Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathoma > Chapter 2 > Flashcards

Chapter 2 Flashcards

1
Q

inflammation

A

inflammatory cells, plasma proteins, and fluid exit vessels into interstitial space;
acute and chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

acute inflammation

A

edema and neutrophils in tissue;
response to infection or necrosis;
immediate response, limited specificity (innate immunity);
includes epithelium, mucus, complement, mast cells, macrophages, dendritic cells, neutrophils, basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

toll-like receptors (TLR)

A

on innate immune cells;
activated by PAMPs (pathogen-associated molecular patterns) - CD14 of macrophage recognizes LPS of gram- bacteria;
upregulation of NF-kappaB and immune response genes;
TLRs also in adaptive immunity and chronic infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Arachidonic Acid (AA) metabolites

A

AA from phospholipase A, acted on by cyclooxygenase or 5-lipoxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

cyclooxygenase

A

acts on AA to produce prostaglandins;
PGI2, PGD2, PGE2 mediate vasodilation of arteriole and vascular permeability of post capillary venule;
PGE2 causes pain and fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

5-lipoxygenase

A

acts on AA to produce leukotrienes;
LTB4 attracts and activates neutrophils;
LTC4, LTD4, LTE4 (reactive in anaphylaxis) cause vasoconstriction, bronchospasm, and vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

mast cells

A

activated by trauma, complement C3a and C5a, and cross-linked IgE;
immediate response - preformed histamine granule release (vasodilation, vascular permeability);
delayed response - AA metabolites (mostly LTs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

complement

A

proinflammatory serum proteins;
activated via:
classical pathway - IgG or IgM bind antigen;
alternative pathway - microbial product activation;
mannose-binding lectin - MBL binds mannose on microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

major complement components

A

C3a and C5a (anaphylatoxins) - mast cell degranulation of histamine;
C5a - neutrophil chemotaxis;
C3b - opsonin for phagocytosis;
MAC - membrane attack complex (C5b + C6-9), holes in cell membrane to lyse microbe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hageman factor

A

Factor XII, produced in liver;
activated by subendothelial tissue or collagen;
activates coagulation/fibrinolytic systems, complement, kinin system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

bradykinin

A

made from high-molecular-weight kininogen;
causes vasodilation and vascular permeability (like histamine);
also causes pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

cause pain

A

PGE2 and bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

mast cells activated by?

A

trauma;
C3a and C5a
cross-linked IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

chemotactic for neutrophils

A

LTB4;
C5a;
IL8;
Bacteria products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

opsonins

A

enhance phagocytosis by marking target cell;
IgG;
C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

acute inflammation stages

A

fluid phase;
neutrophile phase;
macrophage phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

signs of inflammation

A 
redness (rubor);
heat (calor);
swelling (tumor);
pain (dolor);
fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

redness and heat of inflammation

A

due to vasodilation;

via relaxation of arteriole smooth muscle - histamine, prostaglandins, bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

swelling of inflammation

A

leakage of fluid from post capillary venule (exudate);

via histamine and tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

pain of inflammation

A

bradykinin and PGE2, sensitize nerve endings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

fever of inflammation

A

macrophages release IL-1 and TNF - increase cyclooxygenase activity in perivascular hypothalamus (temp control);
high PGE2 raises temp set point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

neutrophil movement

A 
margination;
rolling;
adhesion;
transmigration and chemotaxis;
phagocytosis;
destruction of material;
resolution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

neutrophil margination

A

vasodilation slows blood flow;

cells move to periphery of blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

neutrophil rolling

A

endothelial cells upregulate selectin “speed bumps”;
P-selectin from Weibel-Palade bodies via histamine;
E-selectin from macrophages via TNF and IL-1;
selectins bind sialyl Lewis X on leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

neutrophil adhesion

A

upregulation of ICAM and VCAM on endothelium by TNF and IL-1;
integrins of leukocytes upregulated by C5a and LTB4;
firm adhesion between CAMs and integrins;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

leukocyte adhesion deficiency

A

defect of integrins;
leukocytes will not bind CAMs;
delayed separation of umbilical cord, increased circulating neutrophils, recurrent bacterial infections without pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

neutrophil transmigration and chemotaxis

A

neutrophils attracted by LTB4, C5a, IL-8, bacterial products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

neutrophil phagocytosis

A

enhanced by opsonins;

pseudopods extend from leukocytes, form phagosomes, merge with lysosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Chediak-Higashi syndrome

