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ESA 4 Rev > CPT revision > Flashcards

CPT revision Flashcards

1
Q

What is the pathophysiology of rheumatoid arthritis?

A

Hypertrophy of joint synovial to form pannus.
Infiltration of inflammatory cells, release of pro-inflammatory cytokines.
Pannus erodes cartilage and bone

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2
Q

What criteria aids RA diagnosis?

A 
Morning stiffness > 1 hour
> 3 joints affected
Hand joints affected
Symmetrical
Rheumatoid nodules
Serum rheumatoid factor
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3
Q

What are the side effects of corticosteroids?

A 
Hypertension
Osteoporosis
Weight gain
Bruising
Hyperglycaemia 
Infections
Skin thinning
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4
Q

What is the MOA of corticosteroids?

A

Inhibit T cell activation

Prevent IL-1 and IL-6 synthesis by macrophages.

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5
Q

What SE are common to all immunosuppressants?

A

Hepatitis
Infection risk
Malignancy
BM suppression

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6
Q

Name 4 highly protein bound drugs.

A

NSAIDS
Methotrexate
Warfarin
Sulphonylureas

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7
Q

What tests are necessary to monitor if giving calcinuerin inhibitors?

A

eGFR - renal toxicity

BP - accelerates hypertension

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8
Q

What tests must be done before methotrexate treatment?

A

CXR - pnueumonitis
FBC
LFT

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9
Q

What are the side effects of methotrexate, how can they be reduced?

A 
Mucositis 
BM suppression
Liver cirrhosis, hepatitis
Lungs - pneumonitis 
Teratogenic

Folic acid reduces mucositis + BM suppression.

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10
Q

Which DMARD has poor intestinal absorption and can therefore be used to treat IBD?

A

Sulphasalazine

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11
Q

What is the MOA of sulphasalazine?

A

Inhibit T cell proliferation and IL-2 synthesis

Decrease neutrophil chemotaxis and degranulation.

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12
Q

Which DMARD causes haemorrhagic cystitis, how can this be minimised?

A

Cyclophosphamide - acrolein metabolite is toxic to bladder epithelium.
Mesna and hydration - mesna binds bladder ep and prevents interaction

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13
Q

What is the MOA of anti-TNF alpha?

A

Inhibit cytokine cascade and leukocyte recruitment

Decrease angiogenesis

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14
Q

Give 4 conditions methotrexate is used to treat.

A

Cancer
RA
Psoriasis
Crohn’s

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15
Q

How can oseltamivir resistance arise?

A

Neuroaminidase enzyme mutation

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16
Q

Which viral enzyme activates aciclovir?

A

thymidine kinase

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17
Q

What is the MOA of nucleoside RT inhibitors and non-nucleoside RT inhibitors?

A

NRTI - analogues of nucleosides, bind and halt reverse transcriptase.
NNRTI - non-competitive inhibition of HIV reverse transcriptase. Bind to allosteric sight and cause conformational change, inhibiting RT.

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18
Q

What is the MOA of protease inhibitors?

A

Inhibits protease enzyme responsible for cleavage of the viral polyprotein into a number of essential enzymes and proteins.

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19
Q

What is the MOA of integrase inhibitors?

A

Inhibits insertion of viral DNA into host genome

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20
Q

What is the advantage of virus resistance testing?

A

Increases outcome
Reduces costs
No ADRs of ineffective therapy
Decreases resistant virus pool

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21
Q

How is virus resistance testing done?

A

Phenotypic characterisation

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22
Q

What advice should you give to patients when prescribing warfarin?

A

Risk of bruising and bleeding
Teratogenic
Avoid NSAIDs and aspirin - bleeding risk
Food - too many leafy greens reduce effectiveness

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23
Q

What should you check before administering heparin?

A

Renal function - renal clearance

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24
Q

What are ADRs of heparin?

A

Bleeding
Osteoporosis
Thrombocytopenia

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25
Q

What is used to reverse heparin if actively bleeding?

A

Protamine sulphate - dissociates heparin from antithrombin III. Irreversibly binds.

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26
Q

Name 3 anti-platelet drugs and their MOA.

A

Aspirin - COX - 1 inhibitor, inhibits thromboxane A2 synthesis
Clopidogrel - ADP antagonist
Dipyridamole - phosphodiesterase inhibitor

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27
Q

What are the benefits of anti platelet drugs?

A

Decreased risk of intracranial haemorrhage

No monitoring

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28
Q

What are the disadvantages of anti-platelet drugs?

