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ESA 2 > Inflammation > Flashcards

Inflammation Flashcards

0
Q

Function of macrophages

A

Phagocytosis and destruction of debris and bacteria. Long term scavengers

Process and present antigens to the immune system (professional antigen presenting cells)

Synthesise cytokines, complement complexes, clotting factors and proteases

Controls other cells by cytokine release or cell-cell interactions

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1
Q

Ways chronic inflammation can come about

A

Stem from acute inflammation if the damage is severe

De novo (no acute phase) e.g. Autoimmune (rheumatoid arthritis), chronic infection (viral hepatitis) or chronic low level irritants

Alongside acute inflammation with severe persistent or repeated infections e.g. Chronic cholecystitis

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2
Q

Appearance of macrophages

A

Foamy cytoplasm as lots of RER, large nucleus

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3
Q

Function of lymphocytes

A

Complex, many immunological functions.

B cells differentiate to plasma cells which produce antibodies

T cells involved in control and have a cytotoxic function.

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4
Q

Appearance of plasma cells

A

Lots of cytoplasm due to abundant RER
Clock-face chromatin in the nucleus
Perinuclear hof - pale area around the nucleus

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5
Q

Function of plasma cells

A

Produce and secrete antibodies

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6
Q

Appearance of eosinophils

A

Bilobular nucleus with bright pink cytoplasm : ‘sunburnt face with shades’

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7
Q

Eosinophils are seen in

A

Allergies, parasite infestations (esp in the gut), some tumours

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8
Q

Function of fibroblasts/myofibroblasts in chronic inflammation

A

Recruited by macrophages, secrete collagen

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9
Q

How giant cells are made

A

Fusion of macrophages due to frustrated phagocytosis (too much for them to phagocytose)

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10
Q

Appearance of giant cells

A

Multinucleated, horseshoe-shaped aggregation of nuclei around the outside, abundant cytoplasm in the centre.

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11
Q

Types of giant cell

A

Touton seen in fat necrosis and xanthoma. Contains fat.

Langhans seen in TB

Foreign body

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12
Q

Brief overview of possible complications of chronic inflammation

A

Tissue destruction, excessive fibrosis, impaired function, atrophy

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13
Q

Microscopic and macroscopic description of chronic cholecystitis

A

Macro - fibrotic, redness of wall, white mucosa, multiple gallstones

Micro - Thickened muscle, lots of plasma cells, lymphocytes

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14
Q

Describe the cause of chronic cholecystitis

A

Gallstone becomes stuck in the cystic duct, irritating the gall bladder and causing multiple repeated episodes of acute inflammation

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15
Q

Difference in cause between acute and chronic gastritis

A

Acute - alcohol/drugs e.g. NSAIDs

Chronic - Heliobacter pylori

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16
Q

Microscopic and macroscopic appearance of gastric ulceration

A

Punched out area of necrosis with a central ulcer

Polymorphs and fibrin in the centre, lymphoid infiltrate

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17
Q

What is a fistula?

A

Abnormal connection between two epithelial-lined organs (usually when tubular)

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18
Q

Localised and systemic effects of rheumatoid arthritis

A

Localised - joint destruction

Systemic - affects other organs, rarely causes amyloidosis

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19
Q

What is a granuloma?

A

Aggregate of activated macrophages. Modified and immoveable. Other inflammatory cells can be involved.

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20
Q

Causes of granuloma

A

Mild irritants - artificial joints which have broken/ruptured silicone implant

Infections - mycobacterium (TB/leprosy), other (fungi, rare)

Unknown - sarcoidosis, Wegener’s granulomatosis, Crohn’s disease

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21
Q

Cardinal signs of inflammation

A

Rubor, calor, dolor, tumor and loss of function

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22
Q

Describe the changes to blood flow in acute inflammation

A

Transient vasoconstriction of arterioles
Vasodilation of arterioles then capillaries, increasing blood flow which causes heat and redness.
Increased permeability of blood vessels causing exudation of protein-rich fluid and slow circulation as blood is thicker.
Vascular stasis

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23
Q

Describe the meaning of vascular stasis

A

Concentration of erythrocytes increases

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24
Q

Function of histamine

A

Vascular dilatation, transient increase in vascular permeability and pain.

