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Pathology > Cardiovascular pathology > Flashcards

Cardiovascular pathology Flashcards

1
Q

For congenital cardiac defects, insults must occur before the ……

A

16 week of development

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2
Q

Acyanotic heart disease means …..

In the long run, this will lead to …..

A

blood is shunted from the left to the right side of the heart.
* Leads to right heart failure, secondary pulmonary hypertension

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3
Q

Some of the loudest murmurs are heard in ……

A

VSD

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4
Q

Define the Ostium primum defect, and what is the possible cause?

A

It is an ASD in the lower atrial septum above the AV valves.

  • The possible cause is a defect in the AV valve
  • Accounts for 5% of all ASD
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5
Q

Define the Ostium secundum defect, and what is the possible cause?

A

Defect in the center of the atrial septum at foramen ovale

  • The defect is in septum primum or septum secundum, or both
  • Not associated with maldeveloped AV valve
  • Accounts for 90% of all ASD
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6
Q

Atrial septum remains open in some people, however it is closed by …..

A

pressure difference between the right and left atria

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7
Q

Complete endocardial cushion defect results in ….., ….. & …..

A

ASD, VSD & a common AV canal

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8
Q

Define patent ductus arteriosus, and what are the complications?

A

It is the flow of blood from the aorta to the pulmonary artery
* It deprives the systemic circulation of oxygenated blood, leading to pulmonary hypertension

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9
Q

What is the drug used to treat PDA?

A

indomethacin is used to close the shunt

* Prostaglandin E is utilized to keep the shunt open if needed

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10
Q

Cyanotic congenital heart disease means …..

A

blood is shunted from the right to the left side of the heart
* Poorly oxygenated blood enters the circulation, causing cyanosis & permits paradoxic embolism

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11
Q

Define the Tetralogy of Fallot

A

The most common cyanotic congenital heart disease. There is

  1. VSD
  2. Overriding aorta
  3. Right ventricular hypertrophy
  4. Pulmonary stenosis (little blood reaching the lungs)
    * Note: PDA permits survival if the pulmonary artery is completely obstructed
    * The degree depends on the right ventricular flow obstruction
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12
Q

Define the transposition of great vessels

A

The failure of the truncoconal septum to spiral (the aorta arises from the right ventricle, and the pulmonary artery arises from the left)
* PDA, ASD, VSD or patent ovale mixes the venous and systemic blood, permitting survival

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13
Q

Antibiotic prophy is needed for patients with tetralogy of fallout and transposition of great vessels. T/F??

A

True

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14
Q

Obstructive congenital heart disease usually do cause cyanosis. T/F??

A

false
* Obstructive congenital heart diseases like coarctation of aorta, pulmonary stenosis or aortic stenosis. They do not cause cyanosis

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15
Q

Define the coarctation of the aorta, and what are the types?

A

narrowing of the aorta

* It could be preductal, ductal or postductal depending on the site where ductus arteriosus joins the aorta

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16
Q

Unequal division of the truncus arteriosus may cause ……

A

pulmonary valve stenosis or atresia

* may cause cyanosis if severe

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17
Q

Infective endocarditis of the aortic valve causes ……

A

left ventricular overload and sudden death

* The second most common cause of aortic stenosis after rheumatic fever

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18
Q

What are the cardiovascular defects associated with the following

  1. Marfan syndrome
  2. Down’s syndrome
  3. Turner’s syndrome
A
  1. Aortic dissection, ASD
  2. Ostium Primum ASD, VSD
  3. Coarctation of the aorta, pulmonary stenosis
  • Note: Rubella infection (German measles) also causes ASD, VSD, PDA
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19
Q

Fetal alcohol syndrome causes ……

A

VSD

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20
Q

Trimethadione is ……., Isotretionin is ……

A

antiseizure medication
acne treatment & leukemia tx
* They both cause fetal cardiac defect

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21
Q

Narrowing of the coronary arteries could be due …..

