Patho: EXAM 1 (Inflammation & Stress) Study Guide

Patho exam 1

What are the two main components of the acute inflammatory response?

Vascular response (“bring supplies”) and Cellular response (“bring fighters”).

In acute inflammation, what triggers the vascular response?

Tissue injury → release of chemical mediators (histamine, prostaglandins, bradykinin).

What happens during vasodilation in inflammation, and why?

Blood vessels widen → ↑ blood flow → redness (erythema) and heat; brings oxygen and immune cells.

What does increased vascular permeability cause, and why?

Endothelial cells contract → fluid & proteins leak into tissues → swelling (edema); proteins/antibodies help fight microbes and dilute toxins.

What is exudate formation, and what is its purpose?

Fluid + proteins + WBCs leak into tissues → dilute toxins, trap microbes, prepare for healing.

What are the 4 steps of the cellular response in acute inflammation?

1) Margination & adhesion, 2) Diapedesis, 3) Chemotaxis, 4) Phagocytosis.

Why is chemotaxis important in inflammation?

It directs WBCs to the exact site of injury using chemical “signals.”

What is the overall goal of the vascular vs cellular response?

Vascular = open the gates and deliver supplies; Cellular = send soldiers to fight and clean up.

what are included in Vascular response

Vascular response (open the gate and flood the area with supplies): “The Very Inflammatory Event” Tissue injury occurs, Vasodilation, Increased vascular permeability, Exudate formation. 

what are included in Cellular response

Cellular response (bring in soldiers to fight and clean up ): margination & adhesion. diapedesis (transmigration), chemotaxis, phagocytosis

What are microscopic changes in inflammation?

VPEMM: Vasodilation, ↑ Permeability, Exudate formation, WBC Migration, Mediator release.

What are macroscopic signs of inflammation?

Redness, heat, swelling, pain, and loss of function.

What role do mast cells play in inflammation?

Act as “alarm cells” that release histamine, prostaglandins, leukotrienes, and chemotactic factors.

What is the effect of histamine from mast cells?

Vasodilation and ↑ permeability → redness, swelling.

what is the difference between chemotaxis and chemotactic 

chemotaxis is when they guide to the site and chemotactic is just signaling

Which cells are the first responders in inflammation, and what do they do?

Neutrophils → phagocytose bacteria/debris, short-lived.

Which cells arrive later and sustain the response?

Macrophages → long-lasting, secrete cytokines, clean up. Macrophages = Maids/Maintenance (later, long-lasting, cleaning and coordinating).

What role do eosinophils play?

Defend against parasites and regulate allergic responses.

What role do lymphocytes play in inflammation?

T & B cells → adaptive immunity if inflammation persists.

What role do platelets play?

Release growth factors and start clotting.

What are signs of local inflammation?

Redness, heat, swelling, pain, loss of function.

What are signs of systemic inflammation?

FLAME: Fever, Leukocytosis (↑ WBC), Anorexia, Malaise, ↑ Elevated proteins (CRP, ESR).

What are the 3 stages of Hans Selye’s General Adaptation Syndrome?

A.R.E you stressed? :Alarm, Resistance, Exhaustion.

What happens in the alarm stage of stress?

SNS activates → adrenal medulla releases epinephrine (↑ HR, bronchodilation, ↑ glucose) and norepinephrine (vasoconstriction, ↑ BP, ↓ GI/renal perfusion).

What happens in the resistance stage of stress?

HPA axis kicks in. hypothalamus release CRH (Corticotropin-Releasing Hormone), pituitary release ACTH (Adrenocorticotropic Hormone), adrenal cortex release cortisol. Hypothalamus → CRH → Pituitary → ACTH → Adrenal cortex releases cortisol.

What are the effects of cortisol?

Easy hook: Your body runs on GAS during stress, thanks to cortisol. G = glucose, amino acids, fatty acids → fuel for stress. A = arterial pressure, ↑ BP. S = Suppresses immunity/inflammation if prolonged.

What happens in the exhaustion stage of stress?

IPO burnout, I = impaired immunity, P = poor healing. O = organ damage. Prolonged cortisol depletes resources → impaired immunity, poor healing, organ damage.

What are the 3 plasma protein systems in inflammation?

CCK: Complement, Clotting, and Kinin systems.

What does the complement system do?

TAG, SIGNAL, KILL. Opsonization, chemotaxis, and direct killing of microbes with MAC (membrane attack complex).

What is the function of the clotting system in inflammation?

Creates fibrin mesh to stop bleeding, trap pathogens, and form a scaffold for healing.

What does the kinin system produce and what are its effects?

Produces bradykinin → vasodilation, ↑ permeability, pain.