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pathoanatomy > circulatory disturbances > Flashcards

circulatory disturbances Flashcards

1
Q

Venous stasis (congestion) definition

A

Engorgement of capillaries and veins due to impaired drainage.

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2
Q

Venous stasis (congestion) - etiologic factors

A
  • Right heart insufficiency leading to hyperemia
  • Stenosing venous disease (obliteration of a vein)
  • Dilatative venous disease (varices).
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3
Q

Acute venous stasis involves

A

hypoxic injury only

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4
Q

Chronic venous stasis involves

A

hypoxic injury and increased hydrostatic pressure

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5
Q

Pulmonary edema is due to

A

an increase of fluid in alveolar wall (interstitium) which, if severe, subsequently affects alveolar spaces

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6
Q

The main cause of pulmonary edema is

A

failure of the left ventricle, causing increased pressure in the alveolar capillaries

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7
Q

heart failure cells

A

Heart failure cells are macrophages in the lungs that contain hemosiderin from phagocytosed red blood cells. They appear after capillary rupture in conditions like pulmonary edema and can be identified with Prussian blue stain.

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8
Q

right – sided cardiac failure

A

causes back pressure in the systemic venous system, which is transmitted back down the hepatic vein to the central veins (particularly seen in tricuspid valve incompetence)

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9
Q

What condition is associated with hepatic congestion in constrictive pericarditis?

A

Chronic passive venous congestion, also known as “nutmeg liver”.

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10
Q

Describe the macroscopic appearance of “nutmeg liver”.

A

Dark areas where centrilobular zones are congested by blood and pale peri-portal areas.

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11
Q

What can occur if arterial hypotension complicates right-sided cardiac failure?

A

Necrosis of the centrilobular hepatocytes.

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12
Q

What biological marker indicates necrosis of centrilobular hepatocytes?

A

Elevated serum transaminase levels.

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13
Q

What does long-term chronic congestion lead to in the liver?

A

Fibrosis of the necrotic parenchyma, producing nodular congestive cirrhosis.

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14
Q

Renal congestion

A

It is a chronic passive venous congestion of the kidney. It occurs in the right ventricular failure or due to obstruction or compression of the renal vein

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15
Q

Atheroma is a

A

a specific degenerative disease affecting large and medium size arteries in systemic circulation

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16
Q

Risk factors for atheroma:

A

Hyperlipidemia
Hypertension
Diabetes mellitus
Cigarette smoking

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17
Q

Atheromatous plaques in coronary arteries may be one of 2 types:

A

eccentric plaques (rich in lipid and affect only one segment of the wall)
concentric plaques (rich in collagen and affect the whole wall of the artery

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18
Q

The stages of evolution of a plaque:

A

fatty streaks
fibro-lipid plaque
complicated plaque

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19
Q

The complications of atherosclerosis:

A

Ischemia
Aneurysm formation
Calcification
Thrombus formation

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20
Q

Thrombosis definition

A

A clotted structured, solid mass of blood forming in the circulation in a living individual (intra vitam) is called a “thrombus

21
Q

What distinguishes a thrombus from a coagulum?

A

A thrombus is structured and forms within the circulatory system, while a coagulum is unstructured and forms outside the circulatory system.

22
Q

How can a thrombus be differentiated from an agonic clot?

A

An agonic clot is a soft mass of blood forming in the circulation of a dead body (post-mortem), while a thrombus forms in a living organism.

23
Q

A thrombus is composed of elements derived from activation of the coagulation cascade:

A
  1. Aggregated platelets
  2. Insoluble fibrin derived from soluble plasma fibrinogen
  3. Entrapped red cells
24
Q

Three main factors predispose to thrombus formation

A
  1. Endothelial dysfunction
  2. Change in the flow pattern of blood
  3. Hyper coagulability due to an increased concentration of fibrinogen
25
Q

How do thrombi formed in slow-moving blood in veins differ from those formed in fast-moving blood in arteries?

A

Thrombi in veins have a high proportion of trapped red cells and a low ratio of fibrin to platelets, appearing soft, reddish, and gelatinous (red thrombi). Thrombi in arteries have a relatively high platelet-to-fibrin content, appearing firm, pale, and with prominent laminations (white or hyaline thrombi).

26
Q

What is a mixed thrombus?

A

A mixed thrombus is composed of one or more laminated thrombi with interspersed or apposed red thrombi. They appear as long occlusive casts of the vascular lumen.

