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Pharmo Flashcards

0
Q

What is reasons model of accident causation?

A

A number of factors that come together, all required but non sufficient to cause the error alone. Includes latent conditions, active failure and failure of defences.

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1
Q

What are the different sorts of active failure in prescribing?

A

Violation - Directly contravening known guidelines
Slips - e.g. Copying one dose for multiple drugs
Lapses - e.g. Missing a contraindication
Mistakes - e.g. Not knowing to reduce a drug in renal failure

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2
Q

Why do errors happen?

A 
High expectations from day 1
Exhaustion on nights
Lack of senior support
Routine task boredom
Lack of familiarity with patients 
New drugs
Increased uses of drugs 
Older patients with co morbidities and poly pharmacy
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3
Q

What is the individual vs systems base for medical drug errors?

A

Individuals fault - fear, retrain, litigation, naming and shaming
System fault - safeguards, barriers, acceptance and improvement

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4
Q

What is pharmacovigilance?

What are the aims?

A

The process of id and responding to safety issues about marketed drugs.

  • id previously unrecognised safety hazards
  • what causes the toxicity
  • obtain evidence of safety to allow widening of drugs use
  • identify false positive adrs
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5
Q

What are type a and type b drug reactions?

A

A - predictable, exaggerated pharmocological response, dose dependant, common, high morbidity low mortality
B - unpredictable, not expected, in dependant of dose, rare, high mortality

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6
Q

What are the dissadvantages of a clinical trial vs clinical prescription?

A 
Small number of patients vs millions 
Restricted age, pmh and dhx vs anyone indicated 
Limited duration vs lifelong 
Specialists prescribers vs generalists
High level of clinical monitoring vs low
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7
Q

How are adrs identified?

A

Spontanious reporting
Cohort studies
Case control studies

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8
Q

What is the yellow card scheme?

What drugs should be especially reported?

A

A report of potential adrs to mhra
Mhra then consider the cohort or case control studies

Black triangle drugs (1st year out of trials)
Unusual or serious reactions from established drugs

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9
Q

Problems with yellow card scheme?

A

Significant undereporting
Delays in reporting
Poor data - filled in too fast
Misleading reports
No control group (how many recieve with no issues)
Difficulty recognising previously unknown adrs

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10
Q

Why is reporting of adrs low?

A 
Failure of pt to report
Adr is trivial
Not knowing report
Lack of time
Uncertainty of causal relationship
Experience with process
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11
Q

What is bioavailability? How is it calculated?

A

Fraction of administered drug that reaches systemic circulation
F = AUC (oral) / AUC (iv)

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12
Q

What factors effect bioavailability?

A

Active - gi membrane pumps, enzymatic destruction, first pass metabolism
Passive - lipid solubility, molecular size of drug, pKa of drug

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13
Q

What factors determine drug distribution?

A

Lipophilicity
Plasma protein binding
Tissue protein binding
Variation in compartment size etc. (E.g. Obese with more fat)

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14
Q

How do we work out volume of distribution of a drug?

A 
Calculate concentration (C0) in plasma at time zero by extrapolating backwards from successive concentration measurements.  
Vd = initial dose / C0 
Assumes immediate distribution of the drug

Alternatively plot Vd using initial dose over current concentration against time then extrapolate back to get Vd at time 0

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15
Q

What does Vd show?

What would a reading of 5L, 10L, 200L suggest?

A

Equivalent volume of plasma a drug is distributed within - indicitive of compartments
5 - in plasma
10 - in ECF
200 - in muscle or fat too

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16
Q

How can Vd be expressed?

A

Total (e.g. 8L) or as a propotion of weight (e.g. 0.2 L/kg)

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17
Q

What reactions occur in phase 1 metabolism?

A

Redox reactions, hydroxylation

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18
Q

What enzymes are most commonly involved in phase 1 metabolism? Which subset?

A

CYP450

CYP459 3A4

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19
Q

How does phase 1 metabolism contribute to differing half lives of drugs?

A

CYP enzymes very generalist and therefore have variable rates with different drugs

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20
Q

What non modifiable factors can influence drug metabolism?

A

Ethnicity
Sex
Age
Genetics

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21
Q

What does pharmacogentetics allow?

A

An understanding how different genotypes will relate to different drugs to determine which drugs are effective and which are safe

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22
Q

Give an example of pharmacogenetics applied to antihypertensive drugs
Why? What is given instead?

A

Ace inhibitors is less effective in black people
Afro caribbeans patients have lower RAS activity so medication would not be so effective.
Thiazide or calcium channel blocker.

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23
Q

What adr are afrocaribbean pts more likely to suffer from lisinopril?

A

Angioedema

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24
Q

What is the formula for half life?

A

T1/2 = 0.7 Vd/CL

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25
Q

What is the definition of half life?

A

The constant fraction of a drug eliminated over a certain time period

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26
Q

What are routes for drug elimination?

A 
Urinary
Bile
Exhaled air
Breast milk
Sweat 
Tears
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27
Q

How is steady state concentration calculated in an infusion?

A

CpSS = dose rate / clearence

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28
Q

How long does it take for a drug given at a constant rate to reach steady state?

A

Five. Half lives

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29
Q

Roughly how is a loading dose calculated?

A

Loading dose = Vd x desired CpSS

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30
Q

Should a loading dose be adjusted for renal failure? What about maintainance doses?

A

Loading no, maintenance yes.

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31
Q

What is the most common drug target?

A

Enzymes

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32
Q

What are some examples of unconventional drug action?

A

Being an enzyme (streptokinase)
Reacting with small molecules (antiacids)
Binding free molecules (chelating agents)

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33
Q

What could cause non linear pharmacodynamics?

A

Limitations in second messengers

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34
Q

Define antagonist

A

Has no intrinsic efficacy blocking the receptor

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35
Q

Define partial agonist

A

An agonist that is unable to reach a full response even when all receptors are activated as such also acts as a partial antagonist

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36
Q

Define affinity, how is it recorded from a graph of binding vs concentration?

A

The tendency for a drug to bind to bind to its receptor

Defined by Kd, the concentration at which half the receptors are bound.

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37
Q

What is efficacy, how is it recorded from a graph of concentration against effect?

A

The maximal response of a drug when bound to. Its receptor

Measured by Emax (response where further increase in drug concentration provides any additional effect)

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38
Q

What is potency? How is it recorded from a concentration response graph?

A

The drug concentration at which 50% of emax is obtained

Recorded as EC50

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39
Q

What do competitive antagonists change?

A

Decrease potency, no change to efficacy

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40
Q

What effect on a dose response curve would a non competitive agonist have?

A

No effect on potency, reduced efficacy

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41
Q

In what situation would a noncompetive antagonist not effect efficacy of a drug”

A

Low enough dose with spare receptors

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42
Q

What do selectivity and specificity refer to in pharmocology?

A

Selectivity - the affinity of a drug for a particular receptor (highly selective may still effect others as dose increases)
Sensitivity - the drug effects a specific subtype of receptor (e.g. Beta 1 only)

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43
Q

How is. Therapeutic index calculated?

A

Td50/Ed50

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44
Q

WHat is therapeutic window?

A

The range of drugs concentrations that elicit a desired effect without unacceptable adverse effects.

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45
Q

List some pharmacokinetic dd interactions

A

Absorption - eg. Changes to gut motility (metoclopramide).
Distribution - protein binding interactions (e.g. Aspirin displacing warfarin)
Metabolism - cyp induction or inhibition
Elimination - altered urine pH (e.g. alkanisation of urine to excrete aspirin)

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46
Q

Name some cyp enzyme inducers and inhibitors

A

Inducers - Rifampicin, chronic alcohol, carbamezapine, st johns wort, sulphonureas
Inhibitors - Cimetidine, acute alcohol, isonazid, valporate, sulphonamides

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47
Q

How do cyp induction and inhibition differ (other than the obvious)!

A

Induction - onset over several weeks (increasing expression of the enzyme)
Inhibition - onset over several days (competitive and non competitive inhibition)

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48
Q

How can pharmacodynamic ddis be used beneficially?

A

Enhance therapeutic effect (combination therapy)

Antagonise unwanted effect

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49
Q

Give some examples of direct and indirect unwanted pharmacodynamic ddis

A

Direct - adrenaline and maoi both causing increased sympathetic stimulation
Indirect - furosemide causing hypokalaemia enhancing digoxin

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50
Q

Which drug classes most commonly cause pharmacodynamic ddis?

A 
Anticonvulsants
Antibiotics
Anticoagulants
Antidepressants
Antiarrhythmics
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51
Q

What diseases most prevalently cause drug disease interactions?

