Brainscape's Knowledge GenomeTM

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


See full index

Immunology > Pathology - cell death > Flashcards

Pathology - cell death Flashcards

1
Q

cell death - types and their main difference

A
  1. apoptosis –> intact cell membrane without significant inflammation
  2. Necrosis –> inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Apoptosis? requires?

A

programmed cell death that requires ATP

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

Apoptosis pathways and their common features

A
  1. Intrinsic
  2. Extrinsic
    both activate cytosolic caspases that mediate cellular breakdown (cytosolic proteases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Apoptosis - appearance

A
  1. deeply eosinphilic cytoplasm
  2. cell shrinkage
  3. pyknosis (nuclear shrinkage)
  4. nuclear basophilia
  5. membrane blebbing
  6. Karyorrhexis (nuclear fragmentation)
  7. formation of apoptotic bodies
  8. chromatin condensation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

apoptotic bodies - origin and fate

A

from cytoplasmic bleb –> they have lignands for macrophages receptors –> phagocytes by macrophages

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

Karyorrhexis? (and mechanism)

pyknoseis

A

Karyorrhexis: nuclear fragmentation caused by endonucleases cleaving at internucleosomal regions
nuclear shrinkage: nuclear shrinkage

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

Sensitive indicator (finding) of apoptosis

A

DNA laddering (fragments in multiples of 180bp)

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

Intrinsic pathway is AKA

A

mitochondrial pathway

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

Intrinsic (mitochondrial) pathway is physiologically involved in

A

tissue remodelling in embryogenesis

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

Intrinsic (mitochondrial) pathway occurs when (pathophysiology and examples)

A
  1. a regulating factor is withdrawn from a proliferating cell population (eg. IL-2 after a completed immunologic reaction –> apoptosis of proliferating effector cells)
  2. after exposure to injurious stimuli (radiation, toxins, hypoxia, misfolded proteins) –> P53 activation –> BAX/BAK –> mit and cyt C+ + APAF-1 –> initiator caspases (esp caspase 9) –> Executioner caspases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Intrinsic (mitochondrial) pathway is regulated by

A

Bcl-2 family proteins such and BAX and BAK (proapoptotic) and BCL2 (antiapoptotic)

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

Bcl-2 antiapoptotic effect

A

it prevents cyt C release by binding to and inhibiting APAF 1 (APAF normally binds to cyt C and induce activation of capsase 9, initiating caspase cascade)

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

APAF normally ….

A

binds to cyt C and induce activation of capsase 9, initiating caspase cascade

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

BCL2 overexpression –> …and example

A

APAF-1 is overly inhibited –> decreased capsase activation –> tumorgenesis
example: Follicular lymhoma (t:14:18)

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

Extrinisic (death receptor) pathway - pathways and mechanisms (and aka)

A

aka: death receptor pathway
1. ligand receptor interactions –> FasL binding to Fas (CD95) or TNF-a binding to TNF
2. Immune cell –> cytotoxic T-cells or NK cells release of perforin and granzyme B)

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

Fas-FasL interaction is necessary in …. (and clinical relevance)

A

thymic medullary negative collection –> Mutation in FAS increases numbers of circulating self-reacting lymphocytes due to failure of clonal deletion
Defective Fas-FasL interaction -> autoimmune lymphoproliferatice syndrome

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

Fas-FasL pathway –>

A

FasL bind to Fas –> multiple Fas molecules coalesce, forming a binding site for death domain, containing adapter protein (FADD) –> activation of initiator caspases –> executioner caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Perforin apoptosis - mechanism

A

Cytotoxic cell bind to the cell perforin form a pore between the 2 cells –> granzyme passes through the pore and activate executioner caspases

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

Cell necrosis?