A

Increased risk GI bleed

May not have reversal agent

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29
Q

Which study designs are best for establishing a temporal sequence?

A

RCT
Prospective cohort
Poor -case-control, cross-sectional

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30
Q

What is a side effect of H2 antagonists in males?

A

Gynaecomastia

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31
Q

What are side effects of proton pump inhibitors?

A

Diarrhoea
Infection risk
C.difficile risk
Osteoporosis - increase pH, decrease Ca absorption

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32
Q

What are some causes of GORD?

A

Obesity - raised intrabdo pressure
LOS weakness
Delayed gastric emptying
Hiatus hernia

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33
Q

What is the treatment for peptic ulcer?

A

Stop NSAIDs if can
H2RA or PPI for 6 weeks
H-pylori eradication if relevant

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34
Q

What are SE of B2 agonists?

A

Tremor

Tachycardia, palpitations

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35
Q

What is the MOA of montelukast?

A

Leukotriene receptor antagonist

Mast cells release leukotriene - mucus secretion, mucosal oedema, bronchoconstiction

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36
Q

SE of LTRA?

A

Fever
Angioedema, Arthralgia, Anaphylaxis
Dry mouth

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37
Q

What is the MOA of methylxanthines?

A

Inhibit phosphodiesterase, increase cAMP

Inhibit adenosine receptors

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38
Q

What are the characteristics of methylxanthines?

A

Narrow therapeutic window - monitoring required
Poor efficacy
CYP450 metabolism - interactions

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39
Q

What are the SE of aminophylline?

A

Seizures, convulsions

Arrhythmia

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40
Q

Name 2 long acting anticholinergics?

A

Tiotropium bromide

Ipratropium bromide

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41
Q

What is the MOA of voltage gated Na blockers when treating epilepsy?

A

Bind to depolarised Na channels and prolong inactivation state to inhibit spread of hyperactivity.
Detach once membrane potential normal again = use dependent.

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42
Q

Name 4 VGSC blockers for epilepsy?

A

Carbamezepine
Phenytoin
Lamotrigine
Valproate

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43
Q

Which anti-epileptic drug half life reduces with repeated doses.

A

Carbamezepine - induces CYP450 enzymes which metabolise it.

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44
Q

Which AEDs are highly protein bound?

A

Carbamezepine
Phenytoin
Valproate
BZDs

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45
Q

What is a rare but serious ADR of carbamazepine?

A

Bone marrow suppression - neutropenia

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46
Q

What ADRs are associated with AEDS?

A

CNS - dizziness, drowsiness, ataxia
Rashes
Nausea and vomiting

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47
Q

Outline the pharmacokinetics of phenytoin, what is the significance of this?

A

Non-linear at therapeutic conc - t/12 unpredictable, monitoring required.
Highly protein bound
CYP450 - enzyme inducing - COCP, warfarin (not itself)

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48
Q

How are phenytoin and valproate levels monitored?

A

Salivary levels - indication of free plasma level

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49
Q

What is the MOA of lamotrigine?

A

Na channel blocker

Ca channel blocker

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50
Q

What are the advantages of lamotrigine?

A

Fewer CNS SE
No CYP induction - fewer DDI
Safest in pregnancy

51
Q

What is the interaction between the OCP and lamotrigine?

A

OCP reduces plasma levels of lamotrigine - dose adjustment needed.

52
Q

What are the risks of AEDs during pregnancy?

A

Neural tube defects - valproate in particular

Learning difficulties

53
Q

What dietary supplements should be taken if to reduce risk of AEDs during pregnancy?

A

Folic acid - neural tube

Vit K in T3

54
Q

What is the MOA of valproate?

A

Weak stimulation of GABA synthesis
Weak inhibition of GABA inactivating enzymes
VGSC blocker and weak CCB

55
Q

Which AED is associated with hepatotoxicity and raised transaminase levels?

56
Q

What DDIs are associated with valproate?

A

Anti-depressants inhibit valproate action.
Anti-psychotics antagonist valproate - lower seizure threshold.
Aspirin increases plasma conc by competitive binding.

57
Q

Which AEDs are indicated for absence seizures?

A

Lamotrigine

Valproate

58
Q

Which AED is first line for generalised seizures?

59
Q

What is the protocol used in emergency seizure management or status epilepticus?

A

Benzodiazepines
2nd dose if continuing after 5 mins
Phenytoin IV

60
Q

Name 2 BZDs used to treat epilepsy and their route of administration.

A

IV lorazepam

Rectal diazepam

61
Q

What are the side effects of L-dopa?

