HYMS Y1 > Block 4 W3 > Flashcards

Block 4 W3 Flashcards

(45 cards)

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1
Q

Give examples of immune driven inflammation.

A 
Allergies
Graft vs. Host disease
Autoimmune disease
Contact dermatitis 
Celiac disease
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2
Q

What is arachidonate acid formed from?

A

Cellular phospholipid bilayer by phospholipase A2.

Metabolised by cyclooxygenase into prostaglandins and prostacyclin, thromboxane.

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3
Q

What is the role of prostacyclin, PGI2?

A

Vasodilator, hyperalgesic, stops platelet aggregation.

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4
Q

What is the role of thromboxane, TXA2?

A

Thrombotic, vasoconstrictor.

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5
Q

What is the role of prostaglandin, PGF2a?

A

Bronchoconstrictor, myometrial contraction.

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6
Q

What is the role of prostaglandin, PGD2?

A

Inhibits platelet aggregation and vasodilator.

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7
Q

What is the role of prostaglandin, PGE2?

A

Vasodilator and hyperalgesic.

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8
Q

Define NSAIDs and give examples.

A

Non-steroidal anti-inflammatory drugs
e.g. aspirin, ibuprofen, diclofenac
Prescribed for pain and chronic inflammation - minor aches and pains.

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9
Q

What are the 3 major effects of NSAIDs?

A
  1. Anti-inflammatory - blocks COX from making prostaglandins which regulate inflammation due to vasodilation and increased vessel permeability.
  2. Analgesic - prostaglandins sensitises spinal neurones to pain.
  3. Antipyretic - prostaglandin synthesis inhibited in hypothalamus so reduces firing rate that control thermoregulation.
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10
Q

Describe the mech of action of aspirin.

A

Irreversibly inactivates both isoforms of COX (1 and 2) by acetylating the catalytic serine residue in position 529.
Affects COX2 expression at both transcriptional and post-t level.

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11
Q

What does low dose aspirin do?

A

Preferentially affects thromboxane pathway -> reduced platelet aggregation.

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12
Q

What does high dose aspirin do?

A

Affects both pathways -> risk of bleeding as inhibits prostacyclin, required for inhibition of platelet aggregation.

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13
Q

How does ibuprofen interact with aspirin?

A

Block the anti-platelet effects.

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14
Q

What are the side effects of aspirin?

A

Deaf, swelling of eyes, face, lips, tongue, wheezing, cold clammy hands, hives, nausea, tachycardia, bloody stools, and vomit.

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15
Q

What do 2nd generation NSAIDs target?

A

Selective COX2 inhibitors
e.g. Coxibs
Minimised gastric problems but targeted prostacyclin which increased risk CVD.

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16
Q

Define NO-NSAIDs?

A

Nitric oxide - donating NSAID

have gastro-protective effect and increased anti-inflammatory activity.

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17
Q

What are the adverse events of NSAIDs caused by?

A

Inhibition of COX1 - useful as a housekeeping role.

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18
Q

What are the adverse side effects of NSAIDs?

A
  1. Abdominal discomfort, dyspepsia - reduced PG synthesis in GI -> increased gastric acid secretion, diminished mucus secretion so acid irritates GI lining.
  2. Stomach/duodenal ulceration - PG normally causes mucus release so NSAIDs blocks this.
  3. MI - COX1 expressed in endothelium -> pre-disposes to blood clots and high BP.
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19
Q

Define SAIDs.

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A

Steroidal anti-inflammatory drugs -> glucocorticoids
e.g. hydrocortisone, prednisone, dexamethasone
Synthesised from cholesterol.
Used in inflammatory diseases.
Reduces phospholipase A, COX2 thus reducing prostaglandins.

20
Q

What are the side effects of SAIDs?

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A

Occurs with prolonged systemic use.

  • suppresses IR
  • suppresses endogenous glucocorticoid synthesis
  • iatrogenic Cushing’s syndrome
  • osteoporosis.
21
Q

How does histamine produce the Lewis Triple response?

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A
  1. reddening - vasodilation
  2. wheal - increased permeability
  3. flare - antidromic stimulation of local nerves
22
Q

What is the effect of histamine systemically?

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A
  • stimulation of gastric secretion
  • contraction of smooth muscle
  • cardiac stimulation
  • vasodilation
  • increased vascular permeability
23
Q

Give examples of sedating anti-histamines.

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A

Chlorphenamine and promethazine

24
Q

Give examples of non-sedating anti-histamines.