A

Enzymatc degradation and protein denaturation of cell due to exogenous injury –> extracellular component leak. Inflammatory process (vs apoptosis)

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

Cell necrosis - types

A
  1. coagulative
  2. Liquefactive
  3. Caseous
  4. Fat
  5. Fibrinoid
  6. Gangrenous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

coagulative necrosis - seen in

A

ischemia/infracts in most tissues (except brain)

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

coagulative necrosis - due to/mechanism

A

ischemia or infraction

–> proteins denaturem then enzymatic degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

coagulative necrosis - histology

A
  • Cell outilines preserved

- increased cytoplasmic binding of acidophilic dyes

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

Liquefactive necrosis - seen in

A 
bacterial abscesses
brain infracts (due to high fat content)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Liquefactive necrosis - due to/mechanism

A

Neutrophils release lysosomal enzymes that digest the tissue –> enzymatic degradation first, then proteins denature

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

Liquefactive necrosis - histology

A

early: cellular debris and macrophages
late: cystic spaces and cavitation (brain)
Neutrophils and cell debris seen in bacterial infection

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

Caseous necrosis - seen in

A

TB, systemic Fungi, Nocardia

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

Caseous necrosis - due to/mechanism

A

macrophage wall off the infecting microprganism –> granular debris

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

Caseous necrosis - histology

A

fragmented cells and debris surrounded by lymphocytes and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Fat necrosis - seen in

A

enzymatic: acute pancreatitis (saponification of peripancreatic fat
nonenzymatic –> traumatic (eg. breast injury)

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

Fat necrosis - due to/mechanism

A

damaged cells release lipase, which breaks down triglycerides in fat cells

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

Fat necrosis - histology

A

outlines of dead fat cells without peripheral nuclei

saponification of fat (combined with Ca2+) apears dark blue on H&E stain

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

Fibrinoid necrosis - seen in

A

immune reactions in vessels (eg. polyarterirtis nodosa, giant cell arteritis)

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

Fibrinoid necrosis - due to/mechanism

A

immune complexes combine with fibrin –> vessel wall damage

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

Fibrinoid necrosis - histology

A

vessels walls are thick and pink

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

Gangrenous necrosis - seen in

A

distal extremity, after chronic ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Gangrenous necrosis - due to

A

dry: ischemia
wet: superinfection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Gangrenous necrosis - histology

A

coagulative (dry)

liquefactive superimposed on coagulative (wet)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

H&E stains

A

acidic –> react with basic (cytoplasm) –> eosin

basic –> react with acidic (nuclei) –> basophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Cell injury is divided to

A
  1. reversible with 02

2. irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

reversible with O2 cell injury - histology (and mechanism)

A
  1. cellular/ER/mitochondrial swelling (low O2–> decreased oxidative phosp –> low ATP –> low activity of Na/k pump)
  2. Ribosomal/polysomal detachment –> low protein synthesis (RER swelling –> detachment)
  3. membrane bedding
  4. nuclear chromatin clumping (anaerobic glycolysis –> low ph)
  5. fatty change (low protein synthesis –> decreased apolipoportein synthesis) –> vacuoles of fat accumulate in cytoplasm
  6. low glycogen (anaerobic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

reversible with O2 cell injury - cellular swelling - mechanism

A

low O2–> decreased oxidative phosp –> low ATP –> low activity of Na/k pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

reversible with O2 cell injury - low proteino synthesis

A

low O2 –> decreased oxidative phosp –> low ATP –> low activity of Na/k pump –> RER swelling –> Ribosomal/polysomal detachment –> low protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

reversible with O2 cell injury - nuclear chromatin clumping

A

anaerobic glycolysis –> low ph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

irreversible cell injury - histology

A
  1. mitochondrial permeability
  2. mitchondria vacuolization
  3. phospolipid-contating amorphous densities within mitochondria
  4. Nuclear pyknosis (condensation)
  5. karyorrhexis (fragmentation)
  6. karyolysis (fading)
  7. plasma membrane damage (degradaton of membrane phospholipid
  8. Lysosomal rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

irreversible cell injury - histology of mitochondria

A
  1. mitochondrial permeability
  2. mitchondria vacuolization
  3. phospolipid-contating amorphous densities within mitochondria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

irreversible cell injury - histology of nucleus

A
  1. Nuclear pyknosis (condensation)
  2. karyorrhexis (fragmentation)
  3. karyolysis (fading)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

nuclear karyolysis? and appearance

A

dissolution of the chromatin –> fading

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

ischemia?

