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pathological process' > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

characteristics of acute inflamation

A 
immediate
short duration
innate
stereotyped
limits damage
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2
Q

causes

A 
microbial infections
hypersensitivity reactions
physical agents
chemicals
tissue necrosis
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3
Q

clinical signs

A

Rubor-Redness
Tumor- Swelling
Calor- Heat
Dolor-Pain

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4
Q

what changes occur in the vessels

A 
vasoconstriction few seconds
vasodilations few minutes
permeability increased due to increased capillary hydrostatic pressure
oedema formation
red cell stasis
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5
Q

what pressures do we need for optimum flow into the interstitium

A

we need high capillary hydrostatic pressure and high interstitial oncotic pressure

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6
Q

what is stasis, why is it good

A

reduced flow through the vessel

important because allows more time for exudate + transudate formation

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7
Q

what is exudate

A

type of interstitial fluid - protein rich to areas of injury

increased vascular permeability

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8
Q

what is transudate

A

type of tissue fluid when actually being moved out of the vessel into the interstitium
no change in vascular permeability
heart/renal/hepatic failure

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9
Q

mechanisms of increased vascular permeability

A

endothelial contraction (gaps between the endothelial cells)

direct injury - toxins damage the wall

endothelial cytoskeleton reorganisation

leucocyte dependant injury (enzymes and toxic ROCs)

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10
Q

why does blood increase viscosity

A

fluid moves out of vessel
increased concentration of proteins in blood
increased viscosity
reduced flow

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11
Q

stages of neutrophil emigration into the interstitium

A

Margination- stick to the endothelial cell layer
Rolling-roll along the endothelium
Adhesion-stick more avidly to the cell layer
Emigration-through the blood vessel wall

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12
Q

how do the clinical signs relate

A

increased vascular permeability, transudate and exudate formation- TUMOR
increased concentration of RBC in vascular system- RUBOR
reduced flow due to RBC stasis-CALOR

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13
Q

adhesion molecules

A

SELECTINS-on endothelial cell surface, unregulated by chemical mediators

INTEGRINS- on neutrophil surface, bind to receptors on the endothelial surface

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14
Q

functions of the neutrophils

A

chemotaxis- process of entering the interstitium
phagocytosis-immune response
killing of micro-organisms- lysosome contains hydrolytic enzymes

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15
Q

pls explain the chemotaxis process in more detail

A

movement along a chemical gradient of chemoattractants

  • pseudopod
  • neutrophil cytoskeleton rearrangement
  • bacterial peptides
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16
Q

why is inflammation an effective response

A

delivery of nutrients, oxygen, cells, plasma proteins
dilution of toxins
stimulation of immune response
destruction of dead and foreign material
pain and loss of enforcing rest (malaise)

17
Q

Chemical mediators

A

Important in up regulation of adhesion molecules (selectins)

examples: amines, peptides, cytokines and chemokines, exogenous mediators, phospholipid derivatives

18
Q

local complications of inflammation

A

reduced blood supply to normal tissues
swelling causes obstruction of tubes and structures
loss of fluid (exudate and transudate)- blood is left highly viscous
Pain causes by stasis

19
Q

systemic complications of inflammation

A

fever-pyrogens affecting thermoregulatory centre
leucocytosis-WBC production increased
acute phase response- CRP release and malaise
shock- septic overwhelming infection, widespread vasodilation, leads to rapid death

20
Q

what happens after acute inflammation

A

complete resolution
chronic inflammations with some fibrous repair
continued acute inflammation with chronic inflammation
death

21
Q

what happens in complete resolution

A 
drainage of the exudate
neutrophils phagocytosed
fibrous repair if architecture preserved
mediators are inhibited
no margination, vessel calibre return to normal
22
Q

how does oedema formation reduce damage

A 
dilutes the toxins 
delivers exudate (proteins) to the site of injury- such as immunoglobulins
increased lymphatic draining delivers antigens to the lymph nodes
23
Q

appendicitis

A

blocken lumen, accumulation of bacteria, increased pressure and reduced blood flow

24
Q

pneumonia

A

streptococcus pneumonia, smoking and COPD riskfactors, shortness breath, fever cough, chest pain

25
Q

meningitis

A

inflammation of the meninges
variety of pathogens
neck stiffness, fever photophobia
rapidly fatal

26
Q

abcess

A

accumulation of dead and dying neutrophils, with associated necrosis (liquefactive)
causes compression of the surrounding structures, pain and blockage of the ducts

27
Q

ascending cholangitis

A

bacteria entering the bile duct from the duodenum

28
Q

examples of inherited disorders of acute inflammation disorders

A

hereditary angio-oedema
alpha 1 antitrypsin deficiency
chronic granulomatous disease

pathological process' (12 decks)

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