Kydada's Exam II

Question 1

What factors can induce vasodilation?

Answer 1

Histamine, bradykinin, leukokinins, some prostaglandins (PGI2, D2, E2, F2α)

These substances are involved in the inflammatory response and help increase blood flow to affected areas.

Question 2

Which cell types are involved in acute inflammation?

Answer 2

Neutrophils

Neutrophils emigrate within one hour and have a short lifespan in the tissue.

Question 3

Which cell types are involved in chronic inflammation?

Answer 3

Macrophages, lymphocytes

Macrophages enter after 12-48 hours and are capable of long life in the tissue.

Question 4

What contents are found in mast cell granules?

Answer 4

Histamine, proteolytic enzymes, heparin, chondroitin sulfate, chemotactic factors

These substances play roles in inflammation and immune responses.

Question 5

What are the granule contents of platelets?

Answer 5

Histamine, thromboxane A2, P-selectin, growth factors (PDGF, FGF, TGF), enzymes

These components are involved in hemostasis and inflammation.

Question 6

What is the sequence of leukocyte efflux from the vasculature?

Answer 6

Margination, rolling, adhesion and pavementing, transmigration, migration in tissue

Each step involves specific receptors and ligands.

Question 7

List a few chemotactic molecules.

Answer 7

C5a, bacterial products, leukotrienes (LTB4, 5-HETE), fibrin degradation products, WBC products (IL-8, MCP-1, PAF)

These molecules attract leukocytes to sites of inflammation.

Question 8

What are the steps in phagocytosis?

Answer 8

Opsonization, attachment, ingestion, killing and degradation

This process is crucial for clearing pathogens from the body.

Question 9

What are opsonins?

Answer 9

Antibodies (immunoglobulins), complement proteins (C3b, C3bi)

Opsonins coat cells or pathogens to enhance phagocytosis.

Question 10

What factors are involved in oxygen-dependent killing in macrophages?

Answer 10

ROS produced by NADPH oxidase

Reactive oxygen species are key to the macrophage’s ability to kill pathogens.

Question 11

What factors are involved in oxygen-independent killing in macrophages?

Answer 11

Enzymes and antimicrobial peptides including BPI, defensins, lysozymes, lactoferrin, Nramp-1

These components provide an alternative method for macrophages to eliminate pathogens without oxygen.

Question 12

How can inflammation damage host tissues?

Answer 12

Neutrophil-mediated damage including lysosomal suicide, frustrated phagocytosis, regurgitation while feeding

These mechanisms can lead to tissue injury during inflammation.

Question 13

What are the chemical mediators of inflammation?

Answer 13

Plasma-derived: Hageman factor, complement components (C3a, C5a, C5b-9), kininogens; Cell-derived: histamine, serotonin, lysosomal enzymes, prostaglandins, leukotrienes, PAF, cytokines, nitric oxide

These mediators play diverse roles in regulating the inflammatory response.

Question 14

What are the functions of kinins?

Answer 14

Vasodilation, increased vascular permeability, pain

Kinins are important in the inflammatory process and contribute to symptoms of inflammation.

Question 15

What initiates the three main complement pathways?

Answer 15

Classic pathway: immune complexes; Alternate pathway: contact with fungal and bacterial cell walls; Lectin pathway: plasma mannose-binding lectin binding to carbohydrates on microbes

These pathways converge at C3 leading to the formation of the membrane attack complex (MAC).

Question 16

What are the actions of complement fragments?

Answer 16

MAC: produces pore-like structure; C3b and C3bi: opsonins; C3a and C5a: anaphylatoxins

Each fragment has specific roles in immune response and inflammation.

Question 17

What is the arachidonic acid pathway?

Answer 17

Includes cyclooxygenase and lipoxygenase pathways; produces prostaglandins, leukotrienes

These products are important mediators in inflammation.

Question 18

How do NSAIDs and glucocorticoids affect the arachidonic acid pathways?

Answer 18

NSAIDs are non-selective; glucocorticoids induce lipocortin expression, inhibiting phospholipase and COX-2

This inhibition reduces inflammation and pain.

Question 19

What are the functions of nitric oxide and platelet activating factor?

Answer 19

Nitric oxide: vasodilator; platelet activating factor: mediator of inflammation, platelet aggregation, vascular permeability

Both play critical roles in the inflammatory response.

Question 20

What are the general classes of cytokines?

Answer 20

Regulate lymphocytes: IL-2, 4, 10; Natural immunity: TNF, IL-1, IL-6; Activate inflammatory cells: IFN, TNF; Stimulate hematopoiesis: IL-3, 5, 7, CSFs; Chemokines

Cytokines are key regulators of immune responses.

Question 21

What are the four classes of chemokines and their functions?

