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EMS > Theme 3: Inflammation, Infection and Immunology: Part 1 > Flashcards

Theme 3: Inflammation, Infection and Immunology: Part 1 Flashcards

1
Q

What is acute inflammation?

A
  • initial tissue reaction to injury
  • response is same no matter what causes injury
  • lasts minutes, hours or days
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2
Q

What is the characteristic cell in acute inflammation?

A

neutrophil polymorph

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3
Q

What are the 5 signs of acute inflammation?

A
  1. Redness (rubor) - caused by vasodilation
  2. Heat (calor) - caused by increased blood flow to vessels or systemic fever due to cytokines
  3. Swelling (tumor) - results from oedema - accumulation of fluid extra cellular space
  4. Pain (dolor) - results from distortion of tissues or pus under pressure
  5. Loss of function (functio laesa)
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4
Q

What are the causes of AI?

A
  • physical agents - burns, radiation
  • infections
  • hypersensitivity reactions- autoimmune
  • chemicals
  • tissue necrosis e.g from MI
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5
Q

Where is the inflammation in meningitis?

A

subarachnoid space in brain

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6
Q

What is acute cholecystitis and what is it often caused by?

A

inflammation of the gall bladder

often caused by gallstones

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7
Q

What are empyema?

A

pockets of pus that have collected inside a body cavity - can develop during AI

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8
Q

What is exudate?

A

extra vascular fluid with high protein concentration, containing cellular debris. Implies inflammation

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9
Q

What is transudate?

A

low protein, little or no cellular component

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10
Q

What is oedema?

A

excess fluid in interstitial tissue/serous cavities

can be exudate or transudate

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11
Q

What is pus?

A

inflammatory exudate rich in neutrophils, dead cell debris and microbes

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12
Q

What are the 3 occurrences in acute inflammation?

A
  1. changes in vessel calibre
  2. increased vascular permeability and fluid exudate formation (fluid enters tissue)
  3. cellular exudate formation (cells enter tissue)
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13
Q

Explain the changes in vessel calibre during AI?

A
  • vasodilation
  • increased blood flow
  • heat and redness
  • mediated by histamine and NO on vascular smooth muscle
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14
Q

What is exudation?

A
  • increased permeability of vessels
  • protein rich fluid escapes into tissue
  • hydrostatic pressure increases and plasma proteins escape into extravascular space increasing the osmotic pressure
  • fluid leaves vessel : exudation
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15
Q

What are the 7 effects of fluid exudate?

A
  • dilution of toxins
  • entry of antibodies
  • transport of drugs
  • fibrin formation
  • delivery of nutrients and oxygen
  • stimulation of immune response
  • responsible for swelling
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16
Q

Why does stasis occur in AI?

A
  • loss of fluid into tissues and increased calibre of vessels
  • slower blood flow and increased viscosity
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17
Q

How does the formation of the cellular exudate occur?

A
  1. Margination of neutrophils
  2. Pavementing of neutrophils
  3. Pass between endothelial cells
  4. Pass through basal lamina and migrate into adventitia
  5. Gap seals itself behind

(neutrophils line up along the vascular endothelium, stick to the endothelium and migrate through walls into tissues)

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18
Q

What is margination?

A

usually neutrophil polymorphs travel down the centre but as blood thickens they move to the side and exit the vessel

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19
Q

What is chemotaxis?

A

movement of a motile cell or organism, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance

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20
Q

give 5 features of neutrophils

A
  • produced in bone marrow
  • commonest white cell in blood
  • increased in acute inflammation
  • motile, amoeboid, can move into tissues
  • short lifespan
  • directional chemotaxis
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21
Q

Which chemical mediators of AI are cell derived?

A
  1. histamine - released by mast cells which increases vascular permeability and dilatation
  2. prostaglandins - come from arachidonic acid with vasodilator properties
  3. lysosomal components
  4. leukotrines - come from arachidonic acid with vasodilator properties
  5. cytokines
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22
Q

What are the systemic effects of inflammation?

A
  • pyrexia (fever)
  • lymph node enlargement
  • nausea, malaise, anorexia
  • leukocytosis
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23
Q

What is fibrinous inflammation?

A
  • increased vascular permeability can result in large molecules such as fibrinogen entering tissues and forming fibrin
  • causes inflammation in linings of body cavities
  • can be removed by fibrinolysis and removal of debris by macrophages
  • if not can lead to scarring (organisation)
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24
Q

What is the ideal outcome of AI?

A

Resolution - tissue restores to normal. This only occurs when there is minimal cell death and depends on the regenerative capacity of the organ or tissue

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25
Q

What is suppuration?

A

discharge of pus

26
Q

What might occur is there is a persistent causal agent causing AI?

A

Chronic inflammation

27
Q

What is innate immunity?

A

cells that have pattern recognition receptors so can respond without memory of encounters with pathogens

28
Q

What are the 3 potential outcomes of acute inflammation?

A
  1. Resolution - phagocytosis of insulting agent, fibrinolysis, phagocytosis of debris - tissue returns to normal state
  2. Repair - organisation (replacement by granulation tissue) –> fibrous scar caused by collagen deposition - when there is more extensive disruption and tissue can’t regenerate
  3. chronic inflammation - organisation +macrophages/lymphocytes/plasma cells
29
Q

What is chronic inflammation?

