pt3 Flashcards

(45 cards)

1
Q

In which tissues does coagulative necrosis typically occur?

A

All tissues except the brain following hypoxic injury.

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2
Q

What are the key microscopic features of coagulative necrosis?

A

Preservation of cell architecture with loss of nuclei and coagulated eosinophilic cytoplasm.

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3
Q

What type of necrosis is characteristic of bacterial infections and CNS hypoxic injury?

A

Liquefactive necrosis.

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4
Q

What causes liquefactive necrosis?

A

The accumulation of inflammatory cells, leading to enzymatic digestion of dead cells into a liquid mass.

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5
Q

What is the gross appearance of caseous necrosis?

A

A cheesy, yellow-white appearance due to tissue destruction, commonly seen in tuberculosis.

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6
Q

What disease is most commonly associated with caseous necrosis?

A

Tuberculosis.

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7
Q

What is fat necrosis?

A

A focal area of fat destruction due to pancreatic lipase release, commonly seen in acute pancreatitis.

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8
Q

What is a characteristic feature of fat necrosis?

A

White chalky calcium soap deposits at lipid breakdown sites.

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9
Q

What is apoptosis?

A

A regulated process of programmed cell death that removes unwanted or damaged cells without causing inflammation.

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10
Q

How does apoptosis differ from necrosis?

A

Apoptosis is controlled and does not cause inflammation, whereas necrosis is uncontrolled and triggers inflammation.

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11
Q

What happens when apoptosis is reduced?

A

Cells accumulate, leading to conditions like cancer (neoplasia).

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12
Q

What happens when apoptosis is excessive?

A

Excessive cell loss, leading to conditions like atrophy.

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13
Q

What are the main cellular events in apoptosis?

A
  • DNA fragmentation
  • Cytoskeletal breakdown
  • Mitochondrial dysfunction
  • Cell shrinkage
  • Formation of apoptotic bodies
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14
Q

What nuclear changes occur in apoptosis?

A

Pyknosis (nuclear shrinkage) followed by karyorrhexis (nuclear fragmentation).

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15
Q

How are apoptotic bodies cleared from the body?

A

They are rapidly phagocytosed by neighbouring cells or immune cells.

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16
Q

How is apoptosis regulated?

A

By an intracellular program involving pro-apoptotic and anti-apoptotic factors.

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17
Q

What are two examples of pathological apoptosis?

A
  1. Radiation-induced apoptosis
  2. Viral infection-induced apoptosis
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18
Q

What are the key differences between necrosis and apoptosis?

A
  • Necrosis: Uncontrolled, inflammatory, involves large groups of cells.
  • Apoptosis: Controlled, non-inflammatory, affects individual cells.
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19
Q

What happens to cellular contents in necrosis vs. apoptosis?

A
  • Necrosis: Leakage of cell contents.
  • Apoptosis: Cellular components are neatly packaged into apoptotic bodies.
20
Q

What is the most likely type of necrosis seen in the brain?

A

Liquefactive necrosis.

21
Q

Why does liquefactive necrosis occur in the brain after ischemic injury?

A

The brain lacks structural proteins that can maintain architecture after cell death, leading to complete tissue digestion.

22
Q

What is haemostasis?

A

A tightly regulated process that keeps blood fluid in normal vessels while allowing clot formation at injury sites.

23
Q

What are the three main components of haemostasis?

A
  1. Vascular wall (endothelium)
  2. Platelets
  3. Coagulation cascade
24
Q

How is thrombosis different from haemostasis?

A

Thrombosis is a pathological process where a solid mass of blood components forms inappropriately within the vascular system.

25
What is the main risk of thrombosis in the vascular system?
Thrombi are poorly attached and prone to fragmentation, which can cause embolism.
26
What are the three major factors that contribute to thrombosis?
Virchow’s Triad: 1. Endothelial injury (e.g., trauma, atherosclerosis) 2. Abnormal blood flow (stasis or turbulence) 3. Hypercoagulability (thrombophilia)
27
How does endothelial injury promote thrombosis?
* Exposes the extracellular matrix (ECM) * Allows platelet adhesion * Triggers the release of tissue factor, activating the clotting cascade
28
What type of abnormal blood flow is associated with arterial and venous thrombosis?
* Turbulence → Contributes to arterial and cardiac thrombosis * Stasis → Contributes to venous thrombosis
29
What is hypercoagulability, and what are common causes?
* Increased tendency of blood to clot * Can be due to genetic factors (e.g., Factor V Leiden mutation) or acquired factors (e.g., prolonged immobility, pregnancy, cancer).
30
Where do arterial thrombi typically form?
At sites of turbulence or endothelial injury, often superimposed on atherosclerosis.
31
What are common sites of arterial thrombosis?
* Coronary arteries (heart attack) * Cerebral arteries (stroke) * Femoral arteries (limb ischemia)
32
How do arterial thrombi appear microscopically?
They consist of alternating layers of platelets, fibrin, and red blood cells, known as lines of Zahn.
33
Where does venous thrombosis usually occur?
In superficial or deep veins of the leg (deep vein thrombosis, DVT).
34
Why does venous thrombosis often remain asymptomatic?
Collateral bypass channels can compensate, making about 50% of cases asymptomatic.
35
What are the two main complications of venous thrombosis?
1. Local pain and oedema (due to impaired drainage) 2. Pulmonary embolism (if thrombus dislodges)
36
What is the most common cause of thrombotic lesions in deep veins?
Blood stasis at venous valves, which creates turbulence and promotes clot formation.
37
How can deep vein thrombosis (DVT) be prevented during long flights?
* Leg exercises * Hydration * Compression stockings * Avoiding prolonged immobility
38
What are the four possible outcomes of a thrombus?
1. Propagation – Thrombus enlarges. 2. Embolization – Thrombus dislodges and travels to another site. 3. Dissolution – Thrombus breaks down via fibrinolysis (e.g., t-PA therapy). 4. Organization & recanalization – The thrombus is incorporated into the vessel wall, restoring blood flow.
39
Why are fibrinolytic agents like tissue plasminogen activator (t-PA) most effective when given early?
Because fibrinolysis is most effective within 5 hours of thrombus formation.
40
What are the main complications of arterial thrombosis?
Distal tissue infarction due to obstruction of blood flow.
41
What are the main complications of venous thrombosis?
Congestion, oedema, and embolism due to impaired venous drainage.
42
What is an embolism?
A detached thrombus or fragment that travels through the bloodstream and causes obstruction elsewhere.
43
What happens if a venous thrombus embolizes?
It enters the pulmonary circulation, causing a pulmonary embolism (PE), which can be fatal.
44
What happens if an arterial thrombus embolizes?
It can block downstream organs, leading to stroke, myocardial infarction, or limb ischemia.
45
Why does arterial blood clot formation often occur at sites of atherosclerosis?
Because atherosclerotic plaques cause endothelial injury and turbulent blood flow, promoting clot formation.