25
Q

Cells which produce histamine

A

Mast cells, basophils, platelets

26
Q

An increase in what two types of pressure causes fluid to move out of capillaries?

A

Hydrostatic pressure

Colloid osmotic pressure

27
Q

Describe the changes in acute inflammation that cause oedema.

A

Arterial dilation increases hydrostatic pressure and permeability causing loss of protein.
Net flow is out, causing oedema.

28
Q

What resolves oedema?

A

The lymphatic system

29
Q

Describe Starling’s law

A

The stroke volume of the heart increases in response to an increase in blood filling the heart when all other factors remain constant, as it increases stretching of the ventricular wall.

30
Q

Describe the difference between transudate and exudate.

A

Transudate - protein rich, caused by heart failure or venous outflow obstruction.

Exudate - protein rich, seen in inflammation.

31
Q

Describe different mechanical causes of leakage from capillaries.

A

Endothelial control, gaps formed - histamine/leukotrienes

Cytoskeletal reorganisation causing gaps to form - cytokines e.g. IL-1/TNF

Direct injury e.g. burns/chemicals

Leukocyte-dependent injuries as polymorphs produce toxic oxygen species and enzymes

Increased transcytosis by channels across the endothelium - VEGF (endothelial growth factor)

32
Q

What protein covers an ulcer to prevent leakage?

A

Fibrin

33
Q

Describe the process of diapedesis of neutrophils

A

Margination of neutrophils due to stasis.
They roll along with intermittent sticking, then adhesion occurs so they stop rolling.
Emigrate through the wall to tissue space - extravasion.
Able to escape as inter-endothelial cell junctions relax, digest basement membrane and move.

34
Q

Describe chemotaxis and give examples of chemicals which allow it.

A

The movement along a concentration of chemoattractants. Receptor-ligand binding causes rearrangement of the cytoskeleton, producing a pseudopod.

e.g. C5a (active complement fragment), LTB4 (a leukotriene) and bacterial peptides (context dependent).

35
Q

What does complement do?

A

Forms a tube which punches holes in bacteria, causing death.

C5a etc are produced as by-products.

36
Q

Describe the function of Fc

A

Fixed complement on antibodies, always the same.

Allows neutrophils to recognise anything with antibodies bound.

37
Q

Describe the role of C3b

A

Bonds to microbial cell surfaces and aids opsonisation by macrophages.

38
Q

How are secondary lysosomes formed?

A

Primary lysosome fuses with a phagosome.

39
Q

Describe the two types of killing mechanism utilised by neutrophils.

A

Oxygen dependent - superoxide, peroxidase and HOCl- (by myeloperoxidase) released into a phagosome.
Oxygen/respiratory burst

Oxygen independent - lysozyme, hydrolases, phospholipases. Bacterial permeability increase protein (BPI), catatonic proteins (defensins)

40
Q

Describe the different types of chemical mediators in acute inflammation.

A

Proteases e.g. kinins/complement system/coagulation/fibrinolytic system. They are plasma proteins from the liver.

Exogenous e.g. endotoxin, a lipopolysaccharide produced by gram negative bacteria

Prostaglandins/Leukotrienes - metabolites of arachodonic acid from phospholipids.]

Cytokines (big)/chemokines (small) produced by white blood cells (especially macrophages) to coordinate the inflammatory response e.g. IL-1/TNF-alpha

41
Q

How does oedema enhance an immune response?

A

Increases lymphatic drainage, delivering to the lymph nodes.

42
Q

Give some complications of acute inflammation

A

Swelling blocks tubes e.g. acute epiglottis
Exudation causes compression e.g. cardiac tamponade: into pericardial cavity.
Or appendicitis - perforates causing peritonitis
Loss of fluid e.g. burns

43
Q

Give the systemic effects of acute inflammation

A

Fever as endogenous pyrogens are produced - TNF alpha and IL increase production of E2 prostaglandin in the hypothalamus.

