tertiary Syphilis

180
Q 
Aortic Dissection
Definition
Associations
Presentation
CXR
Can result in...
A

Longitudinal tear forms false lumen
Associated with HTN, Bicuspid Aortic Valve, Cystic Medial Necrosis, Connective Tissue Disorder (i.e. Marfan’s)
Presents with tearing chest pain radiating to the back
CXR shows mediastinal widening with false lumen larger than true lumen
Can result in pericardial tamponade, aortic rupture

181
Q

How narrow must the coronary artery be to produce angina?

A

> 75% but this does not produce myocyte necrosis

182
Q

Stable Angina
Definition
Mostly due to
EKG

A

Retrosternal chest pain with exertion
Mostly secondary to atherosclerosis
ST depression on ECK

183
Q

Prinzmetals Angina
Due to
EKG

A

Secondary to coronary artery vasospasms

ST elevation on EKG

184
Q

Unstable Angina
Definition
Caused by
EKG

A

Worsening chest pain at rest or with minimal exertion. Caused by thrombosis with incomplete coronary artery occlusion. ST depression on ECK

185
Q

Coronary Steal Syndrome

A

Vasodilators aggravate ischemia by shunting blood from affected area to region of higher perfusion

186
Q

Myocardial infarction
Definition
Most often due to…
ECK

A

Complete occulsion of coronary artery producing myocyte necrosis.
Most often due to thrombosis
ST depression progressing to ST elevation

187
Q

ST depression means

A

Subendocardial wall damage

188
Q

ST elevation means

A

Transumarl wall damage

189
Q

Sudden Cardiac Death
Definition
Most commonly due to
Associated with

A

Death from cardiac cause within 1 hour of symptom onset
Most commonly due to lethal arrhythmia (Vfib)
Associated with CAD

190
Q

Chronic Ischemic Heart Disease
Definition
Progresses to

A

Chronic ischemic myocardial damage. Progresses to CHF

191
Q

MI presentation

A

Diaphoresis, naseau, vomiting, retrosternal pain, pain in left arm and/or jaw, dyspnea, fatigue

192
Q

0-4 hours after MI
Gross
LM
Risk

A

Gross: none
LM: none
Risk: Arrhythmias, CHF exacerbation, shock

193
Q

4-12 hours after MI
Gross
LM
Risk

A

Gross: Dark mottling. Pale with tetrazolium stain
LM: Early coagulative necrosis, edema, hemorrhave, wavy fibers
Risk: Arrhythmias

194
Q

12-24 hours after MI
Gross
LM
Risk

A

Gross: Dark mottling. Pale with tetrazolium stain
LM: Contraction bands from reperfusion injury, Release of necrotic cell contents into blood, Beginning of neutrophil migration
Risk: Arrhythmias

195
Q

1-3 days after MI
Gross
LM
Risk

A

Gross: hyperemia
LM: Extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation. Neutrophil migration
Risk: Fibrinous pericarditis

196
Q

2-14 days after MI
Gross
LM
Risk

A

Gross: Hyperemic border with centrally yellow-brown softening (maximally yellow at day 10)
LM: Macs. Granulation tissue at margins
Risk: Free wall rupture –> tamponade, Papillary muscle rupture, Aneurysm, IV septal rupture

197
Q

2-Several weeks after MI
Gross
Risk

A

Gross: Gray-white tissue

Dresslers syndrome

198
Q

Diagnosis of MI

EKG and blood tests

A

EKG is gold standard in the first 6 hours. Troponin I rises after 4 hours and is elevated for 7-10 days (specific). CKMB predominantly found in myocardium but also skeletal muscle. Useful in diagnosing reinfarction because returns to normal after 48 hours

199
Q

Transmural infarct: EKG

A

ST elevation. Pathological Q wave

200
Q

Subendocardial infarcts
EKG
Necrosis?

A

ST depression. Necrosis of <50% of ventricle wall

201
Q

EKG diagnosis of Anterior wall infarct based on leads showing Q waves?

A

“SAL”
Anteroseptal: V1-V2 (LAD)
Anterior: V1-V4 (LAD
Anterolateral: V4-V6 (LCX)

202
Q

EKG diagnosis of Lateral or Inferior wall infarct based on leads showing Q waves?

