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Part 1 > CV System Pathology 1 > Flashcards

CV System Pathology 1 Flashcards

1
Q

What are the two types of hemorrhage?

A

Acute, sudden, massive loss of blood

Chronic - low-grade, mild leakage of blood

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2
Q

What are some of the complications of hemorrhage?

A

(1) Hemorrhagic shock, which occurs when more than 15% of blood volume is lost.

(2) Hemorrhagic strokes, hemopericardium in areas sensitive to hemorrhage.

(3) Iron deficiency from chronic blood loss.

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3
Q

What is an exudate?

A

Edema fluid containing high amounts of protein and inflammatory cells

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4
Q

What is a transudate?

A

Edema fluid with a low protein content, not usually associated with inflammation

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5
Q

Edema due to reduced plasma osmotic pressure can be due to what?

A

Generally this is due to a loss of albumin. For example, nephrotic syndrome and cirrhosis can both lead to low albumin levels and thus edema

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6
Q

Impaired lymphatic drainage leads to what type of edema?

A

Lymphedema

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7
Q

What mechanisms are involved in compensated, early, nonprogressive shock?

A

(1) Increased heart rate and peripheral resistance to increase blood flow to vital organs

(2) Increased respiratory rate to remove carbon dioxide and raise pH

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8
Q

What occurs in the body during decompensated, progressive shock?

A

(1) Oxygen levels fall, causing vasodilation and decreased blood flow to the heart

(2) Cell injury and cell death occurs from lack of oxygen

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9
Q

What occurs in the body during the irreversible stage of shock?

A

(1) Acute tubular necrosis occurs in the kidney, which is initially reversible

(2) Full renal failure occurs as acute tubular necrosis becomes more severe

(3) Metabolic acidosis, coma and heart failure develop

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10
Q

What initiates clot (thrombus) formation?

A

Damage to endothelial cells that causes interactions between platelets, exposed collagen, and blood proteins.

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11
Q

What is the name of the factor that causes platelets to adhere to the exposed subendothelial surface in clot formation?

A

von Willebrand’s factor

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12
Q

The extrinsic coagulation pathway is initiated by what tissue factor?

A

Thromboplastin. Extrinsic pathway is activated by external trauma that causes blood to escape from the vessel. Intrinsic pathway is activated by trauma within the vessel.

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13
Q

What causes thrombosis?

A

Abnormalities within the body that cause damage to endothelial cells, promote coagulation, or disturb blood flow. Thrombosis is a local clot within a blood vessel.

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14
Q

What are the symptoms of chronic deep venous insufficiency in the legs?

A

Pigmentation, edema, skin induration, ulceration

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15
Q

What is the most common cause of death in Western industrialized countries?

A

Arterial thrombosis (atherosclerosis) due primarily to cigarette smoking

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16
Q

What is an embolus?

A

A piece of a thrombus that has broken off, entered the bloodstream, and become trapped in the vasculature (thromboembolism)

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17
Q

Where do leg venous thrombi commonly lodge?

A

In the lung, after entering the right atrium of the heart through the inferior vena cava and passing through the ventricle (pulmonary emboli)

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18
Q

Where do arterial emboli that break off from mural thrombi in the heart or major arteries commonly lodge?

A

(1) Branches of the carotid artery, causing stroke

(2) Branches of the mesenteric artery, causing hemorrhagic infarction

(3) Branches of the renal artery, causing renal cortex infarcts

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19
Q

What is the name of an embolus that lodges at the bifurcation of the main pulmonary artery?

A

Saddle embolus

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20
Q

What are the two types of infarcts?

A

(1) Anemic - white or pale in areas without collateral blood supply

(2) Hemorrhagic - red, in areas where collateral blood supply may be insufficient

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21
Q

What causes infarction?

A

Blockage or lack of blood flow to an organ

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22
Q

What is the primary pathological condition that leads to cardiac tamponade?

A

Pericardial effusion (which is fluid accumulation in the pericardial cavity and thus puts pressure onto the heart and affect its function).

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23
Q

How is arteriosclerosis defined?

A

Sclerosis of the arteries. Sclerosis means to harden.

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24
Q

What types of arteries are affected by atherosclerosis?

A

Atherosclerosis is arteriosclerosis of large elastic arteries, including the aorta, coronary, common iliac, femoral, popliteal, internal carotid, and cerebral arteries

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25
Q

What are atheromas?

