Oedema, Congestion, Infarction and Shock Flashcards

1
Q

What is edema, and how does it manifest?

A

Edema is the accumulation of fluid in tissues, either localized or generalized. It can manifest as mild swelling (e.g., shoes fitting tighter after a long day) or severe conditions like alveolar fluid accumulation, leading to life-threatening hypoxia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What can cause edema?

A

◾ Increased hydrostatic pressure;
◾ Reduced plasma osmotic pressure;
◾ Lymphatic obstruction;
◾ Sodium and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the causes of increased hydrostatic pressure leading to edema?

A

◾ Impaired venous outflow (e.g., deep vein thrombosis, heart failure);
◾ Increased arterial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the effects of reduced plasma osmotic pressure?

A

Loss of fluid from circulation into tissues;
It is commonly caused by reduced albumin levels due to:
◾ nephrotic syndrome,
◾ liver cirrhosis,
◾ protein malnutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does lymphatic obstruction contribute to edema?

A

Prevents fluid reabsorption from interstitial spaces;
Causes include inflammatory or neoplastic obstruction and parasitic infections (e.g. filariasis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What happens in nephrotic syndrome regarding plasma proteins?

A

Increased permeability of glomerular capillaries resulting in loss of plasma proteins (e.g., albumin) in urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the mechanism of edema in heart failure?

A

◾ In heart failure, the heart’s ability to pump blood is compromised. This leads to a backup of blood in the veins, increasing the pressure within the capillaries. This forces fluid out of the capillaries and into the surrounding tissues, hence oedema results.
◾ Additionally, heart failure reduces the cardiac output, leading to decreased renal blood flow. In response, the kidneys activate mechanisms to retain sodium and water (e.g. RAAS) in an attempt to increase blood volume and improve perfusion. This will result in an increase in overall fluid volume in the body, contributing to oedema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the clinical features of nephrotic syndrome that contribute to edema?

A

◾ Massive protein loss in urine (proteinuria);
Hypoalbuminemia, leading to reduced plasma osmotic pressure;
Secondary hyperaldosteronism due to decreased plasma volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does inflammation lead to edema?

A

Increased vascular permeability due to endothelial cell contraction;
Leakage of protein-rich fluid (exudate) into interstitial spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is anasarca?

A

Severe, generalized edema affecting the entire body; Typically associated with hypoalbuminemia or severe systemic conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Briefly describe the morphology of cerebral oedema.

A

The brain appears swollen with narrowed sulci and distended gyri.

[Image 1] [Image 2]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Briefly describe the morphology of pulmonary oedema.

A

The lungs are 2 - 3 times their normal weight.
Sectioning reveals frothy blood tinged fluid; a mixture of air, oedematous fluid and extravasated red blood cells.

[Image 1] [Image 2] [Image 3] [Image 4] [Image 5]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is effusion?

A

Effusion refers to the escape of fluid into a body cavity or tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the different forms of effusion based on fluid type?

A

Transudate: Low protein content, specific gravity < 1.012 (e.g., heart failure)
Exudate: Protein-rich, specific gravity > 1.020 (e.g., inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Give the medical term for the following:
(a) fluid in the pleural cavity
(b) fluid in the pericardial sac
(c) fluid in the peritoneal cavity

A

(a) Hydrothorax
(b) Hydropericardium
(c) Ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define:
(a) serous effusion
(b) serosanguinous effusion
(c) haemorrhagic effusion
(d) chylous effusion

A

(a) serous effusion: accumulation of clear, pale yellow fluid that is similar to serum
(b) serosanguinous effusion: this type of effusion contains both serous fluid and blood; typically light red
(c) haemorrhagic effusion: this type of effusion involves the presence of a significant amount of blood in the effusion fluid. It appears red.
(d) chylous effusion: this type of effusion contains a milky fluid rich in triglycerides, known as chyle. It is often caused by damage to the lymphatic system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Identify the pathology: [Image].

A

hydrothorax (serous plural effusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Identify the pathology: [Image].

A

serosanguinous pleural effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Identify the pathology: [Image].