A

“Love Is Incredible. Nothing Like It”
Lateral: I, aVL (LCX)
Inferior: II, III, aVF

203
Q

Dresslers Syndrome

PathoPhys

A

Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post MI

204
Q

Causes of Dilated Cardiomyopathies

A

Most common cause = idiopathic (>50%)
“A Bold, Devout Christian Crusader Charged Petrified Hindus”
Alcohol, wet Beriberi, Doxorubicin, Chagas, Coxackie B, Cocaine, Postpartum, Hemochromatosis

205
Q 
Dilated Cardiomyopathy
Common?
Sound, US, CXR
What kind of hypertrophy?
What kind of dysfunction?
Treatment
A

Most common cardiomyopathy (90%)
S3, US = dilated heart, CXR = balloon
Eccentric hypertrophy w/ sarcomeres added in series –> systolic dysfunction?
Treat w/ Na restriction, ACEI, diuretics, digoxin, transplant

206
Q

HOCM: PathoPhys
Genetics
Association

A

Hypertrophied IV septum is too close to mitral valve and obstructs aortic outflow
60-70% are caused by autosomal dominant mutation in β myosin heavy chain –> disorganized, tangled myocardial fibers
Associated with Friedreich’s Ataxia

207
Q

HOCM
Classic Pt
Size, Sound, Murmur, Impulses
Treatment

A

Cause of death in young athletes
Normal sized heart, S4, Systolic murmur, apical impulses
Treat with II or nonDHP IV

208
Q

HOCM
Hypertrophy
Kind of dysfunction?
May produce?

A

Concentric hypertrophy with sarcomeres added in parallel
Diastolic dysfunction ensues
May produce syncopal episodes.

209
Q

Causes of Restrictive Cardiomyopathies

A

“A SHELF”

Amyloidosis, Sarcoidosis, Hemochromatosis, Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffers Syndrome (endomyocardial fibrosis with eosinophils), Fibrosis (post radiation)

210
Q

What kind of dysfunction ensues in restrictive cardiomyopathies?

A

diastolic

211
Q

Treatment for CHF
Mortality reducers?
Symptom relief?
Both?

A

Mortality reducers: ACEI, II (except in acute decompensated HF), ATII antagonists, Spironolactone
Symptom relief: Thiazide and Loop Diuretics
Both: Hydralazine and Nitrates

212
Q

CHF presentation

A

Dyspnea, fatigue, edema, rales

213
Q

What produces Cardiac Dilation?

A

Greater EDV

214
Q

Why do Pts experience dyspnea on exertion

A

Failure of CO to Increase

215
Q

Results of LHF?

A

Pul Edema: transudation of fluid into alveoli. Hemosiderin laden Macs in lung
Paroxysmal Nocturnal Dyspnea and Orthopnea: Increased venous return –> pulmonary vascular congestion

216
Q

Results of RHF?

A

Hepatomegaly (nutmeg liver), Peripheral edema, JVD

217
Q

Bacterial Endocarditis Presentation

A

“FROM JANE”

Fever, Roth Spots, Osler’s Nodes, Murmur, Janeway Lesions, Anemia, Nail-bed hemorrhages, Emboli

218
Q

Roth Spots

A

Round, white spots on retina surrounded by hemorrhage

219
Q

Osler’s Nodes

A

Tender raised lesions on finger and toe pads caused by IC deposition

220
Q

Janeway Lesions

A

Small, painless, erythematous lesions on palm or sole. Hemorrhagic

221
Q

Complications of Bacterial Endocarditis

A

Chordae rupture, Glomerulonephritis, Suppurative pericarditis, emboli

222
Q

Site of infection in Bacterial endocarditis?

