RESIDENCY EXAM INFLAMMATION

1) In acute inflamation
Predominant cell is neutrophils
Onset :minute to hours
Systemic signs are less
Predominant cell is macrophages
Neo vascularization occur
2)Exudate formed :
In acute inflammation
Due to increased osmotic pressure
Due to increased hydrostatic pressure
In chronic inflation
Due to vesodialation
3) exudate :
Spesific gravity 1.00
Contain neutrophil
Plasma protein – pnly albumin
Contain fibrinogen
Contain RBC
4)swelling in acute inflamation occur due to
Increased vascular permeability
Accumulation of exudate
Neoplastic changes
Accumulation of neutrophil
New tissue formation
5) in acute inflamation
Transient veso constriction occur
Vesodialation occur
Increase vascular permeability
Increase CRP
High ESR
6)fate of acute inflamation
Chronic inflamation
Resolution
Dysplastic changes
Scar formation
Healing by neo vascularization
7)following are the cell of acute inflamation
Macrophages
Neutrophil
Activated macrophage
B lymphocyte
Eosinophil
8) chronic inflamation:
Oedema present
Exudate present
Transudate presrnt
Tissue destruction
Vascular changes
9) in acute inflamation vascular changes occur
Capillary first
Artery first
Vein first
Lately
Arteriole first
10) Hall mark of chronic inflamation
A) vascular changes.
B) tissue destruction
C) neutrophils
D) eosinophil.
E) fibrosis
11)cells of chronic inflamation
Macrophage
Neutrophil
Fibroblast
Eosinophil
Lipoblasts
12) Enzyme released from activated macrophage
Neutral protease
Acid hudrolase
Elastase
Plasminogen activator
Laipase
13) Enzyme released from lysosome
Ribonuclease
Oxidase
Lipase
Protease
Peroxidase
14) Composition of pus
Transudate
Death tissue
Dead leukocytes
Sebum
Plasma
15) Chemotactic factors :
IL-1 for macrophage
TNF
LT B4
Il-8 for Eosinophil
C3b and iC3b
16) Steps of phagocytosis
Engulfment
Vasodilation
Chemotaxis
Opsonization
Migration of leukocytes
17) following which cell can do phagocytosis.
Macrophage
Neutrophil
Eosinophil
Kupffer cell
B lymphocyte
18) after phagocytes micro organisms are killed by
H2O2
Lactoferrin
Myeloperoxidase
Hydrochloride
Defensin
19) Following mediators are responsible for fever
C3a
IL-8
IL-2
TNF
LT -C4
20) which are the pre formed inflamatory mediators
Histamin
Lysosomal enzyme
NO
Cytokines
Prostaglandin
21) factors cause vasodilation
Pg-I2
LT-E4
Bradykinin
TNF
C3a
22) followings are inflamatory mediators
Prostaglandin
No
Substance -p
Anaphylatoxin( C4a)
Cytokines
23) mediators cause increase vascular permeability
Histamine
LT C4
C5a
PDGF
IL-1
24) mediators responsible for pain
Pg- E2
Pg -I2
Bradykinin
Histamine
Substance -p
25) Tissue damage in chronic inflamation mediated by
Oxygen metabolites
IL-1
NO
LT -C4
Defensin
26)NO :
Synthesized from molecular oxygen
Synthesized from I-arginine
Ca required for synthesis
Required nitric oxide synthase
Released from endothelial cell
27)macrophage
Play central role in chronic inflamation
Can synthesis NO
Control granulopoiasis
Antigen presenting cell
Produce IL -1
28)Arachidonic acid metabolites causing vasoconstriction
Thromboxen A2
LT-D4
LT B4
Prostacyclin
LT -E4
29)acute phase protein are
Alfa 1 antitrypsin
Pasminogen
Ferritin
Prothombin
Mannos binding protein
30)CRP
Produce in liver
IL-6 upregulate its synthesis
Activate complement by classical pathway
Antigen spesific
E)late indicator of acute inflammation
31) CRP rise in –
Malignancy
Acute mi
Leukaemia
Pregnancy
Sle
32) granulomatous inflamation found in
Sarcoidosis
Tb
Acute inflammation
Psoriasis
Healing process
33)following which are granulomatous bacterial diseases
Tuberculosis
Gonorrhea
Histoplasmosis
Leprosy
Shistosomiasis
34) granuloma is composed of –
Macrophage
T lymphocyte
Modified activated macrophage
Modified B lymphocyte
Neutrophil
35)granulomas in TB
Heal by fibrosis
Always contain giant cell
Are discreet in nature
Always show central caseation
Made of epithelioid cell
36) following cells are involved in acute inflamation
Lymphocyte
Neutrophil
Endothelium of blood vessel
Epithelioid cell
Mast cell
37)Following substance are involved in acute inflamation
Peptides
Lectin
Plasmin
LATS
PGE1
38) Giant cell are found in the pathological lesion associated with following diseases
Actinomycosis
Primary biliary cirrhosis
Lepromatus leprosy
Schistosomiasis
Hodgkin diseases
39) Following which are plasma protein derived mediator
IL-1
Kinins
Prostaglandin
C5a
C4a
40) Cytokines
Released from endothelial cell
Cause local endothelial activation
Released from basophil
TNF
NO
41) Inflammatory cells associated with asthma
Eosinophil
Ig E antibody
Neutrophil
Macrophage
Cytokines
42) chronic inflamatory cells asociated with arthritis
Eosinophil
Mast cell
Macrophage
Neutrophil
Lymphocyte
43) Bacterial killing can occur by oxygen independent mechanism through
H2O2
Elastase
Lysozyme
NO
ATP
44) proliferative inflamation :
Transudate formation
Weeks to month
Granulomatous tissue
Tissue destraction minimum
Exudate formation
45) Transudate :
Occur due to increase hydrostatic pressure
Found in liver cirrhosis
Found in acute inflamation
Neutrophil present
Albumin oresent
46) outcome of acute inflamation
Vesodialation
Embolization
Resolution
Fibrosis
Organization
47) inflamation
Is a host defense
Sometime harmful to human body
Autoimmune is is a example
Occur with in minute
Occur in hair
48)exudate :
Dilute irritant or harmful substance
Act as potent media for bacterial growth
It help phagocytosis
Ph is low
Contain fibrin
49) in inflamation mediators has following roles
Histamin cause vesodialation
Substance -p cause pain
No cause tissue damage
LT4 cause fever
Tnf cause pain
50)TNF ( Tumour necrosis factor)
Found in plasma
Inhibit mitocondrial respiration
Is a protein
Beneficial to host
Has anti viral activity
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