MoD week 2-3 chronic and acute inflammation Flashcards

1
Q

what is acute inflammation?

A

response of living tissue to injury

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2
Q

what are the clinical signs of acute inflammation?

A

rubor, color, tumour, dolor, loss of function

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3
Q

what is vasodilation in acute inflammation?

A

increase permeabiity, and hydrostatic pressure to form exudate
gaps in endothelium allows exudation (plasma proteins), adherence, margination and emigration through basement membrane
recruits macro and lymphocytes

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4
Q

what are the mediators of acute inflammation?

A

histamine (stored in mast cells granules), serotonin (stimulate fibroblasts & platelets), prostaglandins (vasodilate, cause pain & fever), leucotrines (permeability), bradykinin (dilator, produce pain), complement (C3a, C4a, C5a), cytokines, endotoxins

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5
Q

conditions of acute inflammation

A

hereditary angiodema
alpha 1 anti trypsin deficiency
CGD (chronic granulomatous disease)

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6
Q

what is hereditary angiodema?

A

C1 esterase inhibitor deficiency
patient has attacks of non-itchy cutaneous angio-oedema
death in larengeal involvement

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7
Q

what is a-1 antitrypsin deficiency?

A

no inhibition of proteases

breaking down lung tissue causing emphysema

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8
Q

what is chronic granulomatous disease?

A

no O2 burst so granulomas formed everywhere
(unable to generate free radicals)
phagocytes can’t kill them and no free radicals leading to chronic infections

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9
Q

what causes chronic inflammation

A

takes over from acute
begins denovo (autoimmune)
alongside acute (abscess) - prolonged exposure to toxic agents
chronic persistent infections (arise denovo)

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10
Q

what are the processes of neutrophils working in acute inflammation?

A

margination - stasis causes neutrophils to line at edge of endothelium
rolling - neutrophils roll along endothelium
adhesion - to endothelium
emigration - of neutrophils out of capillary walls

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11
Q

What are the possible complications of chronic inflammation?

A

granulomas,
excessive fibrosis: fibroblasts stimulated by cytokines (excess collagen production)
impaired function: myofibroblasts contract e.g. blocking flow duct of liver
atrophy: muscle wasting
tissue destruction

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12
Q

What are giant cells?

A

fusion of macrophages due to frustrated phagocytosis

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13
Q

What are the 3 types of giant cells?

A

langans
foreign body
toutons

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14
Q

what are langans giant cells?

A

TB

have a nucleus like horseshoe - periphery

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15
Q

What are foreign body giant cells

A

present if there are foreign bodies

random nuclei

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16
Q

what are toutons giant cells

A

in lesions with high lipid content e.g. fat necrosis + xanthoma
ring nuclei in centre of cell, can see foam cells (macrophage ingest oxidised lipids)

17
Q

what are the principle cells of chronic inflammation?

A

macrophage
lymphocytes
eosinophils
fibroblasts

18
Q

what is the funciton of macrophage?

A

phagocytosis, present antigens to immune system

stimulate angiogenesis

19
Q

function of lymphocyte?

A
B type (plasma cells) produce antibodies
T type (killer cells) + cytotoxic functions, process antigens, secrete cytokines
20
Q

function of eosinophils

A

allergic rections, parasitic infestations

21
Q

function of fibroblasts

A

make collagen, elastin + GAG, differentiate into myofibriblasts (cells that can contract)

22
Q

major clinical examples of chronic inflammation

A
chronic cholecystitis
peptic ulcer
ulcerative colitis
chrons
cirrhosis
grave's
RA
23
Q

what is chronic cholecystitis?

A

repeated acute inflammation leading to fibrosis of the gall bladder

24
Q

what is peptic ulcer?

A

helicobacter pylori
imbalance between mucosal defence and acid production
necrosis

25
Q

what is ulcerative colitis?

A

colon inflammed, superficial, cholectomy

26
Q

what is chron’s disease?

A

chronic inflammation of all of GI, transmural, treat with removal

27
Q

what is cirrhosis?

A

fibrosis and impaired function

scarring of liver

28
Q

what is grave’s?

A

hyperthyroidism

heat intolerance, weight loss, high BMR, tachycardia, anxiety

29
Q

What is rheumatoid arthiritis?

A

localised autoimmune to joints, symmetrical