A

Usually Mitral Valve

Tricuspid in IV drug users

223
Q

Main Causes of Bacterial Endocarditis

A

Acute: S aureus (large vegetations on normal valve)
Subacute: S. viridans (small vegetations on abnormal or diseased valve)
Common after dental procedures

224
Q

Organisms Causing Tricuspid Bacterial Endocarditis

A

S aureus, Pseudomonas, Candida

225
Q

Causes of non bacterial endocarditis

A

Malignancy, Hypercoagulable state, SLE

226
Q

Bacterial endocarditis in colon cancer caused by

A

S bovis

227
Q

Bacterial endocarditis with a prosthetic valve caused by…

A

S epidermidis

228
Q

Rheumatic Fever Presentation

A

“FEVERSS”

Fever, Erythema marginatum, Valve damage, ESR ↑, Red-Hot Joints (migratory polyarthritis), Subcutaneous nodules, St. Vitus dance (Sydenham’s Chorea)

229
Q 
RF
Organisms causing it
Valves affected
Early vs Late
Type of Disease?
A

GAS (β hemolytic strep)
mitral > aortic&raquo_space;> tricuspid
Early MR, late MS
Type II Hypersensitivity Rxn with Abs against bacterial M protein

230
Q

RF
Histology
Blood titers

A

Aschoff Bodies (granuloma with giant cells), Antischkow cells (activated histiocytes), Elevated ASO

231
Q

Acute Pericarditis
Presentation
PE findings
EKG

A

Sharp pleuritic pain relieved by sitting up and leaning forward.
Friction rub
Widespread ST elevation and/or PR depression

232
Q

Fibrinous Pericarditis
Causes
Findings

A

Dressler’s, Uremia, Radiation

Loud Friction Rub

233
Q

Causes of Serous Pericarditis

A

Viral (often resolves spontaneously), noninfectious inflammatory disease (SLE, RA)

234
Q

Causes of SuppurativePurulent Pericarditis

A 
Bacterial infection (Pneumococcus Streptococcus)
Rare now with antibiotics
235
Q

Cardiac Tamponade
What happens to diastolic pressures?
HR? Sounds? BP? PE findings?

A

Diastolic pressures equalize in all 4 chambers. HR↑, Distant heart sounds, hypotension and Pulsus Paradoxus, JVD

236
Q

Pulsus Paradoxus
Definition
Seen in what diseases?

A

↓ in systolic P by >10mmHg during inspiration

Seen in pericarditis, tamponade, asthma, obstructive sleep apnea, croup

237
Q

Syphilitic Hearth Disease
Causative agent
MoA
Risk for

A

Tertiary Syphilis disrupts vasa vasorum of the aorta and vessel wall atrophys and dilates.
Risk for aortic aneurysm (ascending and arch) and aortic insufficiency (dilation of aorta and valve ring)

238
Q

In Syphilitic Hearth Disease, what happens to the aortic root and ascending aortic arch? How does the aorta appear?

A

Calcification

Tree bark appearance

239
Q 
Cardiac Myxoma 
Common?
Usually described as 
Location
Present with
A

Most common primary cardiac tumor in adults. “ball valve” obstruction of LA presents with multiple syncopal episodes

240
Q

Rhabdomyomas
Common?
Associated with?

A

Most common primary cardiac tumor in children. Associated with Tuberous Sclerosis

241
Q

Most common cardiac tumor?

A

Metastatic (melanoma, lymphoma)

242
Q

Kussmaul’s Sign
Definition
Seen in

A

↑ in JVP during inspiration because negative intrathoracic pressure not transmitted to the heart
Constrictive Pericarditis, Restrictive Cardiomyopathy, RA or RV tumors, Cardiac Tamponade

243
Q 
Raynaud's Phenomenon 
PathoPhys
Location
Disease
Syndrome 
Presentation
A

↓ blood flow to skin due to arteriolar constriction in response to cold or stress
Fingers and toes
Disease if primary (idiopathic)
Syndrome if secondary to connective tissue disease, SLE, CREST
Cyanosis of fingertips and toes

244
Q 
Temporal Giant Cell Arteritis
Kind of vasculitis?
Classic Pt Presentation 
Risk of 
Associated with
Affects which vessels?
Histo
Blood
Treatment
A

Large vessel
Old female with unilateral temporal headache and jaw claudication
Risk of blindness due to ophthalmic artery occlusion
Associated with Polymyalgia Rheumatica
Branches of Carotid artery.Focal Granulomatous inflammation, ↑ESR, Treat with corticosteroids

245
Q 
Takayasu's Arteritis 
Kind of vasculitis?
Classic Pt Presentation 
Affects which vessels?
Histo
Blood
Treatment
A

“FAN My Skin On Wed”
Large vessel
Asian female < 40 with weak upper extremity pulses, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
Granulomatous thickening of aortic arch and proximal great vessels, ↑ESR
Treat with corticosteroids