A 
protein trafficking defect;
impaired phagolysosome formation;
risk of pyogenic infections;
neutropenia (intramedullary neutrophil death);
giant granules in leukocytes;
defective primary hemostasis (dense platelet granules);
albinism;
peripheral neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

neutrophil destruction of phagocytosed material

A

O2 dependent most effective;
HOCl made by oxidative burst:
1. O2 to superoxide by NADPH oxidase (oxidative burst)
2. superoxide to peroxide by superoxide dismutase (SOD)
3. peroxide to HOCl by myeloperoxidase (MPO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

chronic granulomatous disease

A

poor O2 dependent killing;
NADPH defect;
recurrent infection and granulomas with catalase+ org. (S. aureus, P. cepacia, S. marcescens, Nocardia, Aspergillus);
nitroblue tetrazolium test to screen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

myeloperoxidase deficiency

A

defective conversion of peroxide to HOCl;
risk of candida infection (most are asymptomatic);
nitroblue tetrazolium test is normal (oxidative burst intact)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

O2 independent killing

A

less effective than O2 dependent;

via enzymes present in leukocyte secondary granules (lysozyme, major basic protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

neutrophil resolution

A

neutrophils undergo apoptosis within 24 hrs of resolution (pus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

macrophage phase

A

2-3 days after inflammation begins;
derived from monocytes;
travel similar to neutrophils;
phagocytosis with O2 dependent and independent destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

outcome of macrophage phase of inflammation

A

resolution and healing - IL-10 and TGF-beta (anti-inflammatory from macrophages);
continued acute inflammation - IL-8 recruits more neutrophils, persistent pus;
abcess - acute inflammation surrounded by fibrosis via fibrogenic growth factors/cytokines;
chronic inflammation - activate CD4+ helper T cells to promote chronic inflammation

37
Q

chronic inflammation

A

presence of lymphocytes and plasma cells in tissue;
delayed response;
specific (adaptive immunity);
via persistent infection, viruses, mycobacteria, parasites, fungi, autoimmune disease, foreign material, some cancers

38
Q

T lymphocytes

A

progenitor T cells from bone marrow develop in thymus;
T cell receptor (TCR) rearranges to CD4+ (helper) or CD8+ (cytotoxic);
activation requires binding of antigen/MHC complex and 2nd signal

39
Q

CD4+ helper T cell

A

extracellular antigen phagocytosed, processed, presented on MHC II via macrophages or dendritic cells;
B7 on antigen presenting cell bind CD28 on CD4+ cell (2nd signal;
secretes cytokines to aid inflammation;

40
Q

TH1 helper T cell

A 
secrete IFN-gamma - activates macrophages, B cell class switching from IgM to IgG, inhibits TH2 phenotype;
CD8+ cell activated via IL-2
41
Q

TH2 helper T cell

A

secretes IL-4 - activates B cell class switching from IgM to IgE;
IL-5 - eosinophil activatione, class switching to IgA;
IL-13 - similar to IL-4;
IL-10 inhibits TH1

42
Q

CD8+ cytotoxic T cell

A

activation from intracellular antigen, IL-2 from TH1 cells;

activated for killing - via secretion of perforins and granzymes, expression of FAS ligand (activates apoptosis)

43
Q

B lymphocytes

A

made in bone marrow;
immunoglobulin rearrangement to become naive B cell with surface IgM and IgD;
activation via IgM/IgD antigen binding or antigen presentation from CD4+ cell on MHC II

44
Q

B cell activation from CD4+ cell

A

via MHC II;
CD40 on B cell bind CD40L on helper T cell (2nd signal);
helper T cell secretes IL-4 and IL-5 (class switching, hypermutation, maturation of plasma cells)

45
Q

granulomatous inflammation

A

subtype of chronic inflammation;
granuloma - collection of epitheliod histiocytes (macrophages with pink cytoplasm) surrounded by giant cells and lymphocytes;
noncaseating and caseating subtypes

46
Q

noncaseating granuloma

A

lack central necrosis;

from reaction to foreign material, sarcoidosis, beryllium exposure, Crohn disease, cat scratch disease

47
Q

caseating granuloma

A

central necrosis from tuberculosis and fungal infections

48
Q

granuloma formation

A

macrophages process/present antigen via MHC II to CD4+ helper cells;
macrophages IL-2 inducing helper T cells to form TH1;
TH1 secrete IFN-gamma to convert macrophages to epitheliod histocytes and giant cells

