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Misc Pharm > Misc > Flashcards

Misc Flashcards

1
Q

What is the PK of Paracetamol?

A

well absorbed by GIT
Bioavailability: 70-90%
Peak Plasma levels 30-60 mins
highly protein bound

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2
Q

How is Paracetamol Metabolised?

A

Hepatic > 95% undergoes glucoronidation + Sulfation
5% metabolism via CYP450 metabolism (phase 1 hydroxylation) to form NAPQI
NAPQI is toxic but usually detoxified by glutathione (glutathione depleted)

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3
Q

what is the toxic dose of paracetamol for adults?

A

150-200mg/kg

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4
Q

What is the mechanism of action for paracetamol?

A

Selective Cox 2 inhibitor

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5
Q

Describe the mechanism of paracetamol toxicity?

A

Zero order toxicities
undergo conjugation with glucoronide and sulfate –> Saturated
increased paracetamol is metabolised by CYP2E1 to NAPQI
(normally NAPQI detoxified by glutathione but depleted = lots of toxic metabolite)

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6
Q

How does NAC work in treatment of Paracetamol Overdose?

A

NAC is a sulphydryl group donor - restores hepatic glutathione or acts as an alternative substitute for conjugation with toxic metabolite

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7
Q

What are the PK characteristics of ibuprofen?

A

Well absorbed, highly protein bound, highly metabolised by Liver (CYP450)

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8
Q

What are the Pd characteristics of ibuprofen?

A 
Inhibition of prostaglandin synthesis
NSAIDs are reversible cox inhibitor
1. anti-inflammatory
2. Analgesic
3. Antipyretic
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9
Q

What are common side effects of ibuprofen?

A

GI: ulcers, GI bleeding, Abdo pain
Skin: Rashes
Renal: Renal Failure
CVS: Oedema, HTN, CCF

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10
Q

What is the difference between aspirin and NSAIDs?

A

Aspirin irreversibly inhibits COX, Newer NSAIDs (ibuprofen, diclofenac) reversibly inhibits

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11
Q

COX1 vs COX2

A

COX 1 - expressed on most cells

COX2 - inducible, expression depends on various ?

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12
Q

What is the mechanism of action for salbutamol?

A

Selective Beta 2 Agonist - stimulates cAMP that 1) Bronchodilates 2) inhibit release of bronchoconstricting (something)

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13
Q

What are the side effects of salbutamol?

A

Muscle tremor - beta 2 receptor skeletal muscle
Hypokalaemia
Tachycardia/SVT - atrial beta 2 receptor stimulation
V/Q Mismatch - pulmonary venodilation -> shunting blood to poorly ventilated areas (decrease arterial O2 tension)

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14
Q

What are the Pk characteristics of salbutamol?

A

Metabolism: 50%, 1st pass
Half life - 3-6 hrs
Excretion: (something) in liver and metabolically excreted in kidney

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15
Q

What is the mechanism of action for clopidogrel?

A

Irreversible blockade of ADP receptor on platelet to inhibit platelet aggregation

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16
Q

What are the Pk characteristics of Clopidogrel?

A

Absorption: prodrug, metabolised to pharmacoligcally active metabolite AND inactive metabolites. Activated in liver by CYP 450
Excretion: half life 0.5-1 hr, effect life 7-10 days, urine 50%, Faeces 46%
Dose: Loading 300, daily 75

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17
Q

Adverse effects of clopidogrel?

A

Bleeding, rash, diarrhoea, abdo pain, gastric ulcer

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18
Q

What are the Pk characteristics of metformin?

A

Absorption: well absorbed, not protein bound
not metabolised
half life 1.5-3 hrs
Excretion: kidney

19
Q

What is the mechanism of action for metformin?

A

biguanide, unclear. not dependent on functioning pancreatic b cells - doesn’t influence insulin release form pancreas

20
Q

What are the side effects of metformin?

A

GI - diarrhoea

Lactic Acidosis

21
Q

What is the mechanism of action of sulfonylureas?

A

Sulphonylurea - increase release of insulin from pancreatic beta cells
binds to G receptor - inhibit K efflux throught ATP sensitive K Channels - deplorisation
deplorisation -> opens voltage Ca Channel -> Ca Influx -> insulin release
Long term use -> decrease serum glucagon

22
Q

What are the pharmacokinetics of Glicazide?

A

Absorbed orally, hepatically metabolised
Half life - 8 hrs
Excreted 80% renally

23
Q

What are the side effects of glicazide?

A

Hypoglycaemia
GI Side effects
Rash
Pruritus

24
Q

What are the pharmacokinetics of Oxycodone?

A 
Good Oral Absorption (something) 1st pass metabolism
High Volume of distribution
Hepatic metabolism by CYP450
Duration of action - 3-4 hrs
Excreted Renally
25
Q

How does Oxycodone produces its analgesic Function?

A

opioid antagonist acts mainly on mu receptor in brain and spinal cord

26
Q

What analgesia can be used when prescribing oxycodone to decrease dependence?

A
  1. use controlled release preparation
  2. smaller doses at longer intervals
  3. combine with non-opioid preparation
  4. establish goals of tx
  5. frequent evaluation of ongoing requirement
27
Q

What is the mechanism of action for insulin?

A

Promotes glucose uptake from blood into tissues - fat, liver, muscle
promote glycogen synthesis

28
Q

What are the types of insulin formulation?

A
  1. Short acting - lispro, actrapid, novorapid
  2. Intermediate - aspart
  3. Long acting - glargine, determir
29
Q

How are differing preparations used to optimise glycaemic control?

A

aim to replace basal insulin requirement and meal requirement

30
Q

What are the other uses of insulin in ED?

A

Hyperkalaemia, CCB, Betablockade

31
Q

How does dexamethasone’s anti-inflammatory function compare to hydrocortisone?

A

30x more potent, longer acting,

32
Q

Explain the anti-inflammatory function and immunosuppression of glucocorticoid

A
  1. Effect of (s.th), distribution, function of peripheral leucocyte
  2. suppression of inflammatory mediator cytokines, chemokines
  3. inhibition function of macrophage and APC
  4. suppress mast cell degranulation
33
Q

What are the side effects of corticosteroids?

A

Short term: hyperglycaemia, peptic ulcer,

Long Term: immunosuppression, adrenal suppression, DM, Osteoporosis, Cushing Syndrome, poor wound healing

34
Q

What are the pharmocodynamics of Ethanol?

A

CNS: sedation, disinhibition, slurring of speech, impaired judgement, ataxia, coma, respiratory depression,
CVS: decrease contractility
Smooth muscle: vasodilation

35
Q

What are the pharmacokinetics of Ethanol?

A

Rapid absorption from GIT, peak level at 30mins
Metabolised - Zero order kinetics via liver (alcohol dehydrogenase)
Excreted in lungs and urine

36
Q

What is the mechanism of action for octreotide?

A
  1. Somatostatin analog, decrease splanchnic and portal blood flow
  2. Inhibit endocrine + paracrine secretion (Insulin, glucagon, TSH, GH)
37
Q

What are the side effects of octreotide?

A

Anaphylaxis, local irritation during injection,
GIT - N+V, decreased intestinal motility, abdo cramp
hypo/hyperglycaemia

38
Q

What are the pharmacokinetics of Octreotide?

A

Absorption via IV
Metabolised 30-40% by liver
Half life 80 mins
excreted 20% unchanged by kidneys

39
Q

What are the clinical uses of octreotide?

A

Control of bleeding from varices
sulphonylurea overdose
decrease symptoms from hormone secretory tumour
(acromegaly, carcinoid)

40
Q

What is the mechanism of action for streptokinase?

A

enzyme that directly converts plasminogen to plasmin

plasmin - major fibrinolytic enzyme

41
Q

What is the mechanism of Pantoprazole?

A

Irreversibly inactivated H/K/ATPase

blocking PPI >90% acid secretion for up to 24 hours

42
Q

Why an IV infusion is preferred over a single bolus dose?

A

only inactivated actively secreted acid pumps (<10%)

single dose only decrease acid secretion for few hours

43
Q

What strategies can increase bioavailability of pantoprazole?

A
  1. Take as inactive pro drugs, begins as acid resistant enteric coated to prevent gastric elimination\
  2. Take on empty stomach (weak bases - pass into acidified parietal cells where it binds to H/K/ATPase
  3. Take 1 hour prior to meal - peak dose occur when pump most active

Misc Pharm (2 decks)

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