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Pathology Block 10 > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

T helper cells are classified as ____ and TH2 cells drive a ____ mediated response

A

CD4

Antibody

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2
Q

Identify the most likely type of necrosis to occur in the brain after a stroke

A

Liquefaction necrosis

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3
Q

Thromboxane A2 (TXA2) and prostacuyclin (PGI2) are products of this pathway

A

Arachidonic acid

Cyclooxygenase

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4
Q

Cardinal signs

A 
Rumor 
Calor 
Tumor 
Dolor 
Function laesa
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5
Q

Why is PGE2 unique

A

Primary one for pain

Associated with fever

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6
Q

What makes up the most abundant population of WBCs

A

Neutrophils

- segs, PMNs

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7
Q

Primary leukocyte in acute infection

A

Neutrophils

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8
Q

Primary cell players in chronic inflammation

A

Macrophages and lymphocytes

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9
Q

Where are the neutrophils at

A

50% in circulating pool, and 50% in amrginating pool, tethered to the side of the blood vessel walls
-doing a blood count gives us the count that is circulating in the blood, not tethered to the wall

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10
Q

Neutrophil distribution is influenced by what

A

Activating or inactivating neutrophil adhesion molecules

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11
Q

Trauma and WBC

A

Trauma causes neutrophils to be released from the marginating pool, causing the WBC to shoot up

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12
Q

Steps of acut inflammation

A
  1. IL-1 and TNFa released and upregulate the expression of E selecting and P selectin
  2. Neutrophils weakly bind to endothelial selectins and roll along the surface
  3. Neutrophils stimulated to express ligand for cellular adhesion molecules
  4. Neutrophils adhere firmly to cellular adhesion molecules (ICAMs and VCAMs)
    - neutrophils then emigrate (via diapedesis), migrate through the tissues (via chemotaxis), phagocytize, degranulate and kill what has been eaten
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13
Q

IL-8 in acute inflammation

A

Clean up on aisle 8: neutrophils are attracted to site of damage via IL-8

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14
Q

Exudates and acute inflammation

A

Neutrophils going into an area and killing themselves, producing pus

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15
Q

Where are a vast majority of mast cells

A

Lungs and skin

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16
Q

Earliest signs and symptoms of reaction

A

Itching and difficulty breathing because of mast cells in skin and lungs

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17
Q

Cause vasodilation and increased vascular permeability

A

Histamine

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18
Q

What is histamine produced by

A

Basophils, platelet, and mast cells– release triggers include iGE mast cell reactions, anaphylatoxins and IL-1

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19
Q

Vasoactive amines

A

Histamine

Serotonin

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20
Q

Causes vasodilation and increased vascular permeability produced by platelets

A

Serotonin

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21
Q

Anaphylatoxins

A

C3a and C5a

Cause degranulation

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22
Q

Neutrophil attractants

A

IL-8

C5a

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23
Q

What does the kinin system produce

A

Bradykinin

-causes vasodilation, pain, increased vascular permeability, bronchoconstrition

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24
Q

Factor 12 of coagulation cascade

A

Causes prekallikrein to kallikren

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25
Q

What produces pain

A

NOT HISTAMINE. Bradykinin

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26
Q

Bad actor of COX pathway in arachidonic acid

A

Thromboxane A2

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27
Q

What does aspirin act on

A

Thromboxane A2

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28
Q

What does aspirin

A

Irreversibly acetylates platelets

-neutralized

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29
Q

Is aspirin reversible or irreversible

A

Irreversible, all other NSAIDs are reversible

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30
Q

What is thromboxane A2 produced by

A

Platelets

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31
Q

Prostacyclin (PGI2)

A

COX
Dilates vessels
Inhibits stickiness of platelets

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32
Q

PGE2

A

COX
Pain
Fever

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33
Q

What causes pain

A

PGE2

bradykinin

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34
Q

LOX pathway

A

Leukotriene

Plays a huge role in the lungs and asthma

35
Q

What does arachidonic acid split into

A

LOX and COX

36
Q

What does COX split into

A

PGI2

TXA2

37
Q

Steroids and arachidonic acid

A

Hit PAL-2

38
Q

When you want to shut down inflammation fast what do you do

A

You want to shut down the arachidonic acid cascade by giving steroid

Cut head off of snake by adding it to the beginning of the arachidonic acid cascade

39
Q

IL-6

A

Causes liver to produce acute phase reactants

40
Q

Activate endothelial cell adhesion molecules; initaties PGE2 synthesis in anterior hypothalamic, leading to production of fever