A

Hepatic
Renal
Heart

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52
Q

Enzyme inducers are

A 
PCBRAS
Phenotoin
Carbamezapine
Barbituates
Rifampicin 
Alcohol (chronic)
st Johns Wort
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53
Q

Enzyme inhibitors are

A 
GODEVICES
Grapefruit juice
Omeprazole
Disulfarim 
Erythromycin
Valproate 
Isoniazid
Ciprofloxacin 
Ethanol (acute)
Sulphonamides
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54
Q

Side effects of COCP

A 
Venous thromboembolism
Htn
Mi/stroke
Ca breast and cervix 
Mood swings
Decreased glucose tolerance
Choleostasis 
Breast tenderness
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55
Q

When should COCP not be given?

A

Contraindicated
Smoker >35
Breast cancer

With advice
Cured breast cancer
Obese

Caution
Migraine 
Young smoker
Htn
Previous vte
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56
Q

Benefits of COCP beyond pregnancy?

A

Menstrual relief
Acne reduction
Decrease risk of endometrial, colorectal and ovarian cancer

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57
Q

Which cocp has extra anti acne effect?
Why?
What is the associated problem?
Other use?

A

Dianette
Contains cyproterone acetate which acts both as a progesterone and an anti testosterone.
Higher risk of thromboembolism vs other COCPs
Hirtuism

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58
Q

What are the constituents of microgynon?

A

Ethinyloestrodiol

Levonorgestrel

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59
Q

Which generations of progesterone are associated with increased risk of thromboembolism?

A

3+4

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60
Q

Side effects of POP?

A 
Weight gain
Acne
Irritability
Depression
Fluid retention
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61
Q

What are the advantages of POP?

A

No associated risk of venous thromboembolism, stroke or MI and Ca breast

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62
Q

Why does cocp increase risk of cancer of the cervix?

A

Causes inversion of cervix exposing columnar epithelium to acid causing metaplasia then dysplasia.

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63
Q

What drugs are used for emergency contraception? What are the timeframes?

A

Levenorgestrel (up to 72 hrs)
Ullipristal (up to 120 hrs)
Copper iud (up to 120 hrs)

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64
Q

What is a big risk of emergency contraception?

A

All increase risk of ectopic pregnancy.

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65
Q

What are the benefits of HRT?

A

Relieves menopause symptoms

May reduce osteoporosis incidence

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66
Q

What does hrt not change?

A

Cvd risk

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67
Q

What are risks of hrt?

A

Ca breast
Ihd/stroke
Venous thromboembolism
Uterine bleeding

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68
Q

What patients can recieve hrt in pure oestrogen form?

A

Hysterectomy patients

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69
Q

When might antioestrogens be used?

A

Tamoxifen - ca breast

Clomipnene - infertility due to decreased ovulation

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70
Q

Why may antiprogesterones be used? Example?

A

Mifepristone

Abortion or labour induction

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71
Q

What do the different lipoproteins carry?

A

Chylomicrons - tag gi to tissues
Vldl - tag liver to tissues
Ldl - cholesterol liver to tissues
Hdl - cholesterol tissues to liver

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72
Q

What is the association between cholesterol, smoking, htn and chd?

A

Risk of chd is higher than the sum of the parts when combined

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73
Q

What study showed the relationship between chd and raised cholesterol? In which ethnicities?

A

Framingham - northern europe and usa

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74
Q

What is the relationship between bmi and cholesterol?

A

Increases with increasing bmi (even within normal range)

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75
Q

How do statins work?

A 
Inhibit hmg coA reductase 
Decreases hepatic cholesterol synthesis
Increases expression of ldl receptors
Hepatic cholesterol returns to normal
But increased ldl receptors mean higher clearence
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76
Q

What are the benefits of statins to someone with a high cholesterol? Someone with a normal cholesterol?

A 
Decrease in cholesterol by 10% reduces cvd risk by 15%
Also
- antiinflammatory
- reduced thrombotic risk
- plaque reduction
- improved endothelial cell function
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77
Q

Side effects of statins

A 
Myopathy (up to rhabdomyolitis) 
Muscle pain (myalgia) 
Elevated transaminase 
Gi complaints
Arthralgia 
Nightmares
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78
Q

What are fibric acid derivatives more commonly known as? Give two examples

A

Fibrates
Benzofibrate
Gemfibrozil

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79
Q

How do fibrates work?

A

Stimulate PPAR increasing trasncription of lipoprotein lipase
Causes reduced ldl, increased hdl (both moderate) and marked reduction in tag (30%)

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80
Q

What is a contraindication for fibrates?

A

Choleocystitis

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81
Q

What is the interaction between statins and gemfibrozil?

A

Both additive effect increasing risk of rhabdomyolisis and gemfibrozil inhibits statin glucuronidation increasing its side effect profile greater than the sum of the parts.

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82
Q

What is nicotinic acid also know as? What is its mechanism of action?

A

Niacin

Inhibits lipoprotein synthesis in liver reducing vldl, tag and tc.

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83
Q

What are adverse effects of niacin?

A 
Flushing
Hepatotoxicity 
Glucose intolerance 
Peptic ulcers
Itching
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84
Q

What must niacin be given with? Why?

A

Aspirin, to reduce itching

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85
Q

What is an example of a cholesterol lipase inhibitor? How do they work?

A

Ezetimibe

In brush border of gi tract, limiting absorption of cholesterol

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86
Q

Side effects of ezetimibe

A

Abdo pain, diarrheoa, flatulance

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87
Q

What dietary control can be applied to hyperlipidemia?

A

Low fats, cholesterol and alcohol

High fish oil, fibre, vit c and e

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88
Q

What are the current nice statin guidelines?

A

Primary prevention 20mg atorvastatin if qrisk above 10% in next 10 years
Secondary prevention 80mg atorvastatin (reduce if risk of adrs or ddis)

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89
Q 
What are the abnormal values of 
Fasting bm
Random bm
Hba1c
Gtt 
In diagnosing diabetes?
A

Fasting >7
Random >11.1
Hba1c >6.5
Gtt >11.1

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90
Q

Classes of non insulin antidiabetics

A 
Biguanides 
Sulphonylureas
Glitazones
Alpha glucosidase inhibitors
Gliptins
GLP1 agonist
SLGT2 ingibitors
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91
Q

Example, pd and adrs/benefits of biguanides

A

Metformin
Increases insulin sensitivity increasing peripheral glucose uptake and decreasing gluconeogenesis
Adrs - gi upset, lactic acidosis (therefor not in cardiac or resp failure)
Benefits - limited weight gain, low hypo risk, low cost

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92
Q

Example, pd and adrs of sulphonylureas

A

Gliclazide
Increases insulin release by blocking k channels
Adrs - hypos, weight gain, gi upset, rashes
Benefits - can use in renal failure

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93
Q

Example, pd and adrs of glitazones

A

Pioglitazone
Increases insulin sensitivity via PPARs
Adrs - weight gain, bladder cancer, chf, fluid retention
Benefits - low risk of hypo

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94
Q

When would you not use a glitazone?

A

Cvd

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95
Q

When would you not use a sulphonurea?

A

When hypos would be an issue (eg driving)

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96
Q

Example, pd and adrs of GLP1 agonist

A

Exenatide
Mimics glucogon like peptide 1 released from GI tract - causes increased insulin release and decreased gastric emptying, increased satiety, and decreased glucagon release
Adrs - expensive! Injection site problems, gi upset
Benefits - weight loss, good efficacy

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97
Q

Example, pd and adrs of gliptins

A

Saxogliptin
Stop dpp4 breaking down glp1, increases glp1 therefore increased insulin, decreased glucagon, satiety and slowed gi emptying
Adrs - gi upset, gord
Benefits - weight loss

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98
Q

Example, pd and adrs of SGLT2 inhibitors

A

Dapagliflocin
Increases renal glucose excretion
Adrs - thrush, uti, hypos, polyurea
Benefits - weight loss

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99
Q

Rapid acting insulin

Long acting insulin

A

Lispro (rapid)

Glargine (long)

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100
Q

Side effects of insulin therapy?

A

Hypos
Lipodystrophy at injection site
Allergies to suspension

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101
Q

Insulin regime for someone unable to administer their own insulin example:

A

Twice daily mix of short and intermediate acting insulin (e.g. Humalog 25 - 75% intermediate lispro protamine and 25% rapid acting lispro)

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102
Q

Insulin regime for someone who can monitor their own bm and administer own insulin

A

Long acting (e.g. Glargine) overnight then short acting (eg. aspart) at meals

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103
Q

In what ways can antibacterials be classifed? Which is the most useful clinically? Why?

A

Bacteriocidal vs bacteriostatic
Broad vs narrow spectrum
Chemical structure
Target site - most useful as we can predict action on certain bacteria

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104
Q

What must an antibiotic be able to do in order to be effective?