246
Q 
Polyarteritis Nodosa
Kind of vasculitis?
Classic Pt Presentation 
Affects which vessels?
Histo
What mediates the disease?
Ages of lesions?
Arteriogram
Treatment
A

“Scalded My Right Hand on the PAN”
Medium vessels
Young Adult with HepB with fever, wt loss, malaise, headache, abdominal pain, melena, HTN, Neuro dysfunction (wrist drop), Cutaneous eruptions, renal damage
Renal and Visceral vessels
Transmural inflammation with fibrinoid necrosis
IC mediated
Typically of different ages
Arteriogram shows many aneurysms and constrictions
Corticosteroid and cyclophosphamide

247
Q 
Kawasaki Disease 
Kind of vasculitis?
Classic Pt Presentation 
Affects which vessels?
Risk of
Treatment
A

Medium vessels
“FEAR ME”
Asian child < 4 with Fever, conjunctival infection (Eye), cervical lymphAdenitis, desquamating Rash, Mouth and Extremity erythema
Coronary vessels
Risk of coronary aneurysm –> MI, Rupture
Treat with IV Igs and Aspirin

248
Q

Buerger’s Disease (Thromboangiitis Obliterans)
Kind of vasculitis?
Classic Pt Presentation
Treatment

A

Medium vessels
“SCRAPS”
Male < 40 with Segmenting Thrombosing vasculitis, Claudication (may lead to gangrene and auto-amputation), Raynaud’s, Smoker, Painful, Superficial Nodular Phlebitis
Treat with smoking cessation

249
Q 
Microscopic Polyangiitis 
Kind of vasculitis?
Histo 
Organs involved w/ manifestation?
Blood
Treatment
A 
Small vessels
Necrotizing vasculitis w/ No Granulomas
Lungs, Kidney (Pauci Immune Glomerulonephritis), and Skin (Palpable Purpura) 
P-ANCA 
Cyclophosphamide and Corticosteroids
250
Q 
Wegener's Granulomatosis (Granulomatosis with Polyangiitis)
Kind of vasculitis?
Presentation
Histo
Blood
CXR
Treatment
A 
Small vessels 
Upper Respiratory Tract: Perforated nasal septum, sinusitis, otitis media, mastoiditis
Lower RT: Hemoptysis, Cough, Dyspnea
Renal: Hematuria, RBC Casts
Focal Necrotizing vasculitis + Necrotizing granulomas in the lung and upper airway + Necrotizing glomerulonephritis
c-ANCA
Large Nodular Densities 
Cyclophosphamide and corticosteroids
251
Q 
Churg Strauss Syndrome 
Kind of vasculitis?
Classic Presentation
But can also affect
Histo
Blood
A

Small vessels
“BEAN SAP? No, Go to Hell”
Blood Eosinophils, Asthma, Neuropathy (food/wrist drop), Sinusitis, Allergies, Palpable Purpura, glomeruloNephritis (pauci immune), GI, Heart
Granulomatous, necrotizing vasculitis w/ eosinophilia
p-ANCA + ↑ IgE

252
Q 
Henoch-Schonlein Purpura 
Kind of vasculitis?
Most common vasculitis in...
Classic Presentation
Disease Mediated by
Associated with
Age of lesions?
A 
Small vessels
Most common vasculitis in children
"NAPA"
Child following URI with Nephropathy, Abdominal pain (melena), Purpura, Arthralgia 
Mediated by IgA complex deposition
Associated with IgA nephropathy
Multiple lesions of same age
253
Q

Essential HTN therapy

A

ACEI, ARB, Diuretics, IV

254
Q

When are II contraindicated?

A

Cardiogenic shock and must be used with caution in decompensated CHF

255
Q

Treatment for Diabetes Mellitus?

