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Therapeutics CP1 > CP1 Therapeutics > Flashcards

CP1 Therapeutics Flashcards

1
Q

Leading Cause of heart failure

A

Ischemic heart disease

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2
Q

Gold standard for CHF diagnosis

A

Echocardiogram showing <45% ejection fraction

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3
Q

Goals of treatment for CHF (6)

A 
Identify/Treat Causes
Reduce Cardiac Workload
Increase Cardiac Output
Counteract neurohormonal maladaptation 
Relieve symptoms
Increase quality of life
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4
Q

Thromboembolism prophylaxis for Atrial Fibrillation

A

High-Med risk = Warfarin

Low risk = Aspirin

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5
Q

Pharmacological action of ACE-inhibitors

A

Inhibit RAAS by preventing conversion of angiotensin 1 to angiotensin 2

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6
Q

Examples of ACE inhibitors

A

enlapril, lisinopril, ramipril

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7
Q

Therapeutic effects of RAAS inhibition

A

Reduce arterial/venous vasoconstriction (reduce preload/afterload)
Reduce salt/water retention (reduce circulating volume)
Inhibit neurohormonal adaptation/cardiac remodelling

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8
Q

How should you implement an ACE-inhibitor regime

A

low dose then titrate upwards (may go past licensed max dose)

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9
Q

What should be monitored during ACE-i therapy

A

Urea/creatinine (renal function)
K+ (before and during treatment - hyperkalaemia)
Blood pressure

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10
Q

ACE-i Contraindications

A

NSAIDS
Severe renal imparment
Hypotension (<100mmHg)

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11
Q

Complications of ACE-i therapy

A

Hyperkalemia
Severe first dose hypotension (especially during concurrent diuretic therapy - should withhold in first few days of ACE-i introduction)
deterioration in renal health
Dry cough

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12
Q

Examples of AT1 receptor antagonists

A

Losartan, Candesartan, Valsartan

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13
Q

Pharmacology of AT1 receptor antagonists

A

Oppose actions of angiotensin at the AT1 receptor

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14
Q

Advantage of AT1 receptor antagonists

A

No cough whilst being equally as effective as ACE-is

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15
Q

Benefits of diuretics in heart failure

A

reduce circulating volume (reduce preload and afterload), cause venodialtion (reduce preload)

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16
Q

Complication of Diuretics

A

Hypokalaemia

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17
Q

Examples of Beta-blockers

A

Metoprolol, Bisoprolol, Carvedilol, Nebivolol

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18
Q

Benefits of using beta-blockers in CHF

A

reduce sympathetic stimulation of heart, oppose neurohormonal adaptation, anti-arrhythmic

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19
Q

What kind of failure are Beta blockers most effective at treating

A

ischemic heart failure

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20
Q

How should you implement a Beta-blocker regime for CHF

A

start low dose and titrate up

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21
Q

What should you counsel a patient for when starting beta-blockers

A

Symptoms may get worse initially

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22
Q

Contraindications of Beta-blockers

A

Asthma, symptomatic bradycardia, severe heart failure

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23
Q

What is the mechanism of Spironolactone

A

Aldosterone receptor antagonist

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24
Q

What is the role of Spironolactone in CHF

A

Reverses left ventricular hypertrophy at sub-diuretic doses - reducing mortality by 35%

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25
Q

How does Digoxin work

A

Na+/K+ ATPase blockage, causing Na+ accumulation in cells leading to increased exchange for Ca2+ , increasing cardiac contractility, impairing atrioventricular conduction (useful in AF) and inducing some bradycardia

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26
Q

What should digoxin therapy be reserved for

A

CHF with AF

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27
Q

Digoxin contraindications

A

concurrent heart block, bradycardia

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28
Q

How should you implement a digoxin therapy

A

Titrate dose to ensure ventricular rate does not drop below 60bpm (this indicates toxicity)

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29
Q

What should always be monitored in a patient with heart failure

A

Renal function, potassium,

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30
Q

What causes thiazides to become ineffective

A

Renal failure (no secretion in distal convoluted tubule)

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31
Q

Signs of Digoxin toxicity

A

Anorexia, nausea, Visual disturbances, Diarrhoea

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32
Q

NICE guidelines for the management of heart failure (full flowchart)

A

1 )Evidence of LV dysfunction = ACE-i + Betablocker (if mild stable failure)
Cough = switch Ace-i to an AT1RA
2) If symptoms still there, add Aldosterone antagonist (spironolactone)/ATRA/Hyrdalazine + Nitrate
3) if symptoms still present consider Digoxin
4) If Odematous use a diuretic (Thiazide/Loop)

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33
Q

What biochemical signalling factors increase acid secretion

A

Histamine acting on H2-receptors
Gastrin acting on CCK receptors
Vagal Ach via M3 receptors

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34
Q

What factors decrease acid secretion

A

Prostaglandins (E2 + I2) which inhibit the proton pump and stimulate bicarbonate release (gastroprotective)

