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Mechanisms of Disease > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

0
Q

List a few causes for acute inflammation

A

Microbial infections, hypersensitivity reactions, physical agents, chemicals and tissue necrosis. NB: reaction to all of these agents looks the same

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1
Q

What is acute inflammation?

A

Response of living tissues to injury. Its initiated to limit tissue damage and has a short duration

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2
Q

What are the five clinical features of acute inflammation?

A

Rubor (redness), tumour (swelling), calor (heat), dolor (pain) and loss of function

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3
Q

What are the main changes in tissues due to acute inflammation?

A

Vascular changes (changes in blood flow and exudation of fluid) and cellular changes (infiltration of inflammatory cells)

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4
Q

What changes in blood flow occur during acute inflammation?

A

Transient vasoconstriction –> vasodilation –> increase blood flow –> increased permeability of BV –> swelling –> increased viscosity leading to stasis –> release of histamine from mast cells, basophils and platelets

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5
Q

What is starlings law?

A

Increased hydrostatic pressure leads to increased fluid flow out of the vessel. Decreased colloid osmotic pressure leads to increased flow of fluid out of the vessel

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6
Q

What is exudate?

How does it differ from transudate?

A

Exudate is a fluid with a high content of protein and cellular debris which has escaped from the blood vessels and been deposited in tissues.
Transudate has a low protein content, high fluidity and low content of cells or solid materials

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7
Q

List the mechanisms of vascular leakage

A 
Endothelial contraction
Cytoskeletal reorganisation
Direct injury
Leukocyte dependent injury
Increased transcytosis
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8
Q

What is the role of fibrin in acute inflammation?

A

Prevents blood leaking out of vessels because it is sticky, thus localising the inflammatory response

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9
Q

What is the primary type of white blood cell involved in acute inflammation?

A

Neutrophil leukocytes

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10
Q

Describe the process of infiltration by neutrophils

A

Margination - stasis causes neutrophils to line up at the edge of BV along the endothelium
Rolling - neutrophils roll along endothelium, sticking to it intermittently
Adhesion - neutrophils stick more avidly
Emigration of neutrophils through BV walls

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11
Q

How do neutrophils leave blood vessels?

A

Relaxation of inter-endothelial cell junctions.
Localised digestion of vascular basement membrane.
Movement from inside the cell to outside the cell.

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12
Q

How do neutrophils move?

A

Chemotaxis (e.g. C5a), receptor-ligand binding, rearrangement of cytoskeleton, production of pseudopod, bacterial peptides

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13
Q

What are the functions of neutrophils?

A

Contact, recognition and internalisation. Cytoskeletal changes. Phagosomes fuse with lysosomes to produce secondary lysosomes

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14
Q

Why does inflammation cause pain?

A

Chemicals that stimulate nerve endings are released, making the nerves much more sensitive.

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15
Q

How do anti-inflammatories work?

A

They block the effects of enzymes which play a key role in making prostaglandins (e.g. Cox-1 and Cox-2 enzymes).Thus production of prostaglandins is inhibited, resulting in reduced swelling and reduced pain.

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16
Q

Describe the oxygen dependent killing mechanisms of neutrophils

A

Produce superoxides and hydrogen peroxide.

H2O2-myeloperoxidase-halide system produces HOCl-

17
Q

Describe the oxygen independent killing mechanisms of neutrophils

A

Lysozyme and hydrolases. Bacterial permeability increasing protein (BPI) - stored in primary azurophillic granula of neutrophils granulocytes. Cationic proteins (defensins) - eosinophil granulocyte

18
Q

What are the chemical mediators of acute inflammation?

A

Proteases
Prostaglandins/leukotrienes
Cytokines/chemokines
Histamines

19
Q

Why is exudate needed?

A

Delivers plasma proteins to areas of injury (e.g. fibrinogen, immunoglobulins and inflammatory mediators), dilutes toxins and increases lymphatic drainage.

20
Q

What causes fever in inflamed areas?