A

ACEI, ARB, Diuretics, II, α blockers, IV

256
Q 
Ca Channel Blockers
Names
MoA
Used to treat
Tox
A

Verapamil, Diltiazem, Nifedipine, Amlodipine
–/ Voltage gated L-type Ca channel in plasma membrane
Used to treat HTN, Angina, Arrhythmias (not N), Prinzmetals Angina, Raynaud’s
Cardiac depression, AV block, Peripheral edema, Flushing, Dizziness, Constipation

257
Q 
Hydralazine 
MoA
Used to treat
First line therapy for 
Coadministration 
Tox
Contraindicated in
A

↑cGMP –> Smooth Muscle relaxation. Vasodilates arterioles > veins –> ↓ afterload
Used to treat HTN, CHF
First line therapy for HTN in pregnancy with methyldopa
Coadministered with II to –/ reflex tachycardia
Compensatory tachycardia, fluid retention, nausea, headache, angina, Lupus.
Contraindicated in Angina/CAD

258
Q

Treatment for MHTN

A

Nitroprusside (short acting) –> Release of NO –> ↑cGMP –> Smooth Muscle relaxation. Can cause cyanide poisoning

Fenoldopam = D1 agonist –> coronary, peripheral, renal, and splanchnic vasodilation. ↓ BP and ↑ Natriuresis

259
Q 
Nitric Oxide (NO) Releasing Drugs 
Names
MoA
Use
Tox
A

Nitroglycerin, Isosorbide, Dinitrate
NO –> ↑cGMP –> Smooth Muscle relaxation. Dilates veins > arteries –> ↓ preload
Used to treat angina and Pul Edema
Reflex tachycardia, Hypotension, Flushing, Headache, Monday disease (industrial exposure)

260
Q

Goal of Antianginal therapy

A

Reduce O2 demand of myocardium

Reduces Contractility, Afterload, Rate, Size (wall tension = Preload)

261
Q 
Nitrates as Antianginal
EDV
BP
Contractility 
HR
Ejection time
MVO2
A 
EDV ↓
BP ↓
Contractility ↑ (response)
HR ↑ (response)
Ejection time ↓ (response)
MVO2 ↓
262
Q 
II as Antianginal
EDV
BP
Contractility 
HR
Ejection time
MVO2
A 
EDV ↑
BP ↓
Contractility ↓  
HR: ↓
Ejection time: ↑
MVO2: ↓
263
Q 
Nitrates + II as Antianginal
EDV
BP
Contractility 
HR
Ejection time
MVO2
A 
EDV: No change or ↓
BP: ↓
Contractility: NC 
HR: ↓
Ejection time: NC
MVO2: ↓↓
264
Q

Which IV are similar to Nitrates?

Which IV are similar to II?

A

Nitrates: Nifedipine
II: Verapamil

265
Q

Partial β blockers contraindicated in angina

A

Pindolol, Acebutolol

266
Q 
Strawberry Hemangioma
Benign or malignant?
What kind of vessels?
Time and frequency
Course
A

Benign capillary hemangioma of infancy
Appears in first few weeks of life
1/200 births
Grows rapidly and regresses spontaneously at ages 5-8

267
Q 
Cherry Hemangioma
Benign or malignant?
What kind of vessels?
Time and frequency
Course
A

Benign capillary hemangioma of the elderly
Does not regress
Frequency increase with age

268
Q

Cystic Hygroma
What kind of growth?
Where on body?
Associated with?

A

Cavernous lymphangioma of the neck. Associated with Turners Syndrome

269
Q

Pyogenic Granuloma
What kind of tumor?
What can it do?
Associations?

A

Polyploid capillary hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy

270
Q 
Glomus Tumor
Benign or malignant
Painful or not?
Color?
Location?
Arises from?
A

Benign, painful, red-blue, tumor of fingernails. Arises from modified smooth muscle cells of glomus body

271
Q 
Bacillary Angiomatosis 
Benign or malignant
Which vessels?
Location?
What kind of Pts?
Cause?
Frequently confused with
A

Benign capillary skin papules found in AIDS pts. Caused by Bartonella henselae infection. Frequently mistaken for Kaposi Sarcoma

272
Q 
Angiosarcoma 
Frequency?
Kind of malignancy?
Location on body?
Associated with what kind of pts?
Prognosis?
A

Rare blood vessel malignancy typically occuring in head, neck and breast areas. Associated with pts recieving radiation therapy (breast cancer, Hodgkin’s lymphoma).
Very aggressive and difficult to resect due to delayed diagnosis

273
Q

Lymphangiosarcoma
What kind of malignancy?
Associated with?