A

Selectively damage pathogen over body cells

Reach the site of action

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105
Q

What are the three main ways a bacteria can become resistant to an antibiotic?

A

Production of inactivating enzymes
Altering the target site
Altering concentration (decreased influx or increased efflux)

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106
Q

What are the three mechanisms of horizontal bacterial resistance?

A

Conjugation
Transduction
Transformation

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107
Q

How can an appropriate antibiotic be chosen for an infection?

A

Disk sensitivity testing

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108
Q

What are issues with disc sensitivity testing?

A

Abx may not be able to reach site of action
Wrong bacteria cultured
Bacteria may develop resistance during treatment
Wrong dose or route may be used for abx

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109
Q

How are doses calculated for sensitive antibiotics like vancomycin?

A

Calculate minimum inhibitory concentration using an E-test

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110
Q

What are the two GENERAL pharmacodynamic principles of antibiotics? Examples of each

A

Time dependant killing - cell wall ABX - achieved with regular dosing or infusion
Dose dependant killing - aminoglyosides and quinolones (e.g. 1 does of ciprofloxacin for gonorrhoea

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111
Q

What are the different classes of anti cell wall antibiotics? (Main and subsidiary). Examples from each

A

Beta lactams
Penicillins (penicillin!)
Cephalosporins (ceftriaxone)
Carbapenems (meropenem)

Glycopeptides (vancomycin)

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112
Q

What antibiotic would be appropriate in a case of MRSA?

A

Vancomycin

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113
Q

What is the spectrum action of meropenem? What does it not work on?

A

G pos and neg
Anaerobes
No action against mrsa

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114
Q

What is the spectrum of cephalosporin?

What does it not work on?

A

G pos and neg

Does not work on anaerobes or mrsa

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115
Q

What side effects are associated with cephalosporin?

A

Allergic reaction

Clostridium difficile infection

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116
Q

Which penicillin abx is naturally active against beta lactamase producing bacteria?
Which penicillin is active against gram neg?

A

Flucloxacillin

Amoxicillin

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117
Q

How do beta lactam abx work?

How do glycopeptides work differently?

A

Competitively inhibit penicillin binding protein stopping cell wall synthesis
Bind to the petidoglycan cell wall stopping penicillin binding protein from binding

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118
Q

What is the basic structure of the cell wall of a bacteria?

A

Peptidoglycan - carbohydrate chains joined by amino acid bridges

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119
Q

What common bacteria would penicillin V not be useful against? What penicillin could be used instead

A

Staphylococci - many produce beta lactamase

Flucloxacillin

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120
Q

What is responsible for enabling the gram neg actions of amoxicillin?

A

Able to penetrate cell membranes

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121
Q

What is a good use of cephalosporins?

A

Penetrate csf thus meningitis

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122
Q

On what bacteria would vancomycin not work?

A

Gram neg

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123
Q

What are the side effects of vancomycin? Which other group of abx share these effects?

A

Ototoxicity

Nephrotoxicity

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124
Q

What are the three main classes of abx that inhibit protein synthesis? Why are they specific to bacteria?

A

Tetracyclines
Aminoglycosides
Macrolides
As they target prokaryotic ribosomes (30s+50s - 70s)

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125
Q

Which of the 3 classes of abx that effect protein synthesis target the 50s subunit? How do they work?

A

Macrolides

Inhibit peptidyl transferase responsible form moving the growing aa chain from the p site to the a site.

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126
Q

What are the tetracyclins? Moa, adrs, spectrum.

A

Tetracyclin, doxycyclin
Bind to 30s subunit inhibing trna binding causing misreading of mrna.
Stained teeth in children, gastric prokinetics thus diarrheoa
Broad spectrum

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127
Q

Example of an aminoglycoside and spectrum.

A

Gentamicin

Gram -ve with slight gram +ve

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128
Q

What are the side effects of the macrolides?

A

Cyp450 inhibitor

Gastric prokinetic

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129
Q

What classes of drugs effect nucleic acid synthesis?

A

Quinolones (ciprofloxacin)
Sulphonamides + trimethoprim (trimethoprim, sulfadazine)
Metronidazol

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130
Q

How do the quinilones work? Example

A

Ciprofloxacin. Inhibits dna gyrase stopping supercoiling of dna

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131
Q

Effect of sulphonamides and trimethoprim?

A

Inhibit folate synthesis (by inhibiting enzymes including dihydrofolate reductase)

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132
Q

What are the anti tb antibiotics?

A

Rifampicin
Isoniazide
Pyrazinamide
Ethanbutol

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133
Q

What drugs would you give to a fungal infection? How do they work?

A

Azoles - inhibit cell membrane synthesis

Nystatin - inhibits cell membrane function

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134
Q

Differentiate antigenic shift and antigenic drift in flu

A

Shift - 2 different flu viruses in one host swap material producing a novel virus - high risk
Drift - slow mutation of the virus seen in the year to year changes in seasonal flu

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135
Q

Which flu subtypes can have an animal resevoir?

A

A only

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136
Q

What are the surface proteins of influenza virus? What do they do?

A

Haemogglutanin - binds to salysiliate receptor on host cell

Neuroaminidase - releases the virus from the cell surface after budding out

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137
Q

How does the virus loose its envelope once in the cell?

A

Ion influx through m2 ion channel for protons (and activated by protons - low pH)

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138
Q

What drugs block M2 ion channels in flu?

ADRs?

A

Amantadine, rimantadine

Antiparkinsons drugs thus serious cns side effects (nervousness, anxiety, agitation, insomnia, exacerbation of seizures in epileptics, exaggerations of psychotic symptoms in scizophrenics

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139
Q

Why are m2 ion channel blockers poor antivirals?

A

Severe cns side effects

Rapidly develop resistance

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140
Q

Give an example of a neuramonidase inhibitor. Side effects?

A

Oseltamivir

Vomiting, abdo pain, epistaxis

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141
Q

What are the effects of neuraminidase inhibitors?

A

Shorten illness duration
Decrease risk of death
Prophylaxis

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142
Q

What is the recommended treatment window for oseltamivir? Too whom should it be given?

A

48 hours

At risk patients with flu like symptoms during a suspected current outbreak of flu

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143
Q

How does acyclovir work?

A

Inhibits viral dna polymerase

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144
Q

What are the aims of asthma therapy?

A 
Minimal symptoms 
No exacerbations
Minimal use of reliever
No limit to physical activity
Normal lung function
Aim for early control then step up and down as needed
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145
Q

What are the steps of asthma therapy?

A

1 - SAB2 agonist
2 - add inhaled steroid 400mcg
3 - add LAB2 agonist, consider increasing steroid to 800mcg
4 - increase steroids up to 2000mcg, add novel drug
5 - oral steroid

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146
Q

Why do we try to limit use of SAB2 in asthma?

A

Indication of poor control

Overuse causes mast cell degranulation

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147
Q

What are the actions of a intermittently used SAB2 agonist?

A

Relax airway smooth muscle

Inhibit mast cell degranulation

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148
Q

How does beta 2 stimulation relax smooth muscle?

A 
Alpha s
AC
Increase cAMP
Activate PKA
Increase K+ conductance
Hyperpolarisation
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149
Q

Give an example of LAB2 agonist that also acts as a SAB2 agonist
What happens if this is used as a reliever too?

A

Formoterol

Decreases exacerbation number

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150
Q

Example of a long acting beta 2 agonist that does not have short acting effect?

A

Salmeterol

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151
Q

What is the advantage of giving a LAB2 with a steroid combined? 2 examples please.

A

Ease of use - increase compliance
Ensures steroid is being given, not just beta agonists

Symbicort - formoterol and budesinide
Seretide - salmeterol and fluticosone

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152
Q

How are inhaled steroids modified to reduce systemic side effects? Why does this work?

A

Lipophilic side chain

Increases receptor affinity, high local uptake, increased hepatic metabolism

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153
Q

How can steroid inhalers get into systemic systems? How can side effects be reduced? Which steroid is good and bad for this?

A

Swallowed rather than inhaled
Use a steroid that is highly metabolised on first pass eg. budesonide
Beclamethasone undergoes little first pass

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154
Q

What novel drugs can be given in asthma - brief moa and side effects please

A

Methylxanthines such as aminophyllin antagonise adenosine and is a phosphodiesterase inhibitor (increases cAMP). Can cause arrhythmia and fits
Leukotrine receptor antagonists such as montelukast block action of leukotrines - not very efficacious - can cause angioedema, anaphylaxis and fever

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155
Q

Where does COX act to convert arachidonic acid into prostaglandins?

