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Phase 2A > ICS: Pharmacology (with Prescribing) > Flashcards

ICS: Pharmacology (with Prescribing) Flashcards

1
Q

two main physiological factors of a patient to consider when prescribing

A
  • renal disease (=kidney!!)
  • hepatic disease (liver!)
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2
Q

define synergy

A
  • where action of two or more drugs combine
  • can be positive or negative
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3
Q

example of synergy

A

paracetamol & codeine: increases analgesic effect

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4
Q

define antagonism

A

one drug blocking the mechanism of another

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5
Q

define pharmacokinetics

A

action of the body on the drug: how it’s broken down

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6
Q

factors affecting pharmacokinetics

A

or = p. kinetics = (ADME)

  • absorption
  • distribution: bloodstream, fats, protein binding
  • metabolism: how is it broken down and
  • excreted
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7
Q

factors affecting absorption of a drug

A
  • motility
  • acidity of the drug
  • solubility of bloods
  • formation of drug
  • action on enterocytes (grapefruit juice inhibit drug transporter!)
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8
Q

What is an important SE of erythromycin?

A

direct GI stimulation therefore affecting motility of drug

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9
Q

Which particular food may change how warfarin is absorbed?

A

Avocado - has been shown to decrease effectiveness of warfarin, therefore increasing risk of clotting.

  • stays in GI tract longer due to high fat content
  • also a CYP450 inductor - increases drug metabolism so gone before it makes a diff

Ginger also reduce effectiveness of anticoag so + risk of bleeding

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10
Q

what is a prodrug?

A

a drug that needs to be broken down in order to work

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11
Q

what are CYP450’s

A

cytochrome P450

  • hemeproteins - in mito or ER
  • metabolises many substrates, most drugs undergo deactivation by CYPs direct or facilitated
  • regulates detox (= defence mechanism)
  • class 1, 2, 3 most important in humans
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12
Q

two ways, involving CYP450, through which the metabolism process of a drug can be affected

A

inhibition & induction

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13
Q

define inhibition?

A

drug A, inhibiting CYP 450, blocks the metabolism of drug B, leaving more free drug B in the plasma therefore increasing effect of drug B

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14
Q

Examples of food CYP450 inhibitors? (3)

A

grapefruit juice (CCB), soya (NSAID, warf)

→ they decrease metabolism of a drug = increase effectiveness / build up toxicity

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15
Q

define induction?

A

drug C induces CYP450 isoenzyme, leading to increased metabolism of drug D resulting in decreased therapeutic effects of drug D

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16
Q

drugs that induces CYP450?

(beautiful mnemonic)

A

CRAP GPS induces my rage (increase drug met so gone before effect)

  • carbamazepine
  • rifampin
  • alcohol
  • phenytoin
  • griseofulvin
  • phenobarbital
  • sulfonylureas
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17
Q

significance of grapefruit juice on medications

A
  • inhibit p-glycoprotein - a drug transporter - therefore affects absorption of the drug
  • CYP450 inhibitor - subtype CYP3A4 → can make a drug more effective/toxic as it stays longer in body
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18
Q

significance of st john’s wort (Hypericum perforatum) on medications

A

CYP450 inductor = increases metabolism of medications = makes them less effective.

on Warfarin, digoxin, cyclosporin, phenytoin, antiretrovirals

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19
Q

how are drugs first broken down in the liver, and in the kidneys?

A
  • most are renal excretion = kidneys, which is pH dependent
  • some are biliary excretion
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20
Q

pH principles in relation to excretion of a drug

A
  • most drugs are excreted renally, which is pH dependent
  • clears faster if urine is opposite pH of drug
  • weak bases - cleared faster if urine acidic
  • weak acids - cleared faster if urine is alkali
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21
Q

define bioavailability

A

amount of drug that reaches the systemic circulation as a proportion of amount administered

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22
Q

method of administration with the highest bioavailability

A

IV

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23
Q

bioavailability formula

A

AUC oral / AUC IV x 100

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24
Q

What other factors can reduce bioavailability other than method administered

A
  • area of gut
  • gastric pH!
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25
Q

define pharmacodynamics

A

action of the drug on the body: how the drug is used and its effect on cellular receptors via signal transduction

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26
Q

what types of ligands can there be?