A

Lymphatic malignancy associated with persistent lymphedema (post-radical masectomy)

274
Q 
Kaposi Sarcoma
What kind of malignancy
Location on body
Associated with
Frequently mistaken for...
A

Endothelial malignancy found on skin, mouth, GI tract, respiratory tract. Associated with HHV8 and HIV. Frequently mistaken for bacillary angiomatosis

275
Q

Sturge Weber Disease
What kind of disease?
Vessels affected?
Manifestation?

A

Congenital
Capillary sized blood vessels
Port-Wine stain (nevus flammeus) on face, Ipsilateral leptomeningeal angiomatosis (intracerebral arteriovenous malformation), Seizures, early onset Glaucoma

276
Q 
HMG CoA Reductase Inhibitors (Statins)
LDL
HDL
Tri
MoA
Tox
A 
LDL ↓↓↓
HDL ↑
Tri ↓
MoA --/ conversion of HMG-CoA to mevalonate (a cholesterol precursor)
Hepatotoxic (↑LFTs), Rhabdomyolysis
277
Q 
Niacin (Vit B3)
LDL
HDL
Tri
MoA
Tox
A

LDL ↓↓
HDL ↑↑
Tri ↓
MoA Inhibits lipolysis in adipose tissue. Reduced hepatic VLDL secretion
Red, flushed face (↓ by aspirin). Hyperglycemia (acanthosis nigricans), Hyperuricemia (exacerbates gout)

278
Q 
Bile Acid Resins
Names
LDL
HDL
Tri
MoA
Tox
A

Cholestyramine, Colestipol, Colesevelam
LDL: ↓↓
HDL: Slightly ↑
Tri: Slightly ↑
Prevents intestinal reabsorption of bile acids forcing liver to use cholesterol to make Bile
Bad taste, GI discomfort, ↓ absorption of soluble vitamins, Cholesterol Gallstones

279
Q 
Cholesterol Absorption Blockers
Names
LDL
HDL
Tri
MoA
Tox
A 
Ezetimibe 
LDL: ↓↓
HDL: - 
Tri: - 
MoA: Prevents cholesterol reabsorption in small intestine brush border
Rare ↑ in LFTs, Diarrhea
280
Q 
Fibrates
Names
LDL
HDL
Tri
MoA
Tox
A

Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate
LDL ↓
HDL ↑
Tri ↓↓↓
Upregulate LPL –> ↑ TG clearance
Myositis, hepatotoxic (↑ LFTs), cholesterol gallstones

281
Q 
Cardiac Glycosides 
Names
Bioavailability
Protein bound?
T1/2
Excretion
A 
Digoxin
75% bioavailability
20-40% protein bound
T1/2 40h
Urinary excretion
282
Q

Digoxin
MoA
Use

A

–/ Na/K ATPase. ↑ Na –/ Na/Ca exchanger –> ↑ Ca –> ↑ contractility
–> Vagus Nerve –> ↓ HR
Used to treat CHF (↑ contractility), Afib (↓ conduction at AV node, depression at SA node)

283
Q

Digoxin
Tox
EKG
Factors predisposing to toxicity

A

Cholinergic –> nausea, vomiting, diarrhea, blurry yellow vision
AV block, Hyperkalemia,
↑ PR, ↓QT ST scooping, T wave inversion, arrhythmias
Predisposition: renal failure (↓ excretion), Hypokalemia (permissive binding of Na/K pump), Quinidine (↓ clearance. displaces digoxin from tissue binding sites)

284
Q

Digoxin OD antidote

A

Slowly normalize K, Lidocaine, Cardiac Pacer, Anti Digoxin Fab Fragment, Mg

285
Q 
Class I antiarrhythmics 
What kind of molecules
What do they do?
Dependence?
Toxicity is aggravated by...
A

Local anesthetics
↓ conduction in depolarized cells. ↓ slope of phase 0. ↑ threshold for firing in abnormal pacemaker cells
Are state dependent (selective depress frequently depolarized tissues)
Hyperkalemia ↑ toxicity

