Pathoma Chapter 8 Cardio

Front 1

location of ischemia in angina. Exception?

Back 1

subendocardial ischemia

EXCEPT in Prinzmetal Angina, which occludes proximally due to vasospasm and causes TRANSmural ischemia

Front 2

nitroglycerin MOA

Back 2

vasodilate arteries and veins

vasodilation of veins decreases preload

NO increases the level of cGMP within the cell. cGMP then activates myosin light chain phosphatase via a cGMP-dependent protein kinase.

Front 3

angina =

Back 3

REVERSIBLE injury to myocytes

Front 4

EKG finding in angina

Back 4

ST segment depression -- representation of subendocardial ischemia

Front 5

Prinzmetal angina

Back 5

episodic chest pain unrelated to exertion

Front 6

ST segment depression indicates

Back 6

subendocardial ischemia

Front 7

ST segment elevation indicates

Back 7

transmural ischemia

Front 8

Disease associated with vasospasm's in the coronary artery

Back 8

prinzmetal angina

Front 9

MOA of Kawasaki's causing MI

Back 9

vasospasm causes inflammation or damage to endothelial tissue exposing sub-endothelial collagen and Tissue Factor and other pro-coagulants leading to formation of thrombus

Front 10

chest pain radiating to left arm or jaw

Back 10

MI

Front 11

Nitroglycerin used for?
Not used for?

Back 11

used for angina. Not used for MI

Front 12

List most common coronary arteries of infarction

Back 12

Left Anterior Descending(LAD)
Right Coronary Artery(RCA)
Left Circumflex Artery(LCX)

Front 13

Left Anterior Descending occlusion affects

Back 13

Anterior wall of left ventricle and septum

Front 14

Right Coronary Artery affects

Back 14

Posterior wall of left ventricle and septum

Front 15

Left Circumflex Artery occlusion affects

Back 15

Lateral wall of left ventricle

Front 16

MI spares which parts of heart?

Back 16

Right Atria, Right Ventricle, Left Atria

Front 17

What cardiac enzyme useful to test for reinfarction after an MI

Back 17

CK-MB.

Troponin would be elevated due to prior MI, but CK-MB is transiently elevated after MI and should go down within 2 days. If a week later, you have ANOTHER infarction, it should obviously be elevated again.

Front 18

Key complication one day after MI

Back 18

arrhythmia

Front 19

Milestones Post-MI

Back 19

Within 1 Day, you get coagulation necrosis
Within 1 Week, you get acute inflammation with recruitment of neutrophils then macrophages
Within 1 Month, you get the creation of granulation tissue
After 1 Month, you get scar formation.

Front 20

Complication associated with neutrophil infiltration post MI

Back 20

1-3 days

fibrinous pericarditis which presents with chest pain with friction rub due to inflammatory debris entering pericardium.

Notably, this ONLY occurs with a TRANSmural infarction

Front 21

Complication associated with macrophage infiltration after an MI

Back 21

4-7 days

RUPTURE
Rupture of left ventricular wall --> cardiac tamponade
Rupture of Interventricular septum --> left-to-right shunt
Rupture of papillary muscle of the mitral valve --> mitral insufficiency(blood re-enters left atria during systole)

Front 22

Which artery feeds papillary muscle of mitral valve?

Back 22

Right Coronary Artery

Front 23

Dressler's Syndrome

Back 23

Exposure of antigens in pericardium to immune systems which causes auto-immune pericarditis that happens 6-8 weeks post-infarction. Fibrinoid pericarditis.

Front 24

Orthopnea

Back 24

Dyspnea while laying flat over just a few minutes

Front 25

Paroxysmal Nocturnal Dyspnea

Back 25

Dyspnea while laying flat over few hours due to increased venous return while lying flat

Front 26

Heart failure cells arise because?

Back 26

capillaries that burst lead to intra-alveolar hemorrhage. Macrophages come in and eat all the RBC's which cause them to accumulate iron. These are called hemosiderin-laden macrophages or "heart failure" cells.

Front 27

What happens in CHF?

Back 27

Pulmonary congestion leads to pulmonary edema
Decreased Forward perfusion

Front 28

Complications of decreased forward perfusion?