A 
Arachidonic acid
COX
Endoperoxides
COX
PGg
COX
PGh
UNKNOWN MECHANISM
PGe
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156
Q

What do prostaglandins cause generally?

A

Vasodilation
Hyperalgesia
Immunomodulation
Fever

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157
Q

Where do prostaglands act to cause pain? In what ways?

A

Peripherally - EP1 receptor - GalphaQ
decreases K channels and increases Na channels causing depolarisation of neurones
Increased sensitivity to bradykinin

Centrally - EP2 receptor - GaplhaS
Increased PKA decreases glycline affinity reducing inhibition of second order neurones

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158
Q

How do prostaglandins cause fever?

A

IL1 stimulates hypothalamus to produce COX2 stimulating Ep3 receptors GalphaI increasing cellular calcium increasing temperature

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159
Q

Where is COX 1 expressed? What about COX2

A

1 - wide spread - gastric mucosa, renal parenchyma

2 - in inflammed areas, hypothalamus

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160
Q

Which of cox one and two has the larger active site?

A

Cox 2

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161
Q

How do nsaids inhibit cox?

A

Competitive antagonsim

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162
Q

What is the Pk of Nsaids?

A

Heavily protein bound

Two groups - t1/2 under 6 hrs or over 10 hrs

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163
Q

Why do nsaids cause gastric symptoms?

A

Decreased cox1 - decreased mucus secretion and decreased mucosal blood flow

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164
Q

When is nsaids action on the kidneys particually important?

A

Heart patients
Renal patients
Hepatic patients

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165
Q

Side effects of nsaids

A 
Gastric
Bleeding
Wheezing
Reyes syndroms
Stevens johnson syndrome
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166
Q

Give some positive and negative ddis of nsaids

A

Positive - with opiate - good relief
Negative - protein displacement - e.g. Warfarin, methotrexate
- nsaid + aspirin - competes for cox 1 site of aspirin decreasing efficacy

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167
Q

What are unique facts about aspirin?

A

Irreversible inhibition of COX1
T1/2 less than 30 minutes but metabolised to salicylate with t1/2 over 4 hours (though this binds reversibly!)
Zero order at higher dose

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168
Q

What is the classification of paracetamol?

A

Non-Opiate Analgesic Drug

nOAD

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169
Q

How is. Paracetamol thought to work?

A

Weak cox 1-3 inhibitor

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170
Q

What are the layers of the adrenal cortex? What do they excrete?

A

Glomerulosa - minralocorticoids
Fasciculata - glucocorticoids
Reticularis - sex steriods

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171
Q

What does cortisol feed back on?

A

Negativly on hypothalams (reducing CRH) and pituitary (ACTH)

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172
Q

Metabolic actions of glucocorticoids?

A

Raises blood glucose - stimulates glygogenolysis and gluconeogeneis
Proteinolysis
Lipolysis at low concentrations
Lipid deposition at high concentrations

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173
Q

Why might corticosteroids cause hypertension?

A

Increased sensitivity of blood vessels to vasoconstrictors

Mineralocorticoid effect on kidney increases salt and water reabsorption

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174
Q

Side effects of glutocorticosteroids

A 
Weight gain
Increased appatite
Fat redistribution (moon face, buffalo hump, central obesity)
Proteinolysis (striae/thin skin)
Glucose intolerance
Hypertension
Infection
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175
Q

Signs of aldosterone deficiency?

A

Hyponatraemia
Dehydration
Hypotension
Hyperkalaemia

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176
Q

Signs of aldosterone excess?

A

Hypernatraenia
Hypertension
Hypokalaemia

177
Q

Describe the process of crossover with respect to steroids

A

Most steroid drugs have both glucocorticoid and mineralocorticoid effects

178
Q

Which drugs have equal glucocorticoid and mineralocorticoid effects?

A

Hydrocortisone1:1

179
Q

Which drugs have very stronger glucocorticoid effects than mineralocorticoid effects? Which ones? much more so

A

Prednisolone 4:1
Dexamethasone 25:1
Betamethasine 25:1

180
Q

Which steroid is mainly mineralocorticoid

A

Fludrocortisone

181
Q

What do you need to consider about a steroid dose before administrating?

A

Crossover
Duration of action
Equivalent dose

182
Q

Describe the absorption of steroids orally

A

Highly lipophyllic so well absorbed with high bioavailability

183
Q

Where are steroids metabolised?

A

Liver and kidney

184
Q

Examples of steroid routes of administration

A

Iv - hydrocortisone
Oral - prendisolone
Inhaled - budesinide
Topical - beclamethasone

185
Q

How do steroids reduce inflammation?

A

Inhibition of t and b cell responses
Inhibit nf kappa b - signalling molecule for inflammation
Reduced cytokine transcription
Reduced expression of cell adhesion molecules
Reduced phagocytic function
Immunosupression

186
Q

What is the molecular moa of steroids?

What is a variation on this?

A

Diffuses in to cell as lipid soluble
Bind to receptor in cytoplasm (often causing it to dissociate from a heat shock protein)
Enters nucleus and binds to point on dna - hormone response element
Activates or inhibits protein transcription

Can bind to receptors within the nucleus as opposed to cytoplasm

187
Q

What is activation of transcription called by steroids?

What about inactivation?

A

Trans-activation

Cis-repression

188
Q

What do steroids transactivate?

A

Annexin one - decreases arachodronic acid synthesis

189
Q

What do steroids cis-repress?

A

POMC (reducing ACTH production)
Keratin (hence thin skin)
Osteocalcin (osteoporosis)

190
Q

As well as transactivation and cisrepression what do steroids do?

A

Transrepression
Binding to proteins causing decreased cytokines, chemokines, adhesion molecules and inflammatory enzymes, receptors etc.

Some surface receptor action - this would create a rapid respone

191
Q

Examples of when to use steroid use

A 
Decrease Inflammation
To Suppress Immunity To An Extent
Replace Insufficiency 
Diagnosis - Dexamethasone Suppression Test
Preterm Labour
192
Q

Why do steroids cause osteoporosis?

A

Inhibit osteoblasts
Increase osteoclasts
Reduce calcium absorption
Reduce sex steroid production

193
Q

How long will it take to suppress the hpa axis with steroids?

A

3 weeks

194
Q

What can occur in hypoadrenal crisis?

A 
Hypotension
Hypoglycaemia
Hyponatraemia
Hyperkalaemia
Severe dehydration
195
Q

Other than steroids name two other immunosuppressants (classes and drugs)

A 
Azathioprine
Calcineurin inhibitors (ciclosporin, tacrolimus)
196
Q

How does azathioprine work?

A

Metabolised to 6mecaptopurine

Decreases dna and rna synthesis

197
Q

What makes azathioprine unpredictable?

What are the side effects?

A

Broken down at different rates in different people

Bone marrow supression
Malignancy
Infection
Hepititis

198
Q

Which class of immunosuppressants is dependant on cyp for metabolism?

A

Calcineurin inhibitors

199
Q

How do calcinurin inhibitors work?

A

Bind to eponimous bonding proteins (e.g. Ciclosporin binding proteins)
Inhbits calcineurin
Inhibiting production of IL2 in t cells needed for costimulation

200
Q

What are side effects of calcineurin inhibitors?

A

Nephrotoxic
Htn
D and v
Mouth ulcers

201
Q

What is the odd sounding immunosuppressant? How does it work?

A

Mycophenolate mofeti

Inhibits guanosine synthesis in b cells only

202
Q

How does methotrexate work as a dmard

A

Inhibits purine metabolism increasing adenosine that has a regulatory effect on immune cells.

203
Q

Side effects of methotrexate

A

Liver failure
Mouth ulcers
Pnemonitis / intersitial lung disease
Teratogenic

204
Q

What dmard would be used in pregnancy?

A

Sulphasalazine

205
Q

Why is methotrexate used only weekly?

A

Metabolised to polygluyamates with long half life

206
Q

What does sulphasalazine consist of? What does each component do?

A

Sulfapyridine - enters body for RA
Salacilate - remains GI for IBD

Overall inhibits t cell proliferation and neutrophil degranulation and chemotaxis

207
Q

What do you need to be careful of with anti tnf agents?

A

Reactivation of latent tb

Increased risk of malignancy if there has been prior malignancy

208
Q

How do anti tnf agents modify disease?

A

Decrease inflammation
Decreased angiogenesis
Decreased joint destruction

209
Q

What are the endogenous opioids?

A

Enkephalins
Endorphins
Dynorphins

210
Q

What are the three sorts of opiod receptors? What are they? Where are they found?

A

M - supraspinal
K - spinal cord
D - widely distributed
GPCRs

211
Q

What happens when an opioid receptor is triggered?