Answer 21

C-X-C (alpha): act on PMNs; C-C (beta): act on cells other than PMNs; C (gamma): act on lymphocytes; C-X-C-C: chemotactic and adhesive for monocytes and lymphocytes

Chemokines guide the movement of immune cells.

Question 22

What are the functions of IL-1 and TNF?

Answer 22

Increase leukocyte adherence, procoagulant potential of endothelium

Both cytokines are critical in the inflammatory response.

Question 23

What are some acute phase proteins?

Answer 23

Complement proteins, coagulation proteins, antiproteinases, metal-binding proteins, LPS binding proteins, Serum Amyloid A

These proteins are involved in the acute phase response during inflammation.

Question 24

What are the potential outcomes of acute inflammation?

Answer 24

Complete resolution, scarring, abscessation, chronic inflammation

These outcomes depend on the severity and context of the inflammatory response.

Question 25

What causes chronic inflammation?

Answer 25

Continuation of acute inflammation, chronic repeated injury, insidious onset without apparent acute phase ## Footnote Chronic inflammation can develop from unresolved acute inflammation.

Question 26

What is a granuloma?

Answer 26

Discrete aggregate of epithelioid macrophages with mantle of lymphoid cells and peripheral fibrosis ## Footnote Granulomas form in response to persistent antigens.

Question 27

What are the mechanisms of healing and repair?

Answer 27

Parenchymal regeneration, replacement by fibrous tissue ## Footnote Replacement occurs when the stromal framework is destroyed or when permanent cells are damaged.

Question 28

What factors influence healing?

Answer 28

Stromal integrity, regeneration capacity of tissue ## Footnote The type of tissue and its environment affect the healing process.

Question 29

Differentiate between labile, stable, and permanent cells, with examples.

Answer 29

Labile: high turnover (e.g., skin cells); Stable: low mitotic activity but capable of rapid replication (e.g., liver cells); Permanent: terminally differentiated (e.g., neurons) ## Footnote Understanding cell types is crucial for knowing how different tissues heal.

Question 30

What are growth factors?

Answer 30

Proteins that regulate growth, regeneration, neoplasia ## Footnote Examples include epidermal growth factor, platelet-derived growth factor, transforming growth factor.

Question 31

What is granulation tissue?

Answer 31

Proliferation of fibrovascular tissue filling tissue defects ## Footnote It provides a framework for fibrous tissue elaboration.

Question 32

What are the phases of wound healing?

Answer 32

Inflammation, cell migration, matrix deposition, vascular proliferation, collagen synthesis, remodeling ## Footnote These phases are critical for proper healing.

Question 33

What is the difference between first and second intention healing?

Answer 33

First intention: wound edges opposed, rapid healing; Second intention: defect filled with granulation tissue, prolonged course ## Footnote Second intention healing has a greater potential for scarring.

Question 34

What are some adverse outcomes of healing?

Answer 34

Excess granulation tissue, keloid, adhesion, ankylosis, stricture, contracture ## Footnote Abnormal healing can lead to significant complications.

Question 35

What is the shock organ for cattle and sheep?

Answer 35

Lung ## Footnote Clinical signs include cough and dyspnea.

Question 36

What are the mediators of the Type I hypersensitivity early phase?

Answer 36

Histamine, PGD2, LTC4, PAF ## Footnote These mediators increase vascular permeability and cause smooth muscle contraction.

Question 37

What are the mediators of the Type I hypersensitivity late phase?

Answer 37

Leukotrienes, cytokines, chemokines ## Footnote These mediators cause sustained edema and accumulation of WBCs.

Question 38

What are the main mechanisms of Type II hypersensitivity?

Answer 38

Complement-mediated (direct lysis, opsonization), antibody-mediated ## Footnote These mechanisms involve the immune system attacking the body's own cells.

Question 39

What is neonatal isoerythrolysis?

Answer 39

Condition where mare's antibodies attack foal's RBCs through colostrum ## Footnote It typically occurs when the foal inherits a different blood type from the mare.

Question 40

List a few antigens that incite a Type III reaction.

Answer 40

Staphylococcus, feline coronavirus, canine adenovirus-1, equine infectious anemia ## Footnote Persistent antigens can trigger Type III hypersensitivity.

Question 41

How does a Type III reaction cause tissue damage?

Answer 41

Formation of antigen-antibody complexes leading to complement activation and neutrophil influx ## Footnote This results in tissue destruction.

Question 42

What is fibrinoid necrosis?

Answer 42

Degenerative changes in blood vessel walls due to fibrin deposition ## Footnote This process affects the structure of the vessel wall.

Question 43

What are the main mechanisms of Type IV hypersensitivity?

Answer 43

Release of soluble cytokines from CD4+ T cells, direct cytotoxicity by CD8+ T cells ## Footnote This type of hypersensitivity involves T cell-mediated immune responses.

Question 44

What is self-tolerance?

