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Pharm ESA 4 > All Content > Flashcards

All Content Flashcards

1
Q

Define Pharmacokinetics.

A

The movement of a drug within the body.

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2
Q

What does ADME stand for?

A

Absorption
Distribution
Metabolism
Excretion

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3
Q

What is PK affected by?

A

Renal function
Liver function
Pyrexia

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4
Q

What is Bioavailability?

A

The percentage of drug that makes it into the desired body compartment from where it can have efficacy

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5
Q

What factors govern the distribution of a drug from the interstitium?

A
  • Blood flow - how vascularised a tissue is
  • Drug lipophilicity and hydrophilicity - lipophilic drugs can travel straight through a membrane, hydrophobic cannot
  • Protein binding eg. Warfarin to Albumin
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6
Q

How does protein binding affect distribution and efficacy?

A

Only free drug can cause a response.
Drug can be displaced from protein binding by another drug.
Relevant in Renal failure (hypoalbuminaemia), Pregnancy (fluid balance), Heart failure etc.

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7
Q

What does a high Vd (volume of distribution) mean?

A

Spread across the entire body and tissues - less in plasma

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8
Q

What does a low Vd mean?

A

Confined to the plasma

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9
Q

What is the equation for Vd?

A

Vd = dose/conc of drug in plasma

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10
Q

What drug has a particularly high Vd?

A

Digoxin

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11
Q

What is the relationship between half life and Vd?

A

T1/2 and Vd are proportional

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12
Q

Would a fat patient have a higher or lower Vd than a skinny patient? Would they need a higher or lower dose of drug?

A

Higher Vd, would need a higher dose of drug.

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13
Q

What is the Phase 1 of metabolism? Give examples

A

(CYP) P450 mediated drug modifications eg. oxidations
Most drugs are inactivated by this, but some can be activated (eg. Levodopa) and others can just be modified (eg. Codeine to Morphine)

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14
Q

Name one example of a CYP enzyme inhibitor, what CYP it inhibits and what this leads to.

A

Grapefruit juice.
Inhibits CYP3A4
Inhibits Statin metabolism

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15
Q

Name one example of how genetics can affect CYP metabolism.

A

CYP2D6
Affected by Race - 7% of whites don’t have, 30% of blacks have it over-active.
Metabolises antiarrhythmics, antidepressants and opioids

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16
Q

Define the “half life” of a drug.

A

The time in which the concentration of a drug in the plasma decreases by half.

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17
Q

Define the relationship between T1/2 and clearance

A

Inversely proportional - T1/2 goes up with reduced clearance (GFR).

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18
Q

Name 4 things that will affect the T1/2 of a drug.

A

Renal stenosis, Hepatic stenosis, Age (muscle mass), fat, Haemorrhage, DDIs

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19
Q

Describe First Order drug elimination kinetics.

A

Concentration dependent - a constant PROPORTION of drug is eliminated per unit time

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20
Q

Describe Zero Order drug elimination kinetics.

A

Independent of Concentration - a constant AMOUNT of drug is eliminated per unit time

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21
Q

What order elimination kinetics do most drugs exhibit?

A

First Order

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22
Q

What does alcohol do to elimination kinetics of aspirin and phenytoin?

A

Makes them zero order

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23
Q

What does CpSS stand for?

A

Steady state plasma concentration (of drug)

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24
Q

How many half lives does it take to reach CpSS?

A

5

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25
Q

What is the clinical significance of CpSS?

A

Therapeutic benefit is optimal at stead state plasma concentration

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26
Q

How many half lives does it take to fully eliminate a drug from CpSS?

A

5

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27
Q

What must be given if a drug has a long half life?

A

A loading dose to reach minimum effective concentration

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28
Q

Why might Digoxin lead to Digitoxicity?

A

Has a very long (40 hour) half life - takes a long time to be eliminated - renal failure can make this even worse

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29
Q

What is the equation for calculating loading dose?

A

Loading dose = Vd x CpSS / Bioavailability

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30
Q

What are the units of Vd?

A

L/Kg

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31
Q

What is the equation for calculating T1/2?

A 
T1/2 = Log(2)/K
T1/2 = 0.693/K
K = clearance/Vd
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32
Q

What is the equation for calculating K in the T1/2 equation?

A

K = clearance/Vd

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33
Q

What are the units of clearance?

A

ml/min

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34
Q

What is the “Selectivity” of a drug?

A

The chance of it interacting with only the intended receptors - chance of it producing adverse effects

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35
Q

What is the “Affinity” of a drug?

A

The likelihood it will bind to a receptor

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36
Q

What is the Kd?

A

Dissociation constant - the concentration of drug at which 50% of a drug will interact with receptors.

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37
Q

What is the “Efficacy” if a drug?

A

The ability of a drug to produce a response on receptor binding.

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38
Q

What is the “Potency” of a drug?

A

Dose required to produce the required response

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39
Q

Define Ec50.

A

The effective concentration - the concentration of drug needed to produce 50% of the maximum response. A measure of potency.

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40
Q

What is the “Therapeutic Index” of a drug?

A

The relationship between a concentration of a drug that causes a desired effect and an adverse (toxic) effect.

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41
Q

What is the equation for the Therapeutic Index of a drug?

A

TI = Toxic conc/Ec50

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42
Q

What is the “Therapeutic Window” of a drug?

A

The range of dosages that produce a safe, effective treatment.

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43
Q

Name one example of a CYP enzyme inhibitor, what CYP it inhibits and what drug it inhibits.

A

Cranberry juice

Inhibits CYP2C9, involved in Warfarin metabolism -> increased hemorrhagic effect

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44
Q

Define “Adverse Drug Reaction”.

A

An unwanted or harmful reaction that occurs after administration of a drug.

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45
Q

Name all 5 types of Adverse Drug reaction, with an explanation of what each is.

A

A - Augmented - dose related eg. overdose of insulin causing hypoglycaemia
B - Bizarre - unpredictable eg. allergy
C - Chronic - due to prolonged use eg. Cushing’s due prednisolone
D - Delayed - effects years after treatment - eg. cancer due to alkylating agents used in chemo
E - End of treatment - eg. Unstable angina when B blockers are stopped

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46
Q

Name 4 causes of drug response variability.

A
  1. Body weight
  2. Age and sex
  3. Genetics eg. race
  4. Health eg. kiney/liver failure
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47
Q

Name 4 things that increase the risk of an ADR.

A
  1. Polypharmacy
  2. DDIs
  3. Co-morbidities and age
  4. Narrow therapeutic index drugs
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48
Q

What is the “Constitutive actvity” of a receptor?

A

Activity caused by endogenous ligands within the body.

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49
Q

What is an “Inverse Agonist”?

A

Causes a response, but the opposite of what is expected.

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50
Q

Give an example of a partial agonist and its therapeutic use.

A

Buprenorphine.
Opioid addiction.
Higher affinity than opioid, but lower response (lower efficacy) - reduces withdrawal while causing fewer side effects.

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51
Q

Describe the pharmacokinetics of a competitive antagonist.

A 
Can be out-competed at high concentrations - higher affinity though. Potency is reduced, so shift of curve to the right.
Max response unchanged.
Lowers Km (conc required to reach half of max speed)
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52
Q

Describe the pharmacokinetics of a non-competitive antagonist.

A

Binds to allosteric site of a receptor - reduces max response
Does not affect potency
Lowers Vmax (max rate of reaction)

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53
Q

What is Km?

A

Concentration of substrate needed to reach half of Vmax

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54
Q

Give an example of an example of a contraindication in asthma that could cause an ADR.

A

B blockers in asthma.

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55
Q

What is the equation for MAP?

A

MAP = CO x TPR

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56
Q

What is the difference between Primary Secondary hypertension?

A 
Primary = idiopathic
Secondary = caused by something
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57
Q

What are the stages of hypertension and what are the BP values?