A

inadequate blood supply to meet demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

region most vulnerable to hypoxia/ischemia and subsequent infraction

A
  1. Brain: ACA/MCA/PCA boundary areas boundary areas (watershed)
  2. Heart: subendocardium
  3. Kidney: a. Straight segment of proximal tubule (medulla) b. Thick ascending limb (medulla)
  4. Liver: area around central vein (zone III)
  5. Colon: splenic flexure, rectum (both watershed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

region most vulnerable to hypoxia/ischemia and subsequent infraction in kidney

A

a. Straight segment of proximal tubule (medulla)

b. Thick ascending limb (medulla)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

region most vulnerable to hypoxia/ischemia and subsequent infraction in colon

A

a. splenic flexure

b. rectum (both watershed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

ischemia - watershed areas (border zones)

A

receive blood from most distal branches of 2 arteries with limited collateral vascularity –> susceptible to ischemia from hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

neurons most valnerable to hypoxic-ischemic insults include

A

Purkinje cells of the cerebellum and pyramidal cells of the hippocampus and neocortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Infarcts are divided to

A
  1. red (hemorrhagic)

2. pale (anemic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

red (hemorrhagic) infarcts occur in

A

venous occlusion and tissues with multiple blood supplies, such as: 1. liver 2. lung 3. intestine 4. tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Reperfusion injury

A

reperfusion (eg. after angioplasty) injury is due to damage by free radicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

pale (anemic) infarcts occur in

A

solid organs with a single (end-arteria) blood supply, such as: 1. heart 2. kidney 3. spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

red (hemorrhagic) - organs example

pale (anemic) infarcts - organs example

A

red: 1. liver 2. lung 3. intestine 4. tests
pale: 1. heart 2. kidney 3. spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

inflammation is characterised by

A
  1. rubor (redness)
  2. dolor (pain)
  3. calor (heat)
  4. tumor (swelling)
  5. function laesa (loss of function)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

vascular component to inflammation

A
  1. increased vascular permeability
  2. vasodilation
  3. endothelial injury
62
Q

cellular component to inflammation

A

Neutrophil extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation and inflammatory mediator release

63
Q

vascular and cellular component to inflammation

A

vascualr 1. increased vascular permeability 2. vasodilation 3. endothelial injury
component: Neutrophil extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation and inflammatory mediator release

64
Q

inflammation is divided to

A
  1. acute

2, chrnic

65
Q

acute inflammation is mediated by

A
  1. neutrophil
  2. eosinophil
  3. antibody
66
Q

acute inflammation - onset and duration / mediated by

A 
rapid onset (sec to mins)
short duration (minutes to days)
mediated by 1. neutrophil  2. eosinophil  3. antibody
67
Q

acute inflammation - outcomes

A
  1. complete resolution
  2. abscess formation
  3. progression to chronic inflammation
68
Q

chronic inflammation is mediated by

A

mononuclear cells (monocytes/macrophages, lymphocytes, plasma cells) and fibroblasts

69
Q

chronic inflammation is characterised by

A

persistent destruction and repair

70
Q

chronic inflammation is associated with

A
  1. blood vessel proliferation
  2. fibrosis
  3. granulomas
71
Q

chronic inflammation outcomes:

A

scarring and amyloidosis

72
Q

granuloma:

A

nodular collection of epithelioid macrophages

73
Q

Chromatolysis - definition and characteristics

A

reaction of neuronal cell body to axonal injury –> increased protein synthesis in effort to repair damaged axon. Characteristics: 1. round cellular swelling 2. Displacement of the nucleous to the periphery 3. dispersion of Nissle substance throughout cytoplasm

74
Q

Chromatolysis is concurrent with ….(explain)

A

Wallerian degeneration: degeneration of the axonal distal to site of injury
Macrophages remove debris and myelin

75
Q

Types of calcification (and the calcium status)

A
  1. dystrophic –> usually normocalcemic

2. metastatic –> not normocalcemic

76
Q

Dystrophic calcification?