Back 28

Decreased forward perfusion causes the activation of the Renin-Angiotensin system. This causes eventual vasoconstriction, which increases afterload and blood volume increase. Both of which cause the heart to work harder ==> BAD.

Front 29

Mainstay treatment of CHF?

Back 29

ACE inhibitors

Front 30

MCC of Right sided heart failure?

Back 30

Left sided heart failure

Front 31

MOA leading to Right heart failure due to Chronic Lung Disease

Back 31

Lung blood vessels have a natural response to constrict when they are hypoxic as a mechanism to accomodate. However, if the entire lung does this, you raise pulmonary resistance and the right heart has to work harder which can lead to failure(cor pulmonale)

Front 32

Cor pulmonale

Back 32

Right heart dilation due to increased resistance in pulmonary vessels

Front 33

Nutmeg liver

Back 33

A result of congestive heart failure and backup of blood into the hepatic veins.

Front 34

Clinical features of right heart failure

Back 34

Jugular Venous Distention(since this feeds into right heart)
Painful hepatosplenomegaly along with possible "cardiac" cirrhosis of liver
Dependent pitting edema due to increased hydrostatic pressure

Front 35

Most common congenital defect?

Back 35

VSD
A/w?

Hint 35

Fetal Alcohol Syndrome

Front 36

Most common type of ASD? Less common ASD A/w?

Back 36

Ostium Secundum

Ostium Primum A/w Down's Syndrome

Front 37

Paradoxical embolus A/w what cardiac defect?

Back 37

ASD

Front 38

Describe the splitting A/w ASD's

Back 38

The extra volume due to the L-->R shunt causes the pulmonic valve to stay open longer. That is, the aortic valve closes and then the pulmonic valve follows.

Front 39

PDA is A/w?

Back 39

Congenital Rubella

Front 40

PDA arises where in relation to the branches of the aorta?

Back 40

After the major upper extremity branches. Therefore after birth, there is a L-->R shunt due to the PDA.

Can lead to Eisenmenger Syndrome due to eventual switch to the R-->L shunt. Will result in LOWER EXTREMITY CYANOSIS.

Front 41

What classic congenital defect causes lower extremity cyanosis?

Back 41

PDA due to it causing a L-->R shunt AFTER the upper main branches of the aorta.

Front 42

What keeps PDA open?

Back 42

Prostoglandins KEEP the PDA open, while indomethacin, a PGE inhibitor closes it.

PGE KEEEEPS the PDA open

Front 43

Tetralogy of Falot

Back 43

1.) Pulmonary Stenosis
2.) Right Ventricular Hypertrophy
3.) VSD
4.) Overriding Aorta

Front 44

Boot shaped heart on x-ray?

Back 44

Right ventricular hypertrophy, associated with Tetralogy of Falot

Front 45

What condition is associated with squatting after a cyanotic spell? Why does this help?

Back 45

Tetralogy of Falot. It increases systemic resistance, decreasing the pressure differential between

Front 46

Transposition of great vessels A/w

Back 46

Maternal Diabetes

Front 47

What clinical presentation occurs with persistent Truncus Arteriosus?

Back 47

Early cyanosis
5 T's of early cyanosis?

Hint 47

Truncus Arteriosus
Tetralogy of Falot
Transposition of Great Vessels
Tricuspid Atresia
Total Anomalous Pulmonary Venous Return

Front 48

Infantile Coarctation of the Aorta A/w?

Back 48

In infantile form, it is associated with a PDA and Turner's Syndrome.

Notably, this shunt will be R-->L since the narrowing creates a relative low pressure locally distal to coarctation. This contrasts a normal PDA which is a L-->R shunt. As such, infants will develop cyanosis of the lower extremities.

Front 49

Infant with cyanosis of lower extremities

Back 49

Coarctation of the Aorta with associated PDA. PDA is distal to coarctation.

Front 50

Adult Coarctation of the Aorta A/w what clincal sign?

Back 50

"notching" of ribs on x-ray due to engorged arteries. Also associated with what cardiac abnormality?

In the adult form, it will present as hypertension of the upper extremities and hypotension/weak pulses of the lower extremities.

Hint 50

bicuspid aortic valve.