A

Nausea
Hypotension (dopamine vasodilator!!)
Tachycardia
Psychosis - hallucinations

62
Q

Name 2 DDI of L-dopa.

A

Vit B6 increases peripheral breakdown of L-dopa

Combined with MAOIs - risk of hypertensive crisis.

63
Q

Describe the pharmacokinetics of L-dopa.

A

Short half life

Competes with AA for gut absorption - decreased after protein meal.

64
Q

Name a non-ergot derived dopamine agonist.

A

Ropinirole

65
Q

What are the disadvantages of dopamine agonists to treat Parkinson’s?

A
  • Less efficacious than L-dopa
  • Psychotic SE are dose limiting
  • Impulse control disorders
66
Q

What must you ask about before prescribing a dopamine agonist?

A

Impulse control disorders:

  • pathological gambling
  • hyper sexuality
  • compulsive shopping
  • punding
67
Q

What are the SE of dopamine agonists?

A

Nausea
Hypotension - dopamine vasodilates!!
CNS - sedation, confusion, hallucinations

68
Q

Name two MAOI’s.

A

Rasagiline, Selegiline

69
Q

What is the MOA of COMT inhibitors?

A

Inhibits peripheral breakdown of L-dopa to 3-methyldopa which competitively inhibits L-dopa active transport into CNS.

70
Q

What are anticholinergics used to treat in Parkinsons?

A

Tremor only - ACh may antagonise dopamine

71
Q

Deep brain stimulation of what structure can be used to treat PD.

A

Subthalamic nucleus.

72
Q

What are the clinical features of Parkinsons plus syndromes?

A 
Early onset dementia
Early onset postural instability
Early onset hallucinations or psychosis
Early onset postural hypotension + incontinence
Ocular signs 
Symmetrical
73
Q

What is the commonest presentation of myasthenia graves?

A

Diplopia, ptosis

74
Q

When might you prescribe MAOIs?

A

Either with L-dopa to reduce wearing off effects

Alone to treat PD

75
Q

What are the 3 theories of depression?

A

Monoamine hypothesis
Neurotransmitter receptor theory
Monoamine hypothesis of gene expression

76
Q

What are common and rare SE of SSRIs?

A

Common - anorexia, nausea, diarrhoea
Rare - mania precipitation, suicidal ideation, tremor
Citalopram - prolongs QT

77
Q

Give one advantage of prescribing SSRs rather than TCAs.

A

Relatively safe in OD.

TCAs - dangerous in OD due to cardiac effects

78
Q

Name 2 TCAs.

A

Amitryptylline, imipramine

79
Q

What is the MAO of TCAs?

A

Non-specific inhibitor of monoamine uptake - NA and 5-HT.

80
Q

What receptors do TCAs have affinity for, what SE do these cause?

A

alpha 1 adrenoceptors - postural hypotension
Muscarinic receptors - dry mouth, blurred vision, constipation
Histamine receptors

81
Q

What other SE do TCAs cause?

A

CNS - sedation, lower seizure threshold
CVS - tachycardia, impaired contractility
ANS - decrease gland secretions

82
Q

Give an example of an SNRI.

A

Venlafaxine.

83
Q

Explain the dose-dependent effects of SNRIs.

A

Low dose - serotonin action = anti-depressant

High dose - NA action = anxiolytic

84
Q

Inhibition of which dopamine pathway leads to sexual dysfunction and infertility?

A

Tuberoinfundibular

85
Q

Name 2 typical antipsychotics.

A

Haloperidol

Chlorpomazine

86
Q

Name 2 atypical antipsychotics.

A

Olanzapine, clozapine.

87
Q

What are 3 features of all antipsychotics?

A

Sedation
Delayed onset - days to weeks
Extrapyramidal SE

88
Q

Compare and contrast the SE of typical and atypical antipsychotics.

A

Typical - more extrapyramidal SE - parkinsonism

Atypical - more metabolic SE - weight gain, hyperprolactinaemia

89
Q

Which atypical antipsychotic is associated with weight gain?

A

Olanzapine

90
Q

Which atypical antipsychotic is associated with sexual dysfunction and hyperprolactinaemia?

A

Risperidone

91
Q

Why is clozapine only 3rd line therapy despite being most effective antipsychotic?

A

Side effects - require weekly FBC
Neutropenia, agranulocytosis
Constipation, weight gain, hypersalivation.

92
Q

What are the side effects of benzodiazepines?

A

Tolerance
Dependence
Drowsiness, dizziness, ataxia

93
Q

What antidote is used for a benzodiazepine OD?