A

Ca2+ deposition in abnormal tissues 2ry to injury or necrosis –> not directly associated with serum Ca2+ levels (normocalcemic)

77
Q

Dystrophic calcification is seen in (9)

A
  1. TB (lungs and pericardium)
  2. liquefactive necrosis of chronic abscess
  3. fat necrosis
  4. infracts
  5. thombi
  6. schistosomiasis
  7. Monckeberg arteriolosclerosis
  8. Congential CMV and toxoplasmosis
  9. psammoma bodies
78
Q

Dystrophic calcification tend to be … (and example)

A

localized (eg. calcific aortic stenosis)

79
Q

Metastatic calcification? (and examples)

A

widespread depositiom of Ca2+ in normal tissue 2ry to

  1. hypercalcemia (eg. 1ry hyperparathyroidism, sarcoidosis, hypervitaminosis D
  2. high calcium-phosphate product (chronic renal failure with 2ry hyperparathyroidims, long-term dialysis, caciphilaxis, warfarin)
80
Q

drug that is associated with metastatic calcification

A

warfarin

81
Q

Calciphylaxis, is a syndrome of

A

vascular calcification, thrombosis and skin necrosis (mostly in patients with chronic kidney disease, but can occur in the absence of renal failure) –> results in chronic non-healing wounds (usually fatal)

82
Q

Metastatic calcification predominantly in (locations) and why

A

interstitial tissues of kidney, lung and gastric mucosa

–> these tissues lose acid quickly –> high pH favors deposition

83
Q

Leukocyte extravasation predominantly occurs in

A

postcapillary venules

84
Q

WBCs exit from blood vessels at site of …… in ….(number) steps (and steps)

A

tissue injury and inflammation in 4 steps

  1. margination and rolling
  2. Tight-binding
  3. Diapedesis
  4. Migration
85
Q

Leukocyte extravasation - margination and rolling - MOLECULES

A

Vascular stroma - Leukocytes
E-selectin - Sialyl-Lewis
P-selectin - Sialyl-Lewis
GlyCAM-1, CD34 - L-selectin

86
Q

Leukocyte extravasation - Tight-binding - molecules

A

Vascular stroma - Leukocytes
ICAM-1 (CD54) - CD11/18 integrins (LFA, Mac-1)
VCAM-1 (CD106) - VLA-4 integrin

87
Q

Leukocyte extravasation - diapedesis?

A

WBC travels between endothelial cells and exits blood vessel

88
Q

Leukocyte extravasation - diapedesis - molecules

A

Vascular stroma - Leukocytes

PECAM-1 (CD31) - PECAM-1 (CD31)

89
Q

Leukocyte extravasation - Migration?

A

WBC travels through interstitium to site of injury or infection guided by chemotactic agents

90
Q

Leukocyte extravasation - Migration - molecules

A

Vascular/stroma: Chemotactic products released in response to bacteria
–> 1. C5a 2. IL-8 3. LTB4 4. Kallikrein
5. Platelet-activating factor
Leukocyte: various

91
Q

Leukocyte extravasation - molecules for every step

A 
1. margination and rolling
E-selectin - Sialyl-Lewis 
P-selectin - Sialyl-Lewis
GlyCAM-1, CD34 - L-selectin 
2. Tight-binding 
ICAM-1 (CD54) - CD11/18 integrins (LFA, Mac-1)
VCAM-1 (CD106) - VLA-4 integrin 
3. Diapedesis 
PECAM-1 (CD31) - PECAM-1 (CD31)
4. Migration 
C5a, IL-8, LTB4, Kallikrein, Platelet-activating factor
92
Q

Leukocyte adhesion deficiency type 1 - mechanism

A

Low CD18 integrin subunit –> defective tight-binding

93
Q

Leukocyte adhesion deficiency type 2 - mechanism

A

low Sialyl-Lewis X –> defective margination and rolling

94
Q

Leukocyte adhesion deficiency (type 1) - mode of inheritance / prestnation / findings

A

(AR)1. reccurent bacterial skin and mucosa infection

  1. absent pus formation
  2. impaired wound healing
  3. delayed separation of umbilical cord (>30 days)
    findings: 1. increased neutrophils 2. no neutrophils at infection site
95
Q

Free radicals damage cell via

A
  1. membrane lipid peroxidation
  2. protein modification
  3. DNA breakage
96
Q

Free radicals damage is initiated via (6)

A
  1. radiation therapy (cancer therapy)
  2. metabolism of drugs (phase 1)
  3. redox
  4. nitric oxide
  5. transition metals
  6. WBC (neutrophils, macrophages) oxidative burst
97
Q