A
  • inflammation of prolonged duration
  • memory is involved (innate and adaptive immunity)
  • involves macrophages, lymphocytes (T and B cells), plasma cells
  • can cause amyloidosis, cachexia (tissue wasting) and anaemia
30
Q

What are 5 circumstances under which chronic inflammation could arise?

A
  1. progression from acute (if no resolution)
  2. recurrent episodes of acute e.g chronic cholecystitis
  3. persistant infection e.g TB, leprosy
  4. prolonged exposure to toxic agents e.g asbestos causing cirrhosis
  5. autoimmunity e.g Hashimoto’s thyroidism, RA
  6. unknown - chrons disease, UC, sarcoidosis
31
Q

What is chronic pyelonephritis?

A

chronic inflammation and infection of the kidney

32
Q

Which cells synthesis collagen?

A

fibroblasts. (explains why they’re pink) - which gives rise to fibrous scars

33
Q

What is a monocyte?

A

circulating form of a macrophage

34
Q

What are macrophages called in the:

  1. CNS
  2. Liver
  3. Lung
  4. Bone
A
  1. Microglia
  2. Kupffer cells
  3. Alveolar macrophages
  4. Osteoclasts
35
Q

What is granulation tissue?

A

new connective tissue and blood vessels that forms on the surface of a wound during healing - chronic inflammation would occur here

36
Q

What are granuloma?

A

collection of activated epithelioid macrophages
two types:
1. caseating - granuloma that has a core of necrosis in middle
2. non-caseating

37
Q

What are multinucleate giant cells?

A

collections of macrophages that have fused together to form one huge cell with multiple nuclei

38
Q

What are the causes of granulomatous inflammation?

A
  • bacterial: TB, leprosy, syphillis
  • parasitic: schistosomiasis
  • fungal: cryptococcus
  • inorganic metals or dust
  • foreign body: suture
  • unknown: sarcoidosis, UC
39
Q

Which is the largest solid organ in the body?

A

the liver

40
Q

Why is the liver red?

A

due to iron storage

41
Q

What are the 7 functions of the liver?

A
  1. Carbohydrate metabolism - storage of glycogen, conversion of galactose and fructose to glucose, gluconeogenesis
  2. Fat metabolism - triglyceride and lipoprotein synthesis
  3. Protein metabolism and synthesis - synthesis of amino acids, albumin, C-reactive protein, complement 1-9
  4. Billirubin metabolism
  5. Vitamin storage - A,D,B12, Iron
  6. Coagulation factors
  7. Chemical detoxification and metabolism
42
Q

How does acute liver injury occur?

A
  • significant proportions of hepatocytes die at once
  • can be caused by drugs, hepatitis etc
  • if repair is not plausible, patient will need transplant
43
Q

How does chronic liver injury occur?

A
  • persistent ongoing damage and injury
  • inflammatory response
  • heal through fibrosis and regeneration –> cirrhosis
44
Q

What does idiosyncratic hepatotoxins mean?

A

most drug reactions are rare and unpredictable

45
Q

What does intrinsic hepatotoxins mean?

A

drugs like paracetamol in high doses cause liver injury in everyone

46
Q

Explain how paracetamol is metabolised (when taken in therapeutic doses)

A
  1. Paracetamol broken down by P450 enzymes and converted into NAPQI
  2. Glutathione binds to NAPQI and this is excreted by kidney
47
Q

What happens when paracetamol is taken in toxic doses?

A

glutathione is quickly depleted and not readily available

so the toxic metabolite NAPQI remains in liver and causes hepatic necrosis

48
Q

What is confluent necrosis?

A

substantial areas of liver cell death

49
Q

what happens when >50% of liver cells die?

A

patient develops acute liver failure (ALF)

50
Q

In liver cell necrosis, which enzymes are released and can be detected by lab tests?

A

increase in AST and ALT

51
Q

Why is jaundice a symptom of ALF?

A

Failure of bilirubin metabolism, mostly conjugated hyperbilirubinaemia

52
Q

Why would patients with ALF have a bleeding tendency?

A

failure to synthesise proteins - factors II, VII, IX, X depleted

53
Q

Why would patients with ALF have renal failure?

A

shock causes low glomerular filtration

54
Q

What is the treatment for ALF?

A
  • Activated charcoal

- N-acetyl cysteine (which produces glutathione)

55
Q

What is the only reliable way of assessing fibrosis of liver?

A

liver biopsy

56
Q

What are acidophil bodies?

A

single dying hepatocytes

57
Q

What is chronic liver disease?

A

any disease that causes ongoing inflammation of liver, resulting in increasing amounts of fibrosis

58
Q

What is cirrhosis?

A
  • end stage of chronic liver disease
  • significant fibrosis with modularity of the parenchyma
  • liver transplant only cure
59
Q

What are the causes of chronic liver disease?

A
  • infection e.g hepB,C
  • autoimmune hepatitis
  • alcohol
  • obesity
  • biliary diseases
  • genetic diseases e.g haemochromatosis
  • drug induced liver injury
60
Q

How does the liver repair and regenerate?

A

regeneration of labile and stable cells

61
Q

What are 4 consequences of liver cirrhosis?

A
  1. Portal hypertension
    - increased blood flow from portal vein, development of oesophageal varies
  2. Oedema
    - development of ascites and peripheral oedema
  3. Risk of infection
  4. Carcinogenesis
    - increased risk of hepatocellular carcinoma

EMS (16 decks)

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