pt5

Question 1

Define “infarction.”

Answer 1

Infarction is an area of ischemic necrosis within a tissue/organ due to occlusion of its arterial supply or venous drainage.

Question 2

What are some non-thrombotic causes of infarction?

Answer 2

Though most infarcts stem from thrombotic or embolic occlusions, other causes include:
* Vasospasm (sudden vessel spasm)
* Hemorrhage into an atherosclerotic plaque
* External compression (e.g., by a tumor)
* Traumatic rupture of a vessel.

Question 3

How are infarcts classified by color, and what does each type imply?

Answer 3

1. White (anemic) infarcts: Occur in solid organs (e.g., heart, kidney, spleen) with end-arterial circulation.
2. Red (hemorrhagic) infarcts: Typically found in tissues like the lung or in organs with dual blood supply or venous occlusion.
3. Septic vs. bland infarcts: Depends on whether infection is present.

Question 4

Which major factors influence the outcome of an infarction in a particular tissue?

Answer 4

1. Nature of the vascular supply (availability of alternate blood routes)
2. Rate of occlusion (sudden vs. gradual)
3. Tissue vulnerability to hypoxia (neurons and myocardial cells are very sensitive)
4. Oxygen content of the blood (e.g., anemia worsens infarction).

Question 5

In myocardial infarction, why can gross changes be difficult to see in the first few hours?

Answer 5

Early after coronary occlusion (2–6 hours), gross morphological changes in heart muscle are not yet visible. Visible or microscopic changes typically appear 24+ hours post-occlusion.

Question 6

Summarize “shock” in medical terms.

Answer 6

Shock is best described as inadequate tissue perfusion due to systemic hypotension, which arises from reduced cardiac output or insufficient circulating blood volume. It results in diminished oxygen/nutrient delivery to tissues and can lead to organ failure and death if untreated.

Question 7

What are the main categories (causes) of shock?

Answer 7

1. Cardiogenic shock: Heart failure (e.g., myocardial infarction) → low cardiac output
2. Hypovolemic shock: Reduced blood/plasma volume (e.g., hemorrhage, severe burns, diarrhea) → decreased preload and output
3. Septic shock: Intense vasodilation and peripheral pooling (often due to systemic infection/toxins) → reduced effective circulating volume.

Question 8

What are common signs/symptoms indicating a person may be in shock?

Answer 8

• Rapid, weak pulse and low blood pressure
• Cool, pale, or bluish skin (poor perfusion)
• Confusion or altered mental status
• Rapid breathing
• Nausea/vomiting
• Excessive thirst
• Cold, clammy extremities.

Question 9

What first-aid steps can be taken if someone appears to be in shock?

Answer 9

1. Lay the person down and elevate the legs (to improve venous return).
2. Keep the person warm (cover with a blanket).
3. If no neck injury is suspected, turn the head to one side to prevent airway obstruction from possible vomiting.
4. Call emergency services promptly; severe shock is life-threatening.

Question 10

Why can severe blood or fluid loss (e.g., from hemorrhage or burns) lead to hypovolemic shock?

Answer 10

The effective circulating blood volume drops too low, reducing venous return to the heart. This leads to decreased cardiac output and systemic hypotension, diminishing tissue perfusion.

Question 11

How does septic shock cause dangerously low blood pressure?

Answer 11

During sepsis or severe infection, inflammatory mediators cause widespread vasodilation and increase vascular permeability. Blood pools in expanded peripheral vessels, and the effective circulating volume plummets, leading to hypotension and inadequate perfusion.

Question 12

Why is shock considered a “final common pathway” of many lethal events?

Answer 12

Various acute conditions (e.g., massive bleeding, severe heart failure, overwhelming infection) can converge on systemic hypotension and inadequate tissue perfusion. Untreated shock rapidly leads to organ dysfunction, multi-organ failure, and death.