A

IL1 and TNFa

41
Q

Makes RBC sticky

A

Fibrinogen

ESR

42
Q

What does fibrinogen do to ESR

A

Causes it to go up

43
Q

Primary cytokines that acts on liver to produce ACP: ferritin, fibrinogen, CRP

A

IL-6

44
Q

Ferritin

A

Iron binder

45
Q

Huge proinflammatory cytokines and initiate PGE2

A

IL1 and TNFa

46
Q

PMN chemotaxis

A

IL-8

47
Q

4 outcome of acute inflammation

A

Complete resolution with regeneration

Complete resolution with scarring

Abscess formation

Transition to chronic inflammation

48
Q

Abscess in brain

A

Usually with infection, but in brain will be from ischemia, sterile abcsess

49
Q

Causes of chronic infection

A
  • persistenc infeections
  • mycobacteria phagocytized by macrophages and cause a larger inflamed lesion and granuloma
  • autoimmune diseases
  • response to foreign material
  • response to malignant tumors
50
Q

Monocytes

A

Macrophages in blood

51
Q

Macrophages in skin

A

Histiocytes

52
Q

Kupffer cels

A

Macrophages int he liver

53
Q

Osteoclasts

A

Macrophages in bone

54
Q

Microglia

A

Macrophages in brain

55
Q

How can macrophages be modified

A

Into epithelioid cells in granuloma

-NOT EPITHELIAL CELLS. Macrophages have been activated in granulomas

56
Q

B cells, plasma cels, and T cells

A

Lymphocytes

57
Q

Key role in parasitic infections and IgE mediated allergic reactions

A

Eosinophils

58
Q

Major basic protein in eosinophils

A

Toxic to parasites and tissue

59
Q

High number in lung and skin

A

Basophils and mast cells

60
Q

Play key role in IgE mediated reactions and can release histamine

A

Basophils and mast cells

61
Q

What kind of response is epitheliof macrophages in a granuloma

A

TH1 response, cell mediated

62
Q

What is in the center of granuloma

A

Central necrosis

63
Q

Purples high protein filled with neutrophils in the exudate

A

Caused by necrosis

64
Q

Irreversible/often uncontrolled death of many cells

A

Necrosis

65
Q

Neutrophils and acute

A

Necrosis

66
Q

May be aseptic due to blood supply loss

A

Necrosis

67
Q

Two processes in necrosis

A

Enzymatic digestions of the cell

Desaturation of proteins

68
Q

Four types of necrosis

A

Coagulative necrosis
Liquefactive
Caseous
Fat

69
Q

Geletin, dead tissues where cells retain their shape but have lost their organelles, structure boundary is maintained

A

Coagulative necrosis

70
Q

Due to ischemia or infarction: heart attack

A

Coagulative necrosis

71
Q

When can regeneration occur in coagulative necrosis

A

If enough viable cells are present around the affected area regeneration may occur

72
Q

What does ischemia cause in the central nervous system

A

Liquefactive necrosis because there is little structural framework in neural tissue

73
Q

Is coagualtive necrosis septic or aseptic

A

Aseptic because its from loss of blood supply

74
Q

Usually infectious, forms an abscess, often associated with bacterial or fungal infections

A

Liquefactive necrosis

75
Q

Exception of liquefactive necrosis

A

In the brain, it is due to ischemia and is ASEPTIC here but none where else

76
Q

When blood supply is cut off somewhere in the body what does it form

A

A triangular block

77
Q

Cheesy proteinaceous dead cell mass, smog often observed in TB infections, may be seen in histo, cryptococcosis, and cocciodomycosis

A

Caseous necrosis

78
Q

White specks. This is death in adipose tissue-small white lesions are formed, most often due to trauma

A

Fat necrosis

79
Q

Programmed cell death

A

Apoptosis

80
Q

This is critical in an embryo and fine tuning the developing retina

A

Apoptosis

81
Q

How many ganglion cells die in the apoptosis

A

70%

82
Q

T helper cells are classified as _____ and TH2 cells drive a ____ mediated response

A

CD4

Ab

83
Q

Identify the most likely type of necrosis to occur in the brain after a stroke

A

Liquefaction necrosis

84
Q

Thromboxane A2 (TXA2) and the prostacyclin (PGI2) are products of this pathway

A
  • arachidonic acid

- cyclooxygenase

Pathology Block 10 (8 decks)

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