A

Flumazenil

94
Q

Outline the pharmacokinetics of Lithium to treat bipolar disorder.

A

Narrow therapeutic window + long half life - monitoring essential.
Renal excretion

95
Q

What tests must be done before starting lithium treatment and every 6 months?

A

Renal function - renal toxicity

Thyroid function - hypothyroidism

96
Q

What are SE of lithium?

A 
Memory problems
Thirst + polyuria (ADH antagonist)
Tremor
Drowsiness
Weight gain
Renal toxicity
Hypothyroidism
97
Q

Other than lithium, name 3 drugs which can act as mood stabilisers.

A

Carbamezepine
Sodium valproate
Lamotrigine

98
Q

Which two drug classes can be used to treat dementia?

A

Mild-moderate: ACh esterase inhibitors - galantine

Mod -severe: NMDA antagonist - Memantine

99
Q

Name 3 endogenous opioids?

A

Enkaphalins
Dynorphin
Endorphins

100
Q

What effect do opioids have on pre-synaptic receptors?

A

Inhibit adenyl cyclase, less cAMP.
Less Ca influx.
Decreased NT release.

101
Q

What effect do opioids have on post-synaptic receptors?

A

Increased K+ efflux, decreased excitability.

102
Q

What ADRs are associated with opioids?

A 
Nausea + vomiting
Constipation
Confusion
Drowsiness, decreased consciousness
Respiratory depression
Constricted pupils
Dependence + tolerance.
103
Q

Why must steroid therapy never suddenly be stopped?

A

Exogenous steroids mimicking cortisol negatively inhibit the hypothalamus and reduce endogenous cortisol release.
If suddenly stopped, low cortisol levels cause hypo-adrenal crisis.

104
Q

Does prednisolone have more or less mineralocorticoid activity than cortisol?

A

Less - more glucocorticoid selective

105
Q

What effect do corticosteroids have on bone?

A

Inhibit osteoblast formation
Increase osteoclast proliferation
Decrease calcium absorption in gut

106
Q

When are cortisol levels the highest?

107
Q

What are the symptoms of addison’s disease?

A 
Hypoglycaemia 
Hypotension
Weight loss
Nausea 
Hyponatraemia 
Hyerkalaemia
108
Q

What are the symptoms of Cushing’s disease?

A

Same as corticosteroid SE:

  • hyperglycaemia
  • weight gain
  • hypertension
109
Q

What is Cushing’s disease?

A

Excess ACTH resulting from a pituitary adenoma.

110
Q

What drug class is tolbutamide?

A

Sulphonylurea

111
Q

What 4 pieces of lifestyle advice might you give someone before prescribing oral hypoglycaemic agents?

A

Diet - low calorie, low sugar
Exercise
Low alcohol
Stop smoking

112
Q

What are the 3 main consequences of inhibiting ACE?

A
  1. Reduced vasoconstriction
  2. Reduced sympathetic activity
  3. Reduced aldosterone leads to reduced salt and water retention.
113
Q

What advice would you give a patient taking SSRIs?

A
  • Can take 2-6 weeks to be effective

- Continue taking for at least 1 year even if feeling better to reduce risk of relapse

114
Q

What is the risk of giving NSAIDs + SSRIs together?

A

GI bleeding + ulcer formation

- Platelets need 5-HT to clot

115
Q

How would you determine a patients fluid status?

A

Skin turgor
HR, BP
Mucous membranes
Urine output + colour

116
Q

How is a viral load used clinically?

A
  • Effectiveness of treatment - dose adjustment
  • Transmissibility
  • When ‘cured’ - undetectable Hep C viral load
117
Q

What is a ‘low genetic barrier to resistance’?

A

Only 1-2 mutations needed before resistance is likely to develop - more likely

118
Q

What is an ‘unfit’ virus?

A

a virus that has mutated to the point where it can no longer replication quickly/at all.

119
Q

What is Zollinger Ellison Syndrome, how does it manifest clinically?

A

Gastrinoma - G cell cancer

Gastrin -secreting tumor - recurrent peptic ulcers.

120
Q

Thiazides + carbamezepine result in what?

A

Hyponatraemia

121
Q

Steroids + thiazide/loop result in what?

A

Hypokalaemia

122
Q

What does a high blood gas partition mean in terms of solubility and potency?

A

High blood gas partition = more soluble = more potent

123
Q

How does oil gas partition effect onset and offset?

A 
High = slower onset as lipid partitioning
Low = faster onset
124
Q

How does pKa of a local anaesthetic alter onset?

A

Low pKa = faster onset

ESA 4 Rev (16 decks)

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