Pathophysiology Module 4 Exam: The body's defenses (part 1), Pathophysiology Module 4 Exam: Inflammatory response (part 2), Pathophysiology Module 4 Exam: Immune response (part 3) fully solved questions with 100% accurate solutions(Latest Update)

Stress

When a demand perceived by an individual or an event exceeds their coping abilities and results in disturbances in the cognition, emotion, behavior, or function of an individual (disruption of homeostasis)

Stressor

Any perception or event that elicits the general adaptation syndrome

Prolonged stress results in:

- Atrophy of the thymus gland

- hypertrophy of adrenal cortex

- gastric and duodenal ulcers (GI upset)

Thymus gland

located in sternum region, T cells mature here (immunity decreases due to thymus atrophy)

Hypertrophy of adrenal cortex results in:

increase secretion of cortisol which increases blood sugar and stabilizes mast cells (decreases immune response)

General Adaptation Syndrome

Came from experiment on rodents. Divided into three parts:

1. Alarm stage

2. Stage of resistance or adaptation

3. Stage of exhaustion

Alarm stage

The first stage of the general adaptation syndrome. Fight or flight The stressor stimulates sympathetic nervous system which causes release of norepinephrine and epinephrine from nerve terminals. Results in stimulation of adrenergic receptors

Alpha 1 stimulation causes:

Stimulated by norepinephrine and epinephrine.

- vasoconstriction of blood vessels (pallor) and arteries (increases cardiac output and raises BP could lead to angina or heart attack)

- mydriasis (pupils dilate)

- piloerection (goosebumps)

- stimulates apocrine glands (sweaty)

- constricts smooth muscle (GI cramping, ulcers, slowed motility/peristalsis, preterm labor, erection/ejaculation, urine retention)

- stimulated liver glycogenolysis and gluconeogenesis (raises blood sugar)

Alpha 2 stimulation causes:

stimulated by norepinephrine and epinephrine.

- Inhibits the release of more norepinephrine by nerve terminals

- pancreas reduces secretion of insulin and increases secretion of glucagon (increases blood sugar)

- inhibits lipolysis

- increases platelet aggregation (blood clot formation)

Beta 1 stimulation causes:

stimulated by norepinephrine and epinephrine.

- increases heart rate, force of contraction (tachycardia and increased cardiac output)

- stimulates kidneys to release renin (increases BP and blood volume)

- Decreases GI motility and peristalsis

- promotes lipolsysis

Beta 2 stimulation causes:

stimulated by EPINEPHRINE ONLY

- bronchodilation (increased respiratory rate and depth)

- vasodilation (increases blood flow and perfusion)

- temporarily increases muscle contraction (strength)

- relaxes smooth muscle (promotes urination, relaxes uterus which stops preterm labor)

- liver increases glycogenolysis and gluconeogenesis (increases blood sugar)

- pancreas increases insulin production

- inhibits histamine release by mast cells and suppresses inflammatory response (stabilizes mast cells)

Beta 3 stimulation causes:

stimulated by norepinephrine and epinephrine.

Causes lipolysis

Catecholamines

epinephrine, norepinephrine

Epinephrine

hormone produced in the adrenal medulla, released with stressor or profound drop in blood pressure. Stimulates ALL adrenergic receptors and is the ONLY catecholamine that stimulates beta 2

Norepinephrine

Hormone produced in adrenal medulla and neurotransmitter released from nerve terminals. It is released by perceived stressor or profound drop in blood pressure. It stimulates mostly alpha receptors and beta receptors to a lesser extent

cortisol

secreted by adrenal cortex in response to stress. It increases blood sugar and suppresses immune and inflammatory responses

Stage of resistance/adaptation

second stage in GAS; continued activation of stress response, can lead to atrophy of thymus, hypertrophy of adrenal cortex, and GI ulcers. Goal is to stop stressor or help manage stress

Stage of Exhaustion

third stage of the general adaptation syndrome; the body's ability to resist stress becomes depleted; illness, disease, and even death may occur

endorphins

help lower the body's reaction to pain and discomfort during acutely stressful situations (sense of euphoria)

ADH

antidiuretic hormone. helps retain water and increase blood volume (increases bp)

What is the hallmark of the stress response?

elevated blood sugar

What is the only catecholamine that activates Beta 2?