A

M - k efflux therefore hyperpolarisation therefore decreased Ca
K - decreased Ca influx
D - decreased Ca release
All decrease Ca so there is less synaptotagmin activation so less neurotransmitter release

212
Q

What opiate adrs are associated with the different receptors? What are general ones?

A

M - nausea, vomiting, resp depression, constipation, drowsiness, hypotension
K - dysphoria
General - allergy, dependance, tolerance

213
Q

Example of a partial opiate agonist?

A

Buprenorphine

214
Q

T1/2 of morphine?

A

1-7 hours

215
Q

Why is heroin so active in the brain?

A

Twin acyl groups so very lipid soluble so crosses bbb prior to metabolism to morphine

216
Q

What drugs do opiates interact with

A

Alcohol
Barbituates
Anaesthetics
Naloxone

217
Q

Why does morphine cause resp depression?

A

M receptor mediated decreased co2 sensitivity

218
Q

How does warfarin work?

A

Inhibits vit K reductase necessary for the convesion of glu to gla domains on clotting factors 2, 7, 9 and 10

219
Q

What drugs interact with warfarin indifferent ways?

A

Cephalosporins kill gut bacteria so low vit K potentiating effects
Cyp inducers and inhibitors influence metabolism
Protein percipitant drugs e.g. Aspirin displace warfarin

220
Q

Comment on the onset and offset of warfarin. What can be done to mitigate both.

A

Onset is slow as it takes time to replace fully functional clotting factors with altered ones - give heparin cover until inr acceptable

Offset also takes several days for the reverse reason. Can reverse with - vit K or fresh frozen plasma (if life threatening bleed)

221
Q

What is INR?

A

A standardised prothrombin time for the kit used

222
Q

What is prothrombin time?

A

Measures extrinsic pathway of coagulation
Blood + citrate
Overwhelm citrate with calcium and add tf
Measure time until clot forms

223
Q

What are risks of warfarin in pregnancy?

A

First trimester teratogenic

Risks child cerebral haemorrhage on delivery and bleeding from mother

224
Q

What inr would you aim for if you had a pe, dvt or af?

A

2-3

225
Q

What inr would you aim for if you have a prosthetic valve or dvt/pe/af were still problematic at 2-3?

A

2.5-4.5

226
Q

How does unfractionated heparin work?

What is different about LMWH?

A

Binds to antithrombin III increasing its affinity for factors II and X
LMWH is small so cant span II so only binds X

227
Q

What are some novel anticoagulants? How do they work?

A

Fondaparinux - selective factor ten a inhibitor

Dabigitran - direct thrombin inhibitor

228
Q

Adverse effects of heparin?

A

Bruising
Bleeding
Osteoporosis
Thrombocytopenia

229
Q

What causes thrombocytopenia in heparin use?

A

Autoimmune response within a couple of weeks directed against platelets

230
Q

What monitoring is needed in LMWH and UFH?

A

LMWH - none!

UFH - APTT (activated partial thromboplastin time)

231
Q

What is APTT

A

Activated partial thromboplastin time

Overwhelm citrate with calcium, add activator (not TF

232
Q

How does aspirin work as an anti-platelet

A

Inhibits cox 1 irreversibly
Decreasing txa2
Decreasing g alpha q stimulation and thus decreasing calcium release via. iP3

233
Q

How does clopidogrel act as an antiplatelet?

A

Blocks adp receptor stopping g alpha i stimulation inhibiting cAMP mediated suppression of calcium release (reducing the reduction of a reducer!)

234
Q

What is an example of a GP IIb/IIIa inhibitor?

A

Tirofiban

235
Q

What are the different sorts of medications required in anaesthesia?

A

Premedication - anxiolytic - mirtazapine
Induction agent - IV anaesthetic - ketamine
Maintenance agent - volatile gas - sevoflurine
Paralytic - neuromuscular blocker - rocuronium
Pain relief - opiate - morphine
Antiemetic - dopamine antagonist - metaclopramide
Regional anaesthesia - sodium channel blocker - lidocain

236
Q

What is the term for general anaesthesia without the use of inhaled anaesthetics?

A

Total intravenous anaesthetic (TIVA)

237
Q

When might you use a volatile gas anaesthetic over a intravenous anaesthetic?

A

Needle phobics

238
Q

What is the most common action of anaesthetic agents?

A

Bind to GABAa receptors potentiating GABA increasing its potency and its efficacy
Have the same effects at glycine channels in the spinal cord

239
Q

What are the unusual anaesthetics?

What do they do differently?

A

Ketamine, Xe, N2O

Bind allosterically to NMDA receptors antagonising glutamate. As allosteric reduces efficacy but not potency

240
Q

Where do anaesthetics act?

To what ends?

A

Reticular formation - decreases arousal
Hippocampus - decreased memory
Dorsal horn - decreased pain and decreased reflexes
Brainstem - depressed respiration and cvs function

241
Q

What does a low blood:gas partition mean for an inhaled anaesthetic?

A

Faster induction and recovery

242
Q

What does a high oil:gas partition mean for an inhaled anaesthetic?

A

High potency but also retention so slow recovery

243
Q

What is MAC

A

Minimal alveolar concentration - the minimum concentration of anaesthetic in the alveoli that induces a state in which 50% fail to move to surgical stimuli

244
Q

What increases MAC (making it harder to anaesthetise

A 
Young age
Hyperthermia
Pregnancy 
Alcoholism
Stimulants
245
Q

What decreases MAC increasing response to ananesthetic

A

Old age
Hypothermia
Other depressants - anaesthetics, opiates, N2O

246
Q

What is a disadvantage of TIVA?

A

Less easily reversed due to high protein binding

247
Q

How do iv anaesthetics distribute?

A

Initially to target tissue then into fat

248
Q

When does high blood gas coefficient lead to slower induction?

A

Indicates higher protein bound state

249
Q

How is the effect of anaesthesia graded?

A

Guedels signs
Stage 1 - slight decreased eye movement
Stage 2 - increased excitability and tone, erratic breathing
Stage 3 - increasing levels of relaxation, breathing decreases
Stage 4 - flaccid, apnoic, paralysed

250
Q

What are the 5 aims of anaesthesia?

A 
Hypnosis
Analgesia
Amnesia
Relaxation
Reflex depression
251
Q

What is the depolarising neuromuscular blocker? How does it work? What may need to be given alongside it?

A

Suxamethonium
Activates prolonged depolarisation that desensitises receptors
Atropine

252
Q

Differentiate local and regional anaesthesia

A

Regional is larger area e.g. Epidural, spinal, femoral

253
Q

What is directly proportional to potency, speed and duration of local anaesthetics

A

Potency - lipid solubility
Speed - lower pKa
Duration - degree of protein binding

254
Q

What is the order of effect of local anaesthetics?

A

Small mylinated
Unmylinated
Large mylinated

255
Q

Name 5 classes of diuretics with examples of each

A

Carbonic anhydrase inhibitors - acetazolamide
Osmotic diuretic - mannitol
Loop diuretic - frusemide
Thiazide diuretic - bendroflumethiazide
Potassium sparing diuretic - spironolactone

256
Q

MOA of carbonic anhydrase inhibitors

A

Inhibit luminal CA decreasing CO2 available for reabsorption and increasing luminal HCO3
Due to lower CO2 in cells decreased H+ thus decreased activity of Na/H antiporter thus decreased Na+ reabsorption
Higher HCO3 and H in lumen so increased water.

257
Q

Problems with carbonic anhydrase inhibitors

A

Hypokalaemia - increased Na to DCT therefore increased Na/K antiporters and increased DCT flow washes away K+ increasing gradient

258
Q

What is the characteristic of an osmotic diuretic? When are they used?

A

Filtered but not reabsorbed

Maintain urine out put during surgery, cerebral oedema

259
Q

How do loop diuretics work?

A

Inhibit NKCC2 channels in ascending loop of henle.

260
Q

Side effects of loop diuretics - why?

A

Hypokalaemia - high Na in DCT = increased Na/K antiporter, increased flow past DCT carries away K increasing gradient
Hypocalcemia/magnesia = loss of luminal positive potential from re-secretion of absorbed K through ROMK thus less drive for other cation absorption
Ototoxicity = high dose alters endolymph composition

261
Q

Mechanism of thiazides

A

Inhibits Na/Cl synporter in DCT

262
Q

Side effects of thiazides

A

Hypokalaemia
Hypoglycemia
Gout (thiazide excreted by same channel as uric acid thus competes)

263
Q

Mechanism spirolactone

A

Blocks aldosterone from binding to receptor thus:
Decreased basal Na/K ATPase
Decreased apical ROMK
Decreased apical ENaC
Thus decreased Na absorption and K secretion

264
Q

Side effects of spironolactone

A

Hyperkalaemia

Gynecomastia

265
Q

Uses of carbonic anhydrase inhibitors

A

Glaucoma

Mountain sickness

266
Q

Diuretics to use in CHF

A

1 Loop

2 Thiazide

267
Q

Diuretic to use in liver disease

A

1 spironolactone

2 loop

268
Q

Why would you not use acetazolamide in liver failure?