A

Endogenous pyrogens e.g. IL-1 & TNF alpha

21
Q

What is the acute phase response?

A

Decreased appetite, raised pulse rate, altered sleep and changes in plasma concentration of acute phase proteins

22
Q

What are the acute phase proteins?

A

CRP, alpha1-antitrypsin, haptoglobin, fibrinogen and serum amyloid A protein

23
Q

What are the four main sequelae of acute inflammation?

A

Complete resolution (yay!)
Abscess - continued acute inflammation with chronic inflammation
Chronic inflammation and fibrous repair
Death (eek :/)

24
Q

What is the significance of damaged tissue architecture?

A

Cannot completely resolve

25
Q

What is the difference between neutrophil margination and migration?

A

Neutrophil margination is adhesion of the neutrophil to endothelial walls whereas neutrophil migration is the movement of neutrophils to a site of injury by chemotaxis

26
Q

What is lobar pneumonia and how does it occur?

How is the patient likely to present?

A

Presence of too many inflammatory cells. Alveoli fill with fluid instead of air. The causative agent is streptococcus pneumoniae (pneumococcus).
Worsening fever, hypoxaemic, dry cough and breathlessness

27
Q

What is an abscess and what causes it?

Where does it occur?

A

Inflammatory exudate forces tissue apart; there is liquefactive necrosis in the centre.
Usually occurs in solid organs (e.g. liver)
NB: in the liver there is no pain innervation therefore it is detected by looking for fever and bacterial presence in blood

28
Q

What effect does alpha 1 trypsin deficiency have?

A

Alpha 1 trypsin is a protease inhibitor. Due to the deficiency patients will be unable to inhibit elastase in the lungs, which will lead to damage to alveoli (emphysema).

29
Q

How does aspirin work?

A

Inhibits the synthesis of prostaglandins by cyclooxygenase. It also inhibits platelet aggregation; it is an antipyretic (reduces fever) and an analgesic drug (reduces pain)

30
Q

How does the inflammatory response cease?

A

Mediators of acute inflammation have short half lives. May be degraded, bound by inhibitors, unstable or diluted in the exudate. Neutrophils die, break up and are carried away or are phagocytosed.

31
Q

What is the consequence of chronic granulomatos disease?

A

Phagocytes can engulf bacteria but due to the defect in the NADPH enzyme they cannot kill the bacteria.

32
Q

What are the possible causes for appendicitis?

A

Bacteria, physical agents, chemical agents, direct trauma, fecalith, worms, obstruction, lymphoma, adeno carcinoma, carcinoid.

33
Q

List two possible outcomes of untreated acute appendicitis

A

Rupture of appendix leading to infected and faecal matter enter the peritoneum, producing life-threatening peritonitis.
Perforation/gangrene after 24 hours, the peritonitis may be localised, or the inflamed appendix may be surrounded by omentum to form an appendix mass or appendix abscess

34
Q

What are the folds in the brain called?

What are grooves called?

A

Gyri

Sulci

35
Q

Why is increased cranial pressure bad?

A

Increased cranial pressure will be compress the brain, compressing the respiratory centre which results in death.

36
Q

What organisms cause meningitis in neonates and children?

A

Streptococci and e coli, listeria monocytogenes. Haemophilis influenza type b

37
Q

What organisms cause meningitis in young adults?

A

Neisseria meningitides and streptococcus pneumoniae

38
Q

What organisms cause meningitis in older people?

A

Neisseria meningitides and streptococcus pneumoniae

39
Q

What are the long term complications of meningitis?

A

Brain damage, vascular thrombosis, deafness, gangrene (meningococcal), clots and haemorrhage, water house fredrickson syndrome (adrenal glands fail)

40
Q

What is the link between gallstones and hepatic abscesses?

A

Gallstones are a result of a build up of bilirubin or cholesterol. This damages block the bile duct, allowing for a build up of infectious agents (e.g. Ameba) which causes hepatic abscesses

Mechanisms of Disease (8 decks)

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