Acute Inflammation 1 Flashcards

1
Q

What tissue does inflam occur

A

In vascularised ue

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2
Q

What does inflam aim to do

A

Destroy dilute wall off injurious agent

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3
Q

What kind of repsonse is inflammation

A

Primarily protectionn

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4
Q

What would happen without inflammation

A

Woudns wouldn’t heal
Injured organs might remain permanet festering sores
Infectious Wouk,d go unchecked

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5
Q

How can inflammation be harmful

A

Life threatening hypersensitivity
Chronic hi diseases (rheumatoid arthritis)
Renoir by fibrosis lead to disfiguring scars

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6
Q

What are the two types of inflammation

A

Acute and chornic

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7
Q

What’s is acute inflammation

A

The initial and often transient serious of tissue reactions to injury

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8
Q

What su chronic inflammation

A

The subsequent and often prolonged tissue reactions following initial response

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9
Q

What can cause acute inflam

A

Microbial infections - viruses, bac

Hypersensitivity reactions - inappropriate or excessive immune reaction which damages tissue incl parasites

Physical agents - physical trauma

Irritant or corrosive chess

Foreign bodies

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10
Q

Why does inflam have redness

A

Rub or acutely inflames tissue is red as blood vessels dilated in damaged area

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11
Q

Why is inflam heat

A

Increase temp of tissue due to increased blood flow through region hyperaemia

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12
Q

Why does inflammation swell

A

Tumor

Results form accumulation of fluid in extravascylar space - fluid exudate

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13
Q

Why is there pain with inflam

A

Dollar
Due to stretching and distortion of tissues caused by increased fluids - various chem mediators including bradykinin known to prod pain

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14
Q

Why dos inflam cause loss of function

A

Movement of inflame area is consciously and reflexly inhib by pain
Severe pain may immobilise limbs

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15
Q

Explain the vascular phase

A

Vascular dilation opening of precap sphincter

Also endothelial cells lining arterioles increased perm and form flid exudate

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16
Q

What is the net increase in extravascylar fluid called

A

Oedema

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17
Q

What is in fluid exudate and why

A

Immunoglobulins -imp for destruction of foreign bodies

Fibrinogen - becomes fibrin when comes in contact with ECm

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18
Q

What continually sholens to the exudate

A

Removed and replaced by lymphatics and new exudate formed

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19
Q

What brings about incised vascular perm

A

Bradykinin histamine - immediate transient
Severe direct vasc injury - immediate sustained
Endothelial cell injury - delayed prolonged

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20
Q

What so the diagnostic feature of acute inflam

A

Neutrophils accumulation in ecm

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21
Q

What are the functions of neutrophils

A
Kill micoro orgas 
Ingest offending agents
Degrade necrotic tissue 
Produce chem mediators 
Prod toxic oxygen radicals 
Prod tissue damaging enzymes
22
Q

How does a neutrophil each the site of an inflam response

A

Many ways

Adhesion to leukocytes to endothelial cells and subsequent migration Thor endothelium

23
Q

What is margination

A

Loss of intra vasc fluid and inc plasma visc slows allowing neurohils flow in plasma tic zone which Is margination
ONLY IN VENULES

24
Q

What so adhesion

A

Increased neurohils adhesion results from between interaction of adhesion mol on its surface and endothelial surface

25
Q

What is transendothelial migration

A

Once adhesion occurred
Neurohils insert pseudopodia into junctions between endothelial cells
Then cross base mem and into extravascylar space

26
Q

What are some predominat molecules in migration

A

Increased selectins on endo
Loose rolling adhesion between selectins and their recep leukocyte
Firm adhesion between integrins on leucocyte and ICAM1 on endo cell
Transmigration mediated by ICAM1, integrins and PECAM1

27
Q

What increases lucocyte adhesion molecule expression

A

Complement component ca
Leukotriene b4
Tumour necrosis factor

28
Q

What increases the endothelial cell expression for adhesion of other things such as neutrophils and other leukocytes

A

IL1
Endotoxins
Tumour Necrosis factor

29
Q

How do neurohils find site of inflam stimulus

A

By chemo taxis - locomotion orientated along conc grad

30
Q

What are chemotactic compounds for neutrophils

A

Bac prods
Complement comps
Cytokines
Products produced by neutrophils themselves

31
Q

What happens when chemotactic agent attaches to neutrophil

A

Release for intracellular calcium

Influx of extracellular calcium

32
Q

What does increased cytosol if calcium tigger

A

Assembly of contractile proteins responsible for cell movement

33
Q

What are the chemical be released form the inflam site called

A

Endogenous

34
Q

What can these endogenous chms cause

A
Vasodilation 
Emigration of neutrophils
Chemotaxis
Increased vasc perm 
Itching and pain
35
Q

What does histamine do for inflammation

A

Vasc dilation
Transient inc in vasc perm
Released by mast cells, eosinophils, basophils and platelets
Release stim by c3a c5a and lysosomal proteins

36
Q

How do lysosomal compounds affect inflammation

A

Released form neurohils

May increase vasc perm

37
Q

What does serotonin do for inflam

A

Inc vasc perm

38
Q

What doe chemekines do in inflam

A

Proteins which attacks of leucocyte to sit of inflam

Various chemekines bind to scm component setting up a gradient of chemotactic mols fixed to ECm

39
Q

What do leukotripenes do in inflam

A

Syn by arachnoid acid especially by neurohils
Vasoactive properties
Involved in type 1 hypersensitivity

40
Q

What do prostaglandins do in inflam

A

Fatty acid syn
Inc vasc perm
Stim platelet aggregation

41
Q

Plasma contains what four enzyme cascades which mediate aspects of inflam in addition to other factors

A

Complement syst
Kinin syst
Coagulation syst
Fibrinolytic system

42
Q

What causes complement activation

A

Enzymes released form dying cells
Antigen-antibody complexes
Products of kin in, coag and fibrinolytic systems
Bac endotoxins

43
Q

What hallens as a result of complement activation

A

Opsonisation of pathogens (phagocytosis)
Increase vasc perm
Recruit inflam cells
Histamine see lease from mast cells vasodilation

44
Q

What does the kinin syst gen

A

Vasoactive peptides form plasma proteins called kininogens by action of specific kallikreins

45
Q

What activates the kinin syst

A

Coag factor 12 leads to form of kinins such as bradykinin

46
Q

What’s does bradykinin cause

A

Increased vasc perm
Arteriolar dilatation
Smooth muscle contraction
Pain

47
Q

What does the coag system do

A

Conversion of fibrinogen into fibrin

48
Q

What is fibrin

A

Component of acute inflam infiltrate

49
Q

What dos the fibrinolytic syst do

A

Counterbalance coag syst as plasminogen activators cleave plasminogen to give plasmin

50
Q

What is plasmin responsible for

A

Lysis of fibrin into fibrin degradation prods which increase vasc perm

51
Q

What’s inflammation. A response to

A

Tissue injury