A

Excretion of NH3 requires proteination in the kidney tubule

269
Q

Why is spironolactone beneficial in liver failure?

A

Avoids hypokalaemia which stimulates ammonia production

270
Q

Which diuretics are used as antihypertensives?

A

Thiazides

Spironolactone off label

271
Q

What is conns syndrome?

A

An aldosterone producing adenoma
Causes sodium and water retention with concurrent htn.
Treat with spironolactome

272
Q

Other than spironolactone name another. K sparing diuretic

A

Amiloride

273
Q

What should be considered when prescribing in renal failure?

A

Potassium levels
Renal function levels
Reduce renal excreted drugs in line with gfr
Stop nephrotoxic drugs

274
Q

Give some examples of nephrotoxic drugs

A 
Ace inhibitors
Aminoglycosides 
Penicillin
Cyclosporins
Metformin
Nsaids 
Calcineurin inhibitors
275
Q

When and why are ace inhibitors ‘nephrotoxic’

A

Bilateral renal artery stenosis
Needs efferent arteriole vasoconstriction to maintaing gfr
Ace inhibitors stop vasoconstriction

276
Q

What is the prevalence of htn?

What is the benefit of lowering bp by 10mmHg?

A

40%

Reduces stroke risk by 60% and CHD by 40

277
Q

What percentage of Htn is secondary? What are causes? What is the commonest?

A 
10%
Renal disease (80%)
Conns syndrome
Phaeochromocytoma
Coarctation of aorta 
Eclampsia
Cushings sydrome
Steroids 
Ocp
278
Q

Lifestyle tx of htn?

A 
Decrease weight to normal
Decrease salt intake
Limit EtOh
Exercise
Fruit and veg
Smoking cessation to reduce cvd risk factors
279
Q

What are the cut off values for htn?

A

Norm - 180/110

280
Q

What is the initial therapy for HTN?

Second line? Third? Fourth?

A

White under 55 - ACEi
Black or over 55 - CC blocker/thiazide

Second line is ACEi and one other
Third line is all three
Fourth line is all three and beta blocker and referral to specialist

281
Q

Side effects of an acei?

A

Hyperkalaemia
Dry cough
Angioedema
Renal failure with bilat renal artery stenosis

282
Q

What might you use if a pt on ace i complains of dry cough?

A

Angiotensin receptor blocker eg. Losartan

283
Q

Example of an alpha 1 blocker
Moa
Side effects

A

Doxazosin
Blocks alpha 1 thus vasodilates
Postural hypotension, dizzyneas, headache

284
Q

What are the two groups of calcium channel blockers?

A 
Dihydropryidines (amelodipine) 
Non dihydropyridines (verampamil, diltazem)
285
Q

Side effects of the dihydropyradines and why

A

Flushing (vasodilation)
Oedema (no venodilation)
Sweating (increased sympathetics)
Tachycardia (reflex from lower bp)

286
Q

Side effects of verapamil/diltazem

A

Bradycardia
Constipation
Negative ionotrophy

287
Q

What study shows the efficacy of the main groups of antihypertensives - what did it conclude about them?

A

Allhat

All three classes showed a 8% reduction in event rate at 5 years with the same bp reduction

288
Q

What medications alter the prognosis of heart failure?

A

Ace inhibitors/ARBs
Beta blockers
Spironolactone

289
Q

Which trials show the efficacy of spironolactone in chf?

A

RALES

290
Q

What medications only show symptom relief in heart failure without effecting prognosis?

A

Loop diuretics

Thiazide diuretics

291
Q

What is the disadvantage of beta blockade in CHF?
How is this mitigated?
How is it thought beta blockers change long term outcomes?

A

Decreased rate and contractility worsting CO
Start at low dose
Over time CO returns to normal but PVR is lowered due to reduced renin secretion by sypathetic stimulation

292
Q

What are mechanisms of SVT generation?

A 
Accelerated automaticity of SA node
Reentry circuit (AVNRT)
Accessory pathway (AVRT)
Ectopic activity (AF/flutter)
293
Q

Why do people get AF?

A 
Usually secondary to something
Htn
Chf
Hyperthyrodism
Alcohol
294
Q

What is the term for a AVRT that passes through the AV node, through the ventricles then up the accessory pathway

A

Orthidromic

295
Q

What is the term for a AVRT that passes through the accessory pathway, through the ventricles then through the AV node in reverse?

A

Antidromic (will have broad QRS)

296
Q

Short term measures to control SVT

A

Cardiovert if unstable
Vasalva / carotid sinus massage
Adenosine
Beta blocker, verapamil or diltiazem

297
Q

Long term measures to control SVT

A

Catheter ablation
Verapamil/diltaziem/beta blocker
Amiodarone
Flecainide

298
Q

How is AF managed if onset has been within 48 hrs?

A

Dc cardioversion

Flecainide/amiodarone

299
Q

What is done to control AF rhythm if onset more than 48 hrs ago?

A

Warfarinise for 6 weeks

300
Q

What can be used for rate control in AF?

A

Beta blockers
Calcium channel blockers
Digoxin

301
Q

What drug shouldn’t be given alone for atrial flutter? Why?

A

Flecainide

Will slow atrial rate allowing one to one conduction to the ventricles paradoxically increasing ventricular rate

302
Q

How should VT be treated graded on severity?

A

Arrest - ALS
Unstable - DC cardioversion
Stable - amiodarone/lidocain then DC cardiovert if necessary

303
Q

How should non sustained VT episodes be treated chronically?

A

Beta blockers, or, if very symptomatic amiodarone/flecainide

304
Q

What are causes of VT?

A

Brugada
Idiopathic
LQTS (congenital, acquired)

305
Q

Examples of each subclass of Na channel blockers and brief MOA

A

1a. = Disopyamide - binds to open NaC, dissociates slowly so lengthens AP
1b. = lidocain - binds to inactive NaC, dissociates rapidly shortening AP. Use dependant block reducing afterdepolerisations
1c. = flecainide - dissociates very slowly, no effect on AP length

306
Q

General action of na channel blockers

A

Blocking voltage gaited na channels decreasing slope of phase 0 of AP. Decreases rate of AP conduction through the heart.

307
Q

When should Na channel blcokers never be used? Which trial showed this?

A

Structural heart disease

CAST

308
Q

Side effects of class 1abc na channel blockers

A

1a - long qt , hypotension
1b - dizzyness, drowsyness
1c - increased ventricular response to atrial flutter

309
Q

Side effects of beta blockers

A

Bronchoconstriction
Hypotension
Lethargy

310
Q

How do beta blockers influence cardiac function?

A

At sa node reduce GalphaS thus decrease cAMP thus decrease HCN and rate
On myocytes decreases PKA reducing calcium channel phosphorylation and activation

311
Q

What are the class three antiarrhythmics?

A

Eg amiodarone and solatol
K channel blockers but useful drugs also other functions as though theoretically k channel blocking is beneficial by prolonging AP it actually is proarrhythmic

312
Q

Amiodarone side effects

A

LQTS
Pulmonary fibrosis
Fucks with thyroid
Hepatic injury

313
Q

How do the non-dihydrophyramidine ccbs effect heart rate?

A

Blocks inward calcium flow in the sa and av node slowing initiation and conduction,
Negative chronotrophy and ionotrophy

314
Q

When would you not give verapamil or diltaziem?

A

Heart failure - they are negative ionotrophs

315
Q

Half life of amiodarone

A

10-100 days

316
Q

How does adenosine work?

A

Binds to A1 receptors in av and sa nodes activating K conductance hyperpolarising the cell causing massive slowing in conductance

However, t1/2 very short so wears off quickly

317
Q

Side effects of adenosine

A

Bronchospasm
Sense of doom
Chest pains
Flushing

318
Q

What are the two main mechanisms of arrhythmia generation? What are the sub sets of each?

A 
Impulse generation (afterpotentials, ectopic focus, enhanced automaticity)
Conduction (re-entry)
319
Q

What are the four classes of chemotherapy?

Examples

A

Antimetabolites - methotrexate
Intercalating agents - doxyrubacin, bleomycin (kind of)
Alkylating agents - cisplatin
Spindle poisons - taxanes, vinca alkaloids

320
Q

Anticancer actions of methotrexate

A

Inhibits dhfr stopping production of tetrahydrofolate which is oxidised back to dihydrolate by thymidylate synthase. This oxidation drives DUMP to DTMP the precursor of thymine.

