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Pathomorph - CREDIT 1 > Hemodynamic disorders, Thrombosis, Atherosclerosis - DONE > Flashcards

Hemodynamic disorders, Thrombosis, Atherosclerosis - DONE Flashcards

1
Q

Blood clot (latin: cruor, coagulum sanguinis):

A

a mass of coagulated blood.

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2
Q

Two types of blood clots:

A
  1. extravascularly during life

2. within the cardiovascular system after death (post mortem blood clot)

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3
Q

Thrombus (latin: ante mortem blood clot):

A

a mass of clotted blood formed within cardiovscular system during life.

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4
Q

Thrombosis:

A

Thrombosis designates the phenomenon of intravital coagulation of blood.

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5
Q

Virchow’s Triad:

A
  • Interrupted blood flow (stasis)
  • Endothelial injury
  • Hypercoagulability
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6
Q

Interrupted blood flow

A
  • Venous stasis
    • Long surgical operations
    • Immobilization
  • Turbulent flow
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7
Q

Endothelial injury:

A
  • Trauma to endothelial cells
    • Hypertension
    • Burn
    • Irradiation
  • Infections
  • Foreign material
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8
Q

Hypercoagulability:

A
  • Factor V (Leiden) mutations
  • Antithrombin III deficiency
  • Trauma or burn
  • Malignant neoplasms
  • Cigarette smoking
  • Obesity
  • Hormonal contraception
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9
Q

Blood clot (latin: cruor, coagulum sanguinis)

A

Macroscopically, intravascular post mortem clot:
a homogenous, gelatinous, elastic, moist coagulum with a smooth, glistening surface.

It produces a mould of the vessel and lacks attachment to its wall. It can be red or yellow.

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10
Q

Thrombus (ante mortem blood clot) macroscopically:

A

Macroscopically, thrombus presents as a dry, matt, friable mass, closely adhering to the vessel wall, and ranging in color from gray to red.

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11
Q

Thrombus (ante mortem blood clot) microscopically:

A

Microscopically both (blood clot and thrombus) are similar – They consist of fibrin framework with confined erythrocytes, leukocytes, platelets

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12
Q

Thrombus may undergo numerous changes. There are 4 main changes of the thrombus:

A
  1. Propagation
  2. Embolization
  3. Dissolution
  4. Organization and recanalization.
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13
Q

Propagation:

A

The thrombus may accumulate more platelets and fibrin (propagate), eventually leading to vessel obstruction.

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14
Q

Embolization:

A

Thrombi may dislodge and travel to other sites in the vasculature.

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15
Q

Dissolution:

A

Thrombi may be removed by fibrinolytic activity.

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16
Q

What does the term „organization” mean?

A

The term „organization” means the replacement of thrombus by connective tissue.

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17
Q

How does the “organization” happen?

A

Thrombus becomes penetrated by macrophages, fibroblasts, smooth myocytes and capillaries.

It is gradually dissolved, phagocytized by macrophages and replaced by proliferating connective tissue.

The vascular lumen becomes narrowed or occluded.

The dilatation of capillaries which are present in the organized thrombus restores to a limited degree the blood flow („recanalization”)

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18
Q

Organized thrombus microsopically:

A

Histological appearance of organized thrombus depends on its age.

In general, lumen of the vessels is obstructed by fibrous connective tissue or, earlier, by highly cellular granulation tissue.

Dilated capillaries are present.

Haemosiderin visible in the slides derives from breakdown of erythrocytes phagocytized by macrophages.

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19
Q

Thrombosis may result in:

A
  1. Ischemia by occlusion or narrowing of arterial lumen
  2. Passive congestion due to the impairment of venous blood outflow without an efficient venous collateral circulation
  3. Thromboembolism after the detachment of an entire thrombus or its fragments
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20
Q

Where does the embolism come from (?*)

A

Embolism consists in occlusion of a vessel by an embolus (=stopper) disloged by blood from broader segment of the circulatory system.

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21
Q

What is Thromboembolism?

A

Thromboembolism is the most frequent representative of solid embolism.

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22
Q

What is thromboembolism?

A

Thromboembolism is the most frequent representative of solid embolism.

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23
Q

Where does the thromboembolism originate from?

A

It may derive from:

  • heart
  • arteries
  • veins (particularly those of the lower limbs and pelvis)
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24
Q

What is the most frequent representative of solid embolism?

A

Thromboembolism

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25
Q

Where does most of the venous emboli originate?

A

In more than 95% of instances, venous emboli originate from deep leg vein thrombi above the level of the knee.

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26
Q

Where does the large emboli derive from?