A

chylous ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define congestion.

A

This refers to the abnormal accumulation of blood within the blood vessels of an organ or tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

State the two broad types of congestion and give a brief description of each.

A

(1) Active congestion (Hyperemia)
This occurs when there is increased blood flow to a particular area due to the dilation of blood vessels. It is often a result of increased metabolic activity, inflammation, or exercise. The affected area typically appears red and warm due to the increased blood supply.

(2) Passive congestion (Venous congestion)
This occurs when there is an obstruction to the outflow of blood, leading to the accumulation of blood in the affected area. It is often caused by conditions such as heart failure or venous thrombosis. The affected area may appear bluish or purplish due to the deoxygenated blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Outline consequences of impaired venous outflow.

A

Congestion: stasis of deoxygenated blood.
Haemorrhage: increase in capillary pressure which can lead to capillary rupture
Oedema: due to increased intravascular pressure
Chronic hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Differentiate between shock and infarction.

A

Shock is a condition where the body’s organs and tissues do not receive enough blood flow, leading to a lack of oxygen and nutrients. It is as a result of overall failure of the circulatory system.
Infarction refers to the death of tissue due to a lack of blood supply. This is usually caused by a blockage in an artery, e.g. a blood clot, which prevents blood from reaching the affected area.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

List the types of shock.

A

🩺 Cardiogenic shock
🩺 Hypovolemic shock
🩺 Septic shock
🩺 Neurogenic
🩺 Anaphylactic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the common causes of shock?

A

◾ Hypovolemia;
◾ Cardiogenic failure;
◾ Sepsis;
◾ Anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the main pathological feature of shock?

A

systemic hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the sequence of vascular events in shock?

A

Vasoconstriction during compensatory stage;
Progressive vasodilation in later stages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the stages of shock progression?

A

(1) Non-progressive (compensated)
(2) Progressive
(3) Irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What happens during the non-progressive stage of shock?

A

◾ Activation of compensatory mechanisms;
◾ Maintenance of organ perfusion

30
Q

What occurs in the progressive stage of shock?

A

Worsening tissue hypoxia; Metabolic acidosis;
Vital organ dysfunction

31
Q

What occurs in the irreversible stage of shock?

A

Widespread cell death; Organ failure; Unresponsiveness to therapy

32
Q

What is the physiological response in early hypovolemic shock?

A

Tachycardia;
Peripheral vasoconstriction; Increased thirst

33
Q

What is the clinical presentation of hypovolemic shock?

A

Rapid, weak pulse;
Cold, clammy skin;
Decreased urine output

34
Q

What is the main difference between hypovolemic and septic shock in terms of skin appearance?

A

Hypovolemic: cold and clammy skin;
Septic: warm and flushed skin (initially)

35
Q

What are the clinical features of irreversible shock?

A

Severe hypotension unresponsive to treatment;
Profound metabolic acidosis;
Multi-organ failure

36
Q

What are the key systemic effects of septic shock?

A

Persistent hypotension;
Metabolic acidosis;
Multi-organ dysfunction syndrome (MODS)

37
Q

List clinical features of septic shock.

A

Hypotension; Warm, flushed skin (initially); Fever or hypothermia; Organ dysfunction

38
Q

What role do bacterial toxins play in septic shock?

A

Activate immune cells;
Induce cytokine release;
Cause endothelial damage

39
Q

What is the role of cytokines in septic shock?

A

TNF-alpha and IL-1 initiate systemic inflammation;
IL-6 and IL-8 amplify immune response; Cause vasodilation, vascular leakage, and activation of coagulation cascade

40
Q

What are the consequences of widespread endothelial activation in septic shock?

A

Increased vascular permeability; Hypotension;
Disseminated intravascular coagulation (DIC)

41
Q

What is the pathogenesis of lung injury in septic shock?

A

Inflammatory mediators damage alveolar capillary membrane; Results in acute respiratory distress syndrome (ARDS)

42
Q

What causes multi-organ dysfunction in septic shock?

A

Persistent hypoperfusion; Microthrombosis leading to ischemia;
Direct cellular injury by inflammatory mediators

43
Q

What are the complications of prolonged septic shock?