321
Q

How does cisplatin work in cancer?

A

Bound to cl- in plasma due to high plasma cl-
Enters cell loosing cl- as low concentration
Now positive it can bind to negative groups on DNA. It has two binding sites so binds two regions interstrand or intrastrand interfering with dna synthesis and rna transcription

322
Q

How does doxyrubacin work in chemo?

A

Intercalates between base pairs interfering with replication and trascription
Creates a complex with dna and topoisomerase inhibiting dna breaking and religation triggering apoptosis
Produces free radicals damaging DNA

323
Q

How does bleomycin act in chemo?

A

Creates superoxides damaging dna activiating a dna cleaving enzyme

324
Q

How do the taxanes work in chemo?

A

Inhibit microtubule degridation by stabilising beta tubulin
Thus cant dissasemble to pull microtubules apart
Cell sticks in metaphase

325
Q

How do vinca alkaloids work in chemo?

A

Inhibits microtubule formation by binding to beta tubulin subunit so cells cant divide

326
Q

In what phases do the different chemo drugs act?

A

Antimetabolites - S
Alkylating - G1 and S
Intercalating - All
Spindle poisons - M

327
Q

What are the different compartments of a tumour defined by cell replication? Which is most amenable to chemo?

A

A - labile
B - stable
C - permanent

A as chemo doesnt tend to work on G0

328
Q

What is the hypothesis for repeated dosing of chemo?

A

Fractional kill hypothesis

Repeatedly killing a set fraction of cancer cells until negligible left

329
Q

What cancers are sensitive to chemo? What arent?

A

Lymphoma - germ cell are

Prostate and brain arnt

330
Q

Indications for chemo?

A

Curative
Palliative
Neoadjuvant

331
Q

What predicts a bad outcome for chemo?

A

Advanced stage
Weak patient
No molecular target markers
Bad scores

332
Q

What is the disadvantage of oral chemo?

A

Taken at home and people think because it is oral it is milder.
People less likely to report serious side effects of chemo as they don’t want it to be stopped

333
Q

General chemo side effects

A 
Bone marrow suppression 
Alopecia 
Mucositis
Nausea and vomiting
Diarrheoa
Myopathy 
Renal failure
334
Q

Specific side effect of bleomycin

A

Pulmonary fibrosis

335
Q

What can cause variability in chemo pharmokinetics?

A

A - d/v, compliance
D - ascities, hypoalbuminia
M - liver dysfunction
E - renal dysfunction

336
Q

DDIs of chemo?

A

Warfarin
NSAIDs with methotrexate
Enzyme inducers / inhibitors

337
Q

What are the problems with most antiepileptics and pregnancy?

A

4 times the risk of OCP failure and teratogenicity (2-8%)

338
Q

What teratogenic consequences are there to antiepileptics? How can they be mediated?

A

Neural tube defects
Digit hypoplasia
Learning difficulties

Give folate and vit K supplement

339
Q

Which antiepileptics act on VGNaC?

A

Carbamezapine
Phenytoin
Lamotrigine

340
Q

How do VGNaC blockers produce a use dependant block?

A

Bind to inactivation gate and must be depolarised to bind thus voltage dependant

341
Q

When can carbamezapine be used? When cant it be used?

A

Complex partial seizures ++
Generalised tonic clonic seizures +
NOT absence seizures

342
Q

General antiepileptic ADRs

A

Ataxia, dizzyness, drowsiness, nausea, vomiting

343
Q

Which antiepileptic can cause stevens johnson syndrome in 2-5%?

A

Phenytoin

344
Q

Which antiepileptic can disturb BP?

A

Carvamezapine

345
Q

Specific side effect of valpourate?

A

Hepatic failure

Weight gain

346
Q

Specific side effects of phenytoin?

A

Gingival hyperplasia
Stevens johnson
Neutropenia

347
Q

What is special about carbamezapine pharmacokinetics?

A

Induces own cyp metabolism reducing own t1/2

348
Q

Are antiepileptics heavily or lightly protein bound? Consequence of this?

A

Heavily

Long t1/2

349
Q

What is special about phenytoin pharmacokinetics

A

Non linear

350
Q

Which antiepileptic needs liver monitoring?

A

Valporate

351
Q

Which antiepileptic needs plasma level monitoring? How else can conc. be measured?

A

Phenytoin

By saliva conc

352
Q

Which antiepileptic can be used in pregnancy? What is the risk of teratogenesis?

A

Lamotragine

2%

353
Q

Which antiepileptic does not effect cyp? Does it still interact with ocP

A

Lamotrigine

Yep - ocp decreases lamotrigine concentration

354
Q

How does valpourate work?

A

Inhibits gaba degridation and increases gaba synthesis

Also some action as a VGNaC blocker

355
Q

What antiepileptics have ddis with aspirin and antidepressants?

A

Carbamezapin

Valproate

356
Q

What is the antidote to benzo od?

A

Flumazenil

357
Q

Adrs of benzos?

A 
Sedation 
Tolerance
Confusion
Resp and cvs depression
Withdrawal and dependance
358
Q

Clinical features of parkinsons disease?

A 
Pill rolling RESTING tremor
Lead pipe rigidity
Bradykinesia 
Instability
Mood changes / cognitive changes
Expressionless facies
359
Q

Differentials of parkinsons? What distinguishes them?

A

Multiple system atrophy - autonomic features
Drug induced parkinsonism (on antipsychotics or metoclopramide)
Progressive supranuclear palsy (opthalmoparesis)
Essential tremor (isolated tremor)

360
Q

How is parkinsons diagnosed?

A

Clinical
Positive response to treatment
DAT scan (tracer absorbed by dopaminergic neurones thus rduced in Parkinson’s - can be used to differentiate from essential tremor)

361
Q

How is adrenaline made?

A 
Tyrosine
- tyrosine hydroxilase
LDOPA
- dopa decarboxilase
Dopamine 
- dopamine hydroxilase
Noradrenaline 
Adrenaline
362
Q

What breaks down dopamine?

A

MAO

COMT

363
Q

Treatment options for parkinsons?

A 
Levodopa (with carbidopa) 
Dopamine receptor agonists
MOAI
COMT inhibitors
Anticholinergics
Surgery
364
Q

When is ldopa most effective? Why? What class of drug can be used when it isnt useful?

A

Early disease when there are still dopaminergic neurones

Use a dopamine receptor agonist

365
Q

Side effects of Ldopa?

A 
On off movements
Freezing
Dystonia
Nausea vomiting
Flushing
Psychosis 
Hallucinations
Tachycardia
366
Q

Pk of LDOPA

How do we alter it

A 
Oral
90% inactivated in intestine
9% converted peripherally
1% in the CNS
Alter with carbidopa to stop peripheral conversion allowing smaller dose with less ADRs
367
Q

What drugs interact with LDOPA

A

MOIs - HTN crisis

Antipsychotics

368
Q

What should you bare in mind when prescribing a COMT inhibitor in parkinsons?

A

Should not be given alone - needs something to work on!

369
Q

Example of a COMT inhibitor

A

Entacapone

370
Q

MOA for entacapone

A

Stops peripheral breakdown of LDOPA increasing amount and also reducing competition for transport into cns against its metabolite
Thus prolongs motor response to LDOPA

371
Q

Example of a MOAI
What does it do?
How should it be used?

A

Selegiline
Prolongs ldopa
Denovo or in combo

372
Q

Example of a dopamine receptor agonist? When are they used?

A

Apomorphine

End stage when there are very few dopaminergic neurones for LDOPA to act on

373
Q

Side effect of Apomorphine

A

Compulsive behaviour (gambling, shopping, hypersexuality)

374
Q

Advantage of apomorphine over levodopa

A

Less motor side effects

375
Q

Why give anticholinergics to parkinsons?
Example
Use

A

Ach antagonises dopamine thus reduce ACh
Amantidine
Drug induced disease

376
Q

What do anticholinergics not help with in parkinsons?

A

Bradykinesia

377
Q

Adrs of anticholinergics

A

Confusion
Blurred vision
Drowsiness
Dry mouth

378
Q

What is the pathology of myasthenia gravis?

A

Autoimmune igg binding to ACh receptor binding site competitivly antagonising acetylcholine
Ach remains in cleft so is broken down by acetylcholinesterase

379
Q

Symptoms of myasthenia gravis

A

Fatiguable weakness esp of extraoccular and bulbar muscles

Symetric limb weakness

380
Q

What exacerbates myasthenia gravis?

A

Neuromuscular blockers

Beta blockers, ccbs, aceis

381
Q

What complications can occur with myasthenia gravis? What participates each?