A

ligands can be exogenous (drugs) or endogenous (hormones, neurotransmitters etc)!

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27
Q

types of receptors a drug can target?

A
  • ligand gated ion channels (nicotinic ACh receptor, binding allows + to move in)
  • G protein coupled receptors (muscarinic, beta 2 adreno)
  • Kinase linked receptors (for growth factors - tyrosine phosphorylation)
  • cytosolic / nuclear receptors (for steroids - can modify gene transcription)
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28
Q

Briefly outline how will a ligand-fated ion channel act as a receptor fro drugs

A
  • pore forming membrane proteins, allows ions to pass through the channel pore
  • ligand is the interactor which allows pore to open and move
  • once open, transduce external signals to inside of the cell
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29
Q

Briefly outline how will a G protein coupled receptor work as a receptor for drugs

A
  • transmembrane receptors, targeted by > 30% of drugs
  • changes conformation: hydrolyse GTP to GDP = switch on or off, elicit downstream signalling for effect of the receptor
  • majority of GPCR interact with PLC or AC
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30
Q

Briefly outline how will a kinase linked receptor work as a receptor for drugs

A
  • kinase = enzymes that catalyze the transfer of phosphate groups between proteins (= phosphorylation)
  • so regulating phosphorylation = way to activate signalling
  • extracellular bind = intracellular activity = transmembrane signalling
  • kinase themselves can be ligands
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31
Q

Briefly outline how will a cytosolic / nuclear receptor work as a receptor for drugs

A
  • works by modifying gene transcription (activate or repress)
  • e.g. tamoxifen
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32
Q

examples of diseases where an imbalance of chemicals led to pathology?

A
  • allergy: increased histamine
  • parkinson’s: decreased dopamine
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33
Q

examples of diseases where an imbalance of receptors led to pathology?

A
  • myasthenia gravis: loss of nicotonic ACh receptors
  • mastocytosis: increase in C-kit receptor
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34
Q

what is the two state model of receptor activation?

A

describes how drugs activate receptors by inducing or supporting a conformational change in the receptor from ‘off’ to ‘on’

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35
Q

define agonist

A
  • binds to receptor and **activates it**
  • can be full or partial
  • e.g. salbutamol (asthma) = beta 2 agonist
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36
Q

define antagonist

A
  • binds to receptor and prevents its activation
  • can be reversible or irreversible
  • main site or allosteric site
  • e.g. propanolol = beta blocker
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37
Q

define potency

A

binding affinity of the drug to the receptor = how well a drug works

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38
Q

What does it mean to say that drug A is more potent than drug B?

A

Lower concentrations of drug A will give an equal or greater response than drug B

= aka drug A is more efficacious than drug B

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39
Q

what is EC50

A

concentration of a drug that gives half the maximal response

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40
Q

significance of a narrow therapeutic range

A
  • increased risk of toxicity
  • decreased chance of effective dose
  • e.g. digoxin, lithium, genta/vancomycin
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41
Q

SE simvastatin when prescribed with a potential interactor

A

Rhabdomyolysis = muscle aches

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42
Q

SE warfarin when prescribed with a potential interactor (antibiotic mycins, amiodarone, opioid)

A

Increased risk of bleeding

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43
Q

How would you combat warfarin interactive SE?

A

Monitor INR (= prothrombin time, time for the blood to clot) at day 3, then weekly up to 4 weeks post commencement

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44
Q

SE SSRI when prescribed with TCA & tramadol

A

serotonin syndrome

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45
Q

What is the triple whammy?

A
  1. NSAID or COX2
  2. ACE-i
  3. Dehydration or furosemide

gives you major renal failure

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46
Q

What does the concentration response curve describe?

A
  • amount of response per amount of stimuli (dose)
    • always on a log scale, sigmoid curve shape
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47
Q

Define efficacy

A

maximum response achievable, how well a ligand activates the receptor

(only agonists show this! antagonist doesn’t activate!)

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48
Q

Define intrinsic activity

A

ability of drug receptor complex to produce a maximum functional response

= Emax of partial agonist / Emax of full agonist

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49
Q

Define affinity

A

describes how well a ligand binds to the receptor

(shown in both antagonist and agonist!)

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50
Q

What is receptor reserve?

A

= spare receptors

property a tissue needs to have should it be targeted by full agonists (full = block all receptors!)

