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FOM > acute inflammation > Flashcards

acute inflammation Flashcards

1
Q

Define acute inflammation

A

Fundamental response maintaining integrity of organism
- dynamic homeostatic mechanism
- higher organisms
Series of protective changes occurring in living tissue as a response to injury

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2
Q

Cardinal signs of inflammation

A 
Rubor - redness
Calor - heat 
Tumor - swelling
Dolor - pain 
Loss of function
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3
Q

Aetiology of inflammation

A

Micro organisms - pathogenic organisms cause infection

Mechanical - Trauma - Injury to tissue
- all injuries even sterile eg surgery

Chemical - upset stable environment

  • acid or alkali - upset pH
  • bile and urine - irritation when in inappropriate place eg peritoneum

Physical - extreme conditions

  • heat - sunburn
  • cold - frostbite
  • ionising radiation

Dead tissue - cell necrosis irritates adjacent tissue

Hypersensitivity
- several classes

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4
Q

Processes of acute inflammation

A

Series of microscopic events
Localised to affected tissue
Take place in microcirculation
Result in clinical symptoms and signs of acute inflammation - cardinal signs

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5
Q

What is microcirculation?

A

Capillary beds, fed by arterioles and drained by venules
Extracellular space and fluid and molecules within it
Lymphatic channels and drainage
Starling forces control flow across membrane
Dynamic balance - hydrostatic and colloid osmotic pressures
Compartments and physical constants

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6
Q

Pathogenesis

A

Changes in vessel radius
Change in permeability of the vessel wall - exudation
Movement of neutrophils from the vessel to the extravascular space

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7
Q

Local changes in vessel radius and blood flow

A

Transient arteriolar constriction - few moments, probably protective
Local arteriolar dilatation - active hyperaemia
Relaxation of vessek smooth muscle - autonomic NS or mediator derived
“Triple response” - flush, flare, wheal

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8
Q

What is an exudate?

A

fluid rich in protein - plasma - includes immunoglobulin and fibrinogen

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9
Q

Effects of exudation

A

oedema

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10
Q

What is oedema?

A

accumulation of fluid in the extravascular space

swelling - causes pain, reduces function

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11
Q

Explain flow in inflammation

A

neutrophil polymorphonuclear leukocyte is most important cell

loss of laminar flow
red cells aggregate in centre of lumen - rouleaux formation
neutrophils found near endothelium - margination

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12
Q

Phases of emigration of neutrophils

A

margination - neutrophils move to endothelial aspect of lumen

pavementing - neutrophils adhere to endothelium

emigration - neutrophils squeeze between endothelial cells - active process - to extravascular tissues

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13
Q

What is diapedesis?

A

passage of blood cells through intact walls of capillaries typically accompanying inflammation

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14
Q

Resolution of acute inflammation - ideal outcome

A 
inciting agent isolated & destroyed
macrophages move in from blood and phagocytose debris; then leave
epithelial surfaces regenerate 
inflammatory exudate filters away
vascular changes return to normal 
inflammation resolves
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15
Q

Benefits of acute inflammation

A

rapid response to non-specific insult
cardinal signs and loss of function - transient protection of inflamed area
neutrophils destroy organisms and denature antigen for macrophages
plasma proteins localise process
resolution and return to normal

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16
Q

Outcomes of acute inflammation

A 
resolution
suppuration
organisation
dissemination
chronic inflammation
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17
Q

examples of conditions

A 
appendicitis
pleural inflammation
bacterial endocarditis
acute pyelonephritis
gingivitis
18
Q

Neutrophils - function

A

They are mobile phagocytes which recognise foreign antigens and move towards them, this is called chemotaxis. Then adhere to organisms.

granules possess oxidants (egH2O2) and enzymes (eg proteases)

release granule contents

phagocytose and destroy foreign antigen

19
Q

Consequences of neutrophil action

A

neutrophils die when granule contents released
produce a “soup” of fluid, bits of cell, organisms, endogenous proteins - pus

might extend into other tissues, progressing the inflammation

20
Q

What is the role of plasma proteins in inflammation?