A

Stage 1 = 140/90
Stage 2 = 160/100
Stage 3 = 180/110

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58
Q

What is the target BP in diabetics?

A

130/80

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59
Q

Name 4 lifestyle changes that can reduce hypertension?

A

Exercise
Stress
Diet
Caffeine reduction

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60
Q

Name the 3 types of drugs used for hypertension treatments.

A

ACD

  • ACE/ARBs - Ramipril/Losartan
  • Calcium channel blockers - Amlodipine
  • Diuretics - Thiazide
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61
Q

Give an example of an ACE inhibitor

A

Ramipril

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62
Q

Give 3 side effects of a Ramipril

A

Dry cough - bradykinin not broken down
Low BP - renal failure
Hyperkalaemia

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63
Q

Give a contraindication of Ramipril

A

Not when breastfeeding - causes infant hypotension

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64
Q

Give an example of an ARB

A

Losartan

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65
Q

Why might you use an ARB over and ACE inhibitor?

A

Does not affect Bradykinin - no cough

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66
Q

How do L-type Calcium channel blockers work?

A

Stop calcium entering cells, preventing smooth muscle contraction

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67
Q

What are the 3 classes of Calcium channel blockers?

A
  1. Dihydropyridine eg. amlodipine
  2. Phenylalkamine eg. verapamil
  3. Benzothiazipine eg. diltiazem
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68
Q

Give one DDI of amlodipine

A

Statins

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69
Q

Why are dihydropyridines better than phenylalkamines for hypertension?

A

They are selective for smooth muscle. Phenylalkamines act on the heart too.

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70
Q

Name 3 side effects of amlodipine

A
  • Sympathetic activation eg. tachy
  • Palpitations
  • Flushing/sweating
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71
Q

Name the best diuretic for hypertension

A

Thiazide

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72
Q

Name 4 side effects of Thiazide

A
  • Hypokalaemia
  • Increased urea
  • Impaired glucose tolerance
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73
Q

Describe the guidelines for treating hypertension.

A

If patient less than 55 years old or has heart failure or diabetes: Give A
If patient is more than 55 years old or black: C
Then A+C
Then D

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74
Q

Why are black people treated differently for hypertension?

A

Naturally have reduced Renin levels

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75
Q

Name 2 other hypertension treatments and their MOAs.

A

A-blockers - block peripheral a channels which usually cause vasoconstriction
B-blockers - reduce cardiac output/contraction (reduced sympathetic stimulation)

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76
Q

What is a contraindication of B-blockers?

A

Do not give to asthmatics

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77
Q

Name 3 side-effects of B-blockers

A

Bronchoconstriction
Bradycardia
Lethargy

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78
Q

Define Heart failure.

A

The inability of the heart to produce enough cardiac output to adequately perfuse the organs

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79
Q

What is decompensation in Heart Failure?

A

Decrease in arterial BP, increased heart rate, heart works harder, condition worsens, heart has to work harder against vasoconstricted arteries

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80
Q

Name 4 treatments of Heart failure and how they help.

A
  1. Diuretics - furosemide - oedema
  2. ACE - reduces afterload due to due to less vasoconstriction and fluid
  3. Spironolactone - given with ramipril and furosemide, reduces “Aldosterone escape”
  4. B-blockers - reduces heart rate, improves filling
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81
Q

What is “Aldosterone escape”?

A

Hyperaldosteronism after heart failure

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82
Q

Name every type of diuretic and where it acts.

A 
Osmotic - mannitol
Loop - furosemide - NKCC2
Thiazides - NCC in DCT 1 - Thiazide
Aldosterone antagonists - Spironolactone + Amiloride - DCT 2 + CD
ADH anatagonists - Lithium
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83
Q

Name a Loop diuretic and the channel it acts on

A

Furosemide

NKCC2

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84
Q

Name 4 side effects of Loop diuretics

A
  • Hypokalaemia - metabolic alkalosis
  • Hypotension - acute kidney injury
  • Loss of Ca2+
  • Gout
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85
Q

Name a Thiazide diuretic and the channels it acts on

A 
Thiazide
NCC (NaCl channels)
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86
Q

Name 4 side effects of Thiazides

A
  • Hypokalaemia - metabolic alkalosis
  • Hypotension - acute kidney injury
  • Hypercalcaemia - do not give to hypercalcaemics
  • Gout
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87
Q

Name 2 aldosterone antagonists

A

Spironolactone

Amiloride

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88
Q

Describe how Aldosterone works on the kidney to increase reabsorption

A

Increases ENaC expression and Na/KATPase - increased Na and water loss

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89
Q

Describe the MOA of spironolactone

A

Blocks Aldosterone binding

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90
Q

Describe the MOA of amiloride

A

Blocks ENaC channels

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91
Q

What are the Potassium-sparing diuretics?

A

Spironolactone

Amiloride

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92
Q

Name a ADH antagonist

A

Lithium

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93
Q

Name 2 side effects of Spironolactone

A

Hyperkalaemia

Impotence

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94
Q

Name a DDI of Potassium-sparing diuretics

A

ACE - hyperkaemia

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95
Q

Name 2 DDIs of Thiazide and Loop diuretics

A

1 . Digoxin - hypokalaemia

2. Lithium - increased toxicity

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96
Q

Name 4 uses for Diuretics

A
  1. Hypertension
  2. Heart failure
  3. Nephrotic syndrome
  4. CKD
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97
Q

Describe Diuretic resistance

A

Insufficient diuretic reaches the lumen of the kidney tubules, due to:

  • Reduced GFR in pump failure
  • Fewer nephrons in CKD
  • Reduced albumin (furosemide needs to be bound to albumin to be secreted) in nephrotic syndrome
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98
Q

List 4 nephrotoxic drugs

A

Vancomycin, Gentamicin, Aciclovir, NSAIDs

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99
Q

What do ACE inhibitors affect in the kidney?

A

Angiotensin 2 - vasoconstricts the efferent

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100
Q

What is the management of Hyperkalaemia?

A

Calcium gluconate, Insulin, Glucose, Sodium resonium

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101
Q

Give a good case study for Pharmacovigilance

A

Thalidomide in the 50s - caused limb deformities

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102
Q

Give a good case study for Pharmacovigilance

A

Thalidomide in the 50s - caused limb deformities in pregnant women

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103
Q

Give a risk management example

A

The Pill - can cause thromboembolism - however, dose was lowered without compromising effectiveness and risk reduced

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104
Q

What is Pharmacogenetics?

A

How genetics affect response to a certain drug

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105
Q

What is Pharmacogenetics and give an example

A

How genetics affect response to a certain drug

Eg. How ACE is less effective in Black people due to lower Renin levels

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106
Q

What is the precursor for Steroid drugs?

A

Cholesterol

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107
Q

How should progesterone be given? (IV/Oral)

A

IV - bound by albumin in blood

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108
Q

What can reduce the effectiveness of contraceptives?

A

CYPs can be induced (increased) by:

  • Anti-epileptics
  • St John’s wort
  • Rifampicin
  • Soya food - reduces oestrogen storage, faster use
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109
Q

What can HRT be used for?

A

Menopause - reduces symptoms
Reduces osteoporosis
Does not affect heart disease increased risk

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110
Q

What is HRT?

A

Opposed oestrogen - ERT = unopposed, increases endometrial cancer risk

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111
Q

What are the risk factors of HRT?

A
  • Breast cancer
  • Venous thromboembolism - oestrogen is thrombogenic
  • CVS disease increase (lipid profile fucked)
  • Increased stroke risk
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112
Q

Name a Progesterone receptor antagonist

A

Mifepristone

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113
Q

What is Mifepristone?

A

Progesterone receptor antagonist

Pregnancy termination

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114
Q

What does SERM stand for?

A

Selective Oestrogen Receptor Modulator

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115
Q

What are SERMs used for?