Answer 44

Loss of self-tolerance is central to autoimmune disease development ## Footnote It involves both central and peripheral tolerance mechanisms.

Question 45

What are two manifestations of autoimmunity?

Answer 45

Organ-specific, systemic ## Footnote Autoimmunity can affect specific organs or the entire system.

Question 46

What is pemphigus vulgaris?

Answer 46

Autoimmunity directed against extracellular matrix adhesion protein ## Footnote It causes fluid-filled blisters on skin and mucous membranes.

Question 47

What is autoimmune hemolytic anemia?

Answer 47

Condition where the immune system attacks and removes RBCs ## Footnote This leads to severe anemia and jaundice.

Question 48

What is lymphocytic thyroiditis?

Answer 48

Immune response against thyroglobulin or TSH hormone receptor ## Footnote This condition causes hypothyroidism.

Question 49

What is autoimmune hemolytic anemia?

Answer 49

Condition in which the body’s immune system attacks and removes its own RBCs, leading to severe anemia and jaundice or icterus ## Footnote It is classified as a Type II hypersensitivity.

Question 50

What is lymphocytic thyroiditis (hypothyroidism)?

Answer 50

Immune response against thyroglobulin or TSH hormone receptor ## Footnote This condition is also a Type II hypersensitivity.

Question 51

Differentiate between discoid lupus and systemic lupus erythematosus.

Answer 51

SLE affects the dog’s entire body, while DLE affects just the skin. SLE is considered a Type II or Type III reaction. ## Footnote Biopsy and blood tests are required to differentiate them.

Question 52

What are the host defense mechanisms of the skin?

Answer 52

Epithelial barrier and production of antimicrobial substances ## Footnote These mechanisms help protect against pathogens.

Question 53

What host defense mechanisms are present in the GI tract?

Answer 53

Epithelial barrier, acidic secretions, bile and pancreatic enzymes, mucous layer, antimicrobial defensin proteins, IgA produced in Peyer patches, peristalsis, gut flora ## Footnote These components work together to prevent infection.

Question 54

What are the defense mechanisms of the respiratory tract?

Answer 54

Mucus layer, ciliary sweeping, alveolar macrophages, defensins ## Footnote These mechanisms help trap and eliminate pathogens.

Question 55

What are the host defense mechanisms in the urogenital tract?

Answer 55

Micturition, acidic pH, mucosal lining, conformation ## Footnote These features help prevent infections in the urogenital region.

Question 56

What is antigenic variation?

Answer 56

The mechanism by which an infectious agent alters the proteins or carbohydrates on its surface to avoid a host immune response ## Footnote Examples include antigenic drift and shift in viruses, and genetic rearrangement in spirochetes.

Question 57

What is shock?

Answer 57

A state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia ## Footnote It is a common final pathway to death.

Question 58

What are the three major types of shock?

Answer 58

Hypovolemic shock, neurogenic shock, cardiogenic shock ## Footnote Each type has different underlying causes and mechanisms.

Question 59

Identify important pattern recognition receptors (PRRs).

Answer 59

Membrane localized toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-1-like receptors (RLRs) ## Footnote PRRs play a crucial role in the immune response.

Question 60

What are some causal classifications of shock?

Answer 60

Hypovolemic shock: burns, trauma, hemorrhage, fluid loss; Neurogenic shock: anesthetic accident, CNS or emotional trauma; Cardiogenic shock: myocardial failure, cardiac tamponade, pulmonary embolism; Septic shock: endotoxemia, gram positive septicemia, fungal sepsis, superantigens ## Footnote Each classification has specific causes and implications.

Question 61

How is shock characterized?

Answer 61

Hypotension, tachycardia with vasoplegia, hypoxemia, cool skin, lactic acidosis, anxiety, confusion, coma, multiple organ failure ## Footnote These signs indicate the severity of shock.

Question 62

Describe the three phases of shock.

Answer 62

Non-progressive: adaptive neurohumoral responses; Compensatory (reversible) phase: body compensates for decreased tissue perfusion; Decompensated (irreversible) shock: signs of organ dysfunction appear ## Footnote Proper intervention during the compensatory phase can prevent irreversible damage.

Question 63

Identify the critical players in septic shock.

Answer 63

PAMPS, DAMPS, and PRRs; Cytokines and other mediators; Neutrophils, macrophages, platelets, vasculature; Complement and coagulation cascades ## Footnote These components are essential in the pathophysiology of septic shock.

Question 64

What is hypoxemia?

Answer 64

Low oxygen levels in the blood ## Footnote It is related to shock as circulatory shock leads to cellular and tissue hypoxia.

Question 65

What can NOS inhibition do to improve septic shock?

Answer 65

It can temporarily restore blood pressure, myocardial contractility, and improve oxygen extraction and vasomotor responses ## Footnote However, it can also contribute to mortality depending on which isoform is inhibited.