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35
Q

Goals of treatment for Dyspepsia

A

Symptomatic relief/cure
suppress acid release
promote mucosal protection
eradication of underlying cause (e.g. H-pylori)

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36
Q

Common causative foods for dyspepsia

A

chocolates, spicy foods, fatty foods

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37
Q

Examples of antacids

A

Sodium Bicarbonate
Magnesium Hydroxide
Aluminium Hydroxide

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38
Q

How effective are Antacids

A

offer symptomatic relief but no cure

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39
Q

Why are calcium salts bad for long term control of dyspepsia

A

Promote gastrin release

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40
Q

Method of action for antacids

A

raise stomach pH

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41
Q

Method of action for alginates

A

when combined with saliva a viscous foam forms on top of the stomach, protecting the oesophagus during reflux

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42
Q

Examples of H2-antagonists

A

Ranitidine, Famotidine

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43
Q

How effective are H2-antagonists

A

Short term relief

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44
Q

Best time to use H2-antagonists

A

Night time

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45
Q

Why is imetidine no longer used as a H2 -antagonist

A

Cyp450 inhibitor, causing alteration of the metabolism of antigoaculants, phenytoin (anti-epileptic), carbamazepine (anti-epileptic) and TCAs

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46
Q

How to proton pump inhibitors work

A

inihibit H+/K+ proton pump, reducing H+ secretion

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47
Q

Why are PPis selective

A

become active at acid pHs

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48
Q

Complication of PPIs

A

increased risk of campylobacter infection

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49
Q

What do prokinetic drugs do

A

increase movmement of gastric contents from stomach to duodenum

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50
Q

Examples of prokinetic drugs

A

Domperidone, metocloperamide

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51
Q

What condition do prokinetic drugs help the most

A

GORD

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52
Q

What is the regime for Helicobacter Pylori eradication

A

TRIPLE THERAPY
PPi/H2 antagonist + 2 ABx

2 of: Metronidazole, Amoxicillin, Clarithromycin

1 week of triple therapy + 4-6 weeks PPI

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53
Q

What is the stepped approach to non H-pylori dyspepsia

A

Step 1: Antacid/alginate +antacid
Step 2: H2-antagonist
Step 3: PPI

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54
Q

What drugs are associated with peptic ulceration

A 
NSAIDS
Oral steroids (particularly with NSAIDS)
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55
Q

Why do NSAIDS cause peptic ulceration

A

COX inhibition, causing reduced COX-1 production (which is gastroprotective)

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56
Q

Why do Steroids cause peptic ulceration

A

Lipocortin inhibitor causing decreased cytoprotective PLA2 production

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57
Q

What is the best regime for minimisation of gastric damage due to increased risk factors

A

PPI prophylaxis with misoprostol (prostaglandin analogue)

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58
Q

Contraindictions to misoprostol

A

pregnancy (can cause uterine contraction causing increased abortion risk)

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59
Q

What are the red flag signs for a patient with dyspepsia

A

ALARMS 55, anorexia, loss of weight, anaemia, recent onset/progressive symptoms, malaena/haematemesis, swallowing dificulty), >55 y/o

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60
Q

Flow chart for dyspepsia management

A

mild = antacid/H2 antagonist
recurrent = PPI
ALARMS 55 present = GP referral for endoscopy/H-pylori test
if H-pylori +ve = Triple therapy with PPI + 2 of metronidazole, amoxicillin and clarithromycin for 1 week ,then 4-6 weeks of a PPI
If negative just a PPI

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61
Q

Goals of treatment for Hypertension

A

Reduction in BP to specific targets with as few side effects as possible
SBP <140mmHg
DBP <90mmHg (<80mmHg in diabetes and CKD)

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62
Q

When are ACI-is nephroprotective

A

In diabetics

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63
Q

Apart from hyperkalaemia, what is another important side effect of ACE-is

A

Angioedema

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64
Q

Examples of Calcium channel inhibitors

A

Verapamil (rate limiting) , Amlodipine, felodipine, nifedipine

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65
Q

examples of alpha blockers

A

Doxazosin, prazosin

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66
Q

Why are alpha blockers last choice for Hypertension

A

Widespread side effects making them poorly tolerated

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67
Q

What line are diuretics for Hypertensive control

A

3rd

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68
Q

How do Thiazide Diuretics work

A

inhibit Na+/Cl- in DCT reducing circulating volume

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69
Q

Important side effects of Thiazides

A 
Hypokalaemia
Hypercalcaemia
Postural hypotension
Impaired glucose control
altered lipid profile
Impotence
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70
Q

Contraindications for thiazides

A

Gout

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71
Q

Examples of Thiazide Diuretics

A

Chortalidone, Indapamide

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72
Q

Adverse effects of Calcium channel blockers

A

Peripheral odema
Postural hypotension
Constipation

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73
Q

Side effects of beta blockers

A

Bronchospasm

Reduced Hypoglycaemic awareness `

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74
Q

What lifestyle changes can be done to treat hypertension

A

decreased consumption of alcohol, caffeine, fat, salt, smoking

Increased: weight loss, fruit, oily fish, exercise

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75
Q

How do you confirm hypertension, knowing the patient has implemented lifestyle changes already

