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CP1 > Therapeutics online course > Flashcards

Therapeutics online course Flashcards

1
Q

What is the difference between ADRs and Side effects?

A

side effect maybe beneficial or a disadvantage

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2
Q

what is a type A ADR?

A
  • the normal pharmacological response is undesirable
  • dose-relate
  • predictable
  • usually managed by dose adjustment
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3
Q

How can you minimise GI damage due to NSAIDs?

A
  • identify patients at risk e.g. 65 years, history of ulcers, infection with H.pylori
  • prophylaxis with PPI
  • give in combination with misoprostol- a stable PGE1 analogue, acts on prostanoid receptors to inhibit gastric H+ secretion
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4
Q

What is agranulocytosis?

A

absence of neutrophils

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5
Q

What are the symptoms of agranulocytosis?

A

mouth ulcers, severe sore thread, infections

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6
Q

What medications can cause agranulocytosis?

A

clozapine, carbimazole, carbmazepine

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7
Q

How do NSAIDs damage the kidneys?

A

inhibit renal PGs

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8
Q

What drugs can cause Stevens-Johnson syndrome?

A

carbamazepine and phenytoin

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9
Q

What allele is associated with Stevens-johnson syndrome?

A

HLA-B*1502

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10
Q

What drugs are known to increase activity of metabolising enzymes?

A
  • rifampicin
  • phenytoin
  • ethanol
  • carbamazepine
  • St John’s Wort
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11
Q

What does enzyme induction do to plasma concentration of drugs?

A

decreases

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12
Q

What drugs inhibit Cy P450?

A
  • erythromycin/ clarithromycin
  • ciclosporin
  • psoralen (from grape fruit juice)
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13
Q

What has a quicker effect: enzyme induction or inhibition?

A

inhibition

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14
Q

What drugs does simvastatin react with?

A
  • macrolides
  • amlodipine
  • verapamil
  • ditiazem
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15
Q

How can you prescribe a statin with amlodipine?

A

pravastatin does not interact or use 20mg simvastatin as maximum dose

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16
Q

What can NSAIDS prevent being eliminated from the kidney?

A

methotrexate

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17
Q

which diuretic cause hypokalaemia?

A

loops and thiazide

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18
Q

What do you prescribe with caution with non potassium sparing diuretics?

A

ACEi- increase risk hypotension

digoxin-increase toxicity

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19
Q

What is prescribed with caution with potassium sparing diuretics?

A

ACEi-risk hyperkalaemia

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20
Q

What are the potassium sparing diuretics?

A

sprinolactone

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21
Q

which calcium channel blockers should not be prescribed with beta blockers?

A

verapamil and diltiazem

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22
Q

Which calcium channel blocker can be prescribe with beta blockers?

A

dihydropyridines

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23
Q

Give an example of a direct oral anticoagulant

A

rivaroxaban

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24
Q

How do DOACs work?

A

factor x inhibitor

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25
Q

What are the benefits of DOACs?

A

fewer interactions

no requirement to monitor

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26
Q

What should be avoided with St. Johns wart?

A 
oral contraceptives
antiepileptics
some HIV drugs
ciclosporin
warfarin
simvastatin
MAOIs and SSRIs
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27
Q

What are two food interactions?

A

cranberry juice and warfarin

grape juice and simvastin and some Ca-antagonists

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28
Q

what are the key warfarin interactions?

A

NSAIDs-increased risk of bleeding

antibiotics (esp erythromycin and ciprofloxacin) enhanced Gi bleeding

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29
Q

What are the key NSAID interactions?

A

warfarin

methotrexate- methotrexate toxicity

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30
Q

What should not be prescribe with ACE inhibitors?

A

potassium sparing diuretics

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31
Q

What should not be perescribed with verapamil?

A

beta-blockers-asystole

digoxin- digoxin toxicity

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32
Q

What can cause digoxin toxicity?

A

amiodarone and varapamil

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33
Q

what can cause myopathy?

A

statins and macrolides

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34
Q

What are the steps of WHO good prescribing?

A

Step 1: Define the patient’s problem
Step 2: Specify the therapeutic objective
What do you want to achieve with the treatment?
Step 3: Verify the suitability of your P-treatment
Check effectiveness and safety
Step 4: Start the treatment
Step 5: Give information, instructions and warnings
Step 6: Monitor (and stop?) treatment

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35
Q

What alternative approaches should be taken in renal impairment?

A

-Choose short acting agents (e.g. tolbutamide as a choice sulphonylurea)
-Gentamicin – increase the dosage interval in renal impairment
-Choose non-renally excreted alternatives
E.g. amlodipine in hypertension
Gliclazide in 2DM

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36
Q

What drugs should not be given in renal impairment and why?

A

-Some drugs must be avoided in renal impairment
e.g. metformin
-Some drugs require renal excretion to act may become ineffective in renal impairment
Thiazide diuretics

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37
Q

What drug does not cross the placenta?

A

heparin

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38
Q

what key drug types are issues in pregnancy?

A 
Anti-epileptics
Anticoagulants
Antibiotics –Antihypertensives - labetalol, nifedipine, methyldopa 
Antidiabetics – insulin
Metformin, glibenclamide
Antidepressants
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39
Q

what are the anti-epileptic drugs?

A

phenytoin
valporate
carbamazepine

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40
Q

What risks does phenytoin carry in pregnancy?

A
  • craniofacial abnormalities
  • hypoplasia of distal phalanges
  • growth deficiency
  • mental deficiency
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41
Q

What risk does valproate pose in pregnancy?

A

associated with neural tube defects

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42
Q

What risk does carbamazepine pose in pregnancy?

A

similar to phenytoin but decreased risk

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43
Q

What is the advice for prescribing for epilepsy in pregnancy?

A
  • Continuation of treatment is preferable - counselling
  • Or planned discontinuation
  • Carbamazepine was preferred (5mg folic acid given to reduce chances of neural tube defect)
  • Lamotrigine used first line in generalised tonic-clonic seizures to avoid teratogenic / interacting drugs
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44
Q

What drugs prevent oral contraceptives working?

A
  • AEDs: phenytoin, carbamazepine and phenobarbital

- rifampicin

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45
Q

What are the risks of warfarin in pregnancy?

A
  • chondroplasia punctata (altered bone growth)
  • optic atrophy
  • mental retardation
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46
Q

In which trimesters should warfarin be avoided?

A

1 and 3

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47
Q

What should be prescribe instead of warfarin in pregnancy?

A

LMWH

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48
Q

Aminophylline is used at 500 micrograms per kg per hour (and then adjusted accorded to monitoring)
how much would a 65kg man need?

A

500 micrograms x 65 x 1 = 32.5 mg per hour infusion

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49
Q

What does a 1% solution mean?

A

1g per 100ml

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50
Q

If a solution is 1% how much of the drug is in 2m?

A

20mg

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51
Q

If a solution is 2% how much of the drug is in 5ml?

A

100mg

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52
Q

what ration is equal to a 1% solution?

A

1:100

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53
Q

How much drug is there is a 1:200,000 ratio?

A

5 micrograms/ml

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54
Q

The standard adult dose for anaphylaxis is 500 micrograms i.m.
If the solution is given as 1:1000 how many pls should be administered?

A

So, with 1ml vial of 1:1,000 adrenaline the volume given would be 0.5 ml.
Reason: 1:1000 = 1 mg/ml and need to give 500 micrograms

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55
Q

What abbreviation is used for as required?

A

p.r.n

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56
Q

What are the different abbreviations for drug route?

A

po: oral
im: intramuscular
iv : intravenous
sc: subcutaneous
neb: nebuliser

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57
Q

Define hypertension

A

It may be defined as “A blood pressure which is associated with significant cardiovascular risk”

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58
Q

What can cause secondary hypertension?

A
  • renal disease
  • renovascular disease
  • Conn’s syndrome
  • Cushing’s syndrome
  • hyperthyroidism
  • phaeochromocytoma
  • pregnancy
  • Drugs ( e.g. NSAIDs, corticosteroids, sympathomimetics)
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59
Q

How does renal disease cause an increase blood pressure?

A

not excreting as much fluid

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60
Q

How does renovascular disease increase blood pressure?

A

narrowing renal artery causes an increase in RAAS

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61
Q

How does Conn’s syndrome increase blood pressure?

A

increase in aldosterone which is a fluid retaining hormone

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62
Q

How does Cushing’s syndrome increase blood pressure?

A
  • sodium retention

- increase sympathetic activation

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63
Q

How does hyperthyroidism increase blood pressure?

A

-increase sympathetic activity

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64
Q

What is pheochromocytoma?

A

adrenaline secreting tumor

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65
Q

What contributes to essential hypertension?

A
  • obesity
  • insulin resistance
  • excessive alcohol consumption
  • genetics
  • environment
  • fetal programming –>low birth weight
  • salt sensitivity
  • age
  • ethnicity
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66
Q

How does obesity increase blood pressure?

A

production of angiotensinogen from adipocytes

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67
Q

what are the NICE targets for hypertension treatment?

A
  • SBP < 140mmHg (<140 mmHg in diabetes; <130 mmHg with complications)
  • DBP < 90mmHg (<80mmHg in diabetes)
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68
Q

What is blood pressure the product of?

A

cardiac output x total peripheral resistance

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69
Q

Describe the RAAS pathway?

A
  • Renin is released due to low BP, low Na+ or activation of beta-adrenoreceptors
  • renin converts angiotensinogen into Angiotensin I
  • ACE converts AI into angiotensin II
  • Angiotenin II stimulates the release of aldosterone and causes vasoconstriction
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70
Q

Does vasoconstriction increase cardiac output or total peripheral resistance?

A

total peripheral resistance

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71
Q

When should ACEi not be prescribed and why?

A

renal disease –> blood pressure is very dependent on RAAS so if use ACEi then BP will drop substantially

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72
Q

What may ACEi do to electrolyte levels?

A

increase potassium –> decrease aldosterone causes sodium lose and potassium retention

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73
Q

When should ACEi be considered particularly protective?

A

in DM against nephropathy

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74
Q

What is an alternative to ACEi which do not cause a cough?

A

AT1 receptor antagonists

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75
Q

What do AT1 receptor antagonists block?

A

AII

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76
Q

What are the two types of Calcium channel blocker?

A
  • rate-limiting –> effects on heart and vascular smooth muscule
  • dihydropyridines –> more on vascular smooth muscle
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77
Q

Give an example of a rate limiting calcium channel blocker?

A

verapamil

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78
Q

Give an example a DHP

A

amlodipine

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79
Q

What is a contraindication of rate limiting CCB?

A

heart failure

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80
Q

When are right limiting CCB used?

A

ischaemic heart disease

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81
Q

Which diuretic are second line antihypertensives?

A

thiazide-like

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82
Q

How do diuretics lower blood pressure?

A

Inhibit Na+/Cl- in distal convoluted tubule so secrete more sodium and water

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83
Q

What are the side effects of diuretics?

A
  • Hypokalaemia (monitor potassium)
  • Postural hypotension
  • Impaired glucose control
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84
Q

How do alpha blockers work?

A

competitive receptor antagonists of a1-adrenoreceptors on cardiac muscle

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85
Q

How do beta blockers work?

A
  • Reduction in sympathetic drive to the heart, reducing cardiac output
  • A reduction in sympathetically evoked renin release
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86
Q

What are the side effects of beta blockers and why?

A

Blockade of peripheral b2-adrenoceptors opposes vasodilatation to skeletal muscle ~ cold extremities and fatigue

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87
Q

what is an example of a beta blocker?

A

atenolol

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88
Q

What are the adverse effects of ACEI?

A
  • Cough
  • Severe first dose hypotension
  • Renal damage (monitor eGFR)
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89
Q

What are the adverse effects of calcium channel blockers?

A
  • Peripheral oedema (vasodilation of peripheral small vessels)
  • Postural hypotension
  • Constipation (some due to calcium channels in GI tract)
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90
Q

What are the adverse effects of thiazides?

A
  • Diabetogenic
  • Alter lipid profile
  • Hypokalaemia
  • Postural hypotension
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91
Q

what are the adverse effects of beta-blockers?

A

bronchospasm

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92
Q

What are the adverse effects of alpha-blockers?

A
  • wide spread so poorly tolerated

- postural hypotension

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93
Q

Which antihypertensive do you use for diabetes?

A

ACEi

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94
Q

Which antihypertensive do you use for CHF?

A

ACEi

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95
Q

What antihypertensive do you use for IHD?

A

beta blocker

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96
Q

What are the ACD guidelines?

A
  • hypertension and type 2 diabetes and under 55 and not black = ACEi/ATRA. Then ACEi/ATRA + CCI or diuretic. Then ACEi/ATRA + CCI + diuretic
  • over 55 or black give CCI, then CCI +ACEi/ATRA or diuretic. Then ACEi/ATRA +CCI+ diuretic.
  • FINALSTEP- referral + spironolactone or alpha blocker or beta blocker
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97
Q

What are the risk factors for IHD?

A
  • Male gender
  • Family history
  • Smoking*
  • Diabetes mellitus*
  • Hypercholesterolaemia*
  • Hypertension*
  • Sedentary lifestyle*
  • Obesity *
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98
Q

What causes stable angina?

A

atherosclerotic disease, which limits the heart’s ability to respond to increased demand
symptoms on exertion but are relieved by rest

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99
Q

What causes unstable angina?

A

generally due to plaque rupture and the formation of a non-occlusive thromboembolism, or less commonly vasospasm (Prinzmetal angina)

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100
Q

What is the management for IHD?

A

Lifestyle advice directed at

  • Smoking cessation
  • Increased exercise
  • Healthy diet
  • Weight reduction of appropriate

Coronary artery bypass grafting (CABG) is the most effective approach

Angioplasty with stenting is also used
Using a balloon catheter to dilate / destroy the stenosis and insert a cage intraluminally to prevent restenosis

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101
Q

How do nitrates work?

A
  • nitrates release nitric oxide which activate GC increasing cGMP release
  • Venodilatation, leading to a decrease in preload and a reduction in cardiac work
  • Coronary vasodilatation, improves coronary blood flow
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102
Q

How do beta blockers affect coronary flow?

A

Coronary flow only occurs during diastole, then by slowing the heart the diastolic period will be increased, as will the time for coronary blood flow.

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103
Q

Why do CCB work in IHD?

A
  • Vasodilatation and improve coronary blood flow, so preventing symptoms.
  • Verapamil (and to a lesser extent diltiazem) also have myocardial depressant and bradycardic actions, so reducing cardiac work.
  • Verapamil also exerts Class IV anti-arrhythmic activity.
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104
Q

How does nicorandil work?

A

Nicorandil: combined NO donor and activator of ATP-sensitive K-channels.
The target is the ATP-sensitive K+-channel (KATP):
Potassium leaves the smooth muscle as a result causing hypo-polarisation

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105
Q

How does aspirin work?

A

Favours prostacyclin production over thromboxane as inhibits both endothelial and platelet cyclo-oxygenase (COX). Endothelial cell as nucleated and can regenerate COX, platelets lack nuclei and can not

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106
Q

How does clopidogrel work?

A

ADP receptor antagonist (prevents platelet aggregation)

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107
Q

When is clopidogrel prescribed?

A

Used in pts who can not receive aspirin (e.g. in asthma)

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108
Q

What is the pharmacological treatment of IHD?

A
  • Low dose aspirin and/or clopidogrel
  • BP controlled to < 140/85 mmHg
  • Hypercholesterolaemia (to < 5mmol/l, LDL below 3mmol/l, or a 30% reduction)
  • For symptomatic relief or occasional treatment, a GTN spray or sublingual tablets would be appropriate
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109
Q

What drug treatment is given for long term control of angina?

A

-1st choice: b-blockers for more pronounced stable and unstable angina
But not Prinzmetal angina
Oral long-acting nitrates might be added.
-2nd choice: if a b-blocker is ineffective or contra-indicated, then verapamil (or diltiazem) would be used or failing that a long-acting dihydropyridine (DHP).
Calcium channel blockers are particularity effective at reversing vasospasm
First choice drugs for Prinzmetal angina.
-In refractory disease: a b-blocker plus DHP but not with verapamil. Nicorandil might also be added to therapy.

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110
Q

How is unstable angina treated differently to stable angina?

A

addition of Low molecular weight heparin to therapy

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111
Q

What are the guidelines for pharmacological management of CHF?

A
  • All patients with Left ventricular systolic dysfunction should receive an Angiotensin-converting enzyme inhibitor (ACE inhibitor) and a Beta-blocker
  • All patients with oedema should receive a diuretic
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112
Q

How do ACE inhibitors work in CHF?

A
  • Reduce arterial and venous vasoconstriction (reduce after- and pre-load)
  • Reduce salt/water retention, hence reduce circulating volume
  • Inhibits RAAS, prevents cardiac remodelling?
  • Also used in hypertension
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113
Q

How do you prescribe ACEis?

A
  • Low dose then titrate up

- Monitor creatinine / eGFR and K+ before and during treatment

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114
Q

Which beta blocker is used in CHF?

A

bisoprolol

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115
Q

What type of diuretic is used in CHF?

A

loop

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116
Q

How do diuretics work in CHF?

A
  • Reduce circulating volume
  • Reduces preload on the heart
  • Relieve pulmonary and peripheral oedema
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117
Q

How does spironolactone work?

A
  • Spironolactone – mineralocorticoid (aldosterone) receptor antagonist (MRA)
  • Now being used as an effective agent which reverses the LVH
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118
Q

How does digoxin work?

A

+ve inotrope by inhibiting Na+/K+ ATPase, Na+ accumulates in myocytes, exchanged with Ca2+ leading to increased contractility.

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119
Q

which condition is digoxin good for?

A

AF

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120
Q

What does digoxin do in AF?

A

-Impairs AV conduction and increases vagal activity (via CNS).
-The heart block and bradycardia is beneficial in heart failure with atrial fibrillation
Slowing the heart rate improves cardiac filling

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121
Q

How do you monitor digoxin?

A

measure pulse and make sure >60bpm

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122
Q

What is the management for LV dysfunction?

A
  • ACEi/ATRA and a beta blocker
  • then add aldosterone antagonist or ATRA + ACEi or hydralazine plus nitrate
  • then add digoxin
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123
Q

How does warfarin work?.

A
  • Vitamin K essential for production of prothrombin and coagulation Factors (Vitamin K important for post-ribosomal carboxylation of glutamic acid residues of these proteins).
  • Warfarin blocks Vitamin K reductase, needed for Vit K to act as a cofactor (Vitamin K Epoxide Reductase Complex, VKORC):
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124
Q

When is warfarin used?

A
  • in patients with replaced heart valves
  • atrial fibrillation
  • PE
  • DVT
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125
Q

How is warfarin monitored?

A

INR

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126
Q

What can increased action of warfarin cause?

A

BLEEDING:

  • gastric
  • cerebral
  • haemoptysis
  • blood in faeces
  • blood in urine
  • easy bruising
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127
Q

How do heparins work?

A
  • Activate Antithrombin III (natural protein)

- Antithrombin – inactivates some clotting factors and thrombin by complexing with serine protease of the factors

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128
Q

What is the most important difference between warfarin and heparins?

A

warfarin can take several days to work whilst heparins work immediately

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129
Q

How do you monitor heparins?

A

APTT coagulation screen

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130
Q

How do you monitor DOACs?

A

you don’t have to

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131
Q

How do DACs work?

A

inhibit activated factor X

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132
Q

In which way is warfarin better than DOACs?

A

warfarin is easier to reverse with vitamin K

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133
Q

Describe the arachidonic acid pathway

A
  • Arachidonic acid in the membrane is split by PLA2 to create free AA
  • cyclo-oxygenase converts AA into endoperoxides
  • endoperoxides make prostaglandins. PGI2 in endothelial cells causes vasodilatation and prevents platelet aggregation but thromboxane in platelets causes platelet aggregation.
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134
Q

How is NO produced?

A

L-arginine + O2= NO + citrulline

by nitric oxide synthase

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135
Q

How does aspirin work?

A

inhibit COX (irreversible). Endothelial cells have a nucleus so can produce new COX hence PGI2 is still produced by endothelial cells but platelets do not have a nucleus and hence thromboxane is not produced

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136
Q

How does dipyridamole work?

A

Phosphodiesterase inhibitor. Phosphodiesterase breaks down of cAMP and cGMP which inhibit aggregation

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137
Q

What causes glycoprotein IIb-IIIa expression?

A

ADP binding to platelets

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138
Q

What does glycoprotein IIb-IIIa do?

A

binds bibringen to von Willebrand factor to cross-link platelets

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139
Q

How does clopidogrel work?

A

Blocks ADP receptor

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140
Q

How does Abciximab work?

A

monoclonal antibody against Gp IIb/IIIa

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141
Q

How does alteplase work?

A

breaks down fibrin by converting plasminogen into plasmin

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142
Q

What are the signs and symptoms of peptic ulceration?

A
  • Epigastric pain which may be precisely located by the patient by pointing.
  • Relationship of pain to food is variable
  • Hunger pain, which is relieved by eating.
  • Night pain which is relieved by food, milk or antacids.
  • Waterbrash – appearance of water in the mouth
  • Nausea and less frequently vomiting.
  • Vomiting blood.
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143
Q

What are the causes of peptic ulceration?

A
  • H.pylori

- NSAIDs

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144
Q

How do you test for H.pylori?

A
  • Urea breath test - 13C urea: pt given 13C urea and bacterial ureases convert it to 13CO2 which is absorbed and exhaled from the lungs
  • H.pylori antigens / antibodies in blood, saliva, stools.
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145
Q

What are the warning signs of serious disease with dyspepsia?

A

-Aged over 45 (or 55?) years
-Weight loss
-Anaemia
-Dysphagia (difficulty in swallowing)
-Haematemesis (vomiting blood)
-Melaena (tarry stools)
-Upper abdominal masses
-Persistent symptoms with repeat requests for OTC remedies
Onset of new symptoms

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146
Q

What stimulates gastric acid secretion?

A
  • Histamine via H2 receptors
  • Gastrin
  • Acetylcholine via M-receptors – M3 on parietal cells
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147
Q

What decreases gastric acid secretion?

A
  • Prostaglandins (E2 and I2)

- Also cytoprotective via bicarbonate and mucus release

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148
Q

what are examples of antacids?

A
  • sodium bicarbonate
  • magnesium hydroxide
  • aluminum hydroxide
149
Q

How does sodium bicarbonate work?

A

HCO3- + H+ =CO2 + H20

150
Q

How does magnesium hydroxide work?

A

Mg(OH)2 + 2HCl = MgCl2 + 2H2O

151
Q

How does aluminium hydroxide work?

A

Al(OH)3 + 3HCl = AlCl3 + 3H2O

152
Q

How do alginates work?

A

The alginic acid, when combined with saliva, forms a viscous foam which floats on the gastric contents forming a raft which protects the oesophagus during reflux.

153
Q

How do H2 receptors work?

A

Histamine H2 receptors: coupled via adenylyl cyclase to increase cAMP which activates the proton pump:

154
Q

Which H2 receptor antagonist is no longer used and why?

A

cimetidine –> drug interactions

155
Q

How do proton pump inhibitors work?

A

Widely used, act via irreversible inhibition of the proton pump (H+/K+-ATPase):

156
Q

What is a complication of PPIs?

A

Increased risk of Campylobacter infection (food poisoning) due to increased pH.

157
Q

What do pro kinetic drugs do?

A

Cause Gastric emptying

Movement of gastric contents from stomach to duodenum - drugs which do this will be of benefit in GORD.

158
Q

How does domperidone work?

A

increased closure of oesophageal sphincter (good for reflux disease) and opens lower sphincter.

159
Q

How does metocloperamide work?

A

acts locally to increase gastric motility and emptying (combined with analgesics to accelerate absorption

160
Q

What is the treatment for H.pylori?

A 
2 from: 
Metronidazole
Amoxicillin
Clarithromycin
	plus 
PPI and/or H2 antagonist.  
for 1 week and then PPI alone for a month
161
Q

How do you treat non-h.pylori dyspepsia?

A

Step 1: antacid or alginate and antacid
Step 2: H2 antagonist
Step3: proton pump inhibitor

162
Q

Why do NSAIDs cause peptic ulcers?

A

-block cox enzyme and so stop production of prostaglandins which are protective

163
Q

How does misoptostol work?

A
  • a stable PGE1 analogue, acts on prostanoid receptors to inhibit gastric H+ secretion.
164
Q

When is misoprostol prescribed?

A

with NSAIDs in at risk patients

165
Q

What is a contraindication of misoprostol?

A

females of child bearing age as it causes contractions

166
Q

What are the signs and symptoms of liver disease?

A
  • Jaundice and pruritus (hyperbilirubinemia)
  • Nausea and vomiting (hyperbilirubinemia)
  • Hepatomegaly
  • Ascites (build up of fluid in abdomen –> aldosterone is normally metabolised in the liver)
  • Dark urine and pale stools in cholestasis
  • Spider naevi in alcoholic liver disease
167
Q

What are the causes of liver disease?

A 
Infection
-Viral hepatitis
Adverse drug reaction
-Halothane
-Paracetamol overdose
-Clavulanic acid in ‘Augmentin’ - co-amoxiclav
-Valproate
-Amiodarone
-Herbals
Alcohol abuse
Obesity ~ cirrhosis
Cancer
-Primary or secondary (metastasis)
168
Q

What liver function tests measure hepatocyte health?

A

amionotransferases (alanine=ALT and aspartate =AST)

169
Q

What LFT measures obstruction?

A 
Alkaline phosphatatse (ALP)
Gamma-glutamyl transpeptidase (gamma GT)
170
Q

What LFT measures function?

A
  • albumin

- coagulation (INR)

171
Q

How does RBC breakdown occur?

A
  • iron and globing are reused, biliverdin is formed from harm and reduced o bilirubin
  • bilirubin is uncogaugated and water insoluble
  • the liver conjugates bilirubin to make it water soluble and excreted as bile
  • bile salts are used to emulsify fats via enterohepatic cycling
  • remaining bile is secreted as sterecobilinogen in stools
172
Q

Why do aminotransferases rise out to acute liver damage?

A

they are in high concentration in hepatocytes so if the liver is damaged they leak out

173
Q

Where is alkaline phosphatase usually present?

A

membranes of the liver

174
Q

When is alkaline phosphatase raised?

A
  • choleostasis

- metastasis of liver

175
Q

When is Gamma GTs raised?

A
  • induced by alcohol and some other drugs
  • cholestasis
  • cellular damaged
176
Q

What are the LFT results of acute hepatitis?

A
  • ALT & AST: increased
  • ALP: increased or normal
  • Bilirubin: increased or normal
  • GGT: increased or normal
  • Albumin: normal (long half life)
  • INR: increased or normal
177
Q

What are the LFT results for choleostasis?

A
  • ALP: increased
  • GGT: increased
  • Bilirubin: increased
  • ALT & AST: normal or increased
  • Albumin: normal
  • INR: normal or increased (reduced vit K absorption)
178
Q

What are the LFT results for chronic liver disease?

A
  • GGT: increased
  • Bilirubin: increased
  • Albumin: decreased
  • INR: increased
  • ALP, ALT & AST: normal or increased
179
Q

What is prehepatic jaundice?

A

Water insoluble unconjugated bilirubin produced faster than liver can conjugate it for excretion

180
Q

What can cause prehepatic jaundice?

A
  • Often due to haemolysis – haemolytic anaemias such as spherocytosis
  • Gilbert’s syndrome – 5% of pts have reduced levels of UDP-glucuronosyl transferase which conjugates bilirubin
181
Q

What is heptocellular jaundice?

A
  • Transaminases leak out
  • Liver can not convert insoluble bilirubin from the blood to water soluble bilibubin
  • Reduced bilirubin excretion
182
Q

Define cholestasis?

A

Bile cannot flow from the liver to the duodenum

183
Q

What are the types of cholestasis?

A

intraheptic or extra hepatic

184
Q

What can cause intrahepatic cholestasis?

A
  • Primary biliary cirrhosis: autoimmune damage to bile ducts
  • Hepatocellular damage
  • In pregnancy with unknown cause (~3rd trimester
185
Q

What can cause extra hepatic cholestasis?

A
  • Gallstones

- Carcinoma head of pancreas

186
Q

Why are stools pale and urine dark in obstructive jaundice?

A
  • can not excrete bilirubin in the bile=Pale stools

- Water soluble bilirubin excreted in the urine =Dark urine, Bilirubin in the urine confirms obstructive jaundice

187
Q

What is prescribed for jaundice and how does it work?

A

colestyramine –> bile binding agent and prevents it being recycled

188
Q

What complications can arise due to ascites?

A
  • oedema secondary to hypoproteinaemia
  • sodium retention due to secondary hyperaldosteronism
  • portal hypertension
189
Q

What is prescribed for ascites?

A

spironolactone (+ furosemide? + NaCl restriction due to aldosterone keeping sodium)

190
Q

What are the symptoms of encephalopathy?

A
  • Changes in personality
  • Disorientation
  • Confusion and drowsiness
  • Sensitivity to centrally acting drugs
191
Q

Why does encephalopathy occur due to liver disease?

A

The gut flora produce many nitrogenous products, including ammonia, which are normally cleared by the liver.

192
Q

What is prescribed for encephalopathy?

A

neomycin/metronidazole (anti-bacterial) and lactulose (flush bowel out or bacteria)

193
Q

What is prescribed for gastric bleeding and how does it work?

A

ranitidine (H2 receptor antagonists –> reduces acidity)

194
Q

What is prescribed for osophageal varicies?

A

beta blockers, octreotide

195
Q

What causes osophageal varicis?

A

increased portal vein pressure

196
Q

What are the common causes of diarrhoea?

A
  • Rotavirus: damages small bowel villi
  • Invasive bacteria: damage epithelium.
  • Adhesive enterotoxigenic bacteria: adhere to brush border, increase cAMP leading to Cl- and Na+ secretion followed by water:
  • antibiotics
  • orlistat
  • PPIs
197
Q

What is oral rehydration therapy?

A

Solution of electrolytes to replace the electrolytes lost in diarrhoea e.g. Dioralyte.
Must be isotonic
Glucose allows transport of Na via a symporter

198
Q

why may anti motility agents not be prescribed in diarrhoea?

A

In infection they may reduce clearance of infective organisms from the GI tract, possibly prolonging infection.

199
Q

How do opioids work as anti motility agents?

A

Reduce tone and peristaltic movements of GI muscle by inhibiting presynaptically (via µ-opioid receptors) the release of acetylcholine which allows more time for water reabsorption

200
Q

How do osmotic laxatives work?

A

Enters the colon unchanged and converted by bacteria to lactic and acetic acid - raise fluid volume osmotically.

201
Q

How does magnesium work as a laxative?

A
  • Osmotic effect.

- Mg2+ also release cholecystokinin which increases GI motility.

202
Q

How does Senna work?

A

Senna extracts, enter colon metabolised to anthracene derivatives which stimulates GI activity.

203
Q

What is IBS?

A
  • This is a common, long-standing disorder
  • Present for at least 12 weeks within 1 year
  • Pain, bloating - relieved by defecation
  • Episodes of diarrhoea and/or constipation.
204
Q

How is IBS treated?

A

-Lactulose or loperamide for respective symptoms?
-Antispasmodic agents:
Antimuscarinics e.g. inhibit parasympathetic activity
-Mebeverine: direct relaxant of GI smooth muscle - probably acting as a phosphodiesterase inhibitor:
-Amitriptyline (TCA)
Low doses widely used + effective
Provide some pain relief
Antimuscarinic effects
Alters the sensitivity of sensory nerves in low GIT?

205
Q

What is inflammatory bowel disease?

A

Encompasses both ulcerative colitis and Crohn’s disease

206
Q

What are the clinical features of inflammatory bowel disease?

A
  • Diarrhoea
  • Faecal incontinence
  • Rectal bleeding, bloody diarrhoea
  • Passing of mucus
  • Cramping pains
  • Weight loss
  • In Crohn’s disease there may also be mouth ulcers and anal skin tags
207
Q

What are the complications of crohn’s disease?

A

there may be malabsorption, leading to deficiencies of folate, and iron associated with iron-deficiency anaemia respectively.

208
Q

What are the complications of ulcertative colitis?

A

Blood loss in ulcerative colitis may also lead to iron-deficiency anaemia.

209
Q

What conditions are associated with inflammatory bowel disease?

A

arthritis, uveitis and an increased risk of thromboembolism

210
Q

What is ulcerative colitis?

A
  • Inflammation which involves the rectum and spreads to the colon.
  • Inflammation tends to be superficial, affecting the mucosa.
211
Q

What is Crohn’s disease?

A
  • May affect any part of the GI tract but mostly the ileum and / or colon are involved.
  • T-lymphocytes are activated and lead to transmural inflammation and the extensive involvement may lead to the formation of fistulae.
212
Q

How do 5-aminosalicylates work?

A

inhibits leukotriene and prostanoid formation, scavenge free radicals, decrease neutrophil chemotaxis.

213
Q

What else can be used to treat IBD?

A

corticosteroids and immunosuppressants

214
Q

What is mesalazine?

A

5-aminosalicylate

215
Q

How do you cancel a patient for Mesalazine?

A

Risk of blood dyscrasia, pts should report:

  • Sore throats
  • Fevers
  • Easy bruising or bleeding

Aminosalicylates are associated with side effects which include rashes, headaches, and diarrhoea.

216
Q

What is aziothioprine?

A

immunosuppressant

217
Q

What are the risks and how do you cancel for azithioprine?

A 
-Risk of pancreatitis
Requires FBC monitoring (6-8 weeks)
-Counsel risk of myelosuppression
Bruising &amp; bleeding
Infections
218
Q

How do you monitor methotrexate use?

A
  • Full blood count, renal function and LFT
  • Report fever/cough – may indicate infection due to neutropenia
  • Report cough/dyspnoea – may indicate pulmonary toxicity
219
Q

What is asthma?

A

It is defined as reversible increases in airway resistance, involving bronchoconstriction and inflammation

220
Q

How is asthma characterised?

A

Characterised by reversible decreases in the FEV1:FVC (less than 70-80% suggests increased airway resistance)
Variations in PEF which improve with a b2 agonist (+ morning dipping)

221
Q

How is bronchial calibre controlled?

A

Parasympathetic

  • Acetylcholine (A.Ch.) acts on muscarinic M3–receptors:
  • Bronchoconstriction
  • Increase mucus

Sympathetic

  • Circulating adrenaline acting on beta2-adrenoceptors on bronchial smooth muscle to cause relaxation
  • Plus sympathetic fibres releasing noradrenaline (NA), acting at b2-adrenoceptors on parasympathetic ganglia to inhibit transmission
  • Beta2-adrenoceptors also on mucus glands to inhibit secretion
222
Q

What is COPD?

A
  • It is a combination of Chronic bronchitis + Emphysema in varying proportions
  • Chronic bronchitis – increased mucus, airway obstruction, intercurrent infections
  • Emphysema – involves destruction of alveoli
223
Q

What are the characteristics of COPD?

A
  • FEV1 is reduced

- There is little variation in PEF

224
Q

What are the clinical features of asthma?

A
  • Wheezing
  • Breathlessness
  • Tight chest
  • Cough (worse at night /exercise)
  • Decreases in FEV1, reversed by a b2-agonist
225
Q

Describe the pathophysiology of an asthma attack

A
  • mast cells and mononuclear cells are activated
  • release of spasmogens causes bronchospasm which results in the early phase
  • at the same time chemotaxis are released resulting in the inflammatory response recruiting white cell and so causing the late phase response hours later
226
Q

What are the spasmogens?

A
  • histamine
  • prostaglandin
  • leukotrines
227
Q

Which enzyme produces prostaglandins?

A

COX

228
Q

Which enzyme produces leukocytes?

A

LOX

229
Q

What are the chemotaxis?

A

leukotriene

230
Q

How does salbutamol work?

A

B2 adrenoreceptor agonist –> increase cAMP

231
Q

What are xanthine?

A

bronchodilators- given iv in an emergency

232
Q

What is an example of a xanthine?

A

aminophylline

233
Q

What is reflumilast?

A

selective PDE IV inhibitor (stops breakdown of CAMP)

234
Q

When is reflumilast used?

A

COPD

235
Q

How do Muscurinic M-receptor antagonists work?

A

-block parasympathetic bronchoconstriction.

236
Q

how do corticosteroids work in asthma?

A

preventativ- anti-inflammatory by activation of intracellular receptors, leading to altered gene transcription (decrease cytokine production) and production of lipoortin which interfere with the arachidonic acid pathway by inhabitation of PLA2 which converts membrane arachidonic acid into free AA

237
Q

Why are steroids given with Beta2-agonists?

A

reduces receptor down-regulation

238
Q

what are the side effects of steroids?

A

-throat infections, hoarseness

239
Q

How do leukotriene receptor antagonists (LTRA) work?

A

work as a relieved a receptor and prevent leukotrienes causing bronchospasm

240
Q

What is the stepwise treatment of asthma?

A

Step 1: short acting B2 agonist plus regular inhaled steroid
Step 2: + trial of long actin beta 2 against or LTRA or xanthine
Step 3: increase steroid dose
Step 4: add oral steroid

241
Q

What is the treatment for COPD?

A
  • bronchodilators (shot and long acting)
  • inhaled steroids? (biology of disease makes less effective but effective in 15%)
  • antibiotics for intercurrent infections
  • stop smoking
  • oxygen therapy
242
Q

What are the stepwise guidelines for COPD?

A

Step 1: short acting beta agonist or short-acting antimuscurinic as required
Step 2: if FE1> 50% add long-acting beta2 agonist or long-actin antimuscurinic instead of short acting. If FEV1<50% then add long acting beta agonist and inhaled steroid or replace short acting antimuscurinic with long acting antimuscurinic
Step 3: long acting antimuscurinic plus long acting beta 2 agonist plus inhaled steroid

243
Q

How can NSAIDs cause asthma attacks?

A

they can increase leukotriene production as they inhibit cox enzyme so arachidonic acid is converted into leukotrienes

244
Q

What is the time course of human insulin analogues?

A

have a rapid onset but short duration of action

245
Q

When are human insulin analogues used?

A
  • May be injected just before a meal or when necessary just after a meal.
  • Increase flexibility and are useful for pts prone to pre-lunch hypoglycaemia and those who tend to eat late in the evening and may be at risk of nocturnal hypoglycaemia.
246
Q

What is the time course of short acting insulins?

A

Soluble insulins have relatively short-lived effects of 6-8 hours, with peak effects at 2-5 hours.

247
Q

How can you create intermediate and long-acting insulins?

A
  • Combination of insulin with protamine gives rise to intermediate acting insulin (isophane insulin)
  • binding to zinc gives intermediate to long acting insulin
  • combination with protamine plus zinc gives long-acting insulin.
  • Crystalline insulin zinc suspensions are also long-acting.
  • Biphasic preparations contain both an intermediate-acting agent (e.g. isophane insulin) with a shorter acting form (e.g. soluble insulin).
248
Q

Describe a twice daily regime of insulin

A

2 daily injections, one 30 minutes before breakfast and one before the evening meal of short- and longer-acting insulins in combination, with two thirds of the insulin given as the morning dose. This is the most common regimen.

249
Q

Describe the basal bolus regimen

A

a single dose of medium-acting insulin is given at bedtime and doses of short acting insulin are given 30 minutes before each meal. This allows more flexibility with the timing of meals

250
Q

What is the lifestyle advice for type 2 diabetes?

A
  • to reduce the amount of simple carbohydrates in the diet
  • limit the intake of mono and disaccharides, increase non-starch polysaccharides
  • reduce the intake of fat to reduce the risk of atherosclerosis, such that fat is 30-35% calorific intake and carbohydrate is 50-55% .
  • weight loss in obese
  • increased exercise
251
Q

How long do you wait for lifestyle changes to take effect before moving onto medication for type II DM?

A

3 months

252
Q

How do sulphonylureas work?

A
  • Inhibit ATP-sensitive potassium (KATP) channels.
  • Glucose leads to ATP production which inactivate these channels, leading to cellular depolarisation, which results in calcium influx and insulin secretion.
  • When glucose is low, ATP levels fall and ADP rises, channels open, with membrane hyperpolparization and this decreases insulin release.
  • Sulphonylureas bind to a receptor associated with these channels, resulting in channel closure, which leads to insulin release.
253
Q

What are the side effects of sulphponylureas?

A

-Cause weight gain (+increase insulin resistance), often avoided in obesity
-Awareness may be lost when using beta-blockers
-Associated with causing hypoglycaemia, especially
in the elderly,with long acting agents such as glibenclamide and missing meals

254
Q

How dod meglitinide analogues work?

A

These also act on beta-cells but at a site distinct from the sulphonylurea receptor to cause closure of the KATP-channels, leading to depolarisation and insulin release.

255
Q

What is the time course of meglitinide analogues?

A

Rapid rate of onset and are given at meal times to stimulate post-prandial insulin secretion, which is relatively short-lived.

256
Q

What is another name for meglitinide analogues?

A

prandial glucose regulators (PGRs).

257
Q

What kind of drug is metformin?

A

biguanide

258
Q

When is metformin recommended?

A

in obese patients as does not cause weight gain

259
Q

When is metformin contraindicated?

A

renal impairment

260
Q

How do thiazolindiediones work?

A

Activate nuclear peroxisome proliferator-activated receptors gamma (PPAR-g), which alters gene expression and results in insulin-like effects.
‘Insulin sensitisers’ which work by enhancing glucose utilization in tissues, and so reduce insulin resistance

261
Q

What are the effects of thiazolindieiones?

A
  • reduced hepatic glucose output
  • increased glucose transporters (GLUT) in skeletal muscle with increased peripheral glucose utilization
  • Increased fatty acid uptake into adipose cells
262
Q

What is the stepwise management of DM II?

A

step 1:diet
step2: metformin if normal renal function or sulphonylurea if renal function poor
step 3: 2 from metformin, sulphonylureas or glitazonne

263
Q

How do thionamides work?

A

Decrease the production of thyroid hormones by inhibiting the iodination of thyroglobulin and this occurs via inhibition of thyroperoxidase.

264
Q

What is a complication of thionamides?

A

May cause agranulocytosis leading to leucopenia.
If patients report with sore throats, mouth ulcers, bruising or non-specific illness, a full blood count should be carried out and the drug withdrawn if there is leucopenia.

265
Q

Why are beta-blockers used in hyperthyroidism?

A

They will reduce the actions of catecholamines at beta-adrenoceptors, which are augmented in this condition. Non-selective beta-blockers (e.g. propranolol) are required to relieve the tremor.

266
Q

What is the block and replace regime for hyperthyroidism?

A

-high foes carbimazole to suppress all thyroid activity then add thyroxine to treatment

267
Q

How do glucocorticoids act?

A
  • Inhibit synthesis of COX-2 and inducible nitric oxide synthase
  • Inhibit synthesis of cytokines (interleukins, tumour necrosis factor) and chemokines
  • Stimulate production of lipocortin (which inhibits PLA2 and the synthesis of prostaglandins leukotrienes)
268
Q

What are the uses of glucocorticoids?

A

Anti-inflammatory / immunosuppressive therapy

  • Allergic/ septic emergency i.v.
  • Asthma, COPD – inhaled, oral (see Asthma tutorial)
  • Ulcerative colitis, Crohn’s disease – oral, rectal (see lower GI tutorial)
  • Rheumatoid arthritis - oral
  • Skin conditions, e.g eczema, psoriasis – topical, oral
  • Organ transplantation
  • Others, inc. rhinitis, conjunctivitis

Replacement therapy
-Addison’s disease – need for steriod replacement, life-long.

Others

  • Neoplastic disease
  • Pre-term labour (enhance fetal lung maturation)
269
Q

What are the side effects of oral glucocorticoids?

A
  • Diabetes
  • Osteoporosis
  • Mental disturbances
  • Peptic ulceration (esp. with NSAIDs)
  • Visual: cataract and glaucoma
  • Cushing’s syndrome (at high doses)
  • Suppression of growth (children)
  • Adrenal suppression – sudden withdrawal can cause acute adrenal insufficiency, hypotension and death
  • Infections- increased susceptibility/ severity, particularly chickenpox (and measles)
270
Q

What are the side effects of mineralocorticoids and why?

A
  • Sodium and water retention
  • With potassium loss
  • And may cause hypertension/ worsen CHF
271
Q

What is hypercholestolemia?

A

elevated plasma cholesterol

272
Q

What is atherosclerosis?

A

focal lessons (plaques) on the inner surface of an artery.

273
Q

What diseases does atherosclerosis lead to?

A
  • Ischaemic heart disease (IHD)
  • Peripheral vascular disease (PVD)
  • Cerebrovascular disease
274
Q

What are the risk factors for atherosclerosis?

A
  • Genetic
  • Hypercholesterolaemia (raised LDL or lowered HDL)*
  • Hypertension*
  • Smoking*
  • Obesity*
  • Hyperglycaemia*
  • Reduced physical activity*
  • Infection??
275
Q

What drugs can cause dyslipidaemia?

A
  • Beta-blockers
  • Thiazides
  • Corticosteroids
  • Retinoids - monitor
  • Oral contraceptives
  • Anti HIV
276
Q

What are lipoproteins?

A

transport lipids

277
Q

What are the types of lipoproteins?

A

HDL, LDL, VLDL

278
Q

What does HDL do?

A

good cholesterol- mops up cholesterol from around the body and takes it to the liver

279
Q

What is xanthomata?

A

lipid deposits on eyelids

280
Q

How does atherosclerosis form?

A
  • risk factors cause damage to endothelium
  • LDL binds to receptor on endothelium in normal way
  • damage to endothelium causes monocyte and macrophages to migrate to the sub endothelial level and release ROS.
  • This oxidises LDL which damages the LDL receptor
  • there is poor delivery of cholesterol so it starts to accumulate below the endothelium
  • cholesterol rich plaque with connective tissue forms
281
Q

What are the non-pharmacological managements for high cholesterol?

A

Modify risk factors:

  • Stop smoking
  • Treat HT/DM
  • Exercise
  • Drug-induced?

Low cholesterol diet
- but only 25-30% of cholesterol comes from diet (rest synthesised by liver)

282
Q

How do statins work?

A
  • HMG-CoA Reductase Inhibitors
  • HMG-CoA reductase is the 1st committed step in cholesterol synthesis
  • Reduce plasma cholesterol
  • The reduction in hepatic cholesterol synthesis leads to an upregulation of hepatic LDL receptors, promoting LDL uptake
283
Q

What is a genetic cause of hypercholesterolaemia?

A

homozygous familial hypercholesterolaemia,

284
Q

How is treatment for homozygous familial hypercholesterolaemia different?

A

Less effective in homozygous familial hypercholesterolaemia, can not make LDL receptor.
Atorvastatin may be effective.
Statins effective in heterozygous disease

285
Q

How do statins not prevent the production of necessary cholesterol at other sites?

A

Statins are hepatoselective

  • the liver is the main site of cholesterol synthesis, extrahepatic sites synthesise essential cholesterol
  • 1st pass metabolism: 5% reaches systemic circulation
286
Q

what is the common prescription for high risk cardiovascular patient?

A

stain, aspirin, Beta-bloker and ACEi

287
Q

What is the NICE guideline for prescribing statins?

A

> 10% risk CVD in next disease

288
Q

When should statins be taken and why?

A

Taken at night

offsets a nocturnal increase in cholesterol synthesis

289
Q

Which statin does not need to be taken at night?

A

atorvastatin

290
Q

when do you give high intensity statin vs low intensity?

A

high intensity after a cardiac arrest

291
Q

what is a caution for statin?

A

liver dysfunction –> monitor all patients for liver dysfunction

292
Q

what is another risk for statins?

A

-rhabdomyolysis (break down of muscle which can cause renal failure due to toxin release)

293
Q

What increases risk of rhabdomyolysis with statins?

A

fibres

294
Q

What does simvastatin interact with?

A
  • Contraindicated with macorlides
  • Interaction with amlodipine, verapamil, diltiazem

For amlodipine plus statin:
Pravastatin does not interact
Use 20mg simvastatin as maximum dose

295
Q

How do fibrates work?

A
  • Activate: PPAR-a, alters lipoprotein metabolism
  • promote breakdown in VLDL (with small reductions in LDL and increase in HDL).
  • Also reduce trigycerides – used with statins when TGs (+ cholesterol) raised
  • Decrease glucose, use in DM
296
Q

What are the adverse effects of fibres?

A

rhabdomyolysis.

297
Q

When can cholesterol absorption inhibitors be used?

A

in conjunction with a statin

298
Q

Why are fibres not commonly used?

A

reduce IHD but not mortality

299
Q

How does sitostanol work?

A
  • A functional food
  • Present in Benecol margarine
  • Prevents absorption of cholesterol
  • Reduces LDL cholesterol by 10-15%
  • Helpful add on to dietary restrictions and statin therapy
300
Q

what is the stepwise management of dyslipidaemia?

A
  • if hypercholesterolaemia give statin and lifestyle changes
  • if hypertriglyceridaemia alone lifestyle alone and then if that doesn’t work then add a statin
  • if this doesn’t work add ezetimibe (cholesterol absorption inhibitor)
301
Q

How do SSRIs work?

A

Selectively inhibit the neuronal reuptake of 5-HT, thus enhancing synaptic concentrations of 5-HT and downregulating presynaptic 5-HT receptors.

302
Q

How do tricyclic antidepressants work?

A

Inhibit the neuronal uptake of noradrenaline and 5-HT, leading to augmented concentrations in the synaptic cleft.

303
Q

What are the side effects of TCAs?

A
  • dry mouth
  • blurred vision
  • constipation
  • urinary retention
  • sedation
304
Q

In what patients are TCAs contraindicated and why?

A

-TCAs may cause cardiac effects such as QT interval prolongation and the potentiation of catecholamines also predisposes to heart block and arrhythmias.
dangerous in overdose.
-They are not suitable for patients with ischaemic heart disease, aged over 70 years or those patients who are thought to be at high risk of attempting suicide.

305
Q

When are noradrenaline reuptake inhibitors used?

A

Useful for patients who cannot take TCAs but are resistant to the effects of SSRIs.

306
Q

How do serotonin-noradrenaline reuptake inhibitors work and how are they better than TCAs?

A

Inhibits serotonin and noradrenaline reuptake but fails to bind to additional receptors - fewer side-effects ( lack of sedative and antimuscarinic side-effects but does cause gastrointestinal side-effects).

307
Q

What Asan adverse effect of SNRIs?

A

hypertension

308
Q

How do noradrenergic and specific serotonergic antidepressants work?

A

Exhibits alpha2-adrenocepter antagonist activity, inhibiting negative feedback by these presynaptic receptors and thus producing an increase in noradrenaline and 5-HT transmission.

309
Q

How do serotonin receptor modulators work?

A

Inhibition of serotonin reuptake and the selective inhibition of postsynaptic serotonin receptors.

310
Q

How do mono-amine oxidase inhibitors work?

A

MAOIs inhibit the monoamine oxidases, which increases the concentration of these neurotransmitters.MAOIs also prevent the breakdown of the indirectly acting sympathomimetic amine, tyramine (from diet) - causes the release of catecholamines and leads to a hypertension.

311
Q

What are the step managements for Depression?

A

Step 1: if mild give CBT otherwise SSRI

Step 2: alternative SSRI or reboxetine (NRI) or mitazapine (NaSSA) or TCA

312
Q

What is firstling bipolar treatment?

A

lithium

313
Q

When is lithium contraindicated?

A

renal impairment

314
Q

What other drugs are used for bipolar?

A
  • anticonvulsants

- neuroleptics (antipsychotics)

315
Q

What can be used for sympathetic relief of annuity ?

A
  • propanolol (beta blocker)

- benzodiazepines

316
Q

How does buspirone work?

A

Buspirone activates 5-HT1A­ receptors, binds to dopamine receptors.

317
Q

what does buspirone treat?

A

Anxiety

318
Q

what are the side effects of buspirone?

A
  • dizziness
  • nausea
  • headache
319
Q

What is the treatment for generalised seizures?

A
  • 1st choice valproate or carbamazepine or lamotrigine (in females of childbearing age)
  • 2nd levetiracetam
320
Q

What is the treatment for absence seizures ?

A

1st choice: ethosuximde

2nd choice: valproate/lamotrigine

321
Q

How does valproate work?

A
  • Potentiates GABA

- Causes Na-channel blockade

322
Q

What are the side effects of valproate?

A
  • sedation
  • weight gain
  • tremor
  • liver damage (monitor)
323
Q

How does carbamazepine work?

A

use-dependent blockade of NA-channels

324
Q

What are the side effects of carbamazepine?

A
  • rashes
  • dizziness
  • double vision
325
Q

What is the issue with phenytoin?

A

Many side effects

  • increased gum growth
  • nystagmus a toxic effect

Associate with causing birth defects

Zero order kinetics
-metabolism saturates and so get disproportionate increases in plasma concentration on increasing dose
-Rates of metabolism varies between patients
– requires plasma conc monitoring

326
Q

How does lamotrigine work?

A

-use-dependent blockade of Na-channels, reduces release of glutamate

327
Q

What is the risk of lamotrigine?

A

bone marrow toxicity

328
Q

How can you detect bone marrow toxicity?

A

rash/flu like illness

329
Q

What monitoring is required for anti-epileptic drugs?

A

Haemtological effects

  • Many may cause leucopenia (fever, sore throat, rash, mouth ulcers )
  • FBC should be monitored
  • If severe leucopenia, withdraw under cover of another drug
  • Lamotrigine – associated with aplastic anaemia
  • Valproate – may cause thrombocytopenia

Liver

  • Carbamazepine & valproate may affect hepatic function ~ altered liver function tests (LFTs)
  • LFT (essential with valproate) & INR monitoring

Skin

  • May cause rashes
  • More serious may cause Stevens-Johnson syndrome; toxic epidermal necrolysis (carbamazepine, lamotrigine, phenytoin, valproate)
330
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

331
Q

What are the causes of acute pain?

A
  • injury

- post-operative flare

332
Q

What are the types of chronic pain?

A
  • nociceptive
  • neuropathic
  • visceral
  • mixed
333
Q

What are the examples of nociceptive pain?

A
  • osteoarthritis

- rheumatoid arthritis

334
Q

What are the different types of neuropathic pain?

A

central and peripheral

335
Q

What causes central neuropathic pain?

A
  • post-stroke
  • multiple sclerosis
  • spinal cord injury
  • migraine
  • HIV
336
Q

what causes peripheral neuropathic pain?

A
  • post-herpetic neuralgia

- diabetic neuropathy

337
Q

what causes visceral pain?

A
  • internal organ
  • pancreatitis
  • inflammatory bowel syndrome
338
Q

What causes mixed pain?

A
  • lower back
  • cancer
  • fibromyalgia
339
Q

Describe the WHO pain ladder

A

Step 1: simple analgesics e.g. Aspirin and paracetamol
Step 2: opioids suitable for use in mild to moderate pain +simple analgesics
step 3: opioids suitable for sever pain +simple analgesics

340
Q

What are the actions of paracetamol?

A

Analgesic and antipyretic actions

341
Q

What is the treatment for paracetamol overdose?

A

acetylcysteine

342
Q

How do NSAIDs work?

A

Inhibit cyclo-oxygenase (COX) responsible for arachidonate metabolism to cyclic endoperoxides, preventing formation of prostaglandins and thromboxanes

343
Q

What are the actions of NSAIDs?

A

Analgesic, antipyretic and anti-inflammatory properties

344
Q

What are the adverse effects of NSAIDs?

A

GI tract:

  • GIT erosion and ulceration
  • Ibuprofen (< 1200 mg daily) has best GI profile

Renal

  • Reduce renal blood flow
  • Acute renal failure
  • Sodium, potassium and water retention

‘A’ (airway) Respiratory-Bronchospasm

‘B’ (blood) Haematological
-Reduce platelet aggregation
Aspirin - Irreversible
NSAIDs - Reversible

345
Q

Why is dicofenac not suggested to be prescribed?

A

increases cardiac risk

346
Q

What are the weak opioids?

A
  • Codeine
  • Dihydrocodeine
  • Tramadol (po)
347
Q

What are the strong

opioids?

A
  • Morphine
  • Diamorphine
  • Oxycodone
  • Buprenorphine
  • Fentanyl
348
Q

Why do some people not respond to codeine?

A

Codeine metabolised to morphine via Cyp P450 2D6

  • 10 % Caucasian population unable to convert
  • 90 % Chinese population unable to convert
349
Q

What are the opioid adverse effects?

A
  • Nausea & vomiting
  • Constipation
  • Sedation
  • Respiratory depression (overdose)
  • Hypotension
  • Urinary retention

Need to anticipate adverse effects and provide treatment

350
Q

What are the steps for prescribing morphine?

A

Pain assessment, including current analgesia

Determine opioid requirement

  • Use short acting preparation, regularly plus prn doses
  • E.g. 5 mg 4 – 6 hr, 5 mg prn
  • onvert total daily dose to Modified release formulation
  • Taken every 12 or 24 hours
351
Q

What is breakthrough pain?

A

Transient exacerbation or recurrence of pain in patient who has mainly stable or adequately relieved background pain

  • End of dose failure
  • Incident pain
  • Spontaneous, unpredictable pain
352
Q

How do you treat breakthrough pain?

A
  • 10% total daily regular dose prescribed prn

- Marked variability between patients (5 – 20%)

353
Q

How do you convert to an alternative opioid?

A
  • palliative care section of BNF
  • Determine 24 hour requirement
  • Use conversion factor for alternative opiate to determine new 24 hour requirement
  • Convert to appropriate dosage regimen
354
Q

What drugs are used for patient controlled analgesia?

A
  • morphine

- Tramadol, oxycodone or fentanyl if morphine allergy

355
Q

What are the advantages of patient controlled analgesia?

A
  • Rapid analgesia once pain at steady state
  • Ready prepared
  • Patient satisfaction
  • No dose delay
  • Patient acceptability
  • No peaks or troughs
356
Q

What are the disadvantages of patient controlled analgesia?

A
  • Expensive
  • Requires IV access
  • Training
  • Monitoring
357
Q

What is given in an epidural usually?

A

Commonly fentanyl with (levo)bupivicaine (local anaesthetic + opioid)

358
Q

What are the adverse effects?

A
  • hypotension
  • wrong route
  • infection
359
Q

How do syringe drivers work?

A

continuous subcutaneous infusion

360
Q

what are the indications for syringe drivers?

A
  • Unable to take medicines by mouth (e.g. N&V, dysphagia)
  • Bowel obstruction
  • Patient does not wish to take regular medication by mouth
361
Q

What is used for syringe drivers?

A

Diamorphine is opioid of choice due to excellent aqueous solubility

Possible to mix with other drugs:

  • Haloperidol, cyclizine (N&V)
  • Levomepromazine, midazolam (restlessness & confusion)
  • Midazolam (seizures)
  • Hyoscine N-butylbromide (excessive respiratory secretions)
362
Q

How do you monitor opioid therapy?

A
  • Pulse
  • BP
  • Respiration rate
  • Oxygen saturation
  • Pain intensity
  • Sedation score
  • Opioid usage
  • Opioid side effects
363
Q

How does tramadol work?

A 
mum agonist (30 % of analgesic effect)
Inhibits noradrenaline uptake and 5-HT release
364
Q

How do you manage an opioid overdose?

A

naloxone –> Opioid antagonist

Higher affinity for opioid receptor than agonist

365
Q

What are the symptoms of neuropathic pain

A
  • Burning
  • Electric shock
  • Pins and needles
  • Scalding
  • Shooting
  • Stabbing
366
Q

What are the signs of neuropathic pain?

A
  • hyperalgesia (more sensitive to pain)

- allodynia (non-pain stimuli cause pain)

367
Q

What are the pharmacological treatments for neuropathic pain?

A
  • Tricyclic antidepressants
  • Anticonvulsants (Carbamazepine, Gabapentin, Pregabalin)
  • Opioids
  • Local anaesthetics
  • Capsaicin
368
Q

How do anticonvulsants work against pain?

A
  • Prevent voltage dependent Ca2+ channel activation in dorsal horn neurones
  • Do not affect voltage gated Na+ channels

CP1 (2 decks)

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