Epinephrine

Inflammatory response

rapid and nonspecific. It begins with the release of chemicals from mast cells following injury. Always occurs in the same sequence

-itis

inflammation

Acute inflammation

short-term, 8-10 days

Chronic inflammation

long-term, >14 days (2 weeks)

Functions of inflammatory response

1. Defends against infection

2. Facilitates tissue repair & healing

3. Destroys injurious agents

4. Wall off and confines those agents to limit their effects on host

5. Stimulates & enhances immune response

6. Promotes healing

Inflammation

response to tissue injury or invasion by bacteria, parasites, or fungi)

Cardinal signs of inflammation:

Rubor: redness

Tumor: swelling, edema

Calor: heat, increased temperature

Dolar: pain

(5th is loss of function)

When injury occurs:

1. vascular stage

2. cellular stage

3. plasma protein stage

Vascular stage of inflammation

vasoconstriction (vessel spasm, blanching, < 1 minute) followed rapidly by vasodilation (weeping, leaking, swelling)

Cellular stage of inflammation

WBCs enter injured tissue and destroy ineffective organisms, remove injured cells, and release inflammatory mediators. Mast cells/basophils, neutrophils, and eosinophils; monocytes/macrophages

Mast Cells (tissue)/Basophils (blood)

Initiate inflammatory response through degranulation and the synthesis/release of inflammatory mediators (histamine, chemotactic factor, and arachidonic acid)

Mast cell release of histamine:

Released during degranulate. It causes vasodilation (redness/erythema), warmth, and swelling/edema (capillary weeping/leaking), as well as bronchoconstriction and abdominal cramping (due to smooth muscle constriction)

Mast cell release of chemotactic factor:

released during degranulation. It attracts neutrophils to the site of injury/inflammation

Mast cells synthesis of arachidonic acid:

Arachidonic acid mixed with COX creates prostaglandins and arachidonic acid mixed with LOX creates leukotrienes (SRS-A)

Prostaglandins

cause PAIN, vasodilation, and platelet aggregation

Leukotrienes

cause bronchoconstriction and vasodilation

Neutrophils

drawn to the site of injury by chemotactic factor released by mast cell degranulation. First meal is their last meal

- Role: phagocytosis of bacteria (and some fungi/parasites)

- after phagocytosis, the release cell contents and digestive enzymes causing liquefaction of surrounding tissue (pus)

- removed through lymph

- high number in bacterial infections

Eosonophils

Control inflammatory response. 2nd to arrive.

- Role: mediates histamine (releases more by stimulating mast cells to degranulate), helps dissolve clots, high number in parasitic infections (and some asthmas/allergies)

Monocytes (blood)/Macrophages (tissue)

Largest and slowest WBC. Last to arrive at site of injury

-Role: phagocytosis of large foreign particles

- High number in chronic inflammation

- produces IL-1 and TNF

Immature Neutrophil

Band cell, high in bacterial infections

Cell Derived mediators of inflammation:

arachidonic acid (+cox = prostaglandins, + lox = leukotrienes), cytokines (interleukin-1 and tumor necrotic factor), histamine, serotonin, nitric oxide, platelet aggregating factor (PAF)

Granulocytes

neutrophils, eosinophils, basophils/mast cells

Agranulocytes

lymphocytes and monocytes/macrophages

Interleukin-1

produced by macrophages/monocytes and dendritic cells in response to bacteria (primarily), endotoxins, antigens, and antigen-antibody complexes

Functions:

- PRIMARY ROLE: works on hypothalamus to increase temperature (fever)

- mobilizes neutrophils

- stimulates growth of B cells

Tumor Necrotic Factor

produced by macrophages in response to gram negative bacteria

Functions:

- PRIMARY ROLE: increases neutrophil emigration and phagocytosis and inhibits tumorigenesis

- works on hypothalamus to increase temperature (fever)

- high levels indicate endotoxic shock (sepsis)

Nitric oxide

naturally found in the body. acts as a vasodilator and kills virally infected cells/tumor cells/parasites, regulates O2 binding, and stimulates production of new mitochondria

Plasma Protein systems

1. Complement system

2. Clotting system

3. Kinin system

Complement System activation

Activated by antigens, antibodies, bacteria, and stimulation of clotting/kinin systems

Complement system functions:

1. opsonization (coats bacteria to make them more enticing to macrophages)

2. release of chemotactic factor (attracts more phagocytes/neutrophils)

3. vasodilation

4. Membrane attack Complex (lysis of cell membranes)

Clotting System Functions

stops bleeding, localizes microorganisms, and provides a meshwork for repair and healing.

-vasoconstriction

- platelet plug formation (activated by PAF)

- fibrin web production

- chemotaxis for neutrophils

Can be extrinsic (10 seconds) or intrinsic (10 minutes)

Kinin System

Most active with prolonged/chronic inflammation

-Bradykinin is the primary plasma protein

Bradykinin causes:

- smooth muscle contraction (bronchoconstriction)

- vasodilation of arterioles

- prostaglandin stimulation (pain)

- chemotactic factor

- leukotrienes

- increased capillary permeability

Systemic Inflammation symptoms:

fever, leukocytosis (increase band cells/neutrophils, increased WBC count), lymphadenitis (painful, swollen lymph nodes)

Chronic inflammation symptoms:

incomplete wound healing, persistent signs of local and systemic infection, scarring

Healing

final step in the inflammatory response. Three phases:

1. Resolution (cells return to normal)

2. Repair (replacement of destroyed tissue with scar tissue

3. Healing (primary intention- stitches, minimal tissue loss; secondary intention- heals from inside out, results in scar formation)

Dysfunctional wound healing

Insufficient repair of wound, excessive repair (keloids), or infection

What are the four cardinal signs of inflammation?