A

Overtreatment - cholinergic crisis

Undertreatment - myasthenic crisis

382
Q

Symptoms of a cholinergic crisis

A 
Salivation
Lacrimation
Urination
Deification
Gi upset
Emesis
383
Q

Treatment of myasthenia gravis

A 
Acetylcholinesterase inhbitors (neostigmine)
Corticosteroids
Azathioprine
Iv immunoglobulin
Plasmapheresis
384
Q

Signs of depression?

A

2 of the following that are persistant (>2 week)
Low mood
Anhedoina
Low energy

Also poor sleep, hoplessness, self harm, low libido, low appetite

385
Q

Theories of depression causation

A

Decreased monoamine transmitters (NA and 5HT)
Abnormality of monoamine receptor
Deficiency in molecular functioning distal to receptor

386
Q

ADRs of SSRIs

A 
Anorexia
Mania
Suicidal intention
Extrapyramidal side effects
Serotonin sydrome in od
387
Q

MOA of tricyclics

A

Inhibit NA reuptake
Inhibit 5HT reuptake
Muscarinic blocker
Alpha 1 blocker

388
Q

ADRs of tricyclics

A 
Sedation
Seizure
Arrhythmia
Poor eye accomodation
Postural hypotension
Constipation
389
Q

Other than ssri and tca, what other class of antidepressant are used? Example?

A

Serotonin Noradrenaline Reuptake Inhibitor

Venlafaxine

390
Q

MOA of SNRI

A

Low dose increases serotonin

High dose increases NA

391
Q

Additional side effects of SNRI over SSRI

A

Sleep disturbance
HTN
Dry mouth

392
Q

What drugs work well in bipolar?

A

Antiepileptics

Lithium

393
Q

Why no antidepressants in bipolar?

A

Increase mania

Dont effect the depression

394
Q

Symptoms of mania

A 
Overactivity 
Poor sleep
Rapid speech
Poor judgement
Promiscuous 
Delusions of grandure
395
Q

How does lithium work?

A

? Competes with ca/mg channels
? Increases 5HT
? Attenuates second messengers of neurotransmitter

396
Q

ADRs of lithium

A 
Memory issues
Thirst
Polyuria 
Tremor
Nephrotoxic 
Thyrotoxic
Hair loss
397
Q

What monitoring does lithium require?

A

3 monthly levels and thyroid every 6 months

398
Q

Examples of positive schizophrenia symptoms

A 
Disturbance in thinking
Hallucinations
Delusions
Unusual speech
Behavioural change
Lack of insight
399
Q

Causes of schizophrenia?

A

Biological Genetic Upbringing

Thought to be due to excess dopamine with possible 5HT involvement

400
Q

What is the target pathway for dopamine antagonists in schizophrenia? What effects does this have? What other pathways are effected? Side effects?

A

Mesolimbic - therapeutic reduction in positive symptoms
Mesocortical - increases negative symptoms
Nigrostriatal - extrapyramidal side effects
Tuberoinfundibular - hyperprolactiemia

401
Q

What are extrapyramidal effects?

A

Tarditive dyskinesia
Pseudoparkinsonism
Acute dystonic reactions (muscle spasms of the neck, jaw, back, eyes, tongue)

402
Q

Examples of typical antipsychotics

A

Haloperidol

Chlorpromazine

403
Q

MOA of typical antipsychotics

A

Dopamine blockers
Anticolinergics
Alpha adrenoceptor blockers
Antihistamines

404
Q

Advantages and disadvantages of typical antipsychotics?

A

Ad - known course and side effects

Di - more sedating

405
Q

Side effects of antipsychotics

A

Postural hypotension
Weight gain
Neuroleptic malignant syndrome
Extrapyramidal side effects

406
Q

Name 2 atypical antipsychotics

A

Olanzapine
Rispiridone
Quetiapine
Clozapine

407
Q

Which antipsychotic is most efficacious? Why isnt it used more?

A

Clozapine

Bad side effects

408
Q

What factors stimulate vomiting?

A

Irritation of stomach
Chemoreptor trigger zone
Vestibular apparatus

409
Q

What is released by the stomach on irritation and thus is a drug target for vomiting? What does it stimulate? Where else is this found?

A

5HT stimulating CNX

Chemoreceptor trigger zone

410
Q

What does the vestibular apparatus release in response to noxious stimuli?

A

ACh

Histamine

411
Q

Where do all stimulants for vomiting come together?

A

The medullary vomiting centre

412
Q

What are the different classes of antiemetic?

A

D2 antagonist
5HT antagonist
Antihistamine
ACh antagonist

413
Q

MOA of domperidone?

A

Decreases CTZ activation (dopamine antagonist)

Activates gastric emptying (ACh agonist)

414
Q

MOA metoclopramide

A

Decreases CTZ triggering (D2 antagonist)
Increases gastric emptying (increases ACh)
Decrease stimulation from irritation (5HT atagonist)

415
Q

Which of domperidone and metoclopramide produces worse extrapyramidal effects? Why?

A

Metoclopramide, crosses BBB

416
Q

What other side effects are assocaited with dopamine receptor antagonists used in nausea other than extrapyramidal?

A

Galactorrheoa

417
Q

Example of a 5HT antagonist used in nausea and vomiting

How does it work?

A

Ondansterone

Lowers stimulation of CTZ and stimulation of vagus by irritated stomach

418
Q

Adrs of ondansterone

A

Flushing
Headaches
Constipation

419
Q

Example of ach antagonist in nausea and vomiting

How does it work

A

Hyoscine

Blocks ach from vestibular apparatus

420
Q

What is hyoscine particually useful in?

A

Motion sickness

421
Q

Adrs of hyoscine

A 
Dry mouth
Blurred vision
Paroxismal bradycardia
Low sweating
Itching
422
Q

What h1 antagonist is useful in nausea and vomiting? How does it work?

A

Cyclizine

Crosses bbb and decreases histamine from vestibular apparatus

423
Q

Side effect of cyclizine

A

Qt prolongation

Seditive

424
Q

Types of laxatives and examples?

A

Bulk forming - isphaghula husk
Faecal softners - arachis oil
Osmotically active - macrogel and lactulose
Irritant - senna

425
Q

Wich laxatives are best for soft faeces constipation

A

Stimulants like senna

426
Q

Which laxatives are best for impacted faeces?

A

Osmotic and bulk forming

Lactulose, macrogels and ispaghula husk

427
Q

Major complication of laxatives - how does it happen?

A

Hypokalaemia

Hypokalaemia causes decreased bowel inertia and constipation
Laxative decreases amount of absorbed from bowel (+ feedback) also decreases Na absorption so kidneys raise Na reabsorption increasing renal K loss
Worse hypokalaemia and thus back to the top

428
Q

What is an important consideration when giving a laxative regarding dehydration? Which laxative avoids this problem?

A

Must be given with fluid

Macrogels - powder so must be dissolved mandating fluid intake

429
Q

What laxatives have an immidiate (or rapid) onset?

A 
Magnesium enema (osmotic) - within an hour
Senna (Irritant) - 8 to 10 hours
430
Q

What laxatives are useful in patients with perianal disease?

A

Faecal softners like arachis oil

431
Q

What laxative is used in liver failure? Why?

A

Lactulose

Metabolised by bacteria to acetic and lactic acid acidifying the colon increasing NH4 excretion

432
Q

How do ispaghula husks work?

A

Resistant to digestion
Pull h2o into bowel
Distends bowel triggering contraction and movement

433
Q

Contraindications to bulk forming laxatives

A

Obstruction

Adhesions and ulceration - cause obstruction!

434
Q

What happens if you keep using senna?

A

Colonic atony resulting in constipation

435
Q

What is a good laxitive to use with IBS

A

Ispaghula husks

Absorbs water so is a good laxative if constipated and absorbs water from diarrhoea improving faeces composition

436
Q

Types of anti diarrheoal

A

Antimotility
Bulk forming
Specific treatments

437
Q

What are antimotility antidiarrhoeal?

A

Opiates / loperamide

Decreases bowel motility so increases fluid reabsorption

438
Q

What is a risk of antimotility antidiarrhoeals in IBD

A

Toxic megacolon

439
Q

What specific diseases treatments can aid in diarrhoea

A

Pancreatic supplements

Bile acid suppressants in chrones

440
Q

What would antidiarrhoeals worsten?

A

Overflow constipation

Infection

441
Q

No pharmocological laxatives?

A

Treat underlying cause (dehydration, obstruction, parkinsons)
High fibre diet
Increase fluids
Exercise
Stop causative drugs (codein, calcium, anticholinergics, tca/ssri

PPE (12 decks)

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