A

Large embolus derived from a lower extremity deep venous thrombosis and now impacted in a pulmonary artery branch.

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27
Q

What is the most frequent fat embolism?

A

Pulmonary bone marrow embolism is the most frequent fat embolism.

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28
Q

Microscopic fat globules may be found in the circulation:

A
  • fractures of long bones (which have fatty marrow)

- soft tissue trauma and burns.

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29
Q

Who usually get traumatic fat embolism?

A

Although traumatic fat embolism occurs in some 90% of individuals with severe skeletal injuries, less than 10% of such patients have any clinical findings.

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30
Q

What characterizes fat embolis?

A

Fat embolism syndrome is characterized by pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia.

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31
Q

When does the symptoms of fat embolism occur and what happens?

A

Symptoms typically begin 1 to 3 days after injury, with sudden onset of tachypnea, dyspnea, and tachycardia.

32
Q

Pulmonary bone marrow embolism (Macroscopically)

A

lungs are dark red and oedematous

33
Q

Pulmonary bone marrow embolism (Microscopically)

A

reveals alveolar capillaries distended by globules of fat which present as empty spaces since lipid is removed by fat-solving reagents used in routine processing of the specimen.

Additionally, lung tissue exhibits hyperaemia and sometimes oedema

34
Q

What does the identification of fat emboli require?

A

Identification of fat emboli requires special techniques of preparation i.e. Sudan stain.

35
Q

Infarct (infarction)

A

means a necrotic focus which results from insufficient inflow of arterial blood to a given territory in situation of ineffective collateral circulation or from a sudden stop in the outflow of venous blood, simultanously with inadequate arterial supply.

36
Q

Infarcts are grossly subdivided into:

A
  • ischaemic (white)

- haemorrhagic (red)

37
Q

White infarct =

A

ischaemic infarct

38
Q

Red infarct =

A

haemorrhagic infarct

39
Q

Where does the ischaemic infarct occur?

A

Ischaemic infarct occurs in organs with anatomically or functionally terminal arteries such as:

  • heart
  • spleen
  • kidney
40
Q

What is most commonly caused by arterial occlusion arising from thrombosis or embolism?

A

ischaemic (white) infarct

41
Q

What most commonly cause ischaemic (white) infarct?

A

It is most commonly caused by arterial occlusion arising from thrombosis or embolism

42
Q

How is the ischaemic (white) infarct macroscopically?

A

Macroscopically it has a shape of cone with its base at the periphery of organ and apex pointing towards occluded artery.

In other words: Sharply demarcated white infarct in the kidney.

43
Q

Fresh ischaemic infarct =

A

Infarctus anaemicus recens

44
Q

What is the characteristic sign of fresh ischaemic infarct?

A

Histological examination reveals characteristic signs of ischaemic coagulative necrosis.

45
Q

What does the necrotic tissue look like? What is it composed of?

A

Necrotic tissue is entirely blurred with lost cytological details, and indistinguishable individual cells, although architectural features are preserved for some nuclei.

It is composed of homogenous shadows of cells lacking their nuclei.

In places, however, there are remnants of nuclei representing various phases of damage (under high magnification), such as: pyknosis, karyorhexis, karyolysis.

46
Q

Pyknosis:

A

nuclei are shrunken and more intensively stained with hematoxylin

47
Q

Karyorhexis:

A

nuclei undergo fragmentation

48
Q

Karyolysis:

A

nuclei progressively lose ability to stain with hematoxilin and eventually disappear

49
Q

What surrounds the necrotic area?

A

Necrotic area is surrounded by a rim of neutrophils which in turn is encircled by a zone of hyperaemia.

50
Q

What reflect the inflammatory reaction to the presence of necrotic tissue?

A

Both hyperaemia and cellular exudate reflect the inflammatory reaction to the presence of necrotic tissue

51
Q

Microscopic appearance of a fresh renal infarct:

A

At the far right is normal kidney, then to the left of that hypraemic kidney that is dying, then to the left of that pale pink infarcted kidney in which both tubules and glomeruli are dead

52
Q

Pulmonary haemorrhagic infarct =

A

Infarctus haemorrhagicus pulmonis

53
Q

Haemorrhagic infarct of lung:

A

The term „haemorrhagic infarct of lung” designates local necrosis of lung tissue (interalveolar septa) accompanied by massive haemorrhage within pulmonary parenchyma.

54
Q

What causes haemorrhagic infarct of lung?

A

The lesion results from embolic (very rarely thrombotic) occlusion of a peripheral branch of pulmonary artery but its appearence is determined by efficiency of left ventricle.