A

Used for infertility, ovarian dysfunction and breast cancer eg. Tomoxifen, Clomiphene

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116
Q

Give an example of a SERM

A

Tamoxifen, Clomiphene

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117
Q

What is Clomiphene used for?

A

Induces ovulation, tricks hypothalamus into releasing LH and FSH

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118
Q

What is Tamoxifen used for?

A

Acts as ER (HER 2) receptor antagonist - causes cells to arrest cell cycle in breast.

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119
Q

Why is Tamoxifen only used if endometrium has been taken out?

A

It is an ER agonist in the endometrium

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120
Q

What is synthetic oestrogen called?

A

Oestradiol

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121
Q

What is synthetic progesterone called?

A

Medroxyprogesterone acetate

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122
Q

What is the morning after pill called?

A

Ulipristal acetate

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123
Q

What is Ulipristal acetate?

A

Progesterone receptor modulator (like a SERM) - inhibits ovulation

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124
Q

What is the main target for cardiovascular disease prevention?

A

Cholesterol (LDL)

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125
Q

What is the target cholesterol level?

A

4mmol/L

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126
Q

What is the MOA of statins?

A

HMG-CoA reductase inhibitor - reduces cholesterol synthesis

Upregulates LDL receptors to clear out LDLs via liver

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127
Q

What do statins do to the lipid profile? (LDL, HDL, TAGs)

A

LDL down
HDL up
TAGs down

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128
Q

Name a Statin

A

Atorvastatin, simvastatin (shorter half life)

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129
Q

Name 3 benefits of Statin therapy

A

Reduced CVD risk:

  • Reduced endothelial damage
  • Anti-inflammatory
  • Antioxidant
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130
Q

What CYP metabolises Statins? What must not be taken with them?

A

CYP3A4 - Grapefruit juice

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131
Q

What are the side-effects (ADRs) of Statins?

A
  • Myalgia - test for Creatine Phosphokinase elevation
  • LFT increases
  • Rarely rhabdomyelosis
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132
Q

What should be tested for in myalgia when using statins?

A

Creatine Phosphokinase

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133
Q

Why is atorvastatin better than simvastatin?

A

Simvastatin needed to be taken at night when receptors highest due to low half life.

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134
Q

Name all the drugs used to treat Hypercholesterolaemia (4)

A

Statins
Fibrates
Nicotinic acid
Cholesterol absorption inhibitors

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135
Q

Name a Fibrate

A

Fenofibrate

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136
Q

How do Fibrates work?

A

Increase lipoprotein lipase production, clearing TAGs faster, lowering LDL and raising HDL

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137
Q

How is Fenofibrate given?

A

With statins usually.

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138
Q

What are the side effects of Fenofibrate?

A
  • GI upset
  • Increased Myalgia/Rhabdo risk with Statins
  • Gall stones
  • LFT increases
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139
Q

Name a Nicotinic acid

A

Niacin

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140
Q

What is the MOA for Niacin?

A

Antilipolytic, reduces TAG and LDL, greatly increases HDL

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141
Q

What are the ADRs for Niacin?

A

Flushing, headache, GI disturbance

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142
Q

Name a Cholesterol absorption inhibitor

A

Ezetimibe

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143
Q

What is the MOA for Ezetimibe?

A

Brush border absorption inhibitor - often given with statins

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144
Q

Name a PCSK9 inhibitor

A

Alirocumab

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145
Q

What is Alirocumab?

A

PCSK9 monoconal antibody inhibitor

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146
Q

What other things can lower cholesterol?

A

Exercise
Fish oils
Fibre

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147
Q

What programme measures CVS risk?

A

QRISK

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148
Q

What is always given after an MI?

A

Any lipid lowering agent

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149
Q

Name the types of insulin for Type 1 Diabetes, an example of each and how long each one lasts

A 
Ultrafast acting - Apart - mins
Rapid acting - Novorapid - hour
Short acting - Humulin S - hours
Intermediate acting - Humulin I - one a day
Long acting - DEGLUDEC - two days
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150
Q

What is the most efficient way of administering insulin

A

Insulin pump, detects insulin levels

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151
Q

What are the ADRs of insulin?

A
  • Hypoglycaemia
  • Hyperglycaemia
  • Lipodystrophy - scarring from injections
  • Pain on injection
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152
Q

What is Type 1 diabetes?

A

Autoimmune destruction of Beta cells

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153
Q

What is Type 2 diabetes?

A

Insulin resistance around the body and gradual beta cell failure

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154
Q

What drugs are used to treat Type 2 Diabetes?

A
  • Metformin (Biguanides)
  • Sulphonylureas
  • Pioglitazone (Glitazones)
  • Exenatide (GLP-1 agonists)
  • Sitagliptin (DPP-4 inhibitors)
  • Glifozins (SGLT2 inhibitors)
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155
Q

How does Metformin work?

A

Reduces Insulin resistance, reduces hepatic glucose production

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156
Q

What are the ADRs of Metformin?

A
  • GI upset

- Vitamin B12 deficiency

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157
Q

When should Metformin not be given?

A

If patient has bad CKD or co-morbidities

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158
Q

How do Sulphonylureas work?

A

Stimulate B cells to release Insulin

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159
Q

What are the ADRs of Sulphonylureas?

A
  • Weight gain

- Hypoglycaemia

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160
Q

How does Pioglitazone work?

A

Increased insulin sensitivity within muscle and adipose tissue and reduced glucose production in liver

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161
Q

What are the ADRs of Pioglitazone?

A
  • Weight gain
  • Sodium and fluid retention
  • Heart failure
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162
Q

Name a GLP-1 agonist

A

Exenatide

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163
Q

How does Exenatide work?

A

Increases insulin secretion and reduces glucagon production

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164
Q

Why is Exenatide good?

A

Promotes weight loss

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165
Q

What are the ADRs of Exenatide?

A
  • Hypoglycaemia

- GI upset

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166
Q

Name a DPP-4 inhibitor

A

Sitagliptin

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167
Q

What is the MOA of sitagliptin?

A

Reduces GLP-1 breakdown, then GLP-1 agonist effect - increased insulin, reduced glucagon

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168
Q

Name an SGLT-2 inhibitor

A

Glifozins - add on therapy

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169
Q

Name the 4 classes of antiarrhythmic drugs

A
  • Class 1 - Na channel blockers
  • Class 2 - B-blockers
  • Class 3 - Potassium channel blockers
  • Class 4 - Calcium channel blockers
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170
Q

What are the 5 phases of the non-pacemaker action potential?

A

0 - Depolarisation - Na in
1 - Peak Na opening and K+ starts to open
2 - Calcium channels open - plateau phase
3 - K+ causes repolarisation
4 - NaKATPase maintains baseline

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171
Q

Describe how Class 1 antiarrhythmics work

A

Na channel blockers

Affect Phase 0 - slower depolarisation, but same peak

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172
Q

Describe how Class 2 antiarrhythmics work

A

B-blockers

Affect Phase 2, prolonging plateau and affecting Phase 4 (slower to reach)

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173
Q

Describe how Class 3 antiarrhythmics work

A

K-channel blockers

Increase AP duration (Phase 2 and 3), increase refractory period - can be pro-arrhythmic

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174
Q

Describe how Class 4 antiarrhythmics work

A

Calcium channel blockers
Phase 2 reduced
Decreases Phase 4 spontaneous depolarisation

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175
Q

Describe the Phases of a Pacemaker action potential

A

Phase 4 - Funny channels, gradual depolarisation - Na channels
Phase 0 - Reaches threshold, Ca2+ channels open
Phase 2 - Ca channel peak opening
Phase 3 - K+ repolarisation
No 1

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176
Q

How do Calcium channel blockers affect the pacemaker potential?