Front 51

Etiology of Acute Rheumatic Fever

Back 51

Group A Strep(Strep Pyogenes)

A result of antigenic mimicry due to the virulence factor--M protein. Onset usually 2-3 weeks after strep throat infection

Front 52

Diagnosis of acute rheumatic fever?

Back 52

JONES criteria

J -- Joints(migratory polyarthritis)
O -- Pancarditis
N -- Nodules(subcutaneous)
E -- Erythema Marginatum
S -- Sydenham's Chorea

Main problem is the pancarditis as other symptoms are self-limited

Front 53

Swelling and pain in the wrist that resolves in two days. Then some pain in the ankle that resolves and moves to the knees.

Back 53

Migratory polyarthritis A/w Acute rheumatic fever

Front 54

Describe the pancarditis A/w acute rheumatic fever...

Back 54

Endocarditis -- Generally involves vegetations on Mitral Valve. But can also involve Aortic valve. CAN CAUSE REGURGITATION.

Myocarditis -- Aschoff bodies containing Anitschkow cells(caterpillar nuclei in activated histiocytes).

Pericarditis -- Leads to friction rub and chest pain

Front 55

Most common cause of death during acute phase of acute rheumatic fever

Back 55

myocarditis --
characteristic histologic finding?

Hint 55

Anitschkow cells in Aschoff bodies characteristic

Front 56

"fish mouth" appearance of cardiac valve

Back 56

due to stenosis. A/w chronic rheumatic heart disease as a result of repeat Group A strep infections.

Front 57

How does the mitral valve respond in chronic rheumatic heart disease?

Back 57

thickening of the chordae tendineae and cusps

Front 58

How does the aortic valve respond in chronic rheumatic heart disease?

Back 58

leads to fusion of the commissures

Front 59

Aortic Stenosis etiology...
A/w?

Back 59

due to wear and tear on valves. As such, presents late in life(>60 years)

A/w bicuspid aortic valve(2 leaves doing the work of 3)

Front 60

How can you distinguish stenosis of valves via rheumatic fever vs wear and tear?

Back 60

Rheumatic fever stenosis will always involve mitral valve. Therefore if only aortic valve involved, it must be "wear and tear" etiology.

Also, aortic valve in rheumatic fever will have FUSION of the commissures, whereas in wear and tear, they will just have fibrotic scarring on the surface of the valve.

Front 61

Describe clinical course of aortic stenosis...

Back 61

Long asymptomatic period due to compensation period during which a systolic ejection click is followed by a crescendo-decrescendo murmur is heard.

---This leads to ventricular hypertrophy which can progress to cardiac failure.
---Angina and syncope due to the limited ability to increase blood flow across stenotic valve.
---Microangiopathic hemolytic anemia due to RBC's being damages while crossing the calcified valve.

Front 62

What causes aortic valve regurgitation?

Back 62

Aortic root dilation, Syphilitic Aneurysm(tertiary syphilis) which pulls apart the valve leaflets

or

infectious endocarditis, causing direct damage to the valve

Front 63

Clinical features of aortic regurg...

Back 63

Early, blowing diastolic murmur

diastolic because regurg happens during diastole
blowing because that's the sound that usually happens on blood flowing backwards.

Front 64

When does the pulse pressure widen? Why?

Back 64

The pulse pressure widens because the regurgitating blood increases systolic BP by increasing stroke volume and decreasing diastolic BP by taking away blood from the systemic circulation.

Front 65

head bobbing

Back 65

aortic regurgitation

also a/w bounding pulses and pulsating nail bed.

All this is called "hyperdynamic circulation"

Front 66

eccentric hypertrophy

Back 66

refers to asymmetric hypertrophy of left ventricle generally due to volume overload.

seen in ?

Hint 66

aortic regurgitation.

Front 67

Mitral valve prolapse has a light association with...

Back 67

Marfan syndrome and Ehler-Danlos syndrome

Front 68

heart sound of mitral valve prolapse

Back 68

incidental mid-systolic click followed by a regurgitation murmur.

mid-systolic click is due to the reverse ballooning of mitral valve during contraction of ventricle since the valve is so floppy.(it parachutes out...)

Front 69

Etiology of mitral valve regurg...

Back 69

Mitral valve prolapse, left ventricular dilation, rheumatic heart disease and papillary muscle rupture after MI.

Front 70

heart sound with mitral valve regurg...