49
Q

Digeorge syndrome

A

developmental failure of 3rd and 4th pharyngeal pouches (22q11 microdeletion);
T cell deficiency (lack of thymus);
hypocalcemia (lack of parathyroid);
abnormalities of heart, great vessels, face

50
Q

severe combined immunodeficiency disease (SCID)

A 
defective cell mediated and humoral immunity (T and Be cells);
cytokine receptor defects (necessary for B/T cell maturation);
adenosine deaminase (ADA) deficiency - buildup of adenosine and deoxyadenosine toxic to lymphocytes;
MHC II deficiency (helper T activation, cytokine production);
susceptible to fungal, viral, bacterial, protozoal infections;
sterile isoloation (bubble baby) with stem cell transplant
51
Q

x-link agammaglobulinemia

A

disordered B cell maturation - complete lack of immunoglobulin;
mutated Bruton tyrosine kinase;
after 6 months of life (maternal antibodies present before);
recurrent bacterial, enterovirus (polio and coxsackievirus), and Giardia infections

52
Q

common variable immunodeficiency (CVID)

A

B/helper T cell defects - low immunoglobulin;
risk of bacterial, enterovirus, Giardia infection in late childhood;
risk of autoimmune disease and lymphoma

53
Q

IgA deficiency

A

low serum and mucosal IgA;
most common immunoglobulin deficiency;
risk of mucosal infections (celiac disease)

54
Q

hyper-IgM syndrome

A

elevated IgM;
mutated CD40 (helper T cell) or CD40 receptor (B cell);
2nd signal not delivered to helper T cells, disabling class switching;
low IgA, IgG, and IgE cause recurrent pyogenic infections at mucosal sites

55
Q

Wiskott-Aldrich syndrome

A

thrombocytopenia, eczema, recurrent infections (defective humoral and cellular immunity);
death from bleeding;
mutation in WASP gene (x-linked)

56
Q

complement deficiencies

A

C5-C9 deficiencies - risk of Neisseria infections;

C1 inhibitor deficiency - hereditary angioedema (especially periorbital skin and mucosal surfaces)

57
Q

autoimmune disorders

A 
immune mediated damage of self;
loss of self-tolerance;
more common in women during childbearing age;
usually an environmental trigger;
progressive with relapses and remissions
58
Q

autoimmune loss of self-tolerance

A

central tolerance in thymus leads to thymocyte apoptosis or regulatory T cell generation;
central tolerance in bone marrow leads to receptor editing or B-cell apoptosis;
peripheral tolerance leads to anergy or apoptosis;
regulatory T cells stop autoimmunity by blocking T cell activation and making IL-10/TGF-beta (anti-inflammatory);

59
Q

autoimmune polyendocrine syndrome

A

from AIRE mutation;
no central tolerance in thymus;
hypoparathyroid, adrenal failure, chronic candida infections

60
Q

autoimmune lymphoproliferative syndrome (ALPS)

A

FAS apoptosis pathway mutation;

no peripheral tolerance

61
Q

regulatory T cells

A

CD25 polymorphisms associated with MS and Type I DM;

FOXP3 mutations cause IPEX (immune dysregulation, polyendocrinopathy, enteropathy, x-linked)

62
Q

systemic lupus erythematosus (SLE)

A

chronic, systemic autoimmune disease;
mostly middle-aged females (AA and Hispanic);
antigen-antibody complex damage tissue (type III hypersensitivity);
almost any tissue involved;
hypercoagulabe state;
drug induced lupus from antihistone antibody

63
Q

antigen-antibody complex in SLE

A

UV damage, apoptosis poorly cleared;
self-reactive lymphocytes activated, produce antibodies to host antigens;
complexes taken up by dendritic cells;
activate TLRs, amplify immune respone (IFN-alpha);
deposit on tissues, damage via complement;
deficiency of early complement proteins

64
Q

SLE findings

A

Raynaud sign;
malar butterfly rash, discoid rash (sunlight);
oral, nasopharyngeal ulcers;
arthritis;
serositis (pleuritis and pericarditis);
psychosis, seizures;
renal damage (diffuse proliferative glomerulonephritis) most common and severe injury;
anemia, thrombocytopenia, leukopenia (type II hypersensitivity);
Libman-Sacks endocarditis (plaques on mitral valve);
antinuclear antibody (ANA);

65
Q

antiphospholipid antibody in SLE

A

targets proteins bound to phospholipids;
anticardiolipin (false + VDRL and RPR syphilis tests);
anti-beta2-glycoprotein I;
lupus anticoagulant (false elevated PTT);

66
Q

antiphospholipid antibody syndrome

A

hypercoagulable state from antiphospholipid antibodies (lupus anticoagulant);
arteriole/venous thrombosis;
recurrent pregnancy loss (placental vein thrombosis);
cerebral thrombosis (stroke);
associated with SLE

67
Q

drug induced SLE

A

antihistone antibody;
procainamide, hydralazine, isoniazid;
remission with removal of drugs

68
Q

Sjogren syndrome

A

autoimmune distruction of lacrimal, salvary gland;
lymphocyte-mediated with fibrosis (type IV hypersensitivity);
associated with rheumatoid arthritis;
lymphocytic sialadenitis;
risk of B-cell lymphoma (unilateral parotid enlargement);
ANA can cause neuropathy, neonatal lupus and congenital heart block

69
Q

scleroderma

A

autoimmune sclerosis of skin and visceral organs;
autoimmune mesenchymal damage leads to collagen deposition;
endothelial dysfunction causes inflammation (secretion of growth factors (TGF-beta and PDGF);
perivascular fibrosis leads to organ damage;
limited and diffuse type

70
Q

CREST syndrome

A 
limited type scleroderma (limited skin involvement);
calcinosis;
raynaud sign;
esophageal dysmotility;
sclerodactyly;
telangiectasias of skin
71
Q

diffuse scleroderma

A

any organ involved;
associated with antibodies to DNA topoisomerase I;
commonly:
vessels (raynaud);
GI tract (esophageal dysmotility and reflux);
lungs (interstitial fibrosis and pulmonary HTN);
kidneys (scleroderma renal crisis);

72
Q

mixed connective tissue disease

A

mixed features of SLE, systemic sclerosis, and polymyositis;

ANA with serum antibodies to U1 ribonucleoprotein

73
Q

wound healing

A

initiated when inflammation begins;

combination of regeneration and repair

74
Q

regeneration

A

replace damaged tissue with native tissue;

depends on tissue regenerative capacity;

75
Q

labile tissue

A

possess stem cells and continuously cycle:

  1. bowels (stem cells in mucosal crypts);
  2. skin (stem cell in basal layer);
  3. bone marrow (hematopoietic stem cells);
  4. lung (type 2 pneumocyte)
76
Q

stable tissue

A

cells are quiescent but can reenter cell cycle as needed:

liver compensatory hyperplasia after partial resection

77
Q

permanent tissue

A

lack regenerative potential (myocardium, skeletal muscle, neurons)

78
Q

repair

A

replace damaged tissue with fibrous scar when regenerative stem cells are lost or when tissue lack regen capacity;
granulation tissue leads to collagen and scar

79
Q

granulation tissue

A

consists of fibroblasts (type III collagen), capillaries (nutrient supply), and myofibroblasts (wound contraction);
type III collagen replaced with type I collagen via collagenase (requires zinc cofactor)

80
Q

collagen types

A

I: bone, skin, tendons, most organs
II: cartilage
III: granulation tissue, embryonic tissue, uterus, keloids
IV: basement membrane

81
Q

mechanism of regen/repair

A

paracrine signaling via growth factors;
macrophages secrete growth factors target fibroblasts;
results in gene expression, cell growth

82
Q

growth factors of regen/repair

A

TGF-alpha - epithelial and fibroblast growth factor;
TGF-beta - fibroblast growth factor, inhibits inflammation;
platelet-derived growth factor - for endothelium, smooth muscle, fibroblasts;
fibroblast growth factor - for angiogenesis, skeletal development;
vascular endothelial growth factor (VEGF) - angiogenesis

83
Q

normal wound healing

A

primary intention - wound edges brought together, minimal scar;
secondary intention - granulation tissue fills defect, myofibroblasts contract wound, form scar

84
Q

delayed wound healing

A 
infection (S. aureus most common);
Vit C, copper, zinc deficiency;
foreign body;
ischemia;
diabetes;
malnutrition
85
Q

Vitamin C, copper, zinc in wound healing

A

Vitamin C - cofactor in hydroxylation of proline and lysine procollagen residue (collagen cross-linking);
copper - cofactor of lysyl oxidase (stable collagen cross-linking);
zinc - collagenase cofactor, replace type III collagen with type I

86
Q

dehiscence

A

rupture of wound, common after abdominal surgery

87
Q

hypertrophic scar

A

excess production of scar tissue localized to wound area (type I collagen)

88
Q

keloid

A

excess production of scar tissue disproportional to wound;
excess type III collagen;
genetic predisposistion;
earlobes, face, upper extremities

Pathoma (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions