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** Pharmacology - CF > steroids and non steroidal antiinflammatory drugs > Flashcards

steroids and non steroidal antiinflammatory drugs Flashcards

1
Q

What are Eicosanoids?

A

A precursor generated from phospholipids in the CNS

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2
Q

What are the 3 key groups of Eicosanoids?

A
  • prostaglandins (PGs)
  • thromboxanes (TXA)
  • Leukotrienes
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3
Q

Which enzyme produces Eicosanoids from the phospholipids in the plasma membrane?

A

Phospholipase A2

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4
Q

What activates phospholipase A2 to produce Eicosanoids (5)?

A
  • bradykinin
  • antigen-antibody binding on mast cells
  • thrombin
  • complement C5a
  • cell damage
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5
Q

What is the precursor of Eicosanoids?

A

Arachidonic acid

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6
Q

What other chemical mediator is produced from plasma membrane?

A

Platelet activating factor

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7
Q

Which two Eicosanoids can also be called prostanoids?

A

Prostaglandins

Thromboxanes

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8
Q

What is the nomenclature of prostaglandins?

A

PG = prostaglandin

Letter = basic structure it comes from

Number = the no of C=C

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9
Q

Most often (arachidonic acid is the precursor)

  • how many C=C does PG have?
A

2

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10
Q

Which cells release prostaglandins?

A

ANY injured cell

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11
Q

Which process is Prostaglandin a key mediator in?

A

Inflammation

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12
Q

What are the effects of prostaglandin in blood vessels?

A

Vasodilation (PGE1&2, PGI1)

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13
Q

What are the effects of prostaglandin in healing?

A

Inhibit platelet aggregation (PGI2 & PGE)

n.b. TXA2 = increased platelet aggregation

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14
Q

What are the effects of prostaglandin in the respiratory system?

A

N.b. varies with prostaglandin

Bronchodilation = PGI2 & PGE2

Bronchoconstriction = PGF2 & TXA2

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15
Q

How do prostaglandins affect pain?

A

Sensitise nociceptive neurones to the action of mediators (bradykinin & serotonin) = activate pain fibres

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16
Q

How do prostaglandins affect fever?

A

Act on the hypothalamus = increase body temperatureInflammation = macrophages release IL-1 = AA-> PGE2 = acts on neurones in pre optic area (sets our internal core temp) = increase thermostatic set point = heat generation (shivering, skin vasoconstriction = destroy infection)

When PG production stops (immediately broken down) = decrease set point = heat dissipating (sweating and vasodilation)

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17
Q

Which enzyme converts arachidonic acid (AA) to PG H2 = prostanoid precursor?

A

Cyclo-oxygenases (COX)

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18
Q

How many active sites does COX have?

A

2

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19
Q

What are the actions of the two COX active sites?

A
  • Cycloxegynase site = AA -> PGG2
  • Heme with peroxidase activity = reduces PGG2 to PGH2
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20
Q

How many COX isoenzymes exist?

A

3

COX-1

COX-2

COX-3 (not really understood = splice variant of COX-1)

n.b. different tissues express varying levels of COX-1 & 2= SELECTIVE INHIBITION POSSIBLE

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21
Q

Where is COX-1 found?

A

Consitutive (always there) in most cells

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22
Q

What does COX-1 do?

A

Maintains tissue homeostasis

Housekeeping: gastric protection, blood clotting, renal blood regulation

n.b. inflammation is NOT the main role

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23
Q

What is the key difference between COX-1 & COX-2?

A

COX-1 binding pocket is NARROW

COX-2 binding picket is WIDE

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24
Q

What induces COX-2?

A

Inflammation (abundant in activated macrophages)

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25
Q

When is COX-2 unregulated?

A

In various carcinomas

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26
Q

What does COX-2 produce?

A

Prostanoids = mediate inflammation

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27
Q

What are the two main types of anti-inflammatory agents?

A
  • non steroidal anti-inflammatory drugs (NSAIDs)
  • Glucocorticoids
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28
Q

Which 3 other drugs act as anti- inflammatory agents?

A
  • H1 receptor antagonists
  • chondroprotective drugs
  • immunosupressants
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29
Q

What does NSAIDs stand for?

A

Non steroidal anti-inflammatory drugs

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30
Q

How do NSAIDS target inflammation?

A

inhibit cyclo-oxygenase (COX) = reduced prostaglandin & thromboxane synthesis

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31
Q

When are NSAIDs most commonly used in treatment?

A
  • non-infectious/non-allergenic inflammation (e.g. headache, sprained ankle)
  • control inflammation and pain (e.g. trauma, post-surgery & osteoarthritis)
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32
Q

Which action of cyclo-oxygenase do most NSAIDs inhibit?

A

Endoperoxidase synthase (no PGG2 produced)

n.b. PGG2 & PGH2 = unstable = produced on demand & broken down very quickly

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33
Q

What are the 3 different effects that NSAIDs have?

A
  • Anti-inflammatory (reduce vasodilation, oedema, pain & fever)
  • Analgesic (reduce PG synthesis -> pain from inflammation & tissue damage)
  • Anti-pyretic = anti-fever
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34
Q

NSAIDSs differ in their selectivity for COX isoenzymes…Which NSAID (1) is COX-1 preferring?

A

Salicylates (aspirin)

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35
Q

NSAIDSs differ in their selectivity for COX isoenzymes…Which NSAID (1) has an equal effect on both isoenzymes?

A

Ibuprofen

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36
Q

NSAIDSs differ in their selectivity for COX isoenzymes…Which NSAID (1) is COX-2 preferring?

A

Celecoxib (withdrawn)

Rofecoxib(withdrawn)

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37
Q

What are the 2 additional effects of salicylates (aspirin)?

A
  • reduce platelet aggregation (prophylaxis of strokes & thromboembolism)
  • analgesic- antipyretic (partial)
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38
Q

What are the pharmacokinetics of salicylates (aspirin)?

A

Weak acid = absorbed in stomach

Hydrolysed to salicylic acid in plasma & at low therapeutic doses most is bound to serum albumin

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39
Q

What % of salicylates (aspirin) is excreted unchanged?

A

25%

40
Q

What % of salicylates (aspirin) is oxidised?

A

25%

41
Q

The effects of aspirin are DOSE DEPENDANT!! What are the effects of aspirin at the following doses?

0.5-1 mg/kg

5-10 mg/kg

>30 mg/kg

A

0.5-1 mg/kg = anti-platelet

5-10 mg/kg = analgesic/antipyretic

>30 mg/kg = anti-inflammatory

42
Q

What is the main side effects of salicylates?

A
  • Gastric bleeding(loss of mucosal protection by PGs & inhibition of platelet aggregation)
43
Q

What is salicylism?

A

Overdose

44
Q

What can cause salicylism?

A
  • viral infection (liver/CNS disturbances)
  • repeated ingestion of high doses = chronic toxicity (20-40% fatal)
  • altered acid/base balance (uncouples oxidative phosphorylation
45
Q

What are the effects of overdose?

A

Respiratory & metabolic acidosis (tinnitus, dizziness, hearing loss & nausea;

skin rashes;

reye’s syndrome = serious liver & brain damage)

46
Q

What is the name drug that Aspirin interacts with?

A

Displaces warfarin from plasma proteins = increases the effects of warfarin

47
Q

What are the 3 effects of paracetamol?

A

Weak antipyretic

Mild analgesic

Weak/no anti-inflammatory activity

48
Q

What is the mechanism of action of paracetamol?

A

Uncertain

  • often appears to be COX-2 selective
  • now thought to inhibit COX-1 & 2 by peroxidase function = inhibits PG synthesis of PGs when low levels of arachidonic acid & peroxides are available but little activity at substantial levels of these!

= doesn’t suppress inflammation of rheumatoid arthritis & gout but does inhibit the lesser inflammation from tooth extraction

49
Q

What is the toxic dose of paracetamol?

A

2-3 X normal dose

50
Q

What happens when the toxic dose of paracetamol is taken?

A

= potentially liver toxicity due to saturation of normal liver enzymes

51
Q

How is paracetamol normally metabolised in the liver?

A

Glucuronidation

Sulfation

52
Q

When the toxic dose of paracetamol is take how is it metabolised in the liver?

A

Glucuronidation & sulfination is saturated= mixed function oxidases instead (CYP450) = producs NAPQ (toxic metabolite) -> if not inactivated by conjugation with glutathionine it reacts with cell proteins = cell death

53
Q

Where are ibuprofens derived from?

A

propanoic acids

54
Q

Which COX enzyme does ibuprofen inhibit?

A

All of them! = non selective (COX1 & COX2)

55
Q

What are the 5 effects of ibuprofen?

A

Anti-inflammatory

Anti-pyretic

Analgesic

Mild anti platelet effect

Vasodilation

56
Q

What property of ibuprofen means it can be administered as a topical gel?

A

It is stable in solution (used for sports injuries - absorbed through skin = less risk of digestive problems)

57
Q

What are the common side effects of Ibuprofen (11)?

A

Nausea

Dyspepsia (indigestion)

GI ulceration/bleeding

Raised liver enzymes

Diarrhoea/constipation

Epistaxis (nose bleeds)

Headache

Dizziness

Rash

Salt & fluid retention

Hypertension

58
Q

What are the infrequent adverse effects of ibuprofen?

A

Oesophageal ulceration/bleeding

Heart failure

Hyperkalaemia

Renal impairment

Confusion

Bronchospasm

59
Q

Which condition can be exacerbated by ibuprofen?

A

Asthma -> sometimes fatally!

60
Q

How does COX-1 inhibition cause gastric ulceration?

A

inhibition of PGE2 & PGI2 synthesis

61
Q

Which drugs can cause direct damage to the gastric mucosa?

A

aspirin can precipitate in cells lining the stomach

62
Q

Which two drugs irreversibly inhibit platelet COX-1?

A

Aspirin

Phenylbutazone

63
Q

What other things (4) can increase GI damage?

A
  • concurrent glucocorticoid administration
  • dehydration
  • hypovolemic shock
  • disruption to gastric blood flow
64
Q

Why are selective COX-2 inhibitors beneficial in theory?

A

Target inflammation and reduces the risk of peptic ulceration

65
Q

Why are selective COX-2 inhibitors not used?

A

In clinical trials they caused a significant increase in heart attacks and strokes

66
Q

Which (4) cells produce leukotrienes?

A

Leukocytes

Lung cells

Mast cells

Platelets

67
Q

What are the two different leukotriene receptor classes?

A

BLT (LTB) -> LTB4

= important mediator in all inflammation (activate & targeting of leukocytes & cytokine production)

CysLT (LTC3, LTD4, LTE4)

= mediate bronchoconstriction, vasodilation in most vessels (coronary vasoconstriction), plasma extravasation, role in hayfever & astha treatment

68
Q

Name two CysLT receptor antagonists:

A

Zafirlukast

Montelukast

69
Q

Where are corticosteroids secreted from?

A

Adrenal gland

70
Q

Which area of the adrenal gland secretes mineralocorticoids (e.g. aldosterone)?

A

Outer layer of cortex = zona glomerulosa

71
Q

What action do mineralocorticoids have?

A

regulate water and electrolyte balance

72
Q

Which area of the adrenal gland secretes glucocorticoids (e.g. hydrocortisone & corticosterone)?

A

Middle layer of cortex = zone fascilculata

73
Q

What action do glucocorticoids have?

A

Affect carbohydrate and protein metabolism

74
Q

Which is the most important human glucocorticoid?

A

Cortisol (hydrocortisone)

75
Q

In which fashion are glucocorticoids released?

A

Pulsitile circadian rythmn (highest in morning = declines in evening/night)

76
Q

What are glucocorticoids produced from?

A

Cholestrol

77
Q

Which hormone regulates the initial step of glucocorticoid production?

A

Adrenocorticotrophic hormone

78
Q

What happens in a loss of corticosteroids (4)?

A

muscle weakness

hypotension

hypoglycaemia

weight loss

79
Q

Which disease causes destruction of the adrenal gland?

A

Addison’s disease (autoimmune or due to chronic inflammation)

80
Q

How do glucocorticoids have an anti-inflammatory action?

A

They are part of the immune systems feedback system:

= stimulate Annexin1 (lipocortin) production = blocks phospholipase A2 = blocks parts of inflammatory responseBind to glucocorticoid receptor= up regulates expression of nuclear anti-inflammatory proteins= represses expression of systolic pro-inflammatory proteins (less complement in plasma, less induce NO production, less histamine release from basophils & reduced IgG production)

81
Q

What are the clinical uses of glucocorticoids (8)?

A
  • Asthma
  • Eczema, Rhinitis & allergic conjunctivitis
  • hypersensitivity states (severe allergic reactions)
  • miscellaneous diseases with autoimmune & inflammatory components (e.g. IBD & rheumatoid arthritis)
  • replacement therapy for glucocorticoid deficiency- stop graft rejection
  • cancer treatment
  • acute spinal injury
82
Q

Through which routes can glucocorticoids be administered (4)?

A

Oral

Topical

IV

IM

83
Q

What are the pharmacokinetics of glucocorticoids (3)?

A
  • bound to corticosteroid binding globulin in blood
  • diffuses into cells
  • metabolised by liver
84
Q

What are the unwanted side effects of glucocorticoid use?

A
  • Suppress response to infection
  • suppress endogenous glucocorticoid synthesis
  • metabolic actions
  • osteoporosis
  • cushings syndrome (m. wasting)
85
Q

Which glucocorticoid drug is used to treat asmtha?

A

Flutricansone proprionate

86
Q

Which glucocorticoid drug is used to treat eczema?

A

Hydrocoritsone

Prednisolone

Dexamethasone

87
Q

Which glucocorticoid drug is used to treat rhinitis & allergy?

A

Beclometasone dipropionate

88
Q

Which glucocorticoid drug is used to treat Rheumatoid arthritis?

A

Prednisone

89
Q

Which glucocorticoid drug is used to treat IBS & crohns disease?

A

Budesonide Dexamethasone

90
Q

What is Flutricansone proprionate used to treat?

A

asmtha

91
Q

What is Hydrocoritsone, Prednisolone and Dexamethasone used to treat?

A

eczema

92
Q

What is Beclometasone dipropionate used to treat?

A

rhinitis & allergy

93
Q

What is Prednisone used to treat?

A

Rheumatoid arthritis

94
Q

What is Budesonide and Dexamethasone used to treat?

A

IBS & crohns disease

95
Q

When should use of anti-inflammatory drugs be avoided?

A
  • patients with congestive heart failure or renal insufficiency
  • patients taking ACE inhibitors, methotrexate, blood thinners (warfarin) & some oral hypoglycaemic agents= increased risk of bleeding = possible complications during dental surgery

** Pharmacology - CF (4 decks)

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