A
  1. Atherosclerosis (90% of cases)
  2. Dissecting aortic aneurysm
  3. Arteritis, coronary embolism
  4. Cocaine induced vasospasm
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22
Q

Define angina pectoris, and what are its types

A

Chest pain caused by transient myocardial ischemia without infarction

  1. Stable: associated with exertion, lasts less than 10 mins, relieved with sublingual nitroglycerine. Main cause is narrowing of coronary artery
  2. Prinzmetal angina: it is caused by vasospasm with no atherosclerosis. Mainly in young women
  3. Unstable angina: prolonged chest pain, occurs even at rest, and non responsive to nitroglycerin. Often leads to MI
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23
Q

Define MI, what are the risk factors,

A

Ischemic necrosis due to abrupt decrease in coronary flow or increase myocardial demand that can not be met

  • Often, it is transmural (ST elevated), but may be subendocardial (ST is normal)
  • Risk factors: hypertension, high cholesterol, smoking, family history, DM (due to hypercoagulability of blood), and oral contraceptives
  • MI is more common in men
  • Alcohol increases HDL, which decreases the risk of MI
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24
Q

Which cardiac arteries that when occluded causes infarcts?

A
  1. anterior descending (50%)
  2. Right coronary (35%)
  3. left circumflex (15%)
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25
Q

Subendocardial infarcts are ……

A

infarctions limited to the inner half of the ventricular wall

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26
Q

MI can occur with little or no chest pain in

A

elderly, diabetic patients, and surgical patients

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27
Q

What are the clinical features of MI?

A
  1. Crushing pain radiating to the lower jaw and left arm

2. Diaphoresis, shortness of breath, nausea, anxiety

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28
Q

What are the serum indicators for MI?

A
  1. CK-MB: most common used,
  2. Lactate dehydrogenase (LDH 1): elevated in MI
  3. SGOT (aka aspartate transaminase): also increases, but may indicated liver damage instead
  4. Troponin T & Myoglobin are increased
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29
Q

Ischemia and necrosis of AV node & three fascicles can lead to ….

A

heart block with compromised cardiac function

* Ventricular fibrillation is the most common complication

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30
Q

Thrombus and aneurysm may be formed in MI due to …..

A

lack of contractility of the infarcted area.

* There is outpouching of non contractile scar, however, rupture is uncommon

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31
Q

Patients are most susceptible to myocardial rupture …… days after MI because of ……

A

1-7 days

the myocardium is necrotic but granulation tissue formation has not really began

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32
Q

What are the arteries used to treat angina?

A
  1. Saphenous vein

2. Internal mammary artery

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33
Q

Define Angioplasty

A

Ballon dilatation of the coronary artery

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34
Q

Define the Acute rheumatic fever, and what is its pathogenesis?

A

Recurrent inflammation that follows pharyngitis or scarlet fever caused by group A beta-hemolytic streptococci (rheumatic fever is not an infection)

  • Antistreptococcal antibodies cross react with the host connective tissue (synovial, cardiac, pulmonary, peritoneal) and causes organ damage by autoimmune mechanism
  • Mainly in children 5-15 years old
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35
Q

What is the Major Jones Criteria?

A

the presence of two of the following is enough to diagnose acute rheumatic fever
1. Polyarthritis: involve large joints (swelling & painful)
2. Erythema Marginatum: macular skin rash, in a “bathing suit” distribution
3 Sydenham chorea: involuntary movement of extremities, also called St. Vitus dance
4. Subcutaneous nodules: containing Aschoff bodies
5. Carditis: may cause death during the acute stage, or scarring of the heart valves leading to rheumatic heart disease
* Lab work shows increased ESR

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36
Q

Define the Rheumatic heart disease, and what are the clinical features?

A

deformation of the heart valves through chronic inflammatory insult, deposition of fibrin and then fibrosis

  • Features:
    1. Red, swollen valve leaflets with vegetation
    2. Most commonly affected valve is the mitral & aortic
    3. Valve dysfunction is usually stenosis & insufficiency
    4. Cardiac murmurs
    5. Chronic valvulitis predispose to infective endocarditis. CHF is the end result (takes years to develop)
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37
Q

Rheumatic heart disease is an indication of …… before treatement

A

antibiotic prophylaxis

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38
Q

Define Aschoff bodies

A

lesion of the interstitial myocardial connective tissue

  • The presence of Aschoff bodies means rheumatic heart disease
  • Anitschkow cells (enlarged macrophages) are found in Aschoff bodies
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39
Q

Right side heart failure is caused by left side heart failure due to ……

A

back pressure through the lungs

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40
Q

Salt and water retention is more severe in right heart failure than left heart failure. T/F?

