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Mechanisms of Disease > Session 2 -> Acute inflammation > Flashcards

Session 2 -> Acute inflammation Flashcards

0
Q

What controls acute inflammation?

A

-Chemical mediators, mostly from plasma but some from cells

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1
Q

What is acute inflammation?

A
  • The immediate, innate and stereotyped response of living tissue to any injury
  • It is usually short in duration and involves both vascular and cellular reactions
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2
Q

List the main causes of acute inflammation

A
  • Microbial infection
  • Hypersensitivity immune reactions
  • Physical agents (Heat/UV/Knife)
  • Chemicals (drugs/bleach)
  • Tissue necrosis
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3
Q

What are the main cardinal signs of acute inflammation?

A
  • Rubor
  • Calor
  • Tumor
  • Dolor
  • Loss of function
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4
Q

How does loss of function act as a protective mechanism?

A

-Enforces rest and prevents further injury

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5
Q

Describe the changes in vascular flow which occurs with acute inflammation

A

-Transient vasoconstriction then local vasodilation, resulting in increased bloodflow and then vascular stasis

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6
Q

What is the consequence of local vasodilation in acute inflammation?

A

-Increased stasis results in an increased hydrostatic pressure which causes oedema

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7
Q

Apart from increased hydrostatic pressure, what other factor of acute inflammation contributes to oedema?

A

-There is increased vascular permeability which means plasma proteins leak into the interstitium, reducing colloid oncotic pressure-> less water is drawn back into the blood vessel causing oedema

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8
Q

Why does vascular stasis occur in acute inflammation?

A
  • Decreased colloid oncotic pressure -> reduced fluid resorption
  • Increased hydrostatic pressure -> increased fluid loss
  • Blood becomes viscous and stasis occurs
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9
Q

What causes the vasodilation of arterioles in acute inflammation?

A

-Mast cells, basophils and platelets release prostaglandins, histamine and serotonin which cause vasodilation

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10
Q

What causes rubor/calor in acute inflammation?

A

-Vasodilation -> increased heat loss and increased bloodflow

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11
Q

Why is vasodilation beneficial in acute inflammation?

A
  • Increased temperature

- Increased delivery of cells and chemical mediators

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12
Q

Why does oedema occur in acute inflammation?

A
  • Arterial dilation -> increased HP
  • Increased vascular permeability -> decreased oncotic pressure
  • Increased net outflow of fluid = oedema
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13
Q

What two types of fluid cause oedema?

A
  • Transudate

- Exudate

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14
Q

How does transudate differ from exudate?

A
  • Transudate has a low protein content

- Exudate is protein rich

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15
Q

When does transudate commonly form?

A

-When there is increased hydrostatic pressure as in heart failure

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16
Q

When does exudate commonly form?

A
  • Infection
  • Inflammation
  • Cancer
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17
Q

What type of exudate is commonly found with cancer?

A

-Haemorrhagic exudate

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18
Q

How can oedema be used as a diagnostic tool?

A

-The type of fluid within the oedema can provide information about the pathological cause

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19
Q

How is oedema resolved?

A

-Increased lymphatic drainage

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20
Q

What are the possible mechanisms of vascular leakage?

A
  • Endothelial contraction
  • Cytoskeleton reorganisation
  • Leukocyte-dependant injury
  • Direct injury
  • Increased channels and transcytosis
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21
Q

What chemical mediators influence endothelial contraction?

A
  • Histamines

- Leukotrienes

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22
Q

Why is the formation of fluid exudate beneficial in acute inflammation?

A
  • Delivers nutrients, O2, cells and proteins such as Ab/fibrinogen to site of damage
  • Dilutes toxins
  • Increases lymphatic drainage
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23
Q

WHy is increased lymphatic drainage helpful in acute information?