55
Q

How is the lung tissue supported?

A

Lung tissue is supported by

  • DOUBLE arterial supply pulmonary circulation
  • the bronchial ONE
56
Q

In case of normal cardiovascular condition

A

In case of normal cardiovascular condition (efficient left ventricle), pulmonary embolism does not lead to infarction because bronchial circulation preserves viability of lung tissue; however lead to extravasations into alveolar spaces.

The resulting lesion, identical grossly with haemorrhagic infarct of lung referred to as post-embolic focus.

In favorable cases it entirely disappears with restoration of pulmonary parenchyma to its normal state.

57
Q

In case of passive congestion of lungs:

A

In case of passive congestion of lungs in the course of left ventricular failure, bronchial circulation fails to sustain the pulmonary parenchyma and infarction ensue.

(contrary to normal cardiovascular condition)

58
Q

Pulmonary haemorrhagic infarct (Ma):

A

The lesion is cone-shaped with its base at the pleural surface, dark red, firm

59
Q

Pulmonary haemorrhagic infarct (Mi):

A

histological examination reveals stuffing alveolar spaces with blood;
necrotic alveolar walls, full of blood, are poorly visible within masses of accumulated erythrocytes

60
Q

What does the atherosclerosis afflict?

A

Atherosclerosis afflicts the intima of arteries of the systemic circulation.

61
Q

What characterizes atherosclerosis?

A

It is characterized by intimal lesions called atheromas, or atheromatous plaques, which protrude into and obstruct vascular lumens.

62
Q

Where does the atherosclerotic plaque develop?

A

Atherosclerotic plaques develop primarily in:

  • elastic arteries (e.g., aorta, carotid arteries)
  • large and medium-sized muscular arteries (e.g., coronary arteries).
63
Q

What are the major consequences of atherosclerosis?

A
  • Myocardial infarction
  • Cerebral infarction (stroke)
  • Aortic aneurysms
  • Peripheral vascular disease
64
Q

What are the key processes in atherosclerosis?

A

The key processes in atherosclerosis are intimal thickening and lipid accumulation.

65
Q

What are the earliest lesions of atherosclerosis?

A

Fatty streaks are the earliest lesions of atherosclerosis.

66
Q

What are fatty streaks composed of?

A

They are composed of lipid-filled foam cells.

They are not significantly raised and thus do not cause any disturbance in blood flow.

67
Q

What does the fatty streaks look like in the beginning?

A

Fatty streaks begin as multiple yellow, flat spots less than 1 mm in diameter.

68
Q

What is the size of fatty streaks in the beginning?

A

1 mm in diameter.

69
Q

What does the atheroma or atheromatous (atherosclerotic) plaque constitute of?

A

Initially, as a yellow streak, it constitutes the accumulation of lipoproteins with cholesterol, phagocytized by myocytes and macrophages (yellow plaque).

Then is covered by a firm, white fibrous cap (white plaque)

70
Q

Atheroma or atheromatous (atherosclerotic) plaque (google definition):

A

degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue, and leading to restriction of the circulation and a risk of thrombosis

71
Q

What is the size of atheromatous plaques?

A

from 0.3 to 1-2 cm in diameter

72
Q

What does the atherosclerotic lesions usually involve?

A

Atherosclerotic lesions usually involve only a partial circumference of the arterial wall (focal lesions).

Focal and sparsely distributed at first, atherosclerosis lesions become increasingly numerous and diffuse as the disease progresses.

73
Q

Atherosclerotic plaques have three principal components:

A
  1. cells, including SMCs, macrophages, and other leukocytes
  2. ECM, including collagen, elastic fibers, and proteoglycans
  3. intracellular and extracellular lipids
74
Q

What does the three principal components of atherosclerotic plaques form?

A
  • superficial fibrous cap

- necrotic core

75
Q

Superficial fibrous cap:

A

superficial fibrous cap (composed of SMCs and relatively dense ECM; beneath and to the side of the cap is a cellular area consisting of macrophages, SMCs, and T lymphocytes.

76
Q

Necrotic core:

A

containing a disorganized mass of lipid (primarily cholesterol and cholesterol esters), cholesterol clefts, debris from dead cells, foam cells, fibrin, variably organized thrombus, and other plasma proteins.

Finally, particularly around the periphery of the lesions, there is usually evidence of neovascularization (proliferating small blood vessels).

77
Q

What are foam cells?

A

Foam cells are large, lipid-laden cells that derive predominantly from blood monocytes (tissue macrophages)

Pathomorph - CREDIT 1 (3 decks)

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