A

True

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41
Q

What are the clinical hallmarks of right side heart failure?

A
  1. Jugular venous distention
  2. Hepatosplenomegaly
  3. Generalized edema
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42
Q

Define Cor pulmonale and what are its types?

A

right ventricular failure resulting “specifically” from pulmonary hypertension

  1. Acute: massive pulmonary embolism, leads to “dilatation” of the right ventricle, and even tricuspid regurgitation
  2. Chronic: Hypertrophy of the right ventricle due to pressure overload
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43
Q

What are the main causes for Cor pulmonale?

A
  • Primary pulmonary hypertension: unknown cause
  • Secondary pulmonary hypertension: Cor pulmonale, which is caused by:
    1. pulmonary vascular disease (vasculitis, emboli)
    2. Increase pulmonary vascular resistance (TB, pneumoconiosis, COPD, cancer)
    3. Restrictive chest wall abnormality (rare)
    4. L to R shunts, left heart failure
  • Pneumoconiosis is restrictive disease due to inhalation of dust particles
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44
Q

What are the main causes of shock?

A
  1. Inadequate cardiac output
  2. Reduction in blood volume
  3. Pooling of blood in peripheral vessels (due to loss of vascular tone)
45
Q

What are the stages of compensation in shock??

A
  1. Compensated stage: Early hypotension leads to reflex tachycardia & peripheral vasoconstriction. Occurs via baroreceptor mechanism
  2. Decompensated stage: tachycardia increases but not enough, metabolic acidosis, respiratory distress & decreased renal output
  3. Irreversible stage: irreversible cellular damage, coma & death
46
Q

Define Endocarditis, and describe the lesion grossly and microscopically and state the most common locations

A
  • Colonization of the heart valves &/or endocardium
  • Grossly: vegetative masses overhang the free margin of the valve leaflet, prosthetic valve or other cardiac defect
  • Microscopically: mass of clot, fibrin, and bacteria. When healed leads to fibrosis
  • Most common in the mitral valve
  • In IV drug users, right valves are the most affected
47
Q

What are the causative agents of Endocarditis?

A
  1. Streptococcus Viridans: 65% of infective endocarditis. Usually subacute.
  2. Staphylococcus Aureus: 20 - 30% of infective endocarditis. Common in IV drug users (tricuspid valve is most affected). Usually Acute
  3. Candida: also occurs in drug users. Causes subacute endocarditis
48
Q

How can Streptococcus viridans cause endocarditis? What is the pathogenesis and clinical features?

A

The bacterial by products are removed from the site, leading to absence of inflammatory reaction

  • This occurs although Strep. Viridans are non virulent organisms
  • Turbulent blood flow (due to abnormal valve) permits formation of sterile platelet-fibrin clot on the leaflets that become seeded during transient bacteremia.
  • Features: insidious onset, positive blood culture, low fever without chills, anemia, splenomegaly and hematuria
49
Q

What are the risk factors for the development of Endocarditis?

A
  1. Congenital cardiac anomalies (VSD, stenosis)
  2. Valve abnormalities (mitral prolapse, prosthetic valves, RHD)
  3. Immunosuppression, IV drug use
50
Q

What happens if the bacterial vegetation in the heart becomes large?

A

It may cause myocardial abscess, formation of systemic septic emboli, eat through the heart valve leaflets producing valvular incompetence

51
Q

What are the complications of infective endocarditis?

A
  1. Valve perforation in the acute infections
  2. Myocardial abscess with septum perforation, or even heart block
  3. Mitral annulus and papillary muscle abscess leads to mitral valve prolapse
  4. Right side septic emboli leads to pneumonia or lung abscess
  5. Left side septic emboli leads to stroke, abscesses in the brain, spleen or kidney
52
Q

Mitral valve prolapse is …… . It is clinically characterized by ……

A

the ballooning of the leaflets (usually the posterior one) into the left atrium, causing insufficiency. The chordae tendinae are elongated or ruptured
* midsystolic click & with high pitch murmur.

53
Q

What are the clinical features of mitral valve prolapse? And what are the complications?

