Lecture 21 Flashcards

1
Q

immune complex type hypersensitivity: Involves soluble immune complexes (IgG, IgM, IgA) of antibody and antigen; Only involves complement binding Abs; Complexes are spread to joints/kidneys; Complexes precipitate and activate complement causing tissue damage

A

Type 3

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2
Q

Present in almost all tissues and are the mature form of monocytes.Orchestrate immune responses and help induce inflammation.Secrete signaling proteins that activate other immune cells.General scavenger cells in the body

A

macrophages

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3
Q

release of granules containing histamine and active agents

A

mast cell

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4
Q

3 stages of healing cascade

A

inflammation, proliferation, and remodeling

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5
Q

not true cells, cytoplasmic fragments w/ purple granules that contain chemical for blood clotting (enzymes, serotonin, Ca2+ ions, ADP, and PDGF), normally kept in “inactive” state by molecules secreted by endothelial cells of blood vessels; when activated, form temporary plug that helps to seal breaks in blood vessels

A

platelets

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6
Q

anuclear cell bodies derived from megakaryocytes, which circulate in the vasculature. undergo Adhesion, Activation, and Aggregation during coagulation.

A

Platelets (thrombocytes)

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7
Q

migration of leukocytes (mainly neutrophils or PMNs) into the site of injury (cellular recruitment and activation) associated with acute inflammation

A

cellular events

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8
Q

Cells of the immune system that store and release histamine

A

Mast Cells

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9
Q

is a monoamine neurotransmitter. Derived from tryptophan, primarily found in the gastrointestinal tract (GI tract), blood platelets, and the central nervous system. Released upon degranulation of platelets at site of injury. Functions as a smooth muscle constrictor to immediately act to limit the loss of blood volume

A

Serotonin

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10
Q

activated function of phagocytosis and activation of bactericidal mechanisms; antigen presentation

A

macrophages

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11
Q

antibody dependent hypersensitivity: cell membrane antigens altered to “non self”; could be from complement mediated lysis of host cells, antibody dependent cell mediated cytotoxicity, or direct binding by antibody to stimulate the cell

A

Type 2

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12
Q

balance between constrictor and dilator influences

A

vascular tone

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13
Q

contraction of smooth muscle cells of vessel walls to restrict the loss/flow of blood at site of injury; triggered by sympathetic nerves

A

vasoconstriction

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14
Q

is the most important mediator of a type IV reaction

A

IFNy

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15
Q

cell mediated hypersensitivity: Important mechanism to protect against intracellular pathogens (AIDS patients often get TB); Mediated by T cells rather than by antibody; Either CD4 Helper T cells or CD8 cytotoxic T cells

A

Type 4

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16
Q

anaphylactic hypersensitivity: includes Hayfever, bee sting, allergic asthma, penicillin, and aspirin: allergy and atrophy

A

Type 1

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17
Q

ancestral system designed to keep an individual from bleeding; includes the vascular system, the coagulation system, fibrinolytic system, platelets, kinin system, serine protease inhibitors, and the complement system

A

hemostatic system

18
Q

formed when fluid leaks out because of increased hydrostatic pressure or decreased colloid osmotic pressure; low protein content, few cells

A

transudate

19
Q

3 major components of acute inflammation

A

vascular changes, cellular events, and mediators

20
Q

sympathetic nerves and circulating factors

A

extrinsic factors

21
Q

formed in inflammation where there is high protein content, and may contain some white and red cells; vascular permeability increases as a result of increased interendothelial spaces; protein and fluid leakage

A

exudate

22
Q

____ infiltrate in response to lipid mediators including leukotriene B4 and engulf and degrade pathogens

A

PMNs

23
Q

derived from plasma cells and proteins associated with acute inflammation

A

mediators

24
Q

is a critical factor in initiating the immune response mechanisms to fight inflammation. It causes vasodilation and permits entry of cells and proteins into the site of the infection to engage invading pathogens. It also is a mediator of itching.

A

Histamine

25
Q

Pro-coagulant in its actions (acts as a vasoconstrictor) with short half-life (30 sec). Produced by activated platelets it stimulates activation of new platelets as well as increases platelet aggregation through increasing expression of the GPIIb/IIIa protein complex on platelet membranes. This same effect is also how ADP stimulates platelet activation. Drug Clopidogrel blocks this action. Works by binding to thromboxane A2 receptors (G protein coupled receptor) on platelets. Synthesized by thromboxane-A synthase from prostaglandin H2 in a reaction which also produces equal amounts of 12-Hydroxyheptadecatrienoic acid (12-HHT).

A

Thromboxane A2 (TXA2)

26
Q

your body’s process of fighting against things that harm it, such as infections, injuries, and toxins, in an attempt to heal itself

A

Inflammation

27
Q

increased blood flow (vasodilation) and increased vascular permeability associated with acute inflammation

A

vascular changes

28
Q

Primary cells recruited into site of acute inflammation (PMNs)Most numerous of the phagocytic cells and most important in innate immune responses

A

neutrophil

29
Q

bind to one of four different histamine G-protein coupled receptors on GI, uterus, lung, and vascular smooth muscle cells. Causes vasodilation of vasculature and vasoconstriction of alveolar airways. produced and released from basophils (circulation) and mast cells (connective tissue) during local immune responses

A

Histamine

30
Q

myogenic, endothelial, local substances, and metabolic byproducts

A

intrinsic factors

31
Q

3 stages of hemostatic system

A

vasoconstriction of blood vessels, formation of a platelet plug, and blood clotting which reinforces the platelet plug with a fibrin mesh

32
Q

exposed collagen fibrils represent a site of platelet attachment to initiate blood coagulation.

A

Tissue Collagen

33
Q

normally 1/10,000 bone marrow cells are these large multi-lobulated nuclear cells which give rise to platelets. Number can rise dramatically in disease.

A

Megakaryocytes:

34
Q

earliest stage of inflammation is marked by

A

tissue edema

35
Q

Cell stressors like ischemia activate ________ which cleaves arachidonic acid from membrane phospholipids and facilitates formation of prostaglandins

A

phospholipase A2

36
Q

Anti-coagulant in its actions (it inhibits platelet activation and acts as a vasodilator). produced in endothelial cells, which line the walls of arteries and veins, from prostaglandin H2(PGH2) by the action of the enzyme prostacyclin synthase. has a half-life of 42 seconds, is broken down into 6-keto-PGF1, which is a much weaker vasodilator

A

Prostacyclin PGI2

37
Q

Primary cells recruited into site of acute inflammation. Most numerous of the phagocytic cells and most important in innate immune responses

A

Neutrophils (PMNs)

38
Q

(made and released by damaged endothelial cells). Normally kept in balance by other mechanisms but when overexpressed can contribute to high blood pressure (hypertension) and heart disease among other diseases. Implicated in vascular diseases of heart, lung, kidney and brain.

A

Endothelin-1

39
Q

production of erythrocytes: erythropoiesis

A

hemocytoblast, proerythroblast, erythroblast, normoblast, reticulocyte, and erythrocyte

40
Q

5 cardinal signs of inflammation

A

pain, heat, redness, swelling, and loss of function