A 
ambulatory measurement (around 14 measurements)
on both arms
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76
Q

Classify Hypertension

A

Stage 1 >140/90
Stage 2 >160/100
Severe >180/110

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77
Q

Who should be treated with antihypertensives

A

Stage 1 +end organ disease/diabetes/CV disease/high CV risk (>20% over 10 years)

All Stage 2 + above

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78
Q

When treating hypertension, what factors promote the use of ACE-is/AT1RAs

A

Heart Failure, Left ventricular hypertrophy, diabetes

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79
Q

When treating hypertension, what factors promote the use of Calcium channel blockers

A

afro-caribbean ethnicity

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80
Q

When treating hypertension, what factors promote the use of Thiazides

A

old age

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81
Q

When treating hypertension, what factors promote the use of beta blockers

A

myocardial infarction, IHD, CHF

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82
Q

When treating hypertension, what factors promote the use of alpha blockers

A

resistance to other drugs, prostatic hypertrophy

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83
Q

When treating hypertension, what factors contraindicate the use of ACE-is/AT1RAs

A

renovascular disease

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84
Q

When treating hypertension, what factors contraindicate the use of Thiazides

A

Gout

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85
Q

When treating hypertension, what factors contraindicate the use of beta blockers

A

Asthma/COPD

Heart Block

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86
Q

Flochart for hypertension treatment

A

Step 1: <55/non black/ high renin = Ace inhibitor
>55/black/low renin = calcium channel inhibitor

Step 2: ACE-i + Ca2+ blocker

Step 3: add diuretic (1st line thiazide-like, e.g endapamide/clortalidone)

Step 4: add alpha blocker/spironlactone/other diuretic/beta blocker

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87
Q

aside from hyperlipidaemia patients, Who should be prescribed statins

A

patients with high risk of cardiovascular events (renal failure, diabetes, hypertension)

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88
Q

How do nitrate assist in pharmacological management of ischemic heart disease

A

Release NO, causing venodilation (decreased preload/cardiac work), as well as coronary artery vasodilation, improving coronary blood flow

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89
Q

First line for IHD intervention + why

A

Beta blockers, as coronary flow is only in diastole, so decreasing heart rate prolongs diastole period, increasing coronary blood flow

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90
Q

Names of rate limiting calcium channel blockers

A

verapamil, diltiazem

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91
Q

What did the HOPE trial indicate

A

ACE-is reduce mortality in IHD

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92
Q

Names of potassium channel activator

A

Nicorandil

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93
Q

Method of action of potassium channel activators

A

Donates nitric oxide, promote vasodilation via ATP sensitive K+ channel activation

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94
Q

How does aspirin act as an antiplatelet

A

irreversible inhibition of COX leading to prostacyclin > thromboxane production, endothelial cells regenerate COX via nucleus but platelets cannot as they aren’t nucleated

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95
Q

How does Clopidogrel work

A

ADP receptor antagonist leading to glycoprotein IIb/IIIa inhibition (prevents platelet aggregation)

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96
Q

Aspirin Contraindications

A

Asthma

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97
Q

What is the management of IHD (for someone with the cardiovascular risk needed for intervention)

A

antiplatelet (low dose aspirin or clopidogrel)
BP controlled <140
<5mmol/l cholesterol (<3mmol/L LDL), statin if >
Symptomatic relief of angina use a GTN spray/sublingual tablets

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98
Q

What are the drug choices for the prevention of IHD

A

1st choice - Beta blockers/ if CI use rate limiting calcium channel blocker or a Dihydropyridine calcium blocker (both +/- oral nitrate)
2nd choice - if beta blocker add a Dihydropyridine, if using a dihydropyradine add a beta blocker

3rd choice if still refractory add nicorandil

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99
Q

Whats an important interaction to consider when prescribing prevention for ischemic heart disease

A

Rate limiting calcium channel blockers and beta blockers are contraindicated for concurrent therapy as they may induce life threatening bradycardia

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100
Q

how do you structure IHD intervention (stable angina intervention)

A

Offer GTN for relief, assess CV risk (clotting, lipids and BP lifestyle) and control where necessary, then if there is still symptoms attempt to prevent with beta blockers/ca2+ inhibitors/nicorandil

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101
Q

what is added to management when comparing stable angina and unstable angina

A

LMWH

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102
Q

How does Warfarin work

A

inhibits Vitamin K dependent coagulation

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103
Q

Indications for warfarin therapy

A

artificial heart valves, AF, PE, DVT

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104
Q

How long is Warfarin’s action delayed + why

A

around 3 days, as it inhibits new factor formation, and the stores may last for up to 3 days