Question 13

Approximately how many liters of blood does an average 70-kg adult male have?

Answer 13

About 5 liters of blood. Losing over a third of this volume quickly (e.g., hemorrhage) can induce life-threatening shock.

Question 14

What is the general definition of inflammation, and why is it considered fundamentally protective?

Answer 14

Inflammation is the biological response to noxious or harmful stimuli (e.g., microbes, burns, trauma). It’s fundamentally protective because it aims to eliminate the cause of injury or infection, remove damaged cells, and initiate tissue repair, although it can also lead to tissue damage if excessive.

Question 15

What are the four classical signs of acute inflammation originally described by Celsus?

Answer 15

1. Rubor (Redness)
2. Tumor (Swelling)
3. Calor (Heat)
4. Dolor (Pain) Virchow later added Functio Laesa (Loss of function) as a possible fifth sign.

Question 16

How does “acute” inflammation differ in timing from “chronic” inflammation?

Answer 16

Acute inflammation is a rapid response that typically begins immediately (minutes to hours) and lasts hours to a few days. Chronic inflammation persists much longer (weeks to months or even years).

Question 17

What main goals does the body aim to accomplish during acute inflammation?

Answer 17

To increase blood flow to the site of injury (bringing leukocytes, antibodies, etc.), increase vascular permeability (letting fluid/proteins/cells exit circulation), and recruit and activate leukocytes to eliminate offending agents or debris.

Question 18

Which types of stimuli commonly trigger acute inflammation?

Answer 18

• Infections (bacterial, viral, fungal, parasitic)
• Trauma (blunt or penetrating)
• Burns/frostbite (thermal, chemical)
• Allergic reactions
• Tissue necrosis (e.g., infarction, hypoxia).

Question 19

Name the three major components (steps) of acute inflammation.

Answer 19

1. Vascular dilation → increases blood flow.
2. Microvascular structural changes → plasma proteins and leukocytes leave circulation.
3. Emigration of leukocytes → cells accumulate at the injury site and activate to clear the offending agent.

Question 20

Which mediators are primarily responsible for vasodilation in acute inflammation, and what clinical signs do they produce?

Answer 20

Histamine, bradykinin, and nitric oxide (NO) mediate vasodilation. They cause redness (rubor) and heat (calor) by increasing local blood flow (hyperemia).

Question 21

Why does vascular permeability increase during acute inflammation, and what does this cause?

Answer 21

The endothelium becomes leaky due to endothelial cell contraction, injury, or (less commonly) transcellular transport. This leakage lets plasma fluid and proteins exit into the tissues, causing edema (the swelling or tumor).

Question 22

Describe how leukocytes exit the bloodstream and reach the site of tissue injury (extravasation).

Answer 22

1. Margination & rolling (mediated by selectins on endothelium).
2. Firm adhesion (via integrins like ICAM-1, VCAM-1).
3. Transmigration (diapedesis) across the endothelium.
4. Chemotaxis through tissue along a gradient of chemoattractants until they reach the injury site.

Question 23

What is “chemotaxis,” and which substances commonly act as chemoattractants?

Answer 23

Chemotaxis is the directed migration of leukocytes toward the injury site guided by chemical gradients. Common chemoattractants include:
* Bacterial products
* Complement components (e.g., C5a)
* Cytokines (e.g., IL-8)
* Leukotriene B4.

Question 24

Which leukocytes typically predominate early in acute inflammation, and what is their main function?

Answer 24

Neutrophils usually predominate initially. They phagocytose microbes and cellular debris, release granule enzymes, and generate reactive oxygen species to kill pathogens.

Question 25

What are “phagolysosomes,” and why are they critical for pathogen destruction?

Answer 25

When a leukocyte engulfs a microbe, it forms a phagosome that later fuses with a lysosome. This phagolysosome contains digestive enzymes and often reactive oxygen species that degrade or kill the ingested pathogen.