A

They reduce conduction velocity, increasing the refractory period

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177
Q

Name 2 core mechanisms of inducing arrhythmias

A
  • Abnormal impulse generation

- Abnormal conduction

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178
Q

Name 3 causes of abnormal impulse generation in the heart

A
  • Ectopic foci
  • Early afterdepolarisation - eg. Hypokalaemia
  • Delayed afterdepolarisation - eg. Digoxin toxicity, leads to increased Ca2+
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179
Q

Name 2 causes of abnormal conduction in the heart

A
  • Heart block

- Re-entrant loops

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180
Q

Name a re-entrant loop disease

A

Wolff-Parkinson-White syndrome - accessory pathway into ventricles

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181
Q

Name all the antiarrhythmic drug classes and give an example of each

A 
Class 1 -
b - Lidocaine
c- Flecainide
Class 2 - Bisoprolol/Labetalol
Class 3 - Amiodorone, Sotalol
Class 4 - Verapamil, Diltiazem (NOT AMLODIPINE)
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182
Q

Name the MOA of Lidocaine and its main use

A 
Given IV - relevant
Ventricular tachycardia re-entrant loops
Na channel blocker, only active channels/ischaemic
Phase 0 slow down
Raises QRS time
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183
Q

Name 3 ADRs of Lidocaine

A
  • Dizziness
  • Drowsiness
  • Abdominal upset
184
Q

Name the MOA of Flecainide and its main use

A

Used in AF/WPW

Reduces automaticity in all cells, increases refractory period - can be pro-arrhythmic

185
Q

What must Flecainide be given with?

A

AV node blockers to prevent ventricular arrhythmia

186
Q

Name the MOA of B-blockers

A

Increases refractory period in AV node, increases PR interval, reduces heart rate

187
Q

Name 2 side effects of B blockers

A
  • Bronchoconstriction - asthmatics

- Hypotension - do not use in heart failure or heart block

188
Q

Name the MOA of Amiodorone and its uses

A

Used in most arrhythmias and WPW
Increases action potential duration and refractory period, decreases Phase 0 (Na) too
Also reduces AV node conduction

189
Q

Name 3 ADRs for amiodorone

A
  • Pulmonary fibrosis
  • Hepatic injury
  • LDL increase
190
Q

What 2 drugs must not be given with Amiodorone?

A
  • Warfarin

- Digoxin

191
Q

Name the MOA of Sotalol and its use

A

Used in tachycardia
Increases action potential duration and refractory period and slows AV node conduction
ORAL ONLY

192
Q

Name 3 ADRs of Sotalol

A
  • Pro-arrhythmic
  • Fatigue
  • Insomnia
193
Q

Name the MOAs of Diltiazem and Verapamil and their uses

A

Slow AV node conduction and increase refractory period

  • Controls supraventricular tachycardia ventricles
  • Stops AV node re-entry
194
Q

Name the side-effects of Diltiazem and Verapamil

A
  • Decreased cardiac output

- GI problems

195
Q

What should Verapamil and Diltiazem not be given with and why?

A

B-blockers - can cause AV node block

196
Q

Name 5 other Heart drugs

A
  • Adenosine
  • Vernakalant
  • Ivabridine
  • Digoxin
  • Atropine
197
Q

Describe the MOA of Adenosine

A

Rapid IV bolus, very temporarily (secs) blocks AV node
Hyperpolarises by binding A1 receptors
Stops re-entrant supraventricular arrhythmias

198
Q

Describe the MOA of Vernakalant

A

Slows atrial conduction via K+ blocking

199
Q

Describe the MOA of Ivabridine

A

Blocks funny channel of SA node, slows SA node but does not affect BP - used in sinus tachycardia

200
Q

When must Ivabridine not be given?

A

Pregnancy - teratogenic

Heart failure - reduces heart rate

201
Q

Describe the MOA of Digoxin in AF

A

Used with Ca2+ channel blockers to slow down heart rate in AF
Enhances vagal activity and slows AV node conduction by inhibiting NaKATPase

202
Q

When would Digoxin be used?

A

AF with Bisoprolol

203
Q

Name 2 ADRs of Digoxin

A

Kidney failure due to Digoxin toxicity

Bradycardia

204
Q

Describe the MOA of Digoxin in Heart Failure

A

NaKATPase inhibitor - causes NA build up in the cell
NCX fails, so no Ca2+ pumped out
Ca2+ increases force of contraction

205
Q

Describe the MOA of Atropine

A

Antimuscarinic - speeds up AV conduction and heart rate

206
Q

What is Atropine used for?

A

Bradycardia

207
Q

Describe the course of action for drugs for a patient with AF

A
  1. Bisoprolol - reduce rate
  2. Digoxin
  3. Flecainide (with bisoprolol, reduces VF risk)
208
Q

Describe the course of action for drugs for a patient with VF

A

Amiodorone through central line

Lidocaine/Bisoprolol

209
Q

Name the drug for treating WPW

A

Amiodorone

210
Q

Describe the course of action for drugs for a patient with a re-entrant SVT

A 
Acute -
1. Adenosine
2. Verapamil
Chronic -
1. Bisoprolol
2. Flecainide
211
Q

Describe the course of action for drugs for a patient with a sinus tachycardia

A

Ivabradine

Bisoprolol

212
Q

Name the two types of AF and their treatments

A

Stable - no syncope - Bisoprolol, digoxin, flecainide

Unstable - syncope - Amiodorone, anticoagulant

213
Q

What determines what anticogaulant should be used?

A

Where the clot occurred
Arterial: platelet rich, antiplatelets and fibrinolytics
Venous: low platelet:, use parenteral anticogulants (heparins) and oral anticoagulants (warfarin)

214
Q

Name 4 anti-platelet agents

A
  • Aspirin
  • Clopidogrel/Ticagrelor
  • Abciximab
  • Dipyrimadole
215
Q

Name the MOA of Aspirin

A

COX-1 inhibitor

Prevents Thromboxane A2 formation from arachidonic acid

216
Q

Describe the MOA of Aspirin as an anti-platelet drug

A

COX-1 inhibitor

Prevents Thromboxane A2 formation from arachidonic acid

217
Q

When should Aspirin be given?

A

Secondary prevention of Stroke/TIA, post-op, secondary prevention of MI in stable angina

218
Q

Name the MOA of Clopidogrel/Ticagralor

A

P2Y-12 inhibitor (ADP receptor antagonist)

219
Q

Describe the MOA of Clopidogrel/Ticagralor

A

P2Y-12 inhibitor (ADP receptor antagonist)

Prevents binding of ADP to P2Y-12, inhibits the activation of GP2b/3a receptors, meaning no platelet cascade

220
Q

When should Clopidogrel be given?

A

Post-stroke, post-MI (with aspirin), in people intolerant to aspirin
Given for 12 months post-MI

221
Q

Describe the MOA of Abciximab

A

GP2b/3a inhibitor -> usually lead to binding of fibrinogen to vWF
IV bolus
Also an irreversible binder

222
Q

Name one risk of Abciximab

A

Thrombocytopenia

223
Q

Describe the MOA of Dipyrimadole

A

PDE5 inhibitor - inhibits cellular re-uptake of adenosine, leading to increased plasma adenosine, which inhibits platelet aggregation
Also prevents expression of GP2b/3a via cAMP inhibition

224
Q

When should Dipyrimadole be used?

A

In combination with oral coagulants after valve replacement surgery

225
Q

Name one Fibrinolytic and one group of fibrinolytics

A
  • Streptokinase

- “teplase” group

226
Q

Why can Streptokinase only be given once?

A

Antigenic (from a bacteria), so can cause immune reaction

227
Q

Name 3 anticogulants

A
  • Warfarin
  • Heparin (LMWH)
  • Bempiparin
228
Q

Describe the MOA for Warfarin

A

Inhibits Vitamin K conversion, leading to loss of factors 2, 7, 9 and 10 (need Vitamin K as a co-factor)

229
Q

Why does Warfarin need to be given a few days before effect needed?

