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STEP 1 Pathoma > Chapter 8 > Flashcards

Chapter 8 Flashcards

1
Q

What is stable angina?

A

Chest pain that arises with exertion or emotional stress due to atherolsloersis of coronary arteries with 70+% stenosis where decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion

This represents REVERSIBLE myocyte injury (not necrosis) and presents as chest pain lasting less than 20 minutes that raidates to the left arm or jaw, diasphoresis, and SOB.

Relived by rest or nitroglycerin

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2
Q

What is unstable angina?

A

Chest pain that occurs at rest usually due to rupture of atheroslcerotic plaque with thrombsis and INCOMPLETE occlusion of a coronary artery. Again this represents REVERSIBLE injury to myocytes (no necrosis)

Both stable and unstable angina will show ST segment depression due to subendocardial ischemia

Relived by nitroglycerin but risk of progression to MI

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3
Q

What is Prinzmetal angina?

A

An episode of chest pain unrelated to exertion due to coronary artery vasospasm. Represents reversible cell injury.

Tx with nitroglycerin or CCBs

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4
Q

Myocardial Infarction

A

Necrosis of myocytes usually due to thrombosis with complete occlusion of a coronary artery (can also be caused by Prinzmetal angina or cocaine use), emboli, and vasculitis

Presents with severe, crushign chest pain that is NOT relieved by nitroglycerin

Infarction typically involves the left and right ventricles but spares the atria

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5
Q

What commonly occluded artery causing MI?

A

Left anterior descending artery

Next: RCA

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6
Q

The initial phase of MI leads to subendocardial necrosis involving less than 50% of the thickness (subendocardial infarction) and an EKG showing ST-segment depression. With continued ischemia, this will transition to a transmural infarction with EKG findings of ST-segment elevation

What are the lab findings/enzymes of a MI?

A
  1. Troponin I is the most sensitive and specific marker (gold standrd) for MO and levels typically rise 2-4 hrs after infarction, peak at 24 hrs, and return to normal by 7-10 days
  2. Ck-MB can be useful for detecting reinfarction that occurs days after an intiial MI; These levels rise 4-6 hrs after infarction, peak at 24 hrs, and return to normal with 72 hrs
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7
Q

What is the Tx for an MI?

A

Aspirin and/or heparin- limits thrombosis

  1. Supplemental O2
  2. Nitrates- vasodilate VEINS and coronary arteries
  3. BBs-decreases O2 demand
  4. ACEI-decreases LV dilation
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8
Q

Fibrinolysis or angiplasty can also be used to open occluded vessels in an MI. What are some down sides of that?

A
  1. Reperfusion of irreversibly damaged cells results in calcium influx, leading to hypercontraction of myofibrils (contraction band necrosis; below)
  2. Return of oxygen and inflammatory cells may lead to free radical generation (reperfusion injury)
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9
Q

What are the major complications of an MI within 4 hrs?

A

Cardiogenic shock (massive infarct), CHF, and arrhythmia

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10
Q

What are the major complications of an MI within 4-24 hrs?

A

Gross changes: Dark discoloration

Microscopic changes: Coagulative necrosis

Complciations: Arryhthmias

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11
Q

What are the major complications of an MI within 1-3 days?

A

Gross changes: yellow pallor

Microscopic chnages: Neutrophils

Complications: Fibrinous pericarditis (friction rub)

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12
Q

What are the major complications of an MI within 4-7 days?

A

Gross changes: Yellow palor

Microscopic changes: Macrophages

Complications: Rupture of ventricular free wall leading to tamponade, interventricular septum, or papillary muscle insufficiency/necrosis

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13
Q

What are the major complications of an MI within 1-3 weeks?

A

Gross changes: Red borde emerges as granulation tissue enters the infarct

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14
Q

What are the major complications of an MI within months?

A

Gross: White scar

Microscopic changes: Fibrosis

Complications: Aneurysm, mural thrombosis, or Dressler syndrome

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15
Q

What is Dressler Syndrome?

A

Dressler’s syndrome is a type of pericarditis — inflammation of the sac surrounding the heart (pericardium). Dressler’s syndrome is believed to be an immune system response after damage to heart tissue or to the pericardium, from events such as a heart attack, surgery or traumatic injury. Symptoms include chest pain, which may be similar to chest pain experienced during a heart attack.