A

Acute respiratory distress syndrome (ARDS);
Renal failure;
DIC (disseminated intravascular coagulation)

44
Q

**

How does anaphylactic shock develop?

A

Allergen exposure leads to massive release of histamine and other mediators;
Results in vasodilation and increased vascular permeability

45
Q

What is the role of histamine in anaphylactic shock?

A

Causes systemic vasodilation; Increases vascular permeability; Leads to edema and hypotension

46
Q

What is the most common cause of cardiogenic shock?

A

Myocardial infarction

47
Q

What are the clinical manifestations of an acute myocardial infarction?

A

Chest pain radiating to the left arm or jaw;
Shortness of breath;
Sweating and nausea

48
Q

What causes cold extremities in late-stage shock?

A

Peripheral vasoconstriction to preserve central perfusion

49
Q

What is the hallmark of progressive shock?

A

Worsening lactic acidosis due to impaired tissue oxygenation

50
Q

What is the primary goal of management in shock?

A

Restore adequate tissue perfusion; Maintain oxygen delivery to vital organs

51
Q

What organs are most susceptible to hypoperfusion during shock?

A

Brain; Heart; Kidneys

52
Q

What is the definition of infarction?

A

Tissue death (necrosis) due to inadequate blood supply.

53
Q

What is the morphological difference between acute and chronic infarction?

A

Acute: characterized by necrosis and inflammation; Chronic: replaced by fibrous scar

54
Q

What are the main causes of arterial occlusion in infarction?

A

Thrombosis;
Embolism;
Atherosclerosis

55
Q

What are the microscopic changes seen in an infarct within 6-12 hours?

A

Eosinophilic cytoplasm; Nuclear changes (pyknosis, karyorrhexis, or karyolysis)

56
Q

What are the microscopic features of an infarcted area after 12-24 hours?

A

Coagulative necrosis;
Nuclear changes: pyknosis, karyorrhexis, karyolysis; Surrounding inflammation

57
Q

What happens microscopically in an infarcted area after 1-3 days?

A

Peak neutrophil infiltration; Ongoing necrosis; Surrounding hyperemia

58
Q

What are the key features seen in an infarcted area after 1-2 weeks?

A

Macrophage infiltration;
Fibroblast activation;
Granulation tissue formation

59
Q

What is the primary pathological process of scar formation after infarction?

A

Deposition of collagen by fibroblasts;
Replacement of necrotic tissue with fibrous scar

60
Q

What organs are resistant to infarction and why?

A

Liver: dual blood supply from hepatic artery and portal vein; Lungs: dual blood supply from pulmonary and bronchial arteries

61
Q

What is the role of neutrophils in infarction?

A

Infiltrate the infarcted tissue; Contribute to the removal of necrotic debris

62
Q

What is the time frame for macrophage infiltration in infarction?

A

Begins around 3-7 days after infarction; Peaks during the second week

63
Q

What is the main consequence of prolonged ischemia?

A

Tissue necrosis

64
Q

What are the effects of ischemia on cell organelles?

A

Swelling of mitochondria; Disruption of lysosomal membranes;
Fragmentation of endoplasmic reticulum

65
Q

What are the cellular effects of ATP depletion during ischemia?

A

Sodium-potassium pump failure;
Cellular swelling;
Lactic acid accumulation

66
Q

What are the common sites of venous infarction?

A

Brain (due to venous sinus thrombosis);
Intestines (volvulus or strangulation)

67
Q

What is the role of coagulation in ischemia-reperfusion injury?

A

Reperfusion may trigger platelet aggregation; Formation of microthrombi worsens ischemia

68
Q

What is the significance of granulation tissue in infarction healing?

A

Provides a scaffold for scar formation; Indicates the transition from inflammation to repair

69
Q

What is the gross appearance of a white infarct?

A

Pale, wedge-shaped area; Sharp demarcation between normal and infarcted tissue

70
Q

What is the gross appearance of a red infarct?

A

Hemorrhagic, dark red tissue; Poorly defined margins