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105
Q

How do you monitor warfarin

A

INR (target 2-3)

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106
Q

what drugs does warfarin interact with

A

Cyp450 inducers/inhibitors (potentiated by inhibitors)

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107
Q

Name some cytochrome p450 inhibitors

A

Amiodarone, Fibrates, erythromycin, cimetidine (H2 antagonist)

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108
Q

Name some cytochrome p450 inducers

A

Barbiturates, Carbamazepine, phenytoin

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109
Q

Signs of warfarin potentiation

A

increased bleeding risk

  • gastric ulcer bleeding
  • haemorrhagic stroke
  • haemoptysis
  • haematuria
  • easy bruising
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110
Q

How does warfarin interact in pregnancy

A

Teratogenic, particularly in 1st trimester

can cause fetal vit k deficiency in the 3rd trimester

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111
Q

alternative to warfarin in pregnancy

A

LMWH

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112
Q

Heparin method of action

A

antithrombin 3 activator, inhibiting serine protease, inhibiting factor 9,10,11 formation

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113
Q

What is long term heparin use (>5 days) associated with

A

Thrombocytopenia

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114
Q

What type of heparin requires monitoring

A

Unfractionated

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115
Q

What test monitors heparin’s action

A

Activated partial thromboplastin time (intrinsic pathway)

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116
Q

How does Dabigatran work

A

Oral thrombin inhibitor

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117
Q

What is used to prevent MI in patients who have previously had an MI

A

Low dose aspirin

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118
Q

How does Dipyridamole work

A

Inhibits phosphodiesterase, prevents cGMP/cAMP breakdown causing decreased platelet aggregation

119
Q

How does abciximab work + when is it given

A

Monoclonal antibody against glycoprotein IIb/IIIa, to patients undergoing angioplasty

120
Q

What time of day should statins be taken

A

At night (cholesterol synthesis is highest)

121
Q

What are the actions of paracetamol

A

Analgesia

Antipyrexia

122
Q

Minimum for liver damage with paracetamol

A

14 tablets

123
Q

NSAID actions

A

Analgesia
Antipyrexia
Anti-inflammatory

124
Q

NSAID adverse effects

A

GIT ulceration/erosion
Reduction in renal perfusion
Bronchospasm
Reduced platelet aggregation (reversible)

125
Q

How should you prescribe NSAIDS

A

Lowest effective dose for the shortest period of time necessary to control symptoms,
Regular review required
Consider co-prescription of a PPI, particularly in high GI risk/long term

126
Q

Name some weak opioids

A

Codeine
Dihydrocodeine
Dextropropoxyphene
Tramadol (po)

127
Q

Name some Strong opioids

A 
Morphine
Diamorphine
Oxycodone
Buprenorphine
Fentanyl
128
Q

What are weak opioids most effective with

A

Paracetamol

129
Q

why may Chinese people not respond to codeine

A

90% don’t have a CYP450 2D6 gene

130
Q

Routes of administration of strong opiods

A 
Oral
Rectal
Transdermal
Sublingual
Topical
Intramuscular
Subcutaneous
Intravenous
Epidural
Intrathecal
131
Q

ADR for opioids?

A 
N + V (usually requires an antiemetic) 
Constipation 
Sedation 
Respiratory depression (in toxcicity) 
Hypotension
Urinary retention
132
Q

What is breakthrough pain

A

transient exacerbation/recurrence of pain in patients who have stable pain relief usually

133
Q

What may precipitate breakthrough pain

A

End of dose failure
Incident pain
Spontaneous pain

134
Q

How do you convert to an alternative opioid?

A

Determine 24 hour requirement and use conversion factor for alternative opiate

135
Q

What are some common opioid equivalences for 60mg morphine p.o

A

Hydromorphone p.o - 9.8mg
Oxycodone p.o - 30mg
Fentanyl (transdermal patch) 25 micrograms/hr

136
Q

What opioid should be used in morphine allergy

A

Tramadol, oxycodone or fentanyl

137
Q

Advantages of patient-controlled analgesia

A 
Rapid analgesia
Readily prepared
Patient satisfaction
No dose delay 
Patient acceptabilityNo peaks/troughs
138
Q

Disadvantages of patient-controlled analgesia

A

Expensive
Requires IV access
Training
Monitoring

139
Q

Why would you use diamorphine (heroin) instead of morphine

A

It has better aqueous solubility

140
Q

What should be monitored during opioid therapy

A 
Pulse
BP
O2 Sats
Respiration rate
Pain intensity 
Sedation score
Side effects
Amount of opioid used
141
Q

How does Tramadol work

A

mu-agonist , inhibits NA uptake/5-HT release

142
Q

What is Naloxone

A

Opioid receptor antagonist

143
Q

When would you use Naloxone

A

Opioid overdose

144
Q

Signs/Symptoms of neuropathic pain

A

Burning, Pins and needles, Scalding, shooting, Stabbing

Hyperalgesia, Allodynia

145
Q

Best treatments for neuropathic pain

A 
TCAs
Anticonvulsants (carbamazepine, gabapentin, pregabalin)
Opioids
Local anesthetics
Capsaicin
146
Q