A

Lesions that develop on artery walls comprised of macrophages, low-density lipoprotein (ldl), fibrin, and smooth muscle. They are usually asymptomatic for 20-40 years until they become symptomatic, complicated plaques

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26
Q

How does arteriosclerosis most probably begin?

A

Damage to vascular endothelium’s intima layer. This leads to plaque buildup and thus vessel hardening.

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27
Q

During starvation and poorly controlled diabetes, what form of fuel can the heart use?

A

Ketone bodies. Ketones can be used in the TCA cycle to generate ATP.

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28
Q

When oxidized lipids are ingested by macrophages, what do they form?

A

Foam cells. Foam cells are particularly indicative of early atherosclerosis formation.

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29
Q

What stages are involved in polyarteritis nodosa (pan)?

A

(1) Immune complex deposits in walls of arteries in the first stage, initiating the complement cascade and calling in neutrophils

(2) Macrophages and fibroblasts replace neutrophils in the healing stage, and fibrosis occurs

(3) In the last stage, a cord of collagen forms in the vessel with calcium deposits, occluding the lumen

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30
Q

What is a hallmark of pan?

A

To find lesions in all three stages of development in one vessel

31
Q

What is the most common form of vasculitis?

A

Temporal arteritis. Most patients who develop this condition are over 50 years old.

32
Q

What does thromboangiitis obliterans (Buerger’s disease) cause?

A

Ischemia, pain, gangrene, necrosis of the digits

33
Q

How is Raynaud’s phenomenon different from Raynaud’s disease?

A

Raynaud’s phenomenon is usually secondary to an underlying disorder, such as scleroderma or lupus, while Raynaud’s disease occurs independently.

34
Q

Where do aneurysms occur?

A

Arteries that are weak or thin. Aneurysms is a ballooning of the artery wall at a weakened spot.

35
Q

What are two common types of aneurysms?

A

(1) Atherosclerotic aneurysms - occur in abdominal aorta or iliac arteries

(2) Berry aneurysms - congenital defects in cerebral arteries, most usually the Circle of Willis

36
Q

How does the heart adapt to hypertension?

A

(1) Increase wall thickness –> cardiac hypertrophy

(2) To dilate the heart chamber (Frank-Starling mechanism or law) –> Cardiac dilation

37
Q

What occurs in an aortic dissection?

A

The aortic intima tears, allowing blood to enter other histologic layers, and potentially leading to aortic rupture

38
Q

What is the most dangerous form of varicose veins?

A

Esophageal varices. These may suddenly rupture leading to severe bleeding and thus death.

39
Q

What are the two versions of venous thrombosis?

A

(1) Acute inflammation of the vein (thrombophlebitis)

(2) No inflammation (phlebothrombosis)

40
Q

What conditions promote thrombosis?

A

Blood stasis in the legs from immobilization, cardiac failure, pregnancy or varicose veins.

41
Q

What are common hemangiomas?

A

Port wine stains, strawberry marks, cavernous hemangiomas, and vascular spiders

42
Q

When the heart experiences chronic or acute insults what happens first?

A

Compensation

43
Q

What occurs with right-sided congestive heart failure (chf)?

A

(1) Imbalance in Frank-Starling forces or mechanisms

(2) Leading to dilation

(3) Hypertrophy and enlargement

(4) Failure of the right ventricle

44
Q

What causes right-sided congestive heart failure?

A

Secondary to left-sided chf or lung disease (cor pulmonale). If the left side of the heart is dysfunctional, the blood from that left side of the heart backs up into the lungs and consequently back up into the right ventricle and affects that right side’s function.

45
Q

What occurs with left-sided congestive heart failure?

A

(1) Imbalance in Frank-Starling forces

(2) Dilation

(3) Hypertrophy and enlargement

(4) Failure of the left ventricle

46
Q

What causes left-sided congestive heart failure?

A

Acute myocardial infarction. Myocardial infarctions impair contractility and thus causes dysfunctional systole. This then affects the left side of the heart since it’s responsible for contracting the most.

47
Q

What mechanisms of compensation are involved in congestive heart failure?

A

(1) Baroreceptor response

(2) Shift in oxygen-hemoglobin dissociation curve

(3) Increase in blood volume

(4) Myocyte hypertrophy

48
Q

What four basic syndromes occur with ischemic heart disease?

A

Angina pectoris

Myocardial infarction

Chronic ischemic heart disease

Sudden cardiac death

49
Q

What causes ischemic heart disease?

A

Reduced coronary blood flow, increased myocardial demand, and decreased oxygen in the blood

50
Q

What are the two types of damage that occur with myocardial infarction (MI)?