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51
Q

Difference between a full agonist and a partial agonist

A

in full agonists - all receptors will be blocked so there needs to be a receptor reserve

in partial agonists - even if all receptors are occupied, max response is not seen

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52
Q

What is signal amplification?

A
  • a signal cascade is initiated before a response
  • signal amplification will determine how powerful response will be, but it does not necessarily equal to amplified response!
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53
Q

What is allosteric modulation?

A

Binding of an allosteric ligand to a receptor can affect the effect of an agonist on the receptor

  • can be modulation in affinity or efficacy
  • modulation can be positive = allosteric or negative = orthosteric
  • benzodiazepine = allosteric ligand
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54
Q

Define tolerance?

A

= reduction in drug (agonist) effect over time

  • seen with continuous, repeated high concentration over drug over time
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55
Q

What is desensitisation of receptors?

A
  • three ways: uncoupled, internalised, degraded receptors → binding is affected
  • rapid process!
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56
Q

Term to describe specificity of drug?

A
  • no drug is ever truly specific ;)
  • selective is the better term
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57
Q

Which enzyme is a known clot buster?

A

Streptokinase

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58
Q

How do NSAIDs work?

A

by inhibiting COX enzymes which takes part in prostaglandin synthesis

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59
Q

Actions of NSAIDs?

A
  • analgesic
  • anti-pyretic
  • anti-inflammatory
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60
Q

Role of COX enzymes in prostaglandin synthesis?

A

breaks down arachidonic acid into prostaglandin H2

NSAIDs competitively inhibit COX enzymes so a. acid cannot reach active site

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61
Q

prostaglandin effect

A
  • group of lipids made at site of tissue damage / infection
  • controls inflammation, blood flow, formation of blood clots and induction of labor
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62
Q

Forms of COX enzymes?

A

COX 1 - found normally and widely in the body

COX 2 - this is induced, and found mainly in inflammation only!

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63
Q

Types of NSAIDs and how they act on COX enzymes

A

Aspirin - non-selective, irreversibly blocks active site = inactivation of both COX enzymes
= also reduce platelet aggr

Celecoxib / etoricoxib - selective, only act on COX-2
= reduces GI effects

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64
Q

How do Angiotensin-converting enzyme inhibitors (ACEi) work?

A
  • blocks action of ACE therefore blocks the conversion of angiotensin I to angiotensin II
  • angiotensin II = vasoconstrictor
  • blocked A-II = reduced peripheral vascular resistance (afterload)
  • also aldosterone level is reduced so sodium and water excretion promoted
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65
Q

Indications of ACEi’s

A
  • hypertension
  • chronic heart failure
  • ischaemic heart disease
  • diabetic neuropathy and CKD with proteinuria
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66
Q

Examples of ACEi’s

A

ramipril, lisinopril, perindopril

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67
Q

Important SE of ACEi !!!

A

dry cough!

also dizziness after first dose (from profound hypotension - titrate up)

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68
Q

How do statins work? (3)

A
  • reduce serum cholesterol levels by inhibiting HMG CoA reductase, enzyme involved in making cholesterol
  • decrease cholesterol production by liver and increase LDL clearance from blood
    • indirectly reduce triglyceride and slightly increase HDL levels
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69
Q

Actions of statins?

A
  • reduce cholesterol / triglyceride production, LDL levels
  • slow the atherosclerotic process or reverse it
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70
Q

Indications of statins?

A
  • prim and second prevention of cardiovascular events
  • primary hyperlipidaemia
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71
Q

SE and interactions for statins?

A
  • headache, GI disturbances
  • metabolism reduced by cytochrome P450 inhibitors (amiodarone, macrolides)
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72
Q

three types of protein ports and how they work?

A
  • uniporter - uses ATP to pull one molecule in
  • symporter - uses movement of one molecule to pull in another against [gradient]
  • antiporter - uses movement of one substance moving down the gradient (usually Na+, K+ or H+) to transport another substance against its gradient
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73
Q

Example of medication that targets a symporter to achieve therapeutic effect?

A

loop diuretics e.g. furosemide, bumetanide

  • inhibits sodium-potassium chloride co transporter (NKCC) in ascending loop of henle by binding to it
  • causes Cl & K loss in urine
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74
Q

indications of loop diuretics?

A
  • relief of breathlessness in acute pulmonary oedema
  • fluid overload in both chronic heart failure and other oedematous states
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75
Q

Types of channels a drug can target (major elements)?

A

Sodium, Calcium, Potassium, Chloride

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76
Q

Example of medication that targets epithelial sodium channels?

A
  • amiloride & thiazide
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77
Q

How do thiazides work? Indication?

A
  • thiazide diuretics inhibit the Na/Cl co-transporter in the distal convoluted tube of the nephron → prevents reabsorption of sodium → diuretic
  • also vasodilate but mechanism unknown
  • indication = hypertension, first line alt or add on
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78
Q

SE & CI thiazide diuretics?

A
  • hyponatraemia
  • hypokalaemia → cardiac arrhythmia
  • CI gout as reduce uric acid excretion
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79
Q

Examples of thiazide diuretics?

A

thiazide - bendroflumethiazide

thiazide like - indapamide, chlortalidone (works the same)

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80
Q

Example of medication that targets voltage gated calcium channels?

A

Calcium Channel Blockers = CCB’s

e.g. amlodipine, nifedipine, diliazem, verapamil

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81
Q

How do CCB’s work?

A
  • decreases movement of calcium into vascular smooth muscle and cardiac muscle cells → relaxation and vasodilation
  • within heart, it reduces myocardial contractility, suppress conduction
  • reduced cardiac rate, contractility and afterload reduce myocardial oxygen demand → prevents angina
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82
Q

Types of CCB’s?

A
  • Dihydropyridines = selective for vasculature = amlodipine & nifedipine
  • Non-dihydropyridines = more selective for the heart = verapamil & diltiazem (some effect on blood ves)
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83
Q

CCB indications?

A
  • all CCB’s = stable angina (alt = beta blocker)
  • amlodipine (& nifedipine but less) - 2nd line hypertension & CVD prevent
  • diltiazem & verapamil = rate control in supraventricular tachy, AF, flutter
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84
Q

Important and common SE of amlodipine (& nifedipine)

A
  • peripheral oedema
  • flushing, headaches, palpitations
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85
Q

Common SE verapamil

A
  • constipation
  • more seriously, bradycardia, heart block and cardiac failure
  • diltiazem = any of them
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86
Q

Medication which targets voltage gated sodium channels?

A

lidocaine - anaesthetic

= blocks transmission of action potential in voltage gated sodium channels.

→ reduces arrhythmia!

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87
Q

What does it mean if a channel is voltage gated

A

action potential will induce a conformational change of the channel

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88
Q

Medication which targets voltage gated potassium channels?

A

Sulphonylureas → lowers blood glucose

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89
Q

Where are voltage gated potassium channels found?

A
  • in excitable tissues like muscles and neurones (selective for K=)
  • beta islets of Langerhans - regulates insulin in pancreas
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90
Q

How do sulphonylureas work?

A

stimulates pancreatic insulin secretion by

  • blocks ATP dependent K+ channels in pancreatic beta cells
  • membrane depolarise, calcium channels open → stimulating insulin secretion
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91
Q

Indications for sulphonylureas & SE?

A
  • mono or with metformin
  • DM type 2, but only effective if patient has residual pancreatic function
  • SE weight gain (insulin = anabolic hormone!), GI upset, hypo, rarely hypersensitive reaction (hepatic, blood, rash etc)
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92
Q

Medication that targets the sodium potassium pump?

A

Digoxin

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93
Q

How does the NA/K pump work

A
  • antiporter: moves both against their [gradient]
  • 3 NA out against every 2 K ions
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94
Q

Define inotropic

A

related to force of contraction of the muscle - positive = increase etc

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95
Q

Define chronotropic

A

related to change in heart rate

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96
Q

How does digoxin work?

A
  • competes with K to bind to Na/K ATPase pump
  • inhibits Na/K ATPase pump causing Na to accumulate in cell thereby increasing contractile force (inotropic), treating heart failure
  • increase vagal (parasympathetic) tone, reducing conduction at AV node thereby preventing some impulse transmission to ventricles, treating AF** and **flutter.
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97
Q

Digoxin - SE & CI?

A
  • SE typical present: GI upset, brady, rash, dizziness, visual disturbance (yellow vision)
  • CI renal failure, heart block (2nd and interm), ventricular arrhythm, preexisting electrolyte disturbances (
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98
Q

Digoxin - indication

A
  • AF and flutter but rarely on its own, also beta blocker and CCB better
  • severe heart failure, preexisting AF or later option for those already on ACEi, beta blocker and an ald antag / angiotensin receptor blocker
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99
Q

Medication that inhibits K/H ATP-ase irreversibly to induce therapeutic effect?

A

omeprazole

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100
Q

How do Proton Pump Inhibitors work?

A

They reduce gastric acid secretion - by:

  • irreversibly inhibiting H/K ATPase in gastric parietal cells
  • ( = inhibited proton pump responsible for secreting H+ and generating gastric acid)
  • = almost complete suppression
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101
Q

Proton Pump Inhibitors - indications!

A
  • prevention and treatment of peptic ulcers including those assoc. w/ NSAIDs
  • Symptomatic relief of dyspepsia and GORD
  • eradication of Helicobacter pylori (combined with antibiotics - clarithromycin / metronidazole & amoxicillin & PPI)
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102
Q

Examples of PPI’s!

A

lansoprazole, omeprazole, pantoprazole

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103
Q

PPIs - SE & CI

A
  • SE GI disturbances & headache
  • CI elderly at risk of osteoporosis
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104
Q

3 main fluid compartments of the body?

A
  • intracellular - ⅔ of body weight
  • extracellular - ⅓ of body weight
    • interstitial fluid - ¾ of e.cell
    • plasma fluid - ¼ of e. cell
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105
Q

Principle of drug distribution & exactly how are they distributed to compartments?

A
  • drug is distributed in plasma according to chemical properties and molecular size
  • proteins / large molecules → plasma
  • water soluble molecules → plasma & interstitial compartment
  • lipid soluble molecules → intracellular fluid
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106
Q

How would you calculate the volume of distribution of a drug?

A

Volume of distribution = total amount of drug in body / concentration of drug in plasma

= volume a drug would occupy if it was distributed through all the compartments as if they were all plasma

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107
Q

e.g.’s of drugs found in each fluid compartment?

A

Plasma
- warfarin

Interstitial

  • Aspirin / other NSAIDs
  • antibiotics

Intracellular

  • ster/opioids
  • Paracetamol
  • local anaes
  • Amiodarone!
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108
Q

Define clearance?

A

Removal of drug from plasma by either liver or kidney

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109
Q

From which compartment is a drug eliminated?

A

Plasma!

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110
Q

How can clearance be measured?

A
  • volume of plasma that is completely cleared of drug per unit time
  • rate at which plasma drug is eliminated per unit plasma concentration
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111
Q

What are some ways to measure renal clearance?

A
  • renal blood flow (18% of cardiac output 1L/min)
  • renal plasma flow (60% of blood flow 600ml/min)
  • glomerular filtrate (12% of renal blood flow 130 ml/min)
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112
Q

Marker substance in kidneys?

A

Creatinine

113
Q

How is hepatic clearance measured?

A

Hepatic extraction ratio - proportion of drug removed by one passage through liver

  • affected by liver enzymes
  • high = clearance is only limited by hepatic blood flow = quick
  • low = process is slow and not efficient
114
Q

Define first pass metabolism

A

drug has a high hepatic extraction ratio

metabolism of the drug by the gut and liver before it reaches the bloodstream

115
Q

Where are pro-drugs broken activated usually?

A

liver!

  • where Cytochrome P450 comes in!
  • e.g. hydrocortisone is cleaved into active drug crotisol via metabolism
116
Q

If a drug has limited therapeutic utility it means ..

A

it might not have reached the intended site (lol)

117
Q

Free card for a break

A
118
Q

What are the divisions of the autonomic nervous system?

A

Sympathetic & parasympathetic

119
Q

What is the sympathetic system responsible for?

A
  • fight or flight system
  • sweat glands, blood vessels
120
Q

Features of sympathetic ganglion?

A

ganglion is within a chain next to the spinal cord

121
Q

What is the parasympathetic system responsible for?

A
  • rest and digest
  • heart, gut, bladder
122
Q

Features of parasypathetic ganglion?

A

ganglion is within or very close to the effector organ

123
Q

What are the two main neurotransmitters in the body?

A
  • Acetylcholine - ACh
  • Noradrenaline - NAd
124
Q

What neurotransmitters can be found in the sympathetic system?

A

Both ACh & NAd

125
Q

What neurotransmitter is used in the preganglionic segment in the sympathetic pathway?

A

Acetylcholine ACh

126
Q

What receptor is used in the preganglionic segment in the sympathetic pathway?

A

Nicotinic receptors → used for preganglionic segments in both symp & parasymp pathways

127
Q

What are nicotinic receptors?

A
  • found in preganglionic segments of both symp & parasymp pathways
  • Only ACh acts on them
  • is a channel protein, upon binding by ACh, opens to allow diffusion of cations
    (all you need to know)
128
Q

What neurotransmitter is used in the postganglionic segment of the sympathetic pathway?

A

noradrenaline

129
Q

What is the exception to which noradrenaline is not used in the post-ganglionic sympathetic system (& what receptors are used?)

A

When innervating sweat glands, post ganglionic sympathetic fibres release ACh acting on muscarinic receptors (M3!).

130
Q

What receptors are used in the postganglionic segment of the sympathetic pathway?

A

adrenergic receptors

131
Q

Types of adrenergic receptors?

A

4 in total - alpha 1, 2 & beta 1, 2

132
Q

Differentiate between alpha and beta receptors (general)?

(your trick!)

A

think animal kingdom!

alpha1 (2 is mixed) causes smooth muscle contraction, beta2 (1 is mixed) causes smooth muscle relaxation

alpha also higher affinity for NOradrenalinE as there is NO E in alpha; bEta is adrenaline as there is an E!

133
Q

Noradrenaline is a?

(nature of molecule)

A

neurotransmitter

134
Q

Adrenaline is a?

(nature of molecule)

A

hormone

135
Q

Both adrenaline and noradrenaline are?

(nature of molecules)

A

Catecholamines

136
Q

Production pathway of nor/adrenaline?

A

Tyrosine → DOPA → dopamine → noradrenaline → adrenaline

137
Q

reminder - what are agonists?

A

molecule capable of functionally activating a target

138
Q

reminder - what are antagonists?

A

molecule that binds to a target & prevents others from binding to it. does not activate target!

139
Q

effect of alpha 1 agonists?

(activation of alpha 1)

A
  • causes vascoconstriction, in skin and abdominal bed → will raise BP & cardiac
  • less in brain, lung, heart
140
Q

pharmacological benefit of alpha 1 agonists?

A
  • IV noradrenaline: support septic & anaphylactic shock
  • xylometazoline - nasal decongestion
141
Q

effect of alpha 1 antagonists (alpha blockers) with examples?

A
  • lowers BP through vasodilation - doxazosin
  • treats catecholamine secreting tumour (phaeochromocytoma)- phenoxybenzamine
  • alpha 1A receptor blocking in prostate - treating benign prostatic hypertrophy - tamsulosin
142
Q

effect of alpha 2 agonists?

A
  • reduce BP, but also vascular tone (ex clonidine)
  • neuro - used to help ADHD to help concentration
  • no useful alpha 2 blockers
143
Q

alpha blockers CI?

A

postural hypotension

144
Q

tip to remembering main beta receptor effects respectively?

A

beta 1 - heart!

beta 2 - lungs!

you have 1 heart 2 lungs :)

145
Q

effect of beta 1 agonists?

A

heart and kidneys

  • increase heart rate (chronotropic) & stroke volume
  • release of renin from kidneys - regulates BP
  • lipolysis & hyperglycaemia
146
Q

biggest benefit of beta 1 receptors?

A

equal affinity for nor/adrenaline

= non selective, works at any when used therapeutically

147
Q

effect of beta 1 antagonists (blockers)?

A
  • reduce heart rate & stroke volume, therefore myocardial oxygen demand
  • prolongs refractory period of AV node → tx arrhythmias
  • lowers BP through renin secretion in kidneys
148
Q

beta 1 selective blockers
at this level?

A

atenolol, bisoprolol

(also: metoprolol, betaxolol)
→ means they’re safe to use in COPD (not asthma!!)

149
Q

examples of beta blockers (general)?

A

lol ending: bisoprolol, atenolol, propranolol MAIN then metoprolol. carvedilol

150
Q

Indication for beta blockers (general)?

A