How do TCAs work

A

Inhibit neuronal NA/5-HT reuptake

147
Q

How do Gabapentin and Pregabalin work

A

Prevent ca2+ mediated activation of dorsal horn neurones

148
Q

How does Salbutamol work

A

B2-adrenoreceptor agonist, causing AC activation, increasing intracellular cAMP, promoting muscle relaxation

149
Q

What does prolonged B2-agonist use do

A

Receptor downregulation

150
Q

What may reduce the chance of receptor downregulation in salbutamol use

A

Inhaled corticosteroid

151
Q

What is the requirement when prescribing a Long-acting beta 2 agonist

A

The patient is also on a steroid

152
Q

How does a Xanthine work

A

Adenosine receptor antagonist OR phosphodiesterase inhibitor

153
Q

Examples of Xanthines

A

Theophylline, Aminophylline

154
Q

The best example for Xanthine use

A

Aminophylline intravenously for an acute asthmatic attack

155
Q

How do muscarinic antagonists work

A

Block parasympathetic bronchoconstriction

156
Q

Examples of Muscarinic antagonists

A

ipratropium/tiotropium

157
Q

What role do corticosteroids have in asthma treatment

A

Prevention (do not reverse an attack)

158
Q

Example of steroids used in asthma

A

Beclometasone (becotide inhaled or prednisolone orally)

159
Q

How do steroids work

A

Act on intracellular DNA receptors to influence protein production (anti-inflammatory)

160
Q

Side effects of steroids

A 
Throat infections, hoarseness (inhaled) - advise to wash mouth out after use
Adrenal suppression (oral)
161
Q

Name bronchodilators used in asthma treatment

A

SABAs
LABAs
Xanthines
Muscarinic antagonists

162
Q

Name Anti-inflammatory agents used in asthma treatment

A

Corticosteroids

Leukotrienes receptor antagonists

163
Q

Example of Leukotriene receptor antagonist

A

Montelukast

164
Q

What is a leukotriene

A

Pro-inflammatory product of arachidonic acids

165
Q

What is Omalizumab

A

MAB against free IgE (not bound IgE)

166
Q

What line is Omalizumab used at for asthma treatment

A

Last resort

167
Q

What is the treatment cascade for Asthma

A
  1. SABA (+ inhaled ICS if >2 times a week)
    this will change to everyone gets a SABA+ICS
  2. +LABA trial
  3. if LABA fails, try LTRA/Xanthine
  4. Increase dose of inhaled steroid
  5. Add oral steroid
168
Q

What may require you to step up asthma treatment

A

use of salbutamol inhaler >2 times a week

169
Q

What may assist with poor inhaler technique (in young and old)

A

Spacer devices

170
Q

What order should asthma drugs be taken in

A

Bronchodilator before steroid

171
Q

Treatment cascade for COPD

A
  1. SABA/SAMA
  2. if FEV1 >50% replace SABA/SAMA with LABA/LAMA
    if FEV1<50% add LABA+ICS or replace SAMA with LAMA
  3. LAMA+LABA+ICS
172
Q

How do NSAIDS provoke asthma

A

Increase Leukotriene production (as there is reduced prostaglandin production meaning there is more free AA for LT production)

173
Q

How do statins work

A

HMG-CoA Reductase inhibitors

174
Q

Examples of Statins

A

Simvastatin, Pravastatin, Atorvastatin, Fluvastatin

175
Q

What are the effects of statins

A

Reduction in plasma cholesterol, upregulation of hepatic LDL receptors leading to increased LDL uptake

176
Q

When aren’t statins effective + what is the best to try

A

Homozygous familial disease, atorvostatin

177
Q

When should you consider statin use

A

High cholesterol OR if they have risk factors for CVD

178
Q

Standard prescription following an MI

A

Statin
Aspirin
Beta-Blocker
ACE-i

179
Q

What risk of CVD in the next 10 years requires statin treatment

A

> 10%

180
Q

Cautions for statins

A

Use carefully in liver disease

181
Q

Most important side effect of statins

A

Rhabdomyolysis/myopathy

182
Q

Least likely statin to cause Rhabdomyolysis

A

Pravastatin

183
Q

What should be monitored when starting statins

A

Liver function

184
Q

Drug contraindications for simvastatin

A

Erythromycin
Amlodipine
Verapamil
Diltiiazem

185
Q

Patients with med-high risk of developing CVD

A 
Males >55
Males 45-55/Females >55 with@
1. Family history of IHD
2. Smokers
3. Overweight
4. S Asians
186
Q