A

It only inhibits the production of new clotting factors

Will need heparin cover initially

230
Q

Name 5 therapeutic uses of Warfarin

A
  • DVT prophylaxis
  • PE prophylaxis
  • AF prophylaxis
  • Following orthopaedic surgery
231
Q

What needs to be taken into account when determining Warfarin PK?

A
  • Highly protein bound
  • Needs CYP2C9 - inhibited by Cranberry juice
  • Teratogenic - DO NOT GIVE IN PREGNANCY, GIVE HEPARINS
232
Q

Explain why Warfarin leads to dangerous bleeding and what antidotes exist

A

Can be difficult to manage for long time, causes bleeding

Can use Vitamin K analogue

233
Q

Name 4 Warfarin DDIs

A
  • CYP 2C9 can be affected by Amiodorone, clopidogrel, alcohol, metronidazole
  • Aspirin - increases bleeding
  • Cephalosporin antibiotics reduce Vitamin K
  • NSAIDs displace warfarin from plasma warfarin
  • St John’s wort, Phenytoin increase breakdown speed
234
Q

Name 2 parenteral anticoagulants

A
  • Heparin

- Bempiparin

235
Q

Describe the general MOA of heparins

A

Inhibit the action of coagulation factors

Bind to anti-thrombin and increase action

236
Q

What does anti-thrombin do?

A

Inactivates Thrombin and multiple factors

237
Q

Name an unfractionated heparin

A

Heparin

238
Q

Name a low molecular weight heparin

A

Bempiparin

239
Q

Compare using a low molecular and unfractionated heparin

A

LMWH require less monitoring (more predictable) as they only target factor 10 and so are less likely to cause thrombocytopenia
UFH needs to be IV bolus
LMWH is slower onset

240
Q

Describe the pharmacokinetics of UF Heparins

A

Poorly GI absorbed, must be given via IV bolus or subcutaneously (they are negatively charged large molecules)

241
Q

What does PPCI stand for?

A

Primary Percutaneous Coronary Intervention

242
Q

Give 5 uses of Heparins

A
  • AF
  • DVT
  • PE
    Prior to Warfarin (faster)
    Used in pregnancy as does not cross placenta
243
Q

What is Factor 2?

A

Thrombin

244
Q

Name 3 ADRs of Heparins

A
  • Bleeding/bruising
  • Hepatic and renal damage
  • Thrombocytopenia
245
Q

What is used to determine whether Warfarin should be given?

A

The patient’s INR

246
Q

How is Heparin reversal carried out?

A

Via Protamine Sulphate

247
Q

How does Protamine Sulphate work?

A

Causes Anti-thrombin to dissociate from heparin

248
Q

What is Fondaparinux and how does it work?

A

Inhibits Factor 10 and Thrombin

249
Q

Describe the process of vomiting

A 
CTZ in medulla receives signal to vomit
Nausea occurs
Retrograde peristalsis
Deep inspiration
Epiglottis closes
Abdominal muscles contract
LOS contracts
250
Q

How can the CTZ be activated?

A
  • Vestibular nuclei
  • Gut stretching
  • Drugs/toxins
251
Q

Name 2 anti-emetic drugs that act on the Vestibular nuclei

A
  • Hyoscine hydrobromide

- Cyclizine/Promethazine (pregnancy)

252
Q

Name 3 anti-emetic drugs that act on visceral afferents of the gut

A
  • Ondansetron
  • Metaclopromide
  • Domperidone
253
Q

Name 4 anti-emetic drugs that act on the CTZ

A
  • Haloperidol
  • Dexamethosone
  • Aprepitant
254
Q

Describe the MOA of Hyoscine hydrobromide

A

Antimuscarinic

Blocks AcH in Vestibular nuclei of CTZ

255
Q

Name a reason you would want to use Hysocine hydrobromide

A

Can be used as a patch

256
Q

Describe the MOA of Cyclizine/Promethazine

A

Anti-histamines (H1)

Blocks H1 in Vestibular nuclei of CTZ

257
Q

Give a use of Promethazine

A

Morning sickness in pregnancy

258
Q

Give 2 side-effects of anti-emetics of Vestibular nuclei

A
  • Sedation
  • Dry mouth
  • Consitpation
259
Q

Describe the MOA of Ondansetron

A

5HT antagonist

Reduces GI motility, inhibits CTZ

260
Q

Describe the MOA of Metaclopramide

A

D2 receptor antagonist

Increases gastric emptying by increasing LOS tone and increases peristalsis

261
Q

Describe the MOA of Domperidone

A

D2 receptor antagonist

Can cause significant cardiac side effects

262
Q

Describe the MOA of Haloperidol

A

D2 receptor antagonist

Acts on CTZ

263
Q

Describe the D2 receptor antagonist side-effects

A
  • Sedation

- Parkinsonism

264
Q

Describe the MOA of Aprepitant

A

Neurokinin 1 antagonist
Inhibits CTZ
Side effects: Headache, diarrhoea

265
Q

What drug would you choose for motion sickness?

A

Hyoscine hydrobromide

266
Q

What drug would you give for GORD/paralytic ileus?

A

Domperidone/metaclopramide

267
Q

What drug should be given to women in hyperemesis gravidarum - worse morning sickness due to b-HCG?

A

Promethazine + metaclopramide + ondansetron

268
Q

How is diarrhoea treated?

A

Opioid receptor agonists

269
Q

Name 2 opioid receptor agonists

A
  • Loperamide

- Codeine and morphine

270
Q

Describe the MOA of Loperamide/Codeine

A 
Acts on Micro receptors
Reduces peristalsis (reduced muscle tone)
271
Q

Name 4 side-effects of opioid receptor agonists

A

Paralytic ileus, nausea and vomiting, sedation, addiction

272
Q

Name 2 Osmotic laxatives

A
  • Lactulose

- Movicol

273
Q

What is the MOA of Sodium Docusate

A

Increases intestinal mobility and softens stools

274
Q

What should be given for constipation at different ages?

A

Child: Movicol/Sodium docusate
Adult: Movicol

275
Q

Name 4 gastric acid drugs

A
  • Ranitidine - H2 receptor antagonist
  • Omeprazole - PPI
  • Antacids
  • Alginates
276
Q

Describe the MOA of Omeprazole

A

Destroys active proton pumps - takes hours to have effect, so mainly for long term use
Will take 2-3 days after drug is stopped to recover

277
Q

Name 2 ADRs of Omeprazole

A
  • Diarrhoea
  • Nausea and vomiting
  • Osteoporosis risk
278
Q

Where is arachidonic acid from in the diet?

A

Vegetable oils - Linoleic acid

279
Q

Name the 2 COX isoforms and where they are found

A

COX-1 - constitutively active in most tissues

COX-2 - inducible in inflamed tissues

280
Q

What is COX-1 involved with in the body?

A

GI protection, platelet aggregation, renal blood flow, chronic pain and inflammation

281
Q

What is COX-2 involved with in the body?

A

Tissue repair and healing, inhibition of platelet aggregation, fever, tumour cell growth

282
Q

How do NSAIDs work?

A

Inhibit COX, preventing conversion of arachidonic acid to prostacyclins, such as prostaglandins and thromboxane

283
Q

Describe how the effect of Aspirin changes with dose

A

At low dose - NSAID

At high dose - anti-platelet - irreversible COX inhibitor

284
Q

How do NSAIDs produce an analgesic effect?

A
  • Local action at site of pain to reduce inflammation

- Reduce PGE2 synthesis in dorsal horn, reducing neurotransmitter release in pain relay

285
Q

How do NSAIDs produce an anti-inflammatory effect?

A

Reduce PGE2 synthesis during injury which usually lead to vasodilation and swelling

286
Q

How do NSAIDs produce their anti-pyretic effects?