A

-Stimulates an immune response by delivering microorganisms to the lymph nodes

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24
Q

Describe the process of neutrophil emigration into tissues

A

1) Vasodilation (vascular stasis occurs)
2) Gaps form in the endothelium (endothelial contraction)
3) Exudation (vessels become leaky)
4) Margination (stasis causes neutrophils to line up along edges)
5) Rolling
6) Adhesion
7) Emigration through basement membrane

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25
Q

Why is neutrophil emigration quite a destructive process?

A
  • Enzymes are used to break down the basement membrane of vessels
  • Neutrophils cause relaxation of inter-endothelial cell junctions
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26
Q

Name some chemical mediators involved in vasodilation

A
  • Histamine
  • Prostaglandins
  • Complement factors
  • Serotonin
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27
Q

Name some chemical mediators reaponsible for increased vascular permeability

A
  • Histamines
  • Prostaglandins
  • Kinins
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28
Q

Name some chemical mediators responsible for emigration and chemotaxis?

A
  • Leukotrienes

- Cytokines

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29
Q

Name some proteases which are secreted during acute inflammation

A

-Kinins/C3a/C5a/fibrinolytic system

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30
Q

What are prostaglandins/leukotrienes metabolites of?

A

-Arachodonic acid

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31
Q

What is chemotaxis?

A

-The movement of cells along concentration gradients of chemoattractants to the source of infection

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32
Q

How is chemotaxis initiated?

A

-Ligand-receptor binding of chemoattractant to chemoreceptor on a cell causes the rearrangement of cytoskeleton to produce pseudopods to facilitate movement

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33
Q

What are the three stages of phagocytosis?

A
  • Contact
  • Recognition
  • Internalisation
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34
Q

How do neutrophils recognise cells for phagocytosis?

A

-Facilitated by opsonins-> Neutrophils have many receptors for Fc and C3a to allow detection of Ab-bound or complement-bound material

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35
Q

How do neutrophils digest the material they phagocytose?

A

-They fuse the phagosome with a lysosome, producing a secondary lysosome which destroy contents by digestion with enzymes

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36
Q

What are the killing mechanisms of neutrophils?

A
  • O2-dependant

- O2-independant

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37
Q

What happens in O2-dependant killing in neutrophils?

A

-The neutrophils use superoxide/hydrogen peroxide to kill micro-organisms

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38
Q

What is the O2-independent killing mechanism of neutrophils?

A

-Uses hydrolases, bacteriocidal permeability increasing protein and lysosomes to kill micro-organisms

39
Q

Which killing mechanism of neutrophils is the most efficient?

A

-O2-dependant

40
Q

List some local complications of acute inflammation

A
  • Damage to normal tissue (rubor/calor/tumor/dolor)
  • Obstruction/blockage of tubes by swelling
  • Loss of fluid
  • Pain and loss of function
  • Exudate can compress vita structures (cadriac tamponade)
  • Exudate can lead to the spread of infection eg perotinitis
41
Q

List some systemic complications of acute inflammation

A
  • Fever
  • Leukocytosis
  • Acute phase response
  • Changes in acute phase protein conc
  • Shock
42
Q

How does fever occur in acute inflammation?

A
  • Endogenous pyrogens are produced (substances that induce fever)
  • IL-1, TNF-a and prostaglandins reset the body’s thermastat in the anterior hypothalamus to increase temperature
43
Q

How does leukocytosis occur in acute inflammation?

A
  • IL-1 and TNF-a cause accelerated release of leukocytes from the marrow
  • Macrophages and lymphocytes produce CSF which further stimulates the marrow
44
Q

Which leukocyte is mainly associated with bacterial infection?

A

-Neutrophil

45
Q

Which leukocyte is mainly associated with viral infection?

A

-Lymphocytes

46
Q

What is the acute phase response?

A
  • Decreased appetite
  • Increased Heart rate
  • Altered sleeping patterns
47
Q

What acute phase proteins can become altered in acute inflammation?