286
Q 
Class IA antiarrhythmics 
Name
Action on AP?
Action on EKG?
Regions of heart?
Especially useful in treating
A 
Procainamide, Disopyramide, Quinidine 
↑ AP duration. ↑ effective refractory period
↑ QT 
Affect both Atria and Ventricles 
Reentrant and Ectopic SVT and Vtach
287
Q

Class IA antiarrhythmics

Toxicity

A

Thrombocytopenia, torsades de pointes
Q –> cinchonism (headache + tinnitus)
P –> SLE
D–> heart failure

288
Q 
Class IB antiarrhythmics 
Names
Affect on AP?
Preferentially affects
Useful in
Tox
A

Lidocaine, Mexiletine, Tocainide, (Phenytoin)
↓ AP duration
Preferentially affects ischemic or depolarize Purkinje and ventricular tissue
Useful in acute ventricular (Is Best Post MI) + digitalis induced arrhythmias.
Local anesthetic, CNS↑↓, CV depression

289
Q 
Class IC antiarrhythmics 
Name
Affect on AP?
Useful in 
Usually only used as
Affect on AV node
Toxicity
Contraindicated
A

Flecainide, Propafenone
No affect on AP duration
Useful in Vtach that progresses to Vfib + intractable SVT
Usually used only as a last resort for refractory tachyarrhythmias
Prolongs refractory period in AV node
Tox: Proarrhythmic
Contraindicated Post MI and structural heart disease

290
Q 
Class II antiarrhythmics
Names
MoA
Affect on AP
Area particularly sensitive?
Use
A

Metoprolol, propanolol, esmolol (very short acting), atenolol, timolol
Decrease SA and AV nodal activity by ↓ cAMP –> ↓ Ca currents
Decreases phase 4 slope in pacemaker cells
AV node particularly sensitive (↑ PR interval)
VTach, SVT, Slows ventricular rate during Afib + Aflutter

291
Q

Class II antiarrhythmics

Tox

A

BBC Loses Viewers in Houston
Bradycardia (AV block, CHF), Bronchoconstriction (aggravates asthma), Claudication, CNS effects (sedation), Lipids (metoprolol), Vivid dreams, Hypoglycemia masked

292
Q

Propanolol can exacerbate

A

Vasospasms in Prinzmetal’s angina

293
Q

Beta Blocker OD treatment

A

Glucagon

294
Q 
Class III antiarrhythmics 
Names
MoA
Effect on AP
Used when
EKG effects
A 
"AIDS"
Amiodarone, Ibutilide, Dofetilide, Sotalol 
--/ K channels
↑AP duration, ↑ERP, 
Used when other antiarrhythmics fail
↑QT interval
295
Q

Class III

Toxicity

A

Sotolol: TdP, excessive β Block
Ibutilide: TdP,
Amiodarone: Pul Fibrosis, Hepatotoxic, Hypo/HyperThyroidism

296
Q

Amiodarone Toxicity

Real Classification

A

Pul Fibrosis, Hepatotoxic, Hypo/HyperThyroidism (40% I by weight), Corneal deposits, Skin deposits (blue/gray) –> photodermatitis, neurological effects, constipation, AV affects (bradycardia, heart block, CHF)
Affects lipid membranes so has I, II, III, and IV activity

297
Q 
Class IV antiarrhythmics
Names
Affects on AP
Used to
Tox
A

Verapamil, Diltiazem
↓ conduction velocity, ↑ERP, ↑PR
Used to prevent nodal arrhythmias (SVT)
Constipation, Flushing, Edema, CV (CHF, AV block, Sinus node depression

298
Q 
Adenosine
MoA
Drug of choice for
Speed
Toxicity 
Affects blocked by
A

↑K out of cells –> hyperpolarization and ↓ Ca current.
Drug of choice for SVT (diagnosis and treatment)
Very short acting (15 sec)
Flushing, hypotension, angina
Blocked by caffeine and theophylline

299
Q

Mg used to treat

A

TdP and Digoxin toxicity

300
Q

Names of β1 selective β Blockers

A

Start with A-N

301
Q

Names of non-selective β Blockers (β1 and β2)

A

Start with O-Z

302
Q

Breathing in a pt with CHF

A

Cheyne Stokes Breathing

USMLE (25 decks)

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