A

fibrinogen - coagulation factor - forms fibrin and clots exudate - localises inflammatory process

immunoglobulins in plasma specific antigen - humoral immune response

21
Q

Mediators of acute inflammation

A

molecules on endothelial cell surface membrane
molecules released from cells
molecules in the plasma
molecules inside cells

22
Q

What are the collective effects of mediators?

A 
vasodilation
increased permeability
neutrophil adhesion
chemotaxis
itch and pain
23
Q

What are cell surface mediators?

A

adhesion molecules appear on endothelial cells
eg ICAM-1 help neutrophils stick

P-selectin interacts with neutrophil surface

24
Q

Give examples of molecules released from cells

A

histamine
- preformed in mast cells beside vessels, platelets, basophils
- released as a result of local injury; IgE mediated reactions
- causes vasodilation, increased permeability
- acts via H1 receptors on endothelial cells
5-hydroxytryptamine (serotonin)
- preformed in platelets
- released when platelets degranulate in coagulation
- vasoconstriction

25
Q

other common molecules released from cells

A

prostaglandins

cytokines and chemokines

nitric oxide

oxygen free radicals

26
Q

What are intracellular inflammation pathways?

A

NF-kB - nuclear factor kappa-B pathway

MAPK - mitogen-activated protein kinase

  • stimulated in inflammation via surface receptors eg toll-like receptors
  • regulates pro-inflammatory cytokine production and inflammatory cell recruitment

JAK-STAT - Janus kinase - signal transducer and activator to transcription pathway
- direct translation of extracellular signal to molecular expression

27
Q

Plasma - interaction of 4 enzyme cascades

A

blood coagulation pathways
fibrinolysis
kinin system
complement cascade

28
Q

Blood coagulation pathways

A

clots fibrinogen in exudate

interacts widely with other systems

29
Q

Fibrinolysis

A

breaks down fibrin, helps maintain blood supply

fibrin breakdown products vasoactive

30
Q

Kinin system

A

bradykinin: pain

31
Q

Complement cascade

A

ties inflammation with immune system

active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown

32
Q

immediate systemic effects of inflammation

A

pyrexia

feel unwell - malaise, anorexia, nausea, abdominal pain and vomiting in children

neutrophilia - raised white blood cell count - bone marrow releases/produces

33
Q

Longer term effects of acute inflammation

A

lymphadenopathy - regional lymph node enlargement - immune response

weight loss - catabolic process

anaemia

34
Q

Suppuration - outcome of inflammation

A

pus formation - dead tissue, organisms, exudate, neutrophils, fibrin, RBCs, debris

pyogenic membrane surrounds pus - capillary sprouts, neutrophils, fibroblasts
- walls of pus

35
Q

What is an abscess?

A

collection of pus (suppuration) under pressure
single locule, multiloculated
“points” and discharges
collapses - healing and repair

36
Q

organisation outcome

A

granulation tissue characteristic
healing and repair
leads to fibrosis and formation of a scar

37
Q

What is granulation tissue?

A

“universal patch” - repair kit - for all damage

formed of

  • new capillaries - angiogenesis
  • fibroblasts and collagen
  • macrophages
38
Q

Dissemination outcome

A

spread to bloodstream - patient “septic”

bacteraemia - bacteria in blood
septicaemia - growth of bacteria in blood
toxaemia - toxic products in blood

39
Q

Pathogenesis of septic shock

A

systemic release of chemical mediators from cells into plasma

  • mediators cause vasodilation causing loss of systemic vascular resistance
  • results in catecholamine release
  • tachycardia (increased HR) follows to maintain CO because increased HR compensates
  • CO = SV x HR

bacterial endotoxin released

  • interleukin-1 released
  • acts on hypothalamus - pyrexia

activation of coagulation

  • disseminated intravascular coagulation
  • vasoactive chemical - vasodilatation
  • haemorrhagic skin rash
40
Q

When HR is insufficient to maintain CO

A

SVR low; therefore BP falls

  • BP = CO x SVR
  • increasing HR insufficient (CO = SV x HR)

reduced perfusion of tissues

  • tissue hypoxia
  • loss of cell tissue and organ function

FOM (35 decks)

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