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General Pathology > defense part I > Flashcards

defense part I Flashcards

1
Q

inflammation

A

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

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2
Q

CT cells

A

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

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3
Q

5 signs of inflammation

A

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

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4
Q

vascular changes

A

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)

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5
Q

vascular permeability

A

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)

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6
Q

margination

A

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

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7
Q

leukocyte migration

A

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

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8
Q

selectins

A

1) proteins on platelets

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9
Q

integrins

A

1) protein on the surface of leukocytes adhere to endothelium

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10
Q

toll-like receptors

A

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

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11
Q

G-protein coupled receptors

A

1) short bacterial peptides

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12
Q

opsonin receptors

A

1) thins that coat microbes (antibodies, compliment)

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13
Q

cytokine receptors

A

1) interferons (which activate macrophages)

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14
Q

phagocytosis and degranulation

A

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

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15
Q

myeloperoxidase deficiency

A

1) no burst of OCl- to kill bacteria

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16
Q

chediak-higashi syndrome

A

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

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17
Q

chonic granulomatous disease

A

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

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18
Q

leukocyte adhesion deficiency

A

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

They don’t roll or adhere

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19
Q

chronic granulomatous disease

A

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

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20
Q

chemical mediators of inflammation

A

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

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21
Q

preformed mediators in secretory granules

A

1) histamine, serotonin, and lysosomal enzymes

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22
Q

newly syntheized

A

1) prostaglandins, leukotrienes, etc

23
Q

factor XII

A

1) hagemen factor activation

24
Q

6 main cytokkines

A

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

25
Q

cytokines

A

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

26
Q

acute phase reaction

A

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

27
Q

endothelial effects

A

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

28
Q

fibroblast effects

A

1) collagen proliferation, collagenase

29
Q

leukocyte effects

A

1) more cytokine secretion

30
Q

histamine

A

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

31
Q

serotonin

A

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

32
Q

anaphylatoxins

A

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

33
Q

factor XII (hagemen)

A

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

34
Q

kinin system

A

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

35
Q

oxygen derived free radicals

A

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

36
Q

outcomes of acute inflammation

A

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

37
Q

mediators and chronic inflammation

A

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

38
Q

chronic inflammation

A

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

39
Q

chronic inflammatory cells

A

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

40
Q

activated T cells

A

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

41
Q

a focus forms

A

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

42
Q

plasma cells

A

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

43
Q

eosinophils

A

1) parasitic infections or allergic reactions

44
Q

granulomatous inflammation

A

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

45
Q

necrotizing granulomatous inflammation

A

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

46
Q

role of lymphatics in inflammation

A

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)

47
Q

morphologic patterns of acute and chronic inflammation

A

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

48
Q

purulent

A

1) full of pus

49
Q

fever

A

1) IL1-TNF <=> IL6
2) hypothalamus
3) protaglandins (E)
4) vasculomotor center
5) sympathetic nerves
6) skin vasoconstriction
7) heat dissipation

50
Q

leukocytosis left shift

A

1) WBC count of 15-20k left shift

51
Q

neutrophilia

A

1) usually occurs in bacterial infections

52
Q

lymphocytosis

A

viral infection

53
Q

leukemoid reaction

A

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

54
Q

leukopenia

A

1) decrease in WBC
- ex typhoid fever

General Pathology (10 decks)

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