Dressler’s syndrome may also be called postpericardiotomy syndrome, post-myocardial infarction syndrome and post-cardiac injury syndrome. With recent improvements in heart attack treatment, Dressler’s syndrome is less common than it used to be.

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16
Q

Describe left-sided heart failure

A

Causes include ischemia, HTN, dilated cardiomyopathy, MI, and restrictive cardiomyopathy

Clinical features are due to decreased foward perfusion and pulmonary congestion, leading to pulmonary edema resulting in dyspnea, paroxysmal nocturnal dyspnea due to increased venous return while laying down.

May also result in bursting of small capilaries leading to intraalveolar hemorrhage marked by hemosiderin-laden macrophages (below)

Decreased kidney perfusion leads to activation of the renin system leading to increased fluid retention and edema

Tx with ACEI

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17
Q

Describe right-sided heart failure

A

Most commonly due to left0sides heart failure, left-to-right shunts, and chronic lung disease (cor pulmonale)

Clinical features due to congestion and include JVD, painful HSM with characteristic nutmeg (below) liver that may lead to cirrhosis, and depenent pitting edema

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18
Q

Congenital heart defects most commonly arise during what embryonic period?

A

3-8 weeks

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19
Q

How do left-to-right shunts present?

A

May be relatively asymptomatic at birth but the shunt can reverse eventually due to the following sequence:

  1. Increased flow through the pulmonary circulation results in hypertrophy of the pulmonary vessels and HTN, eventually causing shunt reversal, leading to late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia, and clubbing
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20
Q

How do right-to-left shunts present?

A

Usually with cyanosis shortly after birth

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21
Q

Describe VSDs

A

Defect in the septum that seperates the left and right ventricles; Most common congenital heart defect; associated with fetal alcohol syndrome

Results in a left-to-right shunt and the size of the shunt determines the extent of shunting and age at presentation- shunt can reverse

Tx with surgical closure

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22
Q

Describe ASDs

A

Defect in the septum seperating the right and left atria

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23
Q

Describe Patent Ductus Arteriosus

A

Failure of the ductus arteriosus to close; associated with congential RUBELLA

Resulting in a left-right shunt between the aorta and the pulmonary artery

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24
Q

Auscultation findings of Patent Ductus Arteriosus?

A

Continuous machine-like murmur

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25
Q

Complications of Patent Ductus Arteriosus?

A

It may reverse causing a differential cyanosis (cyanosis of the lower extremities only)

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26
Q

How are PDAs tx?

A

Tx involves Indomethacin, which decreases PGE, resulting in PDA closure (PGE maintains the patency of the ductus arteriosus)

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27
Q

What is the tetrad of tetralogy of fallot?

A
  1. Stenosis of the right ventricular outflow tract
  2. Right ventricular hypertrophy
  3. VSD
  4. An overriding aorta over the VSD
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28
Q

Describe tetralogy of fallot

A

Right-to-left shunt leading to early cyanosis in which pts typically learn to squat in response to a cyanotic spell (increased arterial resistance decreases the shunting and allows more blood to reach the lungs)

Boot shaped heart

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29
Q

Describe Transposition of the Great Vessels

A

Marked by pulmonary artery arising from the left ventricle and the aorta arising from the right ventricle

30
Q

Transposition of the Great Vessels is associated with ________

A

Maternal Diabetes

31
Q

How does Transposition of the Great Vessels present?

A

With early cyanosis (severe; no mixing)

creation of a shunt is needed after birth for survival and PGE can be given to maintain the ductus arteriosus

32
Q

Describe Truncus Arteriosus

A

The formation of a single large vessel arising from both ventricles (truncus fails to divide) presenting with early cyanosis

33
Q

Describe Tricuspid Atresia

A

Occurs when the tricuspid valve orifice fails to develop and the right ventricle becomes hypoplastic

Often associated with an ASD, resulting in a right-left shunt and presenting with early cyanosis

34
Q

Describe coarctation of the aorta

A

narrowing of the aorta- classically divided into infantile and adults forms

35
Q

Describe infantile aortic coarctation

A

Associated with a PDA and coarctation that lies AFTER the aortic arch but BEFORE the PDA and presenting as lower extremity cyanosis in infants, often at birth

36
Q

Infantile aortic coarctation is associated with ________

A

Turner Syndrome

37
Q

Describe adult form aortic coarctation

A

Adult form NOT associated with a PDA and a coarctation that lies after the aortic arch presenting as upper extremity HTN and lower extremity hypotension with weak pulses

Associated with Bicuspid Aortic valves

38
Q

What is the classic finding with adult form aortic coarctation?