Question 26

Name three important pro-inflammatory cytokines and their general effect in acute inflammation.

Answer 26

1. TNF-α 2. IL-1 3. IL-6 They amplify the inflammatory response, promote endothelial activation, and help recruit/activate other immune cells.

Question 27

How can acute inflammation be morphologically classified (patterns)?

Answer 27

1. Serous (thin fluid; e.g., skin blister) 2. Fibrinous (fibrin-rich exudate) 3. Purulent (pus; e.g., abscess) 4. Ulcerative (necrotic tissue loss at surface).

Question 28

Define what “purulent inflammation” is and give an example.

Answer 28

Purulent inflammation is characterized by pus—a thick fluid of neutrophils, necrotic cells, and fluid exudate. An example is abscess formation, often due to Staphylococcus infections.

Question 29

What are the possible outcomes of acute inflammation?

Answer 29

1. Complete resolution (restoration to normal) 2. Healing by connective tissue/fibrosis (scar formation) 3. Progression to chronic inflammation if the injurious agent persists or if the response is dysregulated.

Question 30

Under what conditions does acute inflammation typically resolve completely rather than progress to fibrosis?

Answer 30

When the injury is mild, short-lived, and limited in scope, with minimal tissue damage and the ability for regeneration. Effective elimination of the cause and efficient removal of exudate/debris also favor resolution.

Question 31

Why might extensive acute inflammation lead to scarring (fibrosis)?

Answer 31

If there is substantial tissue damage, or if the tissue cannot regenerate (e.g., destructive infection or severe necrosis), fibroblasts proliferate, depositing collagen and forming a scar that replaces the functional tissue.

Question 32

In an MCQ context, a question states: “Acute inflammation is a rapid host reaction in response to which of the following situations?” and lists infections, trauma, burns, allergy, or “all of the above.” What is the best answer?

Answer 32

All of the above. Acute inflammation can be triggered by infections, trauma (mechanical injury), burns/frostbite, and allergic reactions—among other causes.

Question 33

What fundamentally distinguishes chronic inflammation from acute inflammation in terms of duration and clinical signs?

Answer 33

Chronic inflammation typically persists for months or years, sometimes lifelong, and often lacks the four or five classical acute signs (rubor, tumor, calor, dolor, functio laesa). Acute inflammation lasts hours to days and usually shows those classical signs (e.g., redness, swelling).

Question 34

Under what circumstances can chronic inflammation develop?

Answer 34

1. Progression from unresolved or recurrent acute inflammation. 2. De novo onset (no preceding acute phase), e.g., certain autoimmune or granulomatous conditions.

Question 35

List the three main categories of causes of chronic inflammation.

Answer 35

1. Persistent infection (organisms difficult to eliminate, e.g., Mycobacterium tuberculosis) 2. Immune-mediated inflammatory diseases (autoimmune, allergic, e.g., rheumatoid arthritis, asthma) 3. Prolonged exposure to toxic agents (exogenous like asbestos or endogenous accumulations).

Question 36

Why is chronic inflammation relevant to many prevalent diseases in modern society?

Answer 36

It underlies or contributes to many chronic conditions (e.g., atherosclerosis, autoimmune diseases, neurodegenerative diseases, certain lung pathologies, and cancer), making it a major driver of morbidity and mortality.

Question 37

What are the hallmark morphological features of chronic inflammation?

Answer 37

1. Infiltration with mononuclear cells (macrophages, lymphocytes, plasma cells). 2. Tissue destruction (often progressive). 3. Attempts at healing (angiogenesis + fibrosis) occurring simultaneously with ongoing inflammation.

Question 38

Which cell types typically dominate in chronic inflammation, and how do they contribute?

Answer 38

Macrophages: Key effector cells, secrete cytokines causing further tissue damage/fibrosis, and can form granulomas. Lymphocytes: T-cells produce cytokines (e.g., IFN-γ) activating macrophages; B-cells → plasma cells → antibodies. Plasma cells: Derived from activated B-cells, secrete specific antibodies. Eosinophils/Mast cells: Often present in parasitic infections or allergies.