Rubor, tumor, calor, dolar

Where do mast cells originate? Where do they mature?

Originate in bone marrow, mature in tissues near blood vessels

Basophils release what?

heparin and histamine

SRS-A

slow-reacting substances of anaphylaxis - also called leukotrienes

What are the first cells to arrive after mast cell degranulation?

Neutrophils

Why is a fever sometimes a good thing?

It creates an environment that will most likely inhibit the growth of infectious agents (bacteria, fungi, and parasites)

Body's Lines of defense:

1. Mechanical/chemical barriers (skin, mucous membranes, GI/GU tracts) NON-specific

2. Inflammatory response NON-specific and rapid

3. Immune response SPECIFIC, complex, has memory

Immunity

the protection from disease

- SPECIFIC: every disease has its own set of antibodies

Antigens

a foreign protein or molecule that is recognized by the immune system and induce an immune reaction.

1. alloantigens

2. heteroantigens

Alloantigens

antigens from human proteins other than yourself ex. human proteins, blood, tissues, organs

Heteroantigens

antigens from other species, such as other animals, plants, or microorganisms

Haptens

Very small antigens that do not trigger the immune response and must bind to another immunogen in order to be recognized (classic example is penicillin)

Lymphocytes

The two types of white blood cells that are part of the body's immune system. Includes T cells and B cells

Innate Immunity

Immunity that is present before exposure and effective from birth. It is nonspecific and has no memory; lasts until ~3 months of age

Adaptive Immunity

An antigen specific immune response can be passive or active and naturally or artificially acquired

Passive Natural Adaptive Immunity

antibodies from mother to baby (ex. breast milk)

Active Natural Adaptive Immunity

antibodies are created from exposure to previous illness (you had the disease)

Passive Artificial Adaptive Immunity

Antibody transfer from gamma globulin or immune serum

Active Artificial Adaptive Immunity

Antibodies produced due to vaccination or toxoids

What is the purpose of the immune response?

protects organisms from infection with layered defenses (Innate immunity provides a rapid, nonspecific response; adaptive immunity provides a specific response)

How does the immune response recognize foreign from self?

Every cell carries a surface marker that distinguishes it as "self" called HUMAN LEUKOCYTE ANTIGENS (HLA) or major histocompatibility complex (MHC)

MHC Class 1

protein markers on all cells

MHC Class 2

protein markers on certain specialized cells

How the body handles antigens:

The initial response is that the antigen is recognized by a T helper cell

Epitopes

distinctive markers on antigens that trigger the immune response

Cytokines

The messengers of the immune system.

-Cytokines produced by monocytes/macrophages: IL-1 and TNF (raise temperature)

- Cytokines produced by lymphocytes are leukokines/lymphokines: IL-2 stimulate growth of T cells and activity of NKT cells and interferons interfere with virus replication

Antigen presenting cells

They wear the antigen and show it until T helper sees and activates immune response: dendritic cells, macrophages (place pieces of phagocytized antigen (epitopes) on self to alarm other immune cells), B cells

B cells

produce antibodies

T helper cells (Th)

Master Regulator; increase B cell activity and direct other T cells and entire immune response

Cytotoxic T cells (Tc)

destroy cells by directly attacking antigen. They can also see internal changes of cells and recognize antigens

Natural Killer Cells (NKT)

Innate immunity not antigen specific. Can kill virally infected cells or malignant cells. They release cytokines

T regulator/suppressor cells

Decrease B cell activity

T memory cell

Remembers the antigen and recipe for it

- 21 days for primary response

- seconds for secondary response

Functions of antibodies (immunoglobins)

1. opsonization of bacteria (coats bacteria to make them more enticing)

2. neutralizing toxins

3. Agglutination of viruses (clumping of virus material) The only thing that kills viruses

4. activate inflammatory response

Types of Immunoglobins

IgA: protects portals of entry

IgM: first response (first antibody made for first exposure)

IgG: second response (second exposure, more dominant antibody produced)

IgE: hypersensitivity response (Inappropriate response regulated by Th2)

IgD: dunno. found on surface of B cells

Primary Immune response is ___ and Second immune response is ____

Slow, Rapid

What cell activates the immune response?

T helper cells

What cell activates the B cells (humoral immune response)?

T helper cells

Humoral Immunity

specific immunity produced by B cells that produce antibodies that circulate in body fluids (plasma cells indirectly attack antigens with the production of antibodies)

Complement System

proteins in the plasma activated by antigen-antibody response causes vasodilation, opsonization, chemotaxis, and MAC