A

Rib notching due to the formation of collateral circulation developing across the intercostal arteries

39
Q

What causes acute rheumatic fever?

A

This is a systemic complication of pharyngitis due to GAS affecting children/teens approx 2-3 weeks after an episode of strep pharyngitis due to molecular mimicry against the surface M protein

40
Q

How does ARF present?

A
  1. Migratory polyarthritis- swelling and pain in alarge joint (eg. wrist, keness, ankles) that resolves within days and migrates to another joint
  2. Myocardial Involvement
  3. Subcutaneous nodules
  4. Erythema marginatum
  5. Sydenham chorea
41
Q

Describe the Myocardial Involvement seen in ARF

A
  1. Enocarditis- with mitral vlave most commonly affected, leading to regurg
  2. Myocarditis with Aschoff bodies (described as foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material)
42
Q

Anitschkow cells

A
43
Q

Erythema marginatum-ARF (non-specific)

A
44
Q

What is the major complication of ARF?

A

The persistence and formation of chronic rheumatic heart disease marked by scarring and stenosis with a classic “fish mouth appearance”

45
Q

What are the most common causes of aortic stenosis?

A

Usually due to fibrosis and calcification from wear and tear that presents in late adulthood (congenital bicuspid aortic valve can hasten this progression)

May also arise as a consequence of chronic rheumatic valve disease (will also see mitral stenosis if this is the cause)

46
Q

What are the asucultative findings of aortic stenosis?

A

cardiac compensation leads to a prolonged asymptomatic stage during which a Systolic ejection click followed by a cresendo-descreendo murmur is heard

47
Q

What are the main complications of aortic stenosis?

A
  1. concentric left ventricular hypertrophy
  2. Angina and syncope with exercise
  3. Microangiopathic hemolytic anemia-RBCs are damaged while crossing the calcified valve
48
Q

What is aortic regurg?

A

Backflow from the aorta into the left ventricle during diastole arising due to aortic root dilation (eg. syphilitic aneurysm and aortic dissection) or valve dmaage (e.g. infectious endocarditis)

49
Q

What are the clinical findings of aortic regurg?

A
  1. Early, blowing diastolic murmur
  2. Hyperdynamic circulation ebtween systolic and diastolic pressures
  3. Diastolic pressures that decrease due to regurg, while systolic pressure increases due to increased stroke volume
  4. Presents with a bounding pulse, pulsating nail bed (Quincke pulse) and head bobbing
  5. Results in LV dilation and hypertrophy due to volume overload
50
Q

What is mitral valve prolapse?

A

Ballooning of the mitral valve into the left atrium during SYSTOLE typically due to myxoid degeneration of the valve

51
Q

How does mitral valve prolapse present on asucultation?

A

Mid-systolic click followed by a regurg murmur

NOTE: The click and murmur become softer with squatting due to increased systemic resistance decreasing left ventricular emptying

52
Q

What are some common causes of mitral valve regurg?

A

Reflux of blood from the elft ventricle into the left atrium during systole usually arising due to mitral valve prolapse, LV dilation, infective endocarditis, acute rheumatic heart disease, and papillary muscle infarct after an MI

53
Q

How does mitral valve regurg present on auscultation?

A

Holosystolic blowing murmur;

louder with squatting due to increased systemic resistance decreasing left ventricular emptying and expiration due to increased venous return

54
Q

What are some possible consequneces of mitral stenosis?

A

Narrowing of the mitral valve (usually due to chronic rheumatic valve disease) causes volume overload leading to dilation of the left atrium resulting in pulmonary congestion with edema and alveolar hemorrhage, pulmonary HTN and eventually right sided HF

55
Q

What is the most overall cause of endocarditis?