A
  • C-reactive protein
  • Fibrinogen
  • Haptoglobin
  • a1-antitrypsin
48
Q

What is shock?

A

-Circulatory failure caused by decreased blood volume due to systemic vasodilation and oedema

49
Q

What are the 4 possible resolutions from acute inflammation?

A
  • Complete resolution
  • Continued acute inflammation with chronic inflammation = abscess
  • Chronic inflammation and fibrous repair
  • Death
50
Q

What happens in complete resolution of acute inflammation?

A
  • Morphological changes reverse
  • Vascular changes stop
  • Exudate drains to lymphatics
  • Neutrophils die and are phagocytosed
  • Regeneration of tissue
51
Q

When can regeneration of cells not occur?

A

-When the architecture of the cell has been destroyed

52
Q

How are mediators of acute inflammation removed?

A
  • Mediators have short half lives
  • Enzymes and proteins are inactivated by degredation eg fibrin by plasmin
  • Some mediators are unstable
  • Inhibitors can bind to mediators
  • Specific inhibitors of the acute inflammatory response
  • Dilution by exudate
53
Q

What is the causative organism of lumbar pneumonia?

A

-Streptococcus pneumoniae

54
Q

What are the symptoms of lobar pneumonia?

A
  • Worsening fever
  • Hypoxaemia over a few days as exudate fills alveoli
  • Dry cough
  • Breathlessness
55
Q

What are the predominant features in a skin blister?

A
  • Pain

- Profuse exudate

56
Q

How does exudate result in a blister?

A

-The collection of fluid strips off the overlying epithelia

57
Q

What are the possible outcomes of a skin blister?

A
  • Complete resolution

- Scarring

58
Q

Why is the exudate clear in a skin blister?

A

-Contains relatively few inflammatory cells

59
Q

In what type of tissues do abscesses occur?

A

-Solid tissues

60
Q

How does exudate result in an abscess?

A

-Inflammatory exudate forces the tissue apart and liquefactive necrosis occurs in the centre

61
Q

Why is an abscess painful?

A

-From the high amount of pressure

62
Q

How can abscesses cause damage to other tissues?

A

-Can squash adjacent tissues

63
Q

How does acute inflammation occur in serous cavities?

A

-Through leakage of exudate

64
Q

What is an ascites?

A

-A collection of fluid in the peritoneum causing swelling

65
Q

What is often the cause of acute appendicitis?

A

-Blockage of the lumen by faecolif, tumour or viral infection (swelling of closely associated lymph nodes)

66
Q

How does the blockage of the appendix lead to appendicitis?

A
  • Blockage causes stasis of appendiceal contents
  • Multiplication of bacteria
  • Tissue inflammation, necrosis, ulceration and exudate formation
  • Swelling due to vasodilation and exudate formation = oedema
67
Q

What is ulceration?

A

-Depression in epithelial surface due to loss of epithelia

68
Q

What are the possible outcomes of perforation of the appendix?

A
  • Peritonitis
  • Shock
  • Liver abscess via septicaemia -> hepatic portal vein
69
Q

What is the common cause of bacterial meningitis in neonates?

A
  • GBS
  • E.coli
  • Listeria Monocytogenes
70
Q

What is the common cause of bacterial meningitis in children?

A
  • Streptococcus Pneumoniae
  • Neisseria Meningitidis
  • Haemophilus Influenzae B
71
Q

What is the most common cause of bacterial meningitis in young adults?

A

-Neisseria Meningitidis

72
Q

What is the most common cause of bacterial meningitis in the elderly?

A
  • Listeria Monocytogenes
  • Neisseria Meningitidis
  • Streptococcus Pneumoniae
73
Q

What causes the neurological symptoms in bacterial meningitis?

A

-Purulent pus/exudate rich with neutrophils appears on the brain causing swelling and increasing intracranial pressure leading to neurological symptoms

74
Q

What neurological symptoms are commonly seen in bacterial meningitis?