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A

Cetrizine and fexofenadine.

25
Give examples of immunosuppressive drugs.
Cyclosporine Tacrolimus - prevents transcription of IL-2 Rapamycin - inhibits mTOR and so cell cycle progression.
26
Describe the mech of action of basiliximab.
Monoclonal antibody. | Acts via cytokine or binds receptors directly to limit proliferation of IL-2.
27
Define atopy.
Predisposition for IgE mediated IR.
28
In type I hypersensitivity, describe the immediate reaction caused by the release of mast cells.
Histamine usual effects and chemoattractant for neutrophils and eosinophils. Leukotrienes - bronchial spasms/constrictions, mucus secretion. Prostaglandins effects Th2 cytokines - activates Th2 cells and eosinophils activation.
29
In type I hypersensitivity, describe the late reaction caused by the release of mast cells.
Migration of eosinophils - release peroxidase causing further tissue damage.
30
Describe allergic rhinitis and treatments.
Type I Hay fever due to grass or pollen. Signs - red itchy watery eyes, runny nose. Treatment - reduce exposure, anti-histamines, intranasal corticosteroids.
31
Describe asthma and treatments.
Type I Contraction of bronchial smooth muscle -> SOB. Treatment - reliever inhaler-salbutamol (B2 agonist), preventative inhaler-corticosteroids.
32
Describe allergic eczema and treatments.
Type I Skin breached by allergens, scratching + microbial toxins influx due to unresolved skin -> release of cytokines and chemokine. Chronic disease - Th1 cells and eosinophils. Treatment - reduce itching, emollients, topical corticosteroids.
33
Describe urticaria and treatments.
Type I Release of histamine within skin - leads to angio-oedema. Treatment - anti-histamines, corticosteroids.
34
Describe anaphylaxis and treatments.
Type I Systemic response to allergen -> rapid synthesis of prostaglandins and leukotriene: - systemic vasodilation, increased vascular permeability - fall in BP - severe bronchial constriction, oedema and shock. Treatment - norepinephrine pen -> vasoconstrictor.
35
Describe rhesus disease and treatments.
Type II HDN Treatment - routine antenatal anti-D prophylaxis (RAADP) prevents sensitisation. Anti-D antibodies neutralises any D+ RBC mother is exposed to.
36
Describe antibiotic allergies and treatment.
Type II Drug binds RBC - Abs produced -> destruction of RBCs, drug acts as immunological hapten. Treatment - removal of drug, steroids.
37
Describe Good-pasture syndrome and treatment.
Type II IgG Ab recognise collagen within kidney basement membrane so binding -> complement activation. Treatment - oral immunosuppressants and plasmapheresis.
38
Describe myasthenia gravis and treatment.
Type II Abs block acetylcholine receptors at NMJ - muscle weakness of eyes and face. Treatment - pyridostigmine, immunosuppressants biologics, thymectomy.
39
Describe Graves disease and treatment.
Type II Abs bind thyroid hormone receptor causing activation -> increased thyroid hormone production. Treatment - thionamides, radioactive iodine therapy, surgery.
40
Describe the mechanism of type III hypersensitivity.
Complexes are deposited in organs (kidney, vessels, synovial joints) - constant activation of complement -> tissue damage. Vasculitis, glomerular nephritis, arthritis.
41
Describe systemic lupus erythematous and treatment.
Type III Autoantigens is DNA - anti-DNA antibodies result in systemic damage to tissues i.e. kidney, skin, heart and joints. Treatment - alkylating agent (cyclophosphamide suppressing DNA synthesis), immunosuppressants, rituximab and belimumab.
42
Describe rheumatoid arthritis.
Type IV Cell-mediated joint tissue destruction due to inflammation and cartilage damage. Treatment - NSAIDs, corticosteroids.
43
Describe the mechanism of type IV hypersensitivity.
Sensitisation - haptens cross epidermis -> creates neo-antigens -> presented to APCs = development of memory response. Secondary exposure - memory Th1 cells activates inflammation, macrophages and tissue destruction.
44
Describe contact dermatitis and treatment.
Type IV Nickel, poison ivy 1st contact sensitises, 2nd contact elicits dermatitis. Treatment - trigger avoidance.
45
Describe multiple sclerosis and treatment.
Type IV T cells destroy myelin sheath -> paralysis. Treatment - immunosuppressants, biologic therapy i.e. anti-cytokine and monoclonal Abs.
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