A

Strep viridians (a low virulence organism that infects previously damaged valves (e.g. chronic rheumatic valve disease, prolapse, etc.). This results in small vegetation that do NOT destroy the valve (subacute endocarditis)

56
Q

What is the most common cause of endocarditis in IVDU?

A

S. aureus (most commonly the TRICUSPID; results in large vegetations that destroy the valve (aka acute endocarditis))

Affects previously normal valves

57
Q

__________ is associated with endocarditis of prosthetic valves

A

Staph epi.

58
Q

__________ is associated with endocarditis in pts with underlying colorectal carcinoma

A

Strep. bovis

59
Q

What organisms are most commonly associated with negative blood culture endocarditis?

A

HACEK

Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

60
Q

What are the major clinical findings of endocarditis?

A
  1. Fever due to bacteremia
  2. Murmur due to vegetations
  3. Janeway lesions (soles and palms; proximal), Osler nodes (tender lesions on fingers and toes), splinter hemorrhages and Roth spots due to embolization of septic vegetations
  4. **Anemia of chronic disease** (decreased Hb, elevated ferritin, decreased MCV, decreased TIBC, decreased serum iron, decreased % saturation)
61
Q

Nonbacterial thrombotic endocarditis is associated with what?

A

Sterile vegetations in association with a hypercoag state or underlying adenocarcinoma. Typically seen on the mitral valve

62
Q

Most common causes of dilated cardiomyopathy (dilation of all four chambers resulting in systolic dysfunction)?

A

Genetics (usually AD)

Myocarditis (usually due Coxsackie A and B)

Alcohol and Drugs (doxorubicin)

Seen in late pregnancy

Hemochromatosis

63
Q

How is dilated cardiomyopathy tx?

A

heart transplant

64
Q

Describe hypertrophic cardiomyopathy

A

Massive hypertrophy of the left ventricle usually due to genetic mutations in sarcomere proteins that presents as:

Decreased CO due to a diastolic filling dysfunction and syncope with exercise

Below: myofiber hypertrophy with disarray

65
Q

What is restrictive cardiomyopathy?

A

Decreased compliance of the ventricular endomyocardium that restricts filling during diastole

66
Q

What are some common causes of restrictive cardiomyopathy?

A

Causes inlcude amyloidosis, sarcoidosis, endocardial fibroelastosis (children; below), Loeffler syndrome

67
Q

What is Loeffler syndrome?

A

Löffler’s syndrome or Loeffler’s syndrome is a disease in which eosinophils accumulate in the lung in response to a parasitic infection.

It was first described in 1932 by Wilhelm Löffler in cases of eosinophilic pneumonia caused by the parasites Ascaris lumbricoides, Strongyloides stercoralis and the hookworms Ancylostoma duodenale and Necator americanus.

Although Löffler only described eosinophilic pneumonia in the context of infection, many authors give the term “Löffler’s syndrome” to any form of acute onset pulmonary eosinophilia no matter what the underlying cause. If the cause is unknown, it is specified and called “simple pulmonary eosinophilia”. Cardiac damage caused by the damaging effects of eosinophil granule proteins (ex. major basic protein) is known as Loeffler endocarditis and can be caused by idiopathic eosinophilia or eosinophilia in response to parasitic infection

68
Q

What is a myxoma?

A

A BENIGN mesenchymal tumor with a gelatinous appearance and abundant ground substance on histology (most common primary cardiac tumor in adults)

Usually forms a pedunculated mass in the LEFT ATRIUM that causes syncope due to obstruction of the mitral valve

69
Q

What is a rhabdomyoma?

A

BENIGN hamartoma of cardiac muscle (most common primary cardiac tumor in children)

Usually arises in the ventricles

70
Q

Rhabdomyomas are associated with ________

A

Tuberous sclerosis

71
Q

METs in the heart are more common than primary tumors. Common sources include:

A

Breast and lung carcinoma

melanoma

lymphoma

These most commonly affect the pericardium causing a pericardial effusion

STEP 1 Pathoma (18 decks)

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