27
Q

The clinical rule of thumb for a red thrombus is

A

it arises unnoticed in the leg; a gust of wind will carry it away.

28
Q

The clinical rule of thumb for thrombus adhesion is that:

A

a red thrombus “floats” (hardly adheres at all),
a white thrombus “sticks” (adheres slightly), and
an intermediate thrombus “adheres”.

29
Q

The commonest site for thrombi is in

A

the veins of the lower legs of bedridden patients.

30
Q

Signs of thrombosis include:

A
  • tenderness of veins to palpation
  • foot pain upon dorsiflexion
  • edema in the leg
31
Q

Therapeutic thrombolysis comprises

A

fibrinolytic agents (such as streptokinase or staphylokinase) and oral anti-coagulants (such as heparin)

32
Q

There are 4 main outcomes following vascular occlusion by a thrombus:

A
  • Propagation: enlargement of the thrombus along the vessel
  • Lysis: by the fibrinolytic system (this process may be assisted by therapeutic administration of streptokinase)
  • Organization: by ingrowth of granulation tissue from the vessel wall. New vascular channels develop, bridging the site of occlusion and re-establishing the flow (canalization)
  • Embolism: fragments of thrombus may break off and carried by the circulation to impact in other vessels
33
Q

Embolism definition

A

Process in which certain substances enter the bloodstream in larger vessels as coherent bodies (emboli) and lodge in and occlude smaller vessels.

34
Q

Orthograde Embolism:

A

Occurs in the direction of blood flow, usually in arteries.

Emboli from the left side of the heart impact cerebral, renal, or splenic arteries. Those from the veins of the lower limbs hit the lungs.

35
Q

Retrograde Embolism:

A

Very rare.
Example: Tumor cells embolize opposite to blood flow, from prevertebral venous plexus to cerebral veins due to increased abdominal pressure.

36
Q

Crossed Embolism (Paradoxical Embolism):

A

Rare.
Occurs with an open foramen ovale or left atrial septal defect.
Embolus from pulmonary vessels can pass into systemic circulation.
Example: Embolus from hemorrhoidal veins to the middle cerebral artery.

37
Q

What is the usual precursor to pulmonary embolism?

A

Thrombosis in leg veins, often deep veins in the calf.

38
Q

What is the key principle in preventing pulmonary embolism?

A

Prevention of leg vein thrombosis

39
Q

What is the typical impact of small pulmonary emboli?

A

They affect peripheral branches of the pulmonary artery, causing pulmonary infarcts often associated with pleurisy

40
Q

What are the common clinical symptoms of pulmonary embolism?

A

Chest pain, cough, and bloody sputum.

41
Q

What is the potential consequence of a large pulmonary embolus?

A

It may obstruct a major pulmonary artery, leading to sudden death (massive pulmonary embolus).

42
Q

What is a premonitory embolus?

A

A small embolus with infarction that may precede a much larger, fatal embolus.

43
Q

Types of infarct

A

Anemic Infarct (white infarct): Tissue necrosis due to persistent loss of blood supply from an anatomic terminal artery (without collateral circulation) or a functional terminal artery (with insufficient collateral circulation).

Hemorrhagic Infarct (red infarct):
Tissue necrosis due to persistent occlusion of a terminal artery with slight, insufficient residual blood supply.

44
Q

There are 3 main patterns of myocardial infarction:

A
  1. Regional full thickness (90%)
  2. Regional subendocardial
  3. Circumferential subendocardial
45
Q

Sudden cardiac death is due to

A

either infarction or arrhythmias

46
Q

A well developed infarct has 3 areas:

A

a necrotic area, an inflammatory infiltrate and a hyperemic border

47
Q

Myocardial infarction - Long-term complications (> 2 weeks):

A

Chronic intractable left-heart failure
Ventricular aneurysm
Recurrent myocardial infarction
Dressler’s syndrome

48
Q

Myocardial infarction - Short-term complications (< 2 weeks):

A

Cardiac dysrhythmia
left ventricular failure
Rupture of the ventricular wall
Papillary muscle dysfunction
Mural thrombuCardiac dysrhythmia (ventricular fibrillation, brady-arrhytmias)
Development of left ventricular failure
Rupture of the ventricular wall with cardiac tamponade and rapid death
Papillary muscle dysfunction
Mural thrombus formation with subsequent embolization to: brain, spleen, kidney
Acute pericarditis

49
Q
A

pathoanatomy (7 decks)

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