Back 70

holocystolic blowing murmur louder with squatting and expiration

expiration increases blood flow to atrium and ventricles and as such has more blood to regurg.

Front 71

Acute rheumatic fever influence on mitral valve

Back 71

Mitral valve regurgitation

Front 72

Chronic rheumatic fever influence on mitral valve

Back 72

Mitral valve stenosis

Front 73

heart sounds for mitral valve stenosis

Back 73

opening snap followed by a diastolic rumble

Front 74

Staph aureus in endocarditis

Back 74

acute endocarditis
infects tricuspid valve due to high virulence. Common in IV drug abusers

Front 75

Strep viridens

Back 75

subacute endocarditis

damaged endocardial surface develops thrombotic vegetations that can trap transient bacteria in blood stream

Front 76

endocarditis that is indicative of strep bovis. What do you look for?

Back 76

colorectal carcinoma

Front 77

What kind of organism is strep bovis?

Back 77

Its a group D streptococci. Gram + gamma hemolytic. bile+salt culture?

Hint 77

It will NOT grow on it

the enterococci will.

Front 78

HACEK organisms and relevance

Back 78

Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

Endocarditis with negative blood cultures. These organisms are particularly difficult to grow.

Front 79

Bacterial Endocarditis presenting symptoms...

Back 79

FROM JANE
F - Fever
R - Roth's Spots(round white spots on retina surrounded by hemorrhage)
O - Osler's nodes(painful on finger/toe pads)
M - Murmur(due to vegetative growths on valve)
J - Janeway lesions(painless lesions on palms/soles)
A - Anemia of Chronic Disease(microcytic)
N - Nail-bed hemorrhage
E - Emboli(Rt-PE, Lt-Stroke)

Front 80

Bacterial endocarditis will cause what specific acute phase reactant?

Back 80

Liver releases Hepcidin, which traps iron in the storage sites which raises ferritin levels which reduces total iron binding capacity. Since no access to iron from storage sites, bone marrow will pull iron from blood, causing low serum iron and percent saturation of iron to decrease.

Front 81

Libman-Sacks endocarditis

Back 81

Lupus associated sterile vegetations that form on BOTH sides of mitral valve

Front 82

Dilated Cardiomyopathy etiology

Back 82

commonly idiopathic,
but can be a late complication related to?

Hint 82

Coxsackie A or B virus

Front 83

Hypertrophic Cardiomyopathy etiology

Back 83

Usually due to genetic mutations in sarcomere proteins;
genetics?

Hint 83

autosomal dominant

Front 84

Dilated cardiomyopathy symptoms

Back 84

Systolic dysfuntion(ventricle cannot pump) causing biventricular CHF. Mitral and Tricuspid Regurgitation due to stretching of the walls.

Front 85

Symptoms of hypertroph cardiomyopathy

Back 85

Decreased cardiac output - left ventricular hypertrophy is so massive that it cannot fill.

Syncope with exercise -- subaortic hypertrophy of the ventricular septum results in functional aortic stenosis

Front 86

Sudden death in young athletes

Back 86

hypertrophic cardiomyopathy

Front 87

Histologic appearance of hypertrophic cardiomyopathy

Back 87

Myofiber disarray with hypertrophy. The muscle fibers are going every which way.

Front 88

rare cause of restrictive cardiomyopathy in children

Back 88

endocardial fibroelastosis

Front 89

Classic finding for restrictive cardiomyopathy; ekg?

Back 89

same as congestive heart failure for the most part.
low voltage EKG, dim qrs amplitudes

Hint 89

Low voltage EKG with diminished QRS amplitude

Front 90

Loeffler Syndrome

Back 90

A restrictive cardiomyopathy caused by an endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia

Front 91

Most common primary cardiac tumor in adults

Back 91

Myxoma. Derives from?

Hint 91

MESENCHYME

Front 92

Clinical presentation of myxoma

Back 92

pedunculated mass in the left atrium that causes syncope due to obstruction of the mitral valve

Front 93

Most common primary tumor in children? A/w?

Back 93

Rhabdomyoma
A/w tuberous sclerosis

usually arises in?

Hint 93

in ventricle

Front 94

anti-dnase B

Back 94

same as ASO, Group A strep, Rheumatic Fever