Thermoregulation

Inflammation Fundamentals

100

Q: This granular leukocyte is usually the first to arrive at the site of acute inflammation and is the most abundant in early exudates.

A: What is the neutrophil?

200

Q: This plasma protein system, when activated, results in the formation of C3a and C5a, which are known as these types of inflammatory mediators.

A: What are anaphylatoxins (or chemotactic factors, accepting either but best: anaphylatoxins/chemotactic factors)?

300

Q: This cascade produces bradykinin, which causes vasodilation, increased vascular permeability, and this characteristic sensation often associated with inflammation.

A: What is pain?

400

Q: This process, stimulated by complement fragment C3b, makes bacteria easier for phagocytes to recognize and eat.

A: What is opsonization?

500

Q: The kinin system produces this peptide, which causes vasodilation, increased vascular permeability, and contributes to pain.

A: What is bradykinin?

Acute vs Chronic Inflammation

100

Q: Name two of the classic local signs of acute inflammation (Latin terms not required).

A: Any two of: redness, heat, swelling, pain, loss of function.

200

Q: This type of exudate contains many white blood cells, protein, and cellular debris, and is seen in more severe or advanced inflammation.

A: What is purulent (or suppurative) exudate?

300

Q: In chronic inflammation, these two types of immune cells become more common than neutrophils in the affected tissue.

A: What are lymphocytes and macrophages?

400

Q: Chronic inflammation often leads to fibrosis (scarring). Name one way this can affect the function of the involved organ.

A: Any one of:

• It can stiffen the organ.
• It can distort normal structure.
• It can reduce function, e.g., less gas exchange in fibrotic lung, poor filtration in fibrotic kidney.

500

Q: Give one clear difference between acute and chronic inflammation in terms of either:

• Main cell types involved, OR
• Time course.

• A:
• Cells: Acute – mainly neutrophils; Chronic – mainly lymphocytes and macrophages.
  OR
• Time: Acute – sudden, short‑term; Chronic – long‑lasting, weeks to months or longer.

Wound Healing & Disruption

100

Q: A clean surgical incision that is closed with sutures usually heals by this type of intention.

A: What is primary intention?

200

Q: In normal wound healing, name two of the three major phases.

A: Any two of:

• Inflammatory phase
• Proliferative (reconstruction) phase
• Remodelling (maturation) phase

300

Q: The term for partial or complete separation of a wound that was previously closed (often after surgery) is:

A: What is dehiscence?

400

Q: Healing by secondary intention (e.g., large open wound) usually has more of these two features compared with primary intention.

A: What are more granulation tissue and more scarring?
(You can also accept: higher infection risk.)

500

Q: Name two common risk factors that increase the chance of wound dehiscence after surgery.

A: Any two of:

• Infection at the wound site
• Obesity
• Poor nutrition (e.g., low protein)
• Increased abdominal pressure (coughing, vomiting, straining)
• Diabetes or poor blood supply

Lifespan & Innate Immunity

100

Q: Newborns receive ready‑made antibodies from their mothers. This type of immunity is called:

A: What is passive immunity?

200

Q: Name one reason why newborns are at higher risk for infection compared with healthy adults.

A: Any one of:

• Immature immune system (e.g., less effective neutrophils/complement)
• Thinner skin and mucous membranes
• Less prior exposure to microbes (no built‑up immunity)

300

Q: Name one age‑related change in older adults that can weaken innate immunity.

A: Any one of:

• Decreased phagocyte function (neutrophils/macrophages)
• Reduced chemotaxis
• Thinner, more fragile skin
• Less effective mucociliary clearance in airways

400

Q: Why is it important not to rely only on fever to detect infection in older adults?

A: Because older adults may not develop a strong fever even with serious infection, so we must also watch for changes like confusion, weakness, low BP, or increased RR.

500

Q: Name one key infection‑prevention strategy that is especially important for:
a) Newborns, and
b) Older adults.

A:

• Newborn: e.g., hand hygiene, limiting exposure to sick contacts, maternal/household vaccination (“cocooning”).
• Older adults: e.g., vaccinations (flu, pneumococcal, COVID‑19), good nutrition, skin care, early assessment of subtle infection signs.

Fever & Temperature Disorders

100

Q: The brain structure that acts as the body’s “thermostat” and regulates temperature is the:

A: What is the hypothalamus?

200

Q: Fever is usually caused by chemicals called pyrogens. These make the hypothalamus do this to the body’s “set point.”

A: What is raise (increase) the set point?

300

Q: During fever, the body produces prostaglandin E2 (PGE2) in the hypothalamus. This causes:

• a) Shivering and feeling cold at first, and
• b) Later, sweating as the fever “breaks.”
  Which part (a or b) happens when the set point is raised?

A: a) Shivering and feeling cold happens when the set point is raised (the body is trying to reach the new higher temperature).

400

Q: Explain one key difference between fever and hyperthermia.

A:

• In fever, the hypothalamus raises the set point (controlled response to infection).
• In hyperthermia, the set point is normal, but the body temperature rises because of too much heat or poor heat loss (e.g., heat stroke).

500

Q: Why do medications like acetaminophen help reduce a fever, but are not very helpful in conditions like heat stroke?

A:

• Acetaminophen lowers the hypothalamic set point, so it works when the set point is raised (fever).
• In heat stroke, the set point is normal; the problem is excess heat, so you need cooling and fluid replacement, not just set‑point‑lowering drugs.