A

dyspnea, tachcardia, chest pain, syncope, CHF or sudden death
* Complications are atrial thrombosis, infective endocarditis, PVC, regurgitation, calcification

54
Q

Mitral stenosis is …..

What are the clinical features? and complications?

A

scarring, calcification and fusion of the leaflets that interfere with the opening. Most commonly caused by RHD

  • there is increased left atrium pressure, enlarged left atrium. May be combined with prolapse
  • May eventually lead to atrial fibrillation, which predisposes to thrombosis
55
Q

What are the causes and complications of acute aortic valve insufficiency?

A
  • May result from perforations or tears from infective endocarditis
  • ventricular failure, due to increased filling pressure, decreased diastolic filling time (due to reflex tachycardia), myocardial ischemia
56
Q

What are the complications of chronic aortic valve insufficiency?
And what are the possible causes?

A

The left ventricle will dilate and hypertrophy to accommodate the raise in diastolic volume to maintain adequate CO

  • There is reflex tachycardia, wide pulse pressure
  • Syphilis, RHD, or congenitally bicuspid aortic valve
57
Q

What are the causes and clinical features of aortic valve stenosis?

A
  • Congenitally abnormal bicuspid valve, with fibrosis and thickening of the valve cusps
  • There is Angina, syncope, CHF, left ventricular hypertrophy, decrease in peripheral pulse pressure. Characterized by systolic ejection click
  • May lead to sudden death, arrhythmia, CHF
58
Q

What are the complications in patients with prosthetic valves?

A
  1. Thromboembolism
  2. Paravalvular leak
  3. Infective endocarditis
  4. Microangiopathic hemolysis (trauma to RBC)
59
Q

What is the gross pathology of a heart with myocarditis??

A

Hypertrophy of all four chambers, with hemorrhage and eventual small pale foci of fibrosis

60
Q

What are the causes of infectious myocarditis?

A
  1. Viral: Coxsackie B virus (usually self limited, but recurrent and may lead to cardiomyopathy and death)
  2. Bacterial: Diphtheria, meningococci (these damage the heart directly via toxins)
  3. Protozoal: main cause is Trypanosoma cruzi, which cause Chagas Disease (myocardial necrosis)
61
Q

What are the clinical features of infectious myocarditis?

A
  1. Involvement appears days to weeks after infection with variable severity
  2. May be asymptomatic, with EKG abnormality only. Also, dyspnea, tachcardia, weakness, or severe CHF
  3. Edema is common
  4. Most patients recover fully without long term effects
62
Q

Cardiac tamponade is caused by ….., which affects the heart by …..

A

exudate or transudate in the pericardial space.

* compressing the heart, and decreasing cardiac filling

63
Q

What are the main causes of pericardial effusion?

A
  1. serous effusion: due to hypoproteinemia or CHF

2. Serosanguineous (serum and blood) effusion is caused by trauma from CPR. Hemopericardium is also caused by CPR

64
Q

Arteriovenous fistula is ……

A

abnormal communication between an artery and a vein. Blood flow increases back to the heart (artery —->vein)

65
Q

Arterial hypertension is defined as ……

A

diastolic over 100 (for patients over 60) or over 90 (for patients under 60), with the systolic being over 160 mm Hg

66
Q

Hypertension is the second leading cause of cardiac mortality after ……

A

ischemic heart disease

67
Q

What are the complications of hypertension?

A
  1. Nephrogenic: polyuria nocturia (hypotonic urine), nephrosclerosis, hematuria, proteinuria
  2. Ophthalmologic: retinal hemorrhage
  3. Cardiac: MI, CHF, coronary and peripheral artery disease, claudication, aortic dissection
  4. Neurologic: stroke, headache, nausea, anxiety
68
Q

What are the types of hypertension?

A
  1. Primary: idiopathic, 90% of cases. There is increase in TPR or increased CO. Obesity, stress, Type A personality, oral contraceptives. Common in African american
  2. Secondary: Usually caused second to renal disease. Other causes, Conn’s syndrome, pheochromocytoma, Cushing, Hyperthyroidism, diabetes, coarctation of aorta, preeclampsia & eclampsia
69
Q

What are the most common sites for atheromata formation?