How do fibrates work

A

PPAR-alpha activators, promoting VLDL breakdown

187
Q

What are fibrates useful for

A

reducing triglycerides

188
Q

ADR Fibrates

A

Rhabdomyolysis

189
Q

What does Ezetimibe do

A

Cholesterol absorption inhibitors

190
Q

How do fish oils affect cardiovascular health

A

High omega 3 replaces COX and produces a different balance of TXA/PGI (PGI more potent, TXA less potent)

191
Q

Treatment cascade for Dyslipidaemia

A

IF INCREASED CHOLESTEROL (or high CVD risk)

  1. statin + reduced risks
  2. Add a fibrate
  3. add Ezetimibe

IF INCREASED TRIGLYCERIDES

  1. Lifestyle chances
  2. Fibrate/Fish oil?
192
Q

What action do antipsychotics have

A

Dopamine D2- receptor antagonist

193
Q

What are Extrapyramidal side effects of dopamine receptor blockers

A

drug-induced parkinsonism
Restlessness
abnormal movements
Tardive Dyskinesia

194
Q

Examples of atypical antipsychotics

A

clozapine, olanzapine, risperidose, sertindolequetiapine

195
Q

Metabolic side effects of antipsychotics

A

Weight gain
Hyperglycaemia
Dyslipidaemia

196
Q

Cardiovascular sided effects of antipsychotics

A 
Cardiac arrhythmias (QT-prolongation) 
Severe postural hypotension (Chlorpomazine)
Increase stroke risk (Olanzapine/respirodone)
197
Q

How does Clozapine work

A

D2, D4, 5-HT antagonist

198
Q

Side effect of Clozapine

A

Agranulocytosis (neutropenia)

199
Q

What needs monitoring during clozapine treatment

A

FBC (checking WBC) every week for 18 weeks, every 2 weeks for a year then every 4 weeks after

200
Q

Who is Clozapine restricted to

A

patients who have failed to respond to 2 antipsychotics (including 1 atypical)

201
Q

What is Neuroleptic malignant syndrome

A

life-threatening ADR to antipsychotics causing fever, muscular rigidity, altered mental status, autonomic dysfunction and elevated CK

202
Q

Side effects Chlorpromazine

A

Skin photosensitivity

203
Q

What is needed for an antipsychotic to be considered ineffective

A

4-6 weeks of failure to response

204
Q

What antipsychotic should be used for violent/aggressive patients

A

Haloperidol

Lorazepam

205
Q

What antipsychotics are used for EOL care and what do they do

A

Haloperidol and Lavpromazine due to sedative/anti-emetic effects

206
Q

What is a depot preparation + why would you use it

A

Bolus in oil, given every 1-4 weeks, providing long term control for patients with compliance issues

207
Q

How should Clozapine be counseled

A

Required regular blood tests
Should report signs of infection
Should report any increase/irregularity in pulse

208
Q

How should patients be counselled with respect to antipsychotics

A

May affect driving/enhance alcohol effect
may cause anxiety/headache/insomnia
Should report movement disorders

209
Q

what counts as responding well to antipsychotics

A

only 1 acute episode in 1-2 years = responds well

210
Q

What correlated with clinical efficacy for dopamine antagonists

A

D2 affinity

211
Q

How may Euthyroidism be achieved in hyperthyroidism

A

Antithyroid drugs
Thyroidectomy
Radioactive Iodine

212
Q

How do Thionamides work

A

Decrease thyroid hormone production by inhibiting iodination of thyroglobulin via thyroperoxidase inhibition

213
Q

How long does it take for thionamides to work

A

Several weeks

214
Q

important ADR for thionamides

A

Agranulocytosis

215
Q

Examples of Thionamides

A

Carbimazole, propylthiouracil

216
Q

What role do beta blockers have in hyperthyroidism

A

reduce the action of catecholamines causing symptomatic relief from anxiety, tremors (only in non-selective BBs) and palpitations

217
Q

What are the 2 medical treatment options for hyperthyroidism

A
  1. High dose Carbimazole 1-2 months until remission then 18 month maintenance dose (+BB for symptomatic relief)
  2. ‘Block and replace’ - High dose carbimazole until 0 thyroid activity, then adding thyroxine with the carbimazole + titrate to mimic appropriate thyroid activity (+BB for symptomatic relief)
218
Q

Treatment for hypothyroidism

A

Levothyroxine
50-100 micrograms a day in young, increased after 6 weeks by 25-50 micrograms until appropriate levels are achieved

25 micrograms in elderly + those with IHD, which is then increased by 25micrograms every 3-4 weeks until TSH normalisation 1

219
Q

Important ADR for thyroxine

A

may worsen/uncover angina

220
Q

Length of time for thyroxine treatment

A

lifelong

221
Q

Aim of epilepsy treatment

A

Control seizures with fewest possible side effects

Monotherapy preferred

222
Q

How do antidepressants affect seizure threshold

A

They can lower it

223
Q

1st + 2nd choice for generalized seizures

A

1st Valproate/Carbamazepine (Lamotrigine if childbearing age)
2nd Levetiracetam

224
Q

1st + 2nd choice for absence seizures

A

1st Ethosuximde

2nd Valproate/Lamotrigine

225
Q

How does Valproate work

A

GABA potentiation, inducing Na-channel block

226
Q

Valproate side effects

A

Weight gain, Tremor, sedation

227
Q

Contraindication for Valproate

A

Pregnancy, impaired liver function (essential to have regular LFTs)