A
  • Hearing and vision loss
  • Speech problems
  • Coordination and balance problems
  • Poor memory and concentration
75
Q

How can bacterial meningitis lead to gangrenous limbs?

A

-Septacaemia

76
Q

What is waterhouse-friderchsen syndrome? What is it a sign of?

A
  • Adrenal gland failure caused by bleeding and haemorrhage into the adrenal glands
  • Meningococcal sepsis
77
Q

What is ascending cholangitis?

A

-A bile duct infection which is retreating up the bile duct

78
Q

What is the main cause of ascending cholangitis?

A
  • Gallstone impaction causes blockage of the common bile duct
  • Stasis occurs
  • Replication of bacteria causes acute inflammation of the bile duct which can back up into the liver
79
Q

How can ascending cholangitis cause a liver abscess?

A
  • Inflammation of the liver occurs due to it ascending up the common bile duct
  • Liquefactive necrosis of the liver and inflammation leads to an abscess forming
80
Q

-What is the common bacteria to cause ascending cholangitis?

A
  • Klebsiella Pneumoniae
  • E.coli
  • Enterococcus sp.
81
Q

Why does ascending cholangitis have leukocytosis?

A
  • Many macrophages due to bacterial infection

- Macrophages secrete CSF which stimulates the BM

82
Q

Why is there a raised ALT, bilirubin and alkaline phosphatase when there is a liver abscess?

A

-Leaky cells due to inflammation and destruction of hepatocytes

83
Q

What are possible complications of ascending cholangitis?

A
  • Jaundice
  • Gallstone ileus
  • Acute pancreatitis
84
Q

What is gallstone ileus?

A

-gallstone erodes through gall bladder into duodenum, possibly obstructing the terminal ileum (can lead to rupture as no faeces can pass)

85
Q

Why can gallstones lead to acute pancreatitis?

A

-Gallstone blocks the common bile duct distal to the pancreas resulting in pancreatitis

86
Q

What is hereditary angio-oedema?

A

-Rare autosomal dominant disorder of acute inflammation where there is deficiency of C1-esterase inhibitor leading to angio-oedema

87
Q

Why does c1-esterase deficiency cause angio-oedema?

A
  • C1-esterase inhibits bradykinin.
  • Deficiency of this enzyme means bradykinin is uninhibited
  • Uninhibited bradykinin leads to increased vascular permeability and thus angio-oedema
88
Q

How is hereditary angio-oedema characterised?

A
  • Rapid attacks of non-itchy cutaneous angio-oedema including the dermis, subcutaneous tissue, mucosa and submucosa
  • Possible recurrent abdo-pain due to intesinal oedema
89
Q

How is hereditary angio-oedema treated?

A
  • C1-esterase infusion

- Frozen plasma

90
Q

What is a1-antitrypsin deficiency?

A

-Autosomal recessive disorder of acute inflammation with vary severity caused by deficiency/no a1-antitrypsin

91
Q

What is a1-antitrypsin?

A

-Protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation

92
Q

How does a1-antitrypsin deficiency result in emphysema?

A

-Elastase is not inhibited which results in destruction of the parenchyma of the lung

93
Q

Why does a1-antitrypsin deficiency cause liver sclerosis?

A
  • Misfolding of the protein results in accumulation in the ER as it cannot be exported
  • Hepatocyte damage leading to sclerosis and cirrhosis
94
Q

What is chronic granulomatous disease?

A

-A recessive sex-linked disorder of acute inflammation where immune phagocytes cannot generate superoxide radicals

95
Q

Why is not producing superoxide radicals in chronic granulomatous disease a problem?

A

-Immune phagocytes cannot destroy ingested bacteria resulting in the formation of granulomas and abscesses in the skin, lymph nodes, lung and liver in order to contain the bacteria

96
Q

When does chronic granulomatous disease begin to present?

A

-Chronic infections occur within 1 year of life

Mechanisms of Disease (11 decks)

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