A

(1) Transmural - entire cardiac wall develops myocardial necrosis

(2) Subendocardial - inner one-third of heart wall develops myocardial necrosis

51
Q

What is the most common form of angina?

A

Stable angina. Stable angina is pain that occurs after psychological or physical stress due to less blood flow to the heart. Unstable angina occurs at rest.

52
Q

Which forms of angina are helped by nitroglycerin?

A

Stable angina and Prinzmetal’s angina. Nitroglycerin helps dilate and thus relax the vascular smooth muscle.

53
Q

Which form of angina is not helped by nitroglycerin?

A

Unstable angina

54
Q

What are some of the complications of ischemic heart disease after MI?

A

Arrhythmias

Myocardial rupture

Mural thrombosis and embolism

Ventricular aneurysm

Ruptured papillary muscle

MI occurs when the heart is deprived from oxygen for too long and thus deprived from a vital compound for proper cardiac functions.

55
Q

What is rheumatic heart disease?

A

Negative sequelae from infection with Group A beta hemolytic Streptococcus pyogenes. This bacteria within the bloodstream consequently damages the heart valves.

56
Q

How does rheumatic heart disease develop?

A

A Type II hypersensitivity reaction causes a cross-reaction of strep antibodies with heart tissue. Inflammation of all layers of the heart and damage to heart valves occurs

57
Q

What physical signs are associated with mitral valve prolapse?

A

(1) Audible midsystolic click

(2) A late systolic murmur consistent with mitral regurgitation

58
Q

What is the classic triad of aortic stenosis?

A

(1) Angina (aggravated by exertion and relieved by rest)

(2) Dyspnea (paroxysmal nocturnal and on exertion)

(3) Exertional Syncope

59
Q

Where is an aortic stenosis murmur best heard?

A

The sound radiates to the apex (though it may radiate to the carotids).

60
Q

What causes acute endocarditis?

A

Staphylococcus aureus, secondary to systemic infection. Staph. aureus can cause rapid destruction to the endocardium.

61
Q

What causes subacute bacterial endocarditis?

A

Less virulent organisms, such as Streptococcus viridans. Strep. viridans usually affect people with existing heart damage.

62
Q

What are some common causes of myocardial infections?

A

(1) Bacterial, such as staph, strep and diphtheria

(2) Rickettsial, such as typhus, Rocky Mountain Spotted Fever

(3) Viral, including Coxsackie, influenza and echo viruses

(4) Parasitic, including toxoplasmosis, trichinosis

63
Q

What is dilated cardiomyopathy?

A

Cardiomyopathy leading to ventricular dilation, commonly caused by the death of myocardial cells.

64
Q

What is restrictive cardiomyopathy?

A

Cardiomyopathy with rigid ventricular walls, the most rare type.

65
Q

What is hypertrophic cardiomyopathy?

A

Congenital, acquired or idiopathic cardiomyopathy with significant ventricular hypertrophy.

66
Q

As of 2009, hypertrophic cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic right ventricular dysplasia have been linked with what causative factor?

A

A mutation of a single gene that results in altered structural proteins.

67
Q

Hemopericardium may cause what condition?

A

Cardiac tamponade, a restriction in the filling of the heart. Hemopericardium occurs when blood fills the pericardial sac.

68
Q

What are the three types of acute pericarditis?

A

(1) Fibrinous - caused by uremia, viral infection, myocardial infarction

(2) Purulent - caused by bacterial infection

(3) Hemorrhagic

69
Q

Chronic fibrosing pericarditis may cause what condition?

A

Constrictive pericarditis. When myocytes are replaced by fibrosis, it can’t typically expand as much.

70
Q

Serous pericarditis is also known by what other name?

A

Pericardial effusion

71
Q

What four congenital defects are found in tetralogy of Fallot?

A

Ventricular septal defect

Pulmonary stenosis

Overriding aorta

Hypertrophy of the right ventricle

The combination of these 4 defects defines this condition.

72
Q

What are the most common congenital heart defects?

A

Interventricular septal defects

73
Q

What are some of the causes of chronic cor pulmonale?

A

COPD

Pulmonary interstitial fibrosis

Cystic fibrosis

Pulmonary arteritis

Chest movement disorders

Metabolic acidosis

Cor pulmonale occurs when right-sided heart enlargement is due to lung dysfunction. “Cor” refers to the heart. “Pulmonale” means relating to lungs.

Part 1 (73 decks)

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