228
Q

Carbamazepine side effects

A

Rash, Dizziness, Double Vision, CYP450 induction, teratogenesis

229
Q

Phenytoin side effects

A

increased gum growth, nystagmus if toxic

230
Q

Lamotrigine mechanism

A

Use-dependent blockage of sodium channels, reduction in glutamate release

231
Q

What indicates lamotrigine should be withdrawn

A

Rash + flu like illness (risk of bone marrow toxicity)

232
Q

Why may epilepsy be less controlled during pregnancy

A

enzyme induction and increased volume of distribution

233
Q

What may prevent neural tube defects

A

Folic acid 5mg daily in 1st trimester

234
Q

What is Status epilepticus

A

Continuous seizure for 30+ minutes OR 2 fits without recovery between

235
Q

How do you treat status epilepticus

A

IV benzo

i.v. orazepam
or
Diazepam i.v/rectal
or
Clonazepam
or 
Phenytoin slow i.v

last resort = general anesthetic such as propofol

236
Q

When may treatment withdrawal be considered for epilepsy

A

Seizure free for 2-4 years

237
Q

How do you withdraw a patient from epilepsy treatment

A

Gradual withdrawal, reduce dose every 4 weeks, stop driving during withdrawal

238
Q

How do sulphonylureas work

A

inhibit ATP-sensitive potassium channels in beta cells causing increased insulin release

239
Q

Side effects Sulphonylureas

A

Weight Gain

Hypoglycemia

240
Q

How do Meglitinide analogues work

A

rapid onset beta cell potassium channel closure causing increased insulin release (different receptor to sulphonylureas) `

241
Q

Contraindication for metformin

A

renal impairment

242
Q

Mechanism for Glitazones

A

PPAR-gamma activator, acts as an insulin sensitizer
reduces hepatic glucose output
increased peripheral glucose utlization
increased fatty acid uptake into adipose cells

243
Q

What should be monitored during glitazone therapy

A

Liver function

244
Q

Treatment Cascade for T2DM

A
  1. 3 month trial lifestyle modification
  2. Metformin (SU if renally impaired)
  3. Dual Therapy (Metformin + SU/Glitazone/D4PPi/SGTL2i/GLP1RA)
  4. triple therapy with metformin + 2 other drugs OR Insulin if metformin not tolerated
  5. Insulin
245
Q

Aside from anti-hyperglycaemic drugs, what other drugs that should be considered when treating diabetes

A

Need to control BP and CVD risk factors

Ace-inhibitors nephroprotective in diabetes so 1st line for antihypertensives (however other drugs are just as effective as lowering blood pressure)

Simvastatin should also be prescribed

246
Q

What is the aim for diabetes treatment in terms of glycemic control and Blood pressure

A

<6.5-7.5% HBA1c, <135/75mmHG BP

247
Q

Examples of SSRIs

A

Citalopram, Sertraline, Fluoxetine, paroxetine

248
Q

How do SSRIs work

A

selectively inhibit reuptake of serotonin from neurones, enhancing synaptic concentrations of 5HT + downregulating presynaptic 5HT-Rs

249
Q

Why are SSRIs 1st line treatment for depression

A

better tolerated than TCAs and are safer in overdose

250
Q

Examples of TCAs

A

Amitryptaline, dothiepin, Lofepramine, Nortryptaline

251
Q

Side effects of TCAs

A

Sedation, Dry mouth, blurred vision, constipation, urinary retention (due to antimuscarinic effects), QT interval prolongation, predisposition to heart block/arrhythmias

252
Q

Why may sedation be a benefit for TCA controlled depression

A

sleep is impaired in depression often

253
Q

Who aren’t TCAs suitable for

A

IHD patients, >70 y/o, patients at high risk of suicide

254
Q

Aside from TCAs and SSRIs, what are some other antidepressants in use + give an advantage of each if possible

A
  1. Noradrenaline reuptake inhibitors (Reboxetine, useful for when TCAs are contraindicated but patient is resistant to SSRIs)
  2. Seratonin-noradrenaline reuptake inhibitors (Venlafaxine, less side effects)
  3. Noradrenergic and Specific Serotonergic antidepressents (mirtazapine, limited antimuscarinic effects)
  4. Seratonin receptor modulators (Nefazodone)
255
Q

Complications with Venlafaxine

A

GI issues, Hypertension

256
Q

How do Monoamine oxidase inhibitors work

A

Inhibit monoamine oxidase increasing NT concentration

Also cause indirect increased sympathic stimulation via tyramine metabolism

257
Q

What is the Cheese reaction with MOAIs + how may it be prevented

A

ingestion of high tyramine foods (such as cheese/yeast extract/avocado/banana/pickeled herring) may precipitate a catecholamine storm when taken during MAOI therapy, selective reversible inibitors of MAO-A prevent this reaction, since tyramine is metabolised by MAO-B