Question 39

What role do macrophages play in chronic inflammation, and how do they interact with lymphocytes?

Answer 39

Macrophages ingest pathogens or debris, present antigens to T-cells, and secrete cytokines. In turn, T-lymphocytes secrete IFN-γ to further activate macrophages, creating a positive feedback loop that perpetuates chronic inflammation.

Question 40

Define a granuloma and mention two distinct types.

Answer 40

A granuloma is a specialized form of chronic inflammation where activated macrophages (epithelioid cells) and sometimes giant cells aggregate around a difficult-to-remove agent. Two types are: 1. Caseating (e.g., tuberculosis) 2. Non-caseating (e.g., sarcoidosis).

Question 41

What is the usual pathophysiological reason for granuloma formation?

Answer 41

Granulomas form when the offending agent (microbe, foreign material) cannot be effectively cleared by normal phagocytosis. The immune system walls it off with aggregates of macrophages, giant cells, and lymphocytes.

Question 42

How can chronic inflammation harm host tissues even though it aims to contain the offending agent?

Answer 42

Prolonged inflammation leads to ongoing tissue necrosis, fibrosis, and potentially loss of organ function. Macrophage and lymphocyte products (ROS, cytokines) can damage healthy cells.

Question 43

Name some systemic effects (whole-body manifestations) of chronic inflammation.

Answer 43

1. Fever (low-grade, persistent) 2. Elevated acute-phase proteins (C-reactive protein, fibrinogen, SAA) 3. Leukocytosis (raised white cell count) 4. Mild anemia, weight loss, increased pulse/BP, and general malaise.

Question 44

Why does fever occur in chronic inflammation?

Answer 44

Cytokines (e.g., IL-1, TNF) alter the thermostatic set point in the hypothalamus, causing the body to increase heat production (via shivering, decreased sweating) and reduce heat loss, resulting in fever.

Question 45

What are some lab findings that often increase during chronic inflammation?

Answer 45

CRP (C-reactive protein), Fibrinogen, Serum amyloid A (SAA), White blood cell count (especially in bacterial infections).

Question 46

What are the final outcomes of chronic inflammation if it is not resolved?

Answer 46

Fibrosis (scar formation), Potential loss of organ function, Continual or escalating tissue damage, (In some cases) predisposition to neoplastic changes.

Question 47

How do acute and chronic inflammation differ in vascular changes?

Answer 47

Acute: Marked vascular changes (edema, redness). Chronic: Fewer visible vascular changes (no marked edema).

Question 48

How do acute and chronic inflammation differ in cellular infiltration?

Answer 48

Acute: Neutrophils predominate. Chronic: Macrophages/lymphocytes predominate.

Question 49

How do acute and chronic inflammation differ in tissue repair sequence?

Answer 49

Acute: Repair begins after inflammation ends. Chronic: Ongoing repair (fibrosis, angiogenesis) concurrently with inflammation.

Question 50

Provide an example of a pathological condition that features granulomatous chronic inflammation.

Answer 50

Tuberculosis (Mycobacterium tuberculosis infection) is a classic cause, featuring caseating granulomas with Langerhans giant cells.

Question 51

In an MCQ context, is matching 'Plasma cells' with 'phagocytosis' correct or incorrect?

Answer 51

Incorrect. Plasma cells secrete antibodies; phagocytosis is performed by macrophages and neutrophils, not plasma cells.

Question 52

What are some clinical markers useful in chronic inflammation?

Answer 52

CRP (C-reactive protein), Fibrinogen, Serum amyloid A (SAA), White blood cell count.

Question 53

What are some symptoms of chronic inflammation?

Answer 53

Mild anemia, weight loss, increased pulse/BP, and general malaise.