A

In order of frequency:

  1. Abdominal aorta
  2. coronary arteries
  3. popliteal artery
  4. descending thoracic aorta
  5. internal carotid arteries
  6. Circle of Willis
  • Only in arteries, not veins
70
Q

What are the layers of the atheroma (from inside to outside)? And what are the complications?

A
  1. Fibrous cap (collagen, leukocytes, some smooth muscles)
  2. Cellular zone (smooth muscles, macrophages, lymphocytes)
  3. Central core (foam cells, cholesterol clefts, necrotic cells)
  4. Proliferating capillaries in advanced lesions
    * Thrombus may occur with occlusion of the vessel. Cholesterol emboli may also occur. Hemorrhage in the lesion is possible, or aneurysm
71
Q

Define fatty streaks

A

The first visible lesion before the formation of atheroma. They are yellow intimal lesions composed of lipid containing macrophages

72
Q

How is the atheroma formed?

A
  1. Endothelial injury due to hypertension, hyperlipidemia & high cholesterol, smoking, diabetes (causes hyaline deposition in vessel walls)
  2. Increased inflammatory cells adherence with thrombus formation at the site, with the release of chemical mediators that induce formation of smooth muscle cells
  3. Production of collagen and elastic fibers by the smooth muscle cells, followed by capillary formation from vasa vasorum, subsequent protein leakage with deposition of lipid in the plaque
73
Q

The risk of atherosclerosis correlates more with diastolic than systolic pressure in hypertension. T/F??

A

True

74
Q

The most vulnerable organ to arteriosclerosis is …..

A

the kidney

75
Q

Arteriosclerosis is …..

A

thickening of the intima in arterioles and small vessels, with narrowing of the lumen and ischemia of the involved tissue

76
Q

What are the types of arteriosclerosis?

A
  1. Hyperplastic: associated with malignant hypertension or necrotizing vasculitis. Characterized by onion skin hyperplasia (thickening of intima, deposition of basophilic substance, smooth muscle proliferation, hypertrophy of adventitia)
  2. Hyaline arteriosclerosis: associated with diabetes & old age.
77
Q

Emboli arising the venous circulation usually involve …….

A

the pulmonary circulation

* It may become a paradoxical emboli by passing via right to left shunt

78
Q

Arterial emboli often involves the ……

A

legs, then the brain, other viscera, the arms

* Arterial emboli show the characteristic lines of Zahn

79
Q

Atherosclerotic aneurysm usually occurs in …..

A

abdominal aorta, below the renal arteries

80
Q

Define syphlitic aneurysm

A

Occurs due to chronic damage to vasa vasorum of the aortic media by syphilis

81
Q

Microaneurysm occurs in ……. & ……

A
  1. cerebral vessels, secondary to hypertension
  2. Retinal vessels, as a result of diabetic vasculitis
    * Note that aneurysm occurs only in arteries
82
Q

What is the cause of dissecting aneurysm?

A

degeneration of the tunica media, allowing blood flow from the lumen to enter via an intimal tear and dissect through the layers of the media. Mostly in the aorta
* There is separation of intima and adventitia

83
Q

Define multifocal vasculitis and what is the main cause

A

It is wide spread inflammation of vessels, accompanied by patchy necrosis & thrombi formation
* Usually due to immune reaction

84
Q

Polyarteritis nodosa (PAN) is ……, the main cause is ….. . It is seen mostly in …..

A

systemic necrotizing vasculitis of small and medium sized vessels (at the bifurcations)

  • Hepatitis B is found in 30% of cases. Essentially, all lesions are antigen-antibody complexes
  • Mostly in the kidneys, heart, GIT, while the lungs are spared
85
Q

Define Temporal arteritis and its clinical features

A

Granulomatous inflammation of small and medium sized arteries. Most common in the temporal artery with no know cause
* Features: Headache and facial pain, fever, calcification of the jaw, weight loss, firm temporal arteries, visual disturbances

86
Q

What is the difference between Polyarteritis nodosa and Hypersensitivity (leukocytoclastic) angiitis?

A

Leukocytoclastic angiitis involves smaller vessels.

87
Q

Define thrombophlebitis, and what are the contributing factors for its formation?