258
Q

Treatment cascade for mild depression

A
  1. ‘watchful waiting’ for 2 weeks
  2. SSRIs (TCAs if sleep is an issue) + adjunct psychological treatment should be considered
  3. Consider gradual withdrawl after 6 months if clinical improvement
259
Q

How should non-responsive depression be managed

A

Swap to another SSRI for 6 months, 2+ depressive episodes indicated treatment for 2 years

260
Q

What mechanism does St Johns Wort have

A

similar to SSRIs

261
Q

How does St Johns Wort interact with the metabolism

A

CYP450 inducer

262
Q

Can St Johns Wort be used in conjunction with SSRIs

A

No as it increased toxicity

263
Q

First line treatment for bipolar disorder

A

Lithium

264
Q

When should Lithium be avoided

A

Renal impairment

265
Q

2nd line treatment for bipolar disorder

A

Anticonvulsants (valproate/carbamezepine)

266
Q

Mechanism of action for Benzos

A

GABA potentiation

267
Q

Problematic aspects of Benzos

A

Tolerance + Dependence

Should be limited to 2-4 weeks

268
Q

Drugs to consider in treating anxiety

A

Beta blockers
Benzos
Antidepressants
Buspirone

269
Q

How does Buspirone work

A

Activates 5-HT1a receptors, binds to dopamine receptors

270
Q

Buspirone side effects

A

Dizziness
Nausea
Headaches

271
Q

What drugs may cause secondary diarrhoea

A 
Antibiotics 
Orlistat (lipase inhibitor)
Misoprostol 
PPIs
Digoxin
Metformin
Iron Salts
acarbose
272
Q

First line treatment for diarrhoea

A

Oral rehydration therapy

273
Q

What is the role of antimotility agents in diarrhoea

A

used for symptomatic relief via presynaptic inhibition of Ach release (via mu-opioid receptor)

274
Q

Side effects of using antimotility agents in diarrhoea

A

May prolong infection via reduced clearance of pathogen from GI tract

275
Q

Examples of antimotility agents

A

Codeine, Loperamide, TCA, antimuscarinics

276
Q

First line therapy for constipation

A

balanced diet with good amount of fibre

277
Q

What treatment is available for constipation not responsive to dietary modification

A

Osmotic Laxitives (e.g. lactulose)

278
Q

How do osmotic laxatives work

A

increase fluid volume in colon osmotically

279
Q

Aside from osmotics, what are some types of laxatives

A

Magnesium, Bulking agents, Stimulant Laxatives

280
Q

How do Stimulant laxatives work

A

metabolites stimulate GI activity

281
Q

What are some options for IBS treatment

A 
Lactulose/Loperamide for constipation/diarrhoea 
Antispasmodic agents (antimuscarinics, mebeverine)
TCAs (low dose)
282
Q

Treatment for Ulcerative colitis + Crohns

A

5-Aminosalicylates (more so for UC)
e.g. Sulphasalazine , Mesalazine or 5-ASA
+ corticosteroids 1st line
Prenisolone
Immune suppressants may be required in severe disease (methotrexate, azathioprine, cyclosporine, infliximab)
Surgery is curative in UC, may be a benefit in Crohn’s too

283
Q

How should you counsel Mesalazine (5-aminosalicylate)

A

Patient should report blood dyscrasia (sore throat, fever, easy bruising), side effects may include: rash, headache, diarrhoea

284
Q

What nay exacerbate IBD

A

NSAIDS, Smoking (Crohn’s), alcohol

285
Q

What should be counseled with Aziothioprine (immunosuppressant used in IBD)

A

Pancreatitis, myelosuppresion (bruising/bleeding, infections)

286
Q

What type of IBD is methotrexate effective in

A

Crohn’s

287
Q

How do NSAIDS and Methotrexate interact

A

increase methotrexate toxicity

288
Q

How should methotrexate be monitored

A

FBC, U+E, LFT, report fevers/coughs (indicate neutropenia), report cough/dyspnoea (pulmonary toxcicity)

289
Q

What can happen if ciclosporin is given in addition to steroids

A

increased risk of pneumocystitis carinii

290
Q

what can infliximab lead to the increased risk of

A

TB development

291
Q

In a liver function test, what results most indicate hepatocellular damage

A

Raised ALT/AST

292
Q

In a liver function test, what results most indicate Cholestasis

A

Raised ALP/GGT/Bilirubin

293
Q

In a liver function test, what results most indicate Enzyme induction

A

Raised GGT

294
Q

In a liver function test, what results most indicate Chronic liver disease

A

Raised Bilirubin/INR + Decreased Albumin

Therapeutics CP1 (1 decks)

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