Leukocytosis as IL-1 and TNF-alpha produces accellerated release from bone marrow. Macrophages and T-lymphocytes produce CSFs.

Bacterial infections increase neutrophils and viral increase lymphocytes

44
Q

Describe the acute phase response in acute inflammation.

A

Low appetite, high heart rate, changes to sleep.
Also changes plasma concentration of:
- C-reactive protein (activates complement system and is clinically useful)
- Alpha-1 antitrypsin (inhibits proteases)
- Haptoglobin (scavenges haemoglobin)
- Fibrinogen
- Serum amyloid A (apolipoprotein associated with HDL, can act as a chemotaxin and induce enzymes that degrade the ECM.

45
Q

Describe the condition of shock

A

Clinical syndrome of circulatory failure, caused by widespread vasodilation and a dramatic drop in blood pressure.

46
Q

What are the potential sequelae of acute inflammation?

A

Complete resolution
Continued acute inflammation with chronic, leading to an abcess.
Chronic inflammation and fibrous repair with tissue regeneration (scarring)
Death

47
Q

Describe resolution of acute inflammation

A

Changes reverse and vascular changes stop.
No marginated neutrophils, permeability normal, vessel calibre normal.
Exudate is allowed to drain, fibrin broken down, neutrophils die and damaged tissues may degenerate.
If the tissue arch is destroyed, resolution is not possible.

48
Q

What are the mechanisms of resolution?

A

All mediators have a short half life
May be inactivated by degradation e.g. heparinase
Inhibitors may bind e.g. anti-proteases
May be unstable e.g. some arachnodonic acid derivatives
Diluted in exudate e.g. fibrin degradation products
Specific inhibitors of acute inflammatory changes e.g. lipoxins/endothelin

49
Q

Describe the production of prostaglandins

A

Phospholipids to arachadonic acid by phospholipase A2

Arachadonic acid to prostaglandins by cyclooxygenase

50
Q

Describe the production of leukotrienes

A

Phospholipids to arachadonic acid by phospholipase A2

Arachadonic acid to leukotrienes by lipoxygenase

51
Q

How do corticosteroids suppress the immune system?

A

Inhibit phospholipase A2 so arachadonic acid derivates cannot be made.

52
Q

How does aspirin and other NSAIDs reduce a fever?

A

Inhibits production of prostaglandin E2

53
Q

What is the most potent complement fragment?

A

C5a

54
Q

Describe pus/abcess exudate

A

Creamy/white, rich in neutrophils. Typical of infection by chemotactic bacteria.

55
Q

Describe haemorrhagic exudate

A

Many RBC, appears bloody. Indicates significant vascular damage.
Destructive infections/due to malignancy

56
Q

Describe serous exudate

A

Plasma proteins with few leukocytes so no infection. Seen in blisters.
No fibrinogen.

57
Q

Describe fibrinous exudate

A

Significant fibrin deposition.

Causes friction in pericardial/pleural space.

59
Q

Describe the difference between a Ghon focus and Ghon’s complex in tuberculosis.

A

Focus - Primary site of infection in the lungs, either in the upper part of the lower lobe or lower part of the upper lobe. Inflammation.

Complex - lesion of the lung caused by tuberculosis. Have a calcified focus of infection and an associated lymph node. The centre of the focus undergoes caseous necrosis.

60
Q

Describe a Ranke complex in tuberculosis.

A

A healed primary pulmonary tuberculosis, composed of a Ghon lesion and ipsilateral calcified hilar node.

61
Q

Describe scrofula associated with tuberculosis

A

Lymphadenitis of the cervical lymph nodes

62
Q

Give some associated complications of ulcerative colitis. (not involving the gut)

A 
Ankylosing spondylitis
Erythema nodosum
Pyoderma gangrenosum
Iritis
Scleritis
Hepatitis
Cirrhosis
Sclerosing cholangitis

ESA 2 (46 decks)

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