A

inflammation and thrombus formation of veins. 90% are in the deep veins of the leg (DVT) usually above the popliteal fossa

  • Diagnosed by Virchow’s triad (hypercoagulability, endothelial injury, alteration in blood flow)
  • The thrombus may embolize, cause superinfection or recanalizes restoring flow
88
Q

What are the causes of thrombophlebitis?

A
  1. deficiency of antithrombin III, protein C & protein S
  2. CHF, MI, sluggish blood flow
  3. Immobilization (including bed rest)
  4. Neoplasm producing coagulation promoters
  5. Advanced age with sclerosing veins
  6. Pregnancy with pelvic veins obstruction
  7. Oral contraceptives (activates clotting)
  8. Tissue injury
89
Q

Thrombophlebitis is characterized by ……

A

localized pain, erythema, and edema
* Postphlebitic syndrome is symptoms that may occur as long-term complications of DVT. The symptoms are the same as thrombophlebitis

90
Q

Venous occlusion occurs due to ….., ……. or …….

A

DVT, thrombophlebitis or pregnancy (obstruction of flow)

91
Q

Varicose veins result from …..

A

increased intraluminal pressure (obesity, pregnancy, compression by tumors, valve and wall damage) with inadequate external support.
* More common in women

92
Q

What are the clinical features of varicosites?

A

edema, thrombosis, stasis dermatitis, ulceration

93
Q

Varicose veins are often a source of emboli. T/F??

A

False

* very rare, unlike DVT

94
Q

Define hemangiomas

A

Benign tumor of vascular endothelial cells.

  • In the capillaries, the tumor in unencapsulated
  • Usually in the skin and mucous membrane
95
Q

Define cavernous hemangiomas

A

sponge like tumors composed of dilated cavernous vascular spaces. It is made up of vessels and tissue not from the organ where it is situated
* Unlike capillary hemangioma, this one is disfiguring

96
Q

Define Telangiectasias

A

Developmental abnormality, but closely mimics benign hemangiomas.

  • It is an aggregation arterioles, capillaries and venules.
  • Also called Vascular ectasias
  • Telangiectasias blanch on pressure
97
Q

Define:

  1. Nevus flammeus
  2. Port wine stain
  3. Spider Telangiectasia
A
  1. flat birth mark on the head or neck. Regresses with time
  2. Grow proportionally with child. Appears on skin supplied by trigeminal nerve. Associated with glaucoma, meningeal angioma, and mental retardation
  3. Array of tiny arterioles, common in pregnant women and patients with cirrhosis. In men, it is related to high estrogen levels resulting from liver disease (alcoholism)
98
Q

Define Hemangiosarcoma

A

Atypical, anaplastic endothelial cell tumor that metastasizes. High mortality

99
Q

Hepatic angiosarcoma is ……

A

tumor due to toxins exposure

100
Q

Left side CHF results in ……., while CHF on the right side causes …….

A

pulmonary edema and different dyspneas, S3 & S4
peripheral edema
* Note that isolated right HF doesn’t normally occur

101
Q

What are the types of congestion?

A
  1. Active: due to vasodilation

2. Passive: due to decrease venous return.

102
Q

Saddle embolus is …..

A

large embolus that obstructs the bifurcation of the pulmonary artery

103
Q

The only time a DVT can cause stroke is through ……

A

paradoxical emboli

104
Q

Hypertension is usually accompanied by hypertrophy of …….

A

arteries and arterioles smooth muscle layer (not in capillaries)
* there is an increase in wall to lumen ratio

105
Q

Malignant hypertension is …… . The usual causes are …..

A

severe sudden increase in BP, a complication of secondary hypertension

  • There is renal failure, or eclampsia, preeclampsia
  • Usually in African Americans
  • AKA hypertensive urgency
106
Q

Aortic dissection most often ruptures into …..

A

the pericardial sac (hemopericardium), causing temponade

107
Q

Define Beck’s triad

A

Used to identify possible cardiac temponade

* There is: muffled heart sounds, jugular venous distension, low BP

108
Q

CPK enzyme increase is a clinical indicator for the damage of the following organs …….

A

Heart, skeletal muscles, brain

* Not found in liver

109
Q

The first two signs of heart failure are ….. & ……

A

exertion dyspnea

paroxysmal nocturnal dyspnea

Pathology (18 decks)

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