Free radicals can be eliminated by

A
  1. scavenging enzymes (eg. catalase, superoxide dismutae, glutathione peroxidase)
  2. spontaneous decay
  3. antioxidants (vitamins A,C,E)
  4. certain mental carrier proteins (transferrin, cerulolasmin)
98
Q

glutathione peroxidase requires

A

selenium

99
Q

Free radicals injury - example

A
  1. oxygen toxicity
  2. Drug/chemical toxicity
  3. Mental storage disease
100
Q

Free radicals injury - mental storage disease

A
  1. hemochromatosis (iron)

2. Wilson disease (copper)

101
Q

Free radicals injury - oxygen toxicity

A
  1. retinopathy of prematurity (abnormal vascularization)

2. bronchopulmonanry dysplasia

102
Q

Free radicals injury - Drug/chemical toxicity

A
  1. carbon tetrachloride

2. acetaminophen overdose (hepatotoxicity)

103
Q

Inhalation injury?

A

pulmonary complication associated with smoke and fire

104
Q

Inhalation injury is caused by

many patients 2ry to

A
  1. heats
  2. particules smaller than one μm diameter
  3. irrintants (eg. NH3)
105
Q

Inhalation injury - complications

A
  1. chemical tracheobronchitis
  2. edema
  3. pneumonia
  4. ARDS
106
Q

Inhalation injury - bronchoscopy shows (and when)

A

severe edema, congestions of bronchus and soot deposition

18h after inhalation injury–> resolution 11 days after injury

107
Q

scar formation - tensile strength regained at (when)

A

70-80% of tensile strength regained at 3 months –> little additional tensile strength will be regained afterward

108
Q

scar formation - types

A
  1. hypertrophic

2. keloid

109
Q

hypertrophic vs keloid according to collagen syntehsis

A

hypertrophic –> increased

keloid –> highly increased

110
Q

hypertrophic vs keloid according to organization

A

hypertrophic –> parallel

keloid –> disorganized

111
Q

hypertrophic vs keloid according to extension of scar

A

hypertrophic –> confined to borders of original wound

keloid –> extends beyond borders of original wound with “clawlike” projection

112
Q

hypertrophic vs keloid according to scar evolution over years

A

hypertrophic –> possible spontaneous regression

keloid –> possible progressive growth

113
Q

hypertrophic vs keloid according to frequency

A

hypertrophic –> frequent

keloid –> infrequent

114
Q

hypertrophic vs keloid according to predisposition

A

hypertrophic –> none

keloid –>high incidence in ethnic group with darker skin

115
Q

keloid - high incidence in

A

ethnic group with darker skin

116
Q

Tissue mediators - molecules and action

A
  1. PDGF –> induces vascular remodelling and SMC migratin
    stimulates fibroblast growth for collagen synthesis
  2. FGF –> stimulates angiogenesis
  3. EGF –> stimulates cell growth via tyrosine kinase (eg. EGFR/ErbB1)
  4. TGF-β –> a. Angiogenesis b. fibrosis c. Cell cycle arrest
  5. Metalloproteinases –> tissue remodelling
  6. VEGF –> stimulates angiogenesis
117
Q

Tissue mediators - action of VEGF

A

stimulates angiogenesis

118
Q

Tissue mediators - action of metalloproteinases

A

tissue remodelling

119
Q

Tissue mediators - action of TGF-β

A
  1. Angiogenesis
  2. fibrosis
  3. Cell cycle arrest
120
Q

Tissue mediators - action of EGF

A

stimulates cell growth via tyrosine kinase (eg. EGFR/ErbB1)

121
Q

Tissue mediators - action of FGF

A

stimulates angiogenes

122
Q

Tissue mediators - PDGF is secreted by

A

activated platelets and macrophages

123
Q

Tissue mediators - action of PDGF

A

induces vascular remodelling and SMC migratin

stimulates fibroblast growth for collagen synthesis

124
Q

Phase of wound healing (and when)

A
  1. inflammatory (up to 3 days after wound)
  2. Proliferative (day 3-weels after wounf)
  3. Remodelling (1 week - 6+ months after wound)
125
Q

Phase of wound healing - cells

A
  1. inflammatory: platelets, neutrophils, macrophages
  2. Proliferative: fibroblasts, myofibroblasts, endothelial cells, keratynocytes, macrophages
  3. Remodelling: fibroblasts
126
Q

Phase of wound healing - inflammatory phase?