A

Inhibition of hypothalamic COX-2 where cytokine produced PG synthesis is elevated

287
Q

What is the ending of drugs with lower side-effects profiles that inhibit COX-2 inhibitors?

A

coxib

288
Q

Why are NSAIDs almost completely absorbed in the GI system?

A

They are slightly acidic

289
Q

What happens at high doses of Aspirin?

A

Salicyclic acid, which is produced from aspirin, can conjugate with glycine to form a toxic compound

290
Q

Name 5 NSAID GI ADRs

A 
Dyspepsia
Nausea
Peptic ulceration
Bleeding
Perforation
291
Q

Why do NSAIDs lead to GI ADRs?

A
  • Reduce mucous and bicarbonate release
  • Increase acid secretion
  • Reduce mucosal blood floow
292
Q

Name 3 Renal ADRs of NSAIDs

A
  • Reduce GFR
  • Reduced Renin secretion
    Only problem in CKD/heart failure patients
293
Q

Name a COX-2 inhibitor

A

Celecoxib

294
Q

What is a potential effect of COX-2 inhibitors relative to anti-platelets?

A

Can cause platelet aggregation and oppose COX-1 inhibitors

295
Q

Name 3 CVS ADRs of NSAIDs

A
  • Increased salt and water retention, exacerbates HF and hypertension
  • Vasoconstriction as ADH no longer inhibited by prostaglandins
  • Increased risk of MI
296
Q

Name 6 NSAID DDIs

A

DDIs with highly protein bound drugs - NSAIDs displace the drugs

  • Sulphonylurea - hypoglycaemia
  • Methotrexate - hepatotoxicity
  • Warfarin - increased bleeding
297
Q

Name 6 NSAID DDIs

A

DDIs with highly protein bound drugs - NSAIDs displace the drugs

  • Sulphonylurea - hypoglycaemia
  • Methotrexate - hepatotoxicity
  • Warfarin - increased bleeding
298
Q

Why should Aspirin not be given to under 12s?

A

Reyes syndrome

299
Q

Which is more suitable for pregnant women? Paracetamol or NSAIDs?

A

Paracetamol

300
Q

What is the product of paracetamol in the liver? What does it do? How is it treated?

A

NAPQI
Treated by acetylcystiene
Uses up glutathione

301
Q

What does NAPQI lead to?

A

Nausea, vomiting, abdominal pain, liver damage, death

302
Q

How does Acetylcysteine work?

A

Thiol donor, increases the level of glutathione

303
Q

What do Nociceptors release in response to pain?

A

Substance P and Glutamate

304
Q

How is pain modulated peripherally and centrally?

A

Peripherally: Substantia gelatinosa - reduces pain
Centrally: Peri-aqueductal grey - reduces pain in

305
Q

How do Opioids work?

A

MOP/DOP/KOP receptors activated, cAMP decreased, less Substance P, less nociceptor activation

306
Q

Name 2 strong opioid agonists

A
  • Morphine

- Fentanyl

307
Q

Describe Morphine as a drug

A

Can be taken both orally and IV
Can affect baby
Affects MOP mainly
Does not cross BBB

308
Q

Name 4 side-effects of Morphine

A
  • Respiratory depression
  • Emesis - triggers CTZ
  • Constipation
  • Asthma attack - causes release of histamine
309
Q

Describe Fentanyl as a drug

A 
IV
Highly protein bound, crosses CNS
6 minute half life
100x morphine potency
Safer than morphine as releases less histamine, shorter half life, sedates less
310
Q

Name 3 side-effects of Fentanyl

A
  • Respiratory depression
  • Constipation
  • Vomiting
311
Q

What CYP is Fentanyl metabolised by?

A

CYP3A4

312
Q

Describe Codeine as a drug

A

Oral

Expression dependent on CYP2D6

313
Q

What CYP is Codeine metabolised by?

A

CYP2D6

314
Q

What does Buprenorphine do to opioid receptors?

A

Agonise and antagonise

315
Q

Describe Buprenorphine as a drug

A

Metabolised by CYP3A4

Excreted by biliary system, so safe in renal impairment

316
Q

Compare Buprenorphine and its MOA to morphine

A

Higher affinity for MOP receptor, not easily displaced
Lower efficacy
Antagonises KOP

317
Q

What is Naloxone?

A

Opioid antagonist

318
Q

How must Naloxone be given?

A

IV, slow infusion, not bolus, as needs to antagonise morphine until it is removed from body

319
Q

What is the treatment for the withdrawal of opioid addiction?

A

Methodone - opioid antagonist (full)

320
Q

Define chemotherapy

A

The treatment of cancer with cytotoxic drugs

321
Q

Describe the “Fractional Cell Kill Hypothesis”

A

Chemotherapy will kill all multiplying cells
Bone marrow cells will recover faster than cancer cells
Chemo must then be restarted again quickly

322
Q

Name 3 sites of action of cytotoxic chemo agents

A
  • Antimetabolites
  • Alkylating agents
  • Spindle poisons
323
Q

Describe the MOA of alkylating agents and name one

A

Cisplatin

Forms platinum bonds (adducts), breaks DNA, stops replication

324
Q

Describe 3 mechanisms of resistance to alkylating agents

A
  • Enhanced DNA repair mechanisms
  • Efflux pumps
  • Glutathione increase
325
Q

Describe the MOA of Methotrexate

A

Antimetabolite

Dihydrofolate reductase inhibitor

326
Q

Describe the MOA of 5-fluorouracil

A

Antimetabolite

Thymidylate synthase inhibitor

327
Q

Describe the MOA of Taxanes/Vinca alkaloids

A

Spindle poisons
Prevent spindle formation in mitosis
Vincristine

328
Q

Describe how chemotherapy is administered

A

Via an IV pump into a central line:

  • Hickman line into SVC
  • PICC line into arm - can be an outpatient
329
Q

Why do the Central Lines travel under the skin first?

A

Macrophages in the skin can prevent infection

330
Q

Name 6 side-effects of chemotherapy

A
  • Acute renal failure - from lysis of cells
  • GI perforation at site of tumour
  • DIC
  • Vomiting - drugs act on CTZ
  • Alopecia
  • Thrombophlebitis of veins
  • Bose lines on nails
  • Mucositis
  • Lung fibrosis
331
Q

What is a neoadjuvant?

A

Shrinks cancer before surgery

332
Q

What is an adjuvant?

A

Given after surgery to reduce relapse risk

333
Q

Name 3 Rheumatological conditions

A
  • SLE
  • RA
  • Vasculitis
334
Q

Name 8 Immunosuppressants

A
  • Prednisolone
  • Azathioprine
  • Cyclosporin
  • Mycophenolate mofetil
  • Cyclophosphamide
  • Methotrexate
  • Sulfasalazine
  • Rituximab
335
Q

What is Prednisolone used for?

A

SLE, vasculitis, crohn’s

336
Q

What class of drug is Prednisolone?

A

Corticosteroid

337
Q

What is the MOA of Prednisolone?

A

IL-1 and IL-6 inhibition from macrophages, inhibiting T-cell activation

338
Q

Why do patients need to be taken off Prednisolone gradually?

A

Need to give adrenal glands time to resume their normal function

339
Q

Name 2 side-effects of corticosteroids

A

Increase the progression of age-related diseases:

  • Cataracts
  • Osteoporosis
340
Q

What does DMARD stand for?

A

Disease Modifying Anti Rheumatic Drug

341
Q

What is the main use of Azothiaprine?

A

Steroid-sparing - cuts short the amount of time steroids need to be used

342
Q

What needs to be assessed in patients before giving them Azothiaprine?

