defense part I

Question 1

inflammation

Answer 1

1) protective response intended to eliminate the initial cause of the cell injury and the necrotic cells and tissues arising as a consequence
2) often gets triggered when it shouldn’t

Question 2

CT cells

Answer 2

1) mast cells, fibroblasts, macrophage
2) matrix
- elastic, collagen, proteoglycan

Question 3

5 signs of inflammation

Answer 3

1) heat
2) redness
3) swelling
4) pain
5) loss of function

Question 4

vascular changes

Answer 4

1) antigens are present
2) changes in vascular flow and caliber
- initial vasoconstriction
- then vasodilation (erythema and warmth)
3) exudation of protein rich fluid
- blood viscosity increases (stasis of circulation)
- leukocytes settles along endothelial cells (margination)
- leukocytes adhere to endothelial cells and migrate between (migration)

Question 5

vascular permeability

Answer 5

1) hydrostatic pressure increases
- transudate (protein poor fluid)
2) osmatic pressure increases in arteriole
3) more protein rich filtration (exudate)
4) increased in interstitial osmotic pressure and decrease in intravascular OP (edema)

Question 6

margination

Answer 6

1) begins inflammation by recruitment of WBC by infection or injury

Question 7

leukocyte migration

Answer 7

1) p-selectin
- rolling
2) e-selectin
- rolling and adhesion
3) glycan-1
- rolling
4) ICAM-1
- adhesion, arrest, transmigration
5) VCAM-1
- adhesion

Question 8

selectins

Answer 8

1) proteins on platelets

Question 9

integrins

Answer 9

1) protein on the surface of leukocytes adhere to endothelium

Question 10

toll-like receptors

Answer 10

1) components of macrophages and dendritic cells that recognize viruses and bacteria

Question 11

G-protein coupled receptors

Answer 11

1) short bacterial peptides

Question 12

opsonin receptors

Answer 12

1) thins that coat microbes (antibodies, compliment)

Question 13

cytokine receptors

Answer 13

1) interferons (which activate macrophages)

Question 14

phagocytosis and degranulation

Answer 14

1) immunoglobin and complement are coating the pathogen and engulfed by macrophage
2) lysosomes with granules fuse with it
3) within the phagolysosome, they are killed
- NADPH with cytoplasmic oxidase causes O2 => superoxide
- hydrochlorous acid
- bacteriocidal

Question 15

myeloperoxidase deficiency

Answer 15

1) no burst of OCl- to kill bacteria

Question 16

chediak-higashi syndrome

Answer 16

1) no fusion of the lysosome with phagosome
2) problems in melanocytes (albinism), nervous system cells, and platelets

Question 17

chonic granulomatous disease

Answer 17

1) no superoxide formation (phagocyte oxidase)
2) macrophages come and take over neutrophil job
- make granulomas

Question 18

leukocyte adhesion deficiency

Answer 18

1) type 1
- mutation in an integrin
2) type 2
- mutation in a ligand for selectins

They don’t roll or adhere

Question 19

chronic granulomatous disease

Answer 19

1) patients have defect in the genes that encode phagocyte oxidase
2) because the neutrophils can’t do the job, macrophages come in and take over, making granulomas

Question 20

chemical mediators of inflammation

Answer 20

1) bind to receptors or have direct enzymatic toxic effects
- cellular (histamine) or plasma origin (complement and kinin)
2) may stimulate targets to release 2ndary effector molecules which amplify or counter regulate the initial stimulus
3) decay quickly or are inactivated
4) cause harmful effects

Question 21

preformed mediators in secretory granules

Answer 21

1) histamine, serotonin, and lysosomal enzymes

Question 22

newly syntheized

Answer 22

1) prostaglandins, leukotrienes, etc

Question 23

factor XII

Answer 23

1) hagemen factor activation

Question 24

6 main cytokkines

Answer 24

1) TNF
- release of other cytokines
2) *IL(interleukin)-1: similar to TNF
- BIG ROLE IN FEVER
3) IL-6
- secreted by macrophages; systemic effects
4) IL-12
- secreted by macrophages; increases production of IFN gamma
5) IFN (interferon) gamma: secreted by T cells, tells macrophages to KILL
6) IL-17: secreted by T cells; calls in neutrophils and monocytes

Question 25

cytokines

Answer 25

1) polypeptide products of many cell types that modulate the function of other cell types 2) autocrine, paracrine, or endocrine

Question 26

acute phase reaction

Answer 26

1) fever, feeling sick and tired - IL-1 and TNF 2) shock, neutrophilia

Question 27

endothelial effects

Answer 27

1) leukocyte adherence 2) IL-1 release and friends 3) procoagulant

Question 28

fibroblast effects

Answer 28

1) collagen proliferation, collagenase

Question 29

leukocyte effects

Answer 29

1) more cytokine secretion

Question 30

histamine

Answer 30

1) released in response to - injury - immune rxn - anaphylatoxins - leukocyte derived histamine releasing factors - neuropeptides - cytokines 2) affects arteriolar dilation and permeability

Question 31

serotonin

Answer 31

1) stimulated by platelet aggregation 2) affects arteriolar dilation and permeability

Question 32

anaphylatoxins

Answer 32

1) C3a and C5a - vascular permeability and vasodilation - induce mast cells to release histamine 2) C5a increase leukocyte adhesion to endothelial cells --- 2) C3b and C3bi are opsonins - coats which enhance phagocytosis

Question 33

factor XII (hagemen)

Answer 33

1) when activated, it causes kinin cascade 2) HMWK => bradykinin -important chemical mediator of pain 3) fibrinolytic system - counteracts clotting 4) complement cascade - C3 => C3a

Question 34

kinin system

Answer 34

1 ) bradykinin causes increased vascular permeability, arteriolar dilation, extravascular smooth muscle contraction and PAIN

Question 35

oxygen derived free radicals

Answer 35

1) produced from NADPH oxidase pathway 2) short lives and cause tissue damage - endothelial damage - breakdown of extracellular matrix - direct injury to other cell types

Question 36

outcomes of acute inflammation

Answer 36

1) injury => acute inflammation -> - resolution (back to normal) - abscess (pus) - healing with scarring

Question 37

mediators and chronic inflammation

Answer 37

1) if there is persistent infection, persistent toxins, autoimmune diseases => chronic inflammation => healing with scarring

Question 38

chronic inflammation

Answer 38

1) infiltration by mononuclear cells 2) tissue destruction 3) repair (angiogenesis and fibrosis) --- 1) prolonged duration 2) acute response cannot be resolved 3) persistent infection (granulomatous inflammation / ex TUBERCULOSIS) 4) prolonged exposure to toxic agents 5) autoimmune diseases

Question 39

chronic inflammatory cells

Answer 39

1) monocytes migrate to site of injury 24-48 hours after onset of acute inflammation and are transformed to macrophages 2) macrophages secrete products which destroy tissue and cause angiogenesis and fibrosis - rid cause of injury and initiate repair

Question 40

activated T cells

Answer 40

1) cytokine IFN-gamma 2) cause monocyte or macrophage to be activated

Question 41

a focus forms

Answer 41

1) they stimulate each other until the antigen is removed 2) lymphocytes, macrophages, other inflammatory mediators 3) granulomatous inflammation

Question 42

plasma cells

Answer 42

1) from B lymphocytes 2) secrete antibody and cause chronic inflammation

Question 43

eosinophils

Answer 43

1) parasitic infections or allergic reactions

Question 44

granulomatous inflammation

Answer 44

1) tuberculosis and leprosy, cat scratch disease - MYCOBACTERIUM 2) fungal infection 3) foreign bodies 4) sarcoidosis 5) crohn disease

Question 45

necrotizing granulomatous inflammation

Answer 45

1) necrosis 2) macrophages 3) multinucleated giant cells 4) lymphocytes

Question 46

role of lymphatics in inflammation

Answer 46

1) fluid drains from interstitial space 2) the fluid has inflammatory cells and proteins 3) lymphatic vessels may become inflamed (lymphagitis and reactive lymphadenitis) 4) infection may enter the blood stream from the lymphatics (bacteremia)

Question 47

morphologic patterns of acute and chronic inflammation

Answer 47

1) serous inflammation - water - mild injuries 2) fibrinous inflammation - more cellular components - deposition of fibrin clots 3) suppurative (purulent) inflammation - acute - neutrophilic abscess 4) ulceration

Question 48

purulent

Answer 48

1) full of pus

Question 49

fever

Answer 49

1) IL1 and TNF alpha and IL6 with prostaglandins to elevate body temperature --- 1) IL1-TNF <=> IL6 2) hypothalamus 3) protaglandins (E) 4) vasculomotor center 5) sympathetic nerves 6) skin vasoconstriction 7) heat dissipation

Question 50

leukocytosis left shift

Answer 50

1) WBC count of 15-20k left shift

Question 51

neutrophilia

Answer 51

1) usually occurs in bacterial infections

Question 52

lymphocytosis

Answer 52

viral infection

Question 53

leukemoid reaction

Answer 53

1) WBC from 40-100k - resembles leukemic infiltration - immature

Question 54

leukopenia

Answer 54

1) decrease in WBC - ex typhoid fever