A
  1. clot formation
  2. Increased vessel permeability and neutrophil migration into tissue
  3. macrophages clear debris 2 days later
127
Q

Phase of wound healing - proliferative phase?

A
  1. deposition of granulation tissue and type III collage
  2. angiogenesis
  3. epithelial cell proliferation
  4. dissolution of clot
  5. wound ocontraction (myofibroblasts)
128
Q

Phase of wound healing - remodeling

A
  1. type III collagen replaced by type I collagen

2. increased tensile strength of tissue

129
Q

Granoulomatous disease - mechanism

A

Th1 secrete IFN-γ, activating macrophages –> macrophages secrete TNF-α –> induce and maintains granuloma formation

130
Q

Diagnosing sarcoidosis requires ….. on biospy

A

noncaseating granulomas

131
Q

Granoulomatous disease is associated with

A

hypercalcemia due to calcitriol (1,250OH2 vit D3) production

132
Q

causes of Granoulomatous disease - groups

A
  1. bacterial
  2. fungal
  3. parasitic
  4. chronic granulomatous disease
  5. Autoinflammatory
  6. foreign material
133
Q

causes of Granoulomatous disease - bacterial.

A
  1. Mycobacteria (TB, leprosy)
  2. Bartonella hensele (cat scratch disease)
  3. Listeria monocytogenes (granulomatosis imperfecta)
  4. Treponela pallidum (3ry syphilis)
134
Q

causes of Granoulomatous disease - Fungal

A

endemic mycoses (eg. histioplasmosis)

135
Q

causes of Granoulomatous disease - parasitic

A

schistosomiasis

136
Q

causes of Granoulomatous disease - foreign material

A
  1. berylliosis
  2. hypersensitivity pneumonitis
  3. talcosis
137
Q

causes of Granoulomatous disease - autoinflmmatory

A
  1. sarcoidosis
  2. crohn
  3. Primary biliary cirrhosis
  4. Sabacute (de Quervain/granulomatous) thyroiditis
  5. wegener
  6. Churg-Strauss
  7. Giant cell arteritis
  8. Takayasu arteritis
138
Q

vasculitis that causes Granoulomatous disease

A
  1. wegener
  2. Churg-Strauss
  3. Giant cell arteritis
  4. Takayasu arteritis
139
Q

Exudate vs transudate according to cells and appearance

A

Exudate –> cellular –> cloudy

transudate –> hypocellular –> clear

140
Q

Exudate vs transudate according protein levels

A

Exudate –> high

transudate –> low

141
Q

Exudate vs transudate according LDH

A

Exudate –> high (vs serum)

transudate –> low (vs serum)

142
Q

Exudate vs transudate according specific gravity

A

Exudate –> more than 1.020

transudate –> less than 1.012

143
Q

Exudate is due to

A
  1. lymphatic obstruction (chylous)
  2. inflammation/infection
  3. malignancy
144
Q

Transudate is due to

A
  1. increased hydrostatic pressure (eg. NF, Na+ retention)

2. decreased oncotic pressure (eg. cirrhosis, nephrotic syndrome

145
Q

erythrocyte sedimentation rate (ESR) - description

A

Products of inflammation (eg. fibrinogen) coat RBCs and cause aggregation. The denser RBCs aggregates fall at a faster rate within pipete tube

146
Q

erythrocyte sedimentation rate (ESR) is often co-tested with

A

CRP levels

147
Q

Causes of increased erythrocyte sedimentation rate (ESR)

A
  1. most anemias
  2. infections
  3. inflammation (eg. giant cell, poymyalgia rheumatic)
  4. Cancer (eg. metastasis, MM)
  5. Renal disease (end-stage or nephrotic syndrome)
  6. Pregnancy
148
Q

Causes of decreased erythrocyte sedimentation rate (ESR)

A
  1. sickle cell anemia (altered shape)
  2. polycythemia (increased RBCs dilute aggregation factor)
  3. HF
  4. Microcytosis
  5. Hypofibrinogenemia
149
Q

inhallation injury may present secondary to

A
  1. burns
  2. CO inhallation
  3. arsenic poisoning
150
Q

nephrotic syndrome - ESR

A

increased

Immunology (10 decks)

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