A

TPMT levels - individuals vary in levels (polymorphic)
TPMT metabolises Azothioprine
Low levels of TPMT lead to myelosuppression
Must check bone marrow during treatment

343
Q

Describe the MOA of Azothioprine

A

Decreases DNA and RNA synthesis, reducing inflammation -> reduced amount of new inflammatory cells can be produced

344
Q

Name the side-effects of all immunosuppressants

A
  • Nausea and vomiting
  • Bone marrow suppression
  • Increased cancer risk
  • Increased infection risk
  • Hepatitis
345
Q

Name a Calcineurin inhibitor

A

Cyclosporin

346
Q

When is Cyclosporin used?

A

Transplantation, demratitis etc.
Not used in rheymatology due to renal toxicity
Inhibits cytochrome P450s

347
Q

Describe the MOA of Calcineurin inhibitors

A

Prevent IL-2 production by Calcineurin inhibition, so not T-cells activated

348
Q

Describe the effect of all 5 interleukins

A 
Hot T-Bone Steak
1 - Hot - Fever
2 - T-cell activation
3 - Bone - bone marrow activation
4 - StE - IgE
5 - Ak - IgA
349
Q

Describe the MOA of Mycophenolate Mofetil and when it is used

A

Primarily in transplantation

Inhibits guanosine synthesis, impairing B and T cell proliferation

350
Q

What is inductive and maintenance therapy?

A 
Inductive = induce remission
Maintenance = maintain levels
351
Q

Name 4 side-effects of Mycophenolate Mofetil

A
  • Vomiting
  • Nausea
  • Diarrhoea
  • Myelosuppression
352
Q

Describe the MOA of Cyclophosphamide

A

Strong boi

Alkylating agent - suppresses B and T cell activity

353
Q

What is Cyclophosphamide used for?

A

Lymphoma
SLE
ANCA-vasculitis

354
Q

What must Cyclophosphamide be given with and why?

A

Must be given with Mesna

If not, can lead to hemorrhagic cystitis due to toxic metabolite

355
Q

Name 3 ADRs of Cyclophosphamide

A

Toxicity
Bladder cancer risk
Infertility
- Mycophenolate mofetil is much safer for SLE, don’t use this

356
Q

What is Methotrexate used for?

A 
Gold standard in RA
 Also:
- Malignancy
- Psoriasis
- Crohn's
357
Q

Describe the MOA of Methotrexate in malignancies

A

Dihydrofolate reductase inhibition
Used in thymidine synthesis from tetrahydrofolate - inhibits DNA and RNA synthesis
Greater effect in rapidly dividing cells

358
Q

Describe the MOA of Methotrexate in RA

A

Inhibits Adenosine production

359
Q

Name 3 side-effects of Methotrexate

A
  • Mucositis
  • Marrow suppression
  • Teratogenic and abortion causing
360
Q

What should Methotrexate never be given with?

A

NSAIDs - NSAIDs reducing bloodflow to Kidneys + methotrexate’s toxicity to kidneys = RIP

361
Q

Who should Methotrexate not be given to ideally?

A

Women of child-bearing age

High infertility risk and teratogenic

362
Q

Describe the MOA of Sulfasalazine

A

2 parts
Anti-inflammatory and anti-infection
Inhibits T-cells via IL-2 inhibition
Reduces Neutrophil function

363
Q

Name 5 ADRs of Sulfasalazine

A
  • Myelosuppression
  • Hepatitis
  • Nausea
  • Vomiting
  • Rash
    But very safe in practice and SAFE IN PREGNANCY
364
Q

What is the MOA of Rituximab?

A

Binds CD20 on B cells

365
Q

What is the MOA of Infliximab?

A

Blocks TNF-alpha, reduces inflammation, reduces erosion of joints

366
Q

Name a danger of giving someone a TNF-alpha inhibitor

A

Could cause TB reactivation, as TNF is essential for granuloma formation

367
Q

Name two antibiotic types and give examples of each of antibiotics that target: Cell wall synthesis

A

Beta-Lactams - Penicillin

Glycopeptides - Vancomycin

368
Q

Name two antibiotic types and give examples of each of antibiotics that target: DNA synthesis

A

Quinolones - Ciprofloxin - interact with DNA gyrase

Folic acid antagonists - Trimethoprim

369
Q

Name two antibiotic types and give examples of each of antibiotics that target: Protein synthesis

A

Tetracyclines - Doxycycline

Aminoglycosides - Gentamicin

370
Q

What is an antibiotic breakpoint?

A

The MIC + pharmacokinetic properties of antibiotic are used to predict likely response of infection

371
Q

What is the difference between a bacteriostatic and bactericidal agent?

A 
Bacteriostatic = slows down growth
Bactericidal = will kill
372
Q

Describe the two pharmacokinetic types of antibiotic killing

A
  • Time-dependent

- Concentration-dependent

373
Q

Name 2 nephrotoxic antibiotics

A
  • Vancomycin

- Gentamicin

374
Q

What is Co-amoxiclav?

A

Amoxicillin

Clavulanic acid - B-lactamase inhibitor

375
Q

Name a DDI of Metronidazole

A

Alcohol

376
Q

Describe the pathogenicity of Influenza virus

A

Binds to Sialic acid receptor via Haemagluttinin

Leaves via vesicle - Neuraminidase cleaves off and allows removal

377
Q

Name 3 antiviral targets on influenza virus

A
  • Haemagluttinin
  • M2 ion channel
  • Neuraminidase
378
Q

Name an M2 channel blocker and what this does

A

Amantidine

Inhibits viral uncoating

379
Q

Name a Neuraminidase inhibitor

A

Ostelmavir

380
Q

What class of virus is Varicella Zoster?

A

Herpes virus

381
Q

Where does VZV lie dormant?

A

Dorsal root ganglion

382
Q

Describe the difference between HSV 1 and HSV 2

A

HSV 1 - genital and oral ulceration

HSV 2 - genital ulceration

383
Q

What is the MOA of Acyclovir

A

Guanosine analogue, stops viral DNA synthesis

Needs to be phosphorylated by a viral protein to activate first though, so this could be a method of resistance

384
Q

Name another 2 antivirals

A

Valaciclovir

Tamiflu (ostelmavir)

385
Q

Name all 4 stages of Guedel’s signs

A

1 - Analgesia and conscious, normal
2 - Unconscious, erratic, excitable, erratic breathing
3 - Surgical anaesthesia, patient relaxes
4 - Respiratory paralysis, death

386
Q

What is the MAC of an anaesthetic?

A

Minimum alveolar concentration

Potency (alveolar concentration) at which 50% of subjects fail to move to surgical stimulus

387
Q

What determines MAC?

A

Age, pregnancy, alcoholism, weight, NO (increases MAC)

388
Q

What receptor target do most anaesthetics target?

A

GABA

389
Q

Name 2 regional anaesthetics

A

Lidocaine, bupivacaine

390
Q

What is the MOA of Lidocaine?

A

Use-dependent Na channel blocker - blocks pain fibres

391
Q

What is Asthma hypersensitivity driven by?

A

TH2

392
Q

What are the pathophysiological effects of asthma?

A 
Mucosal oedema
Bronchoconstriction
Mucus plugging
Airway remodelling
Bronchial hyperresponsiveness
393
Q

What is the first step treatment for Asthma?

A

Short acting B2 agonist
Salbutamol, salmetreol, formoterol
Inhibits mast cell degranulation

394
Q

What can happen if Salbutamol is used too much?

A

Can reverse airway control - increase mast cell degranulation

395
Q

Name a selective COX-2 inhibitor

A

Celecoxib

396
Q

What is the second step in the treatment of Asthma?

A

Inhaled corticosteroids
Prednisolone/Beclamethosone
Works better on people with eosinophilic asthma

397
Q

What is the MOA of corticosteroids?

A

Inhibits transcription factors for pro-inflammatory proteins

398
Q

How can steroid effectiveness be increased, biochemically?

A

Addition of a lipophillic side chain

399
Q

What is the risk with using beclamethosone in COPD patients?

A

Immunosuppressive

400
Q

What is the third step in the treatment of Asthma?

A

Long-acting B2 agonist
Formoteral, Salmeterol
Can add in a LABA if not steroid controlled too

401
Q

Why should NSAIDs not be given during labour?

A
  • Delays labour
  • Increases bleeding
  • Prematurely closes Ductus arteriosus - foetal blood supply compromised
402
Q

Name 4 alternative step-three Asthma treatments

A 
Leukotriene receptor antaognist - Montelukast
Methylxanthine - Theophylline
LAMAs
- Tiotropium bromide
- Ipratropium bromide
403
Q

Why is acetylcysteiene used in paracetamol toxicity rather than just glutathione?

A

Acetylcysteiene can enter the liver hepatocytes, while glutathione cannot

404
Q

Describe the MOA of Montelukast

A

Leukotriene receptor antagonist

Prevents mast cells from releasing leukotrienes, which cause bronchoconstriction

405
Q

Name 3 side-effects of Montelukast

A
  • Angioedema
  • Dry mouth
  • Fever
406
Q

What is the MOA of Theophylline and what is it used in?

A

Adenosine antagonist - increased cAMP and PDE inhibitor

Used in severe COPD/Asthma

407
Q

Describe the MOA of LAMAs?

A

M3 inhibitor - stops constriction
Long-acting
In COPD and Asthma

408
Q

Name 3 side-effects of LAMAs

A

Dry mouth, urinary retention, glaucoma

409
Q

Name the treatment steps for acute severe asthma

A
  1. Oxygen
  2. Nebulised salbutamol
  3. Oral prednisolone
  4. Can then give nebulised ipratroprium bromide
410
Q

What should Ipratroprium bromide be given with in life threatening Asthma?

A

Oxygen, as want to oxygenise the blood as much as possible

411
Q

What should Ipratroprium bromide be given with in life threatening COPD?

A

Air - want to prevent shutting off of breathing due to hypoxic drive

412
Q

Why are LAMAs not useful first line therapy in asthma but useful in COPD?

A

Bronchoconstriction in asthma due to B2 receptors

In COPD is due to muscarinic receptors

413
Q

Define a seizure

A

Sudden irregular electrical activity in the brain causing physical mnaifestations

414
Q

Define convulsions

A

Uncontrolled shaking movements due to repeated muscle contraction

415
Q

Define status epilepticus

A

Epileptic seizures occurring without recovery of consciousness in between - emergency

416
Q

Name the two overall classifications of seizures

A

Partial

Generalised

417
Q

Define a partial simple seizure

A

Seizure of a part of the brain

No loss of consciousness

418
Q

Define a complex partial seizure

A

Seizure of a part of the brain

No loss of consciousness

419
Q

What is the first line treatment for partial seizures

A

Carbamazepine

420
Q

Name 5 types of generalised seizures and give a short description of each

A 
Tonic: Increased tone
Atonic: Without tone - drop attack
Tonic-clonic: muscles tense, then conulsions happen
Absence: stop-mid sentence
Myoclonic: shock-like muscle jerking
421
Q

What could give a false-positive EEG result for a seizure?

A

Syncope

422
Q

What other investigations should be carried out on someone who is suspected of having a seizure?

A

ECG - arryhthmias

MRI

423
Q

Name 4 classes of drugs for epilepsy

A

Na channel blockers
GABA potentiators
Ca channel blockers
Levitiracetam

424
Q

Name 3 Na channel blockers used in epilsepsy and describe their MOA

A
  • Lamotrigene
  • Sodium valproate
  • Carbamazepine
425
Q

Name 4 side-effects of Na channel blockers

A

Affects cerebellum and brainstem:

  • Bradycardia
  • Dysdiadokokinisea
  • Ataxic gait
  • Nystagmus
426
Q

Name a Ca channel blocker used in epilepsy and what it is used for

A

Ethosuximide
(sodium valproate)
Absence seizures

427
Q

Name 3 GABA potentiators and their type

A

GABA-transaminase inhibitor - Vigabatrin
Gabapentin - increases GABA production
Diazepam - Benzodiazepines - only used to stop seizures

428
Q

Describe the MOA for Levetiracetam

A

Inhibits pre-synaptic ca channel activity

429
Q

How are anti-epileptics prescribed?

A

Monotherapy only

430
Q

What is the first line for generalised/tonic-clonic seizures?

A

Sodium valproate or Lamotrigene

Second line: Levetiracetam

431
Q

What is Phenytoin?

A

A sodium channel blocker - anti-convulsant
Used for status epilepticus
Has a small therapeutic window

432
Q

Name a liver enzyme inhibitor

A

Sodium valproate

433
Q

Name a liver enzyme inducer

A

Carbamazepine

434
Q

Name 4 side-effects of all anti-epileptic drugs

A

Dizziness
Fatigue
Ataxia
Diplopia

435
Q

Why is Sodium Valproate a teratogenic drug?

A

Reduces folate, leading to neural tube defects

436
Q

What is the initial management of a general seizure?

A

Lorazepam

Midazolam if they are a child or don’t have IV access

437
Q

What is the treatment for status epilepticus

A

Lorazepam

If more than 20 mins, give Phenytoin

438
Q

Name 4 clinical features of Parkinson’s

A
  • Tremor - “pill-rolling”
  • Rigidity - lead pipe, cog-wheeling
  • Bradykinesia
  • Bradyphonia
  • Micrographia
439
Q

What is Dopamine degraded by?

A

COMT

Monoamine oxidase

440
Q

Why is L-dopa given rather than dopamine?

A

Can cross BBB

441
Q

Describe the process of L-dopa being given to a patient and what happens to it in the body

A

Given orally
Absorbed by active transport - competes with amino acids
90% inactivated in abdominal wall by MAO and COMT
9% converted to dopamine in peripheral tissues by DOPA decarboxylase

442
Q

What must L-dopa not be taken with? (2)

A

Protein foods

Pyridoxine - increases peripheral breakdown

443
Q

What must L-dopa be given with?

A

With a DOPA decarboxylase inhibitor and a COMT inhibitor

444
Q

Give an example of a L-dopa mix

A

Co-careldopa

Co-beneldopa

445
Q

Name 4 side-effects of L-dopa

A

Nausea
Hypotension
Psychosis
Tachycardia

446
Q

Name 3 dopamine receptor agonists

A

Ropinirole
Rotigotine
Apomorphine

447
Q

What is a major side-effect of dopamine receptor agonists?

A

Dopamine dysregulation syndrome

  • Gambling
  • Hypersexuality
448
Q

Name 4 side-effects of dopamine receptor agonists

A
  • Sedation
  • Hallucinations
  • Confusion
  • Nausea
  • Hypotension
449
Q

Name 2 Monoamine Oxidase B inhibitors

A

Selegiline

Rasagaline

450
Q

Name 1 COMT inhibitor

A

Entacapone

451
Q

What is important to note about COMT inhibitors?

A

Do not work without L-dopa, just reduce peripheral breakdown of L-dopa - reduces symptoms of “wearing off”

452
Q

What drugs affecting neuromuscular transmission exacerbate Myasthenia Gravis?

A

B-blockers
ACE inhibitors
Aminiglycosides (gentamicin)
Chloroquine

453
Q

Name the complications of not treating and over-treating myasthenia gravis

A

Not treating: Acute exacerbation (myasthenic crisis)

Overtreatment: cholinergic crisis

454
Q

Name the treatment for Myasthenia Gravis

A

Pyridostigmine - AcHesterase inhibitor

455
Q

What are the side-effects of Pyridostigmine?

A

SLUDGE

456
Q

What can Pyridostigmine not be given with?

A

Hypertension medications, as can lead to bradycardia

457
Q

What can be given to a patient before giving them cyclophosphamide to prevent haemorrhagic cystitis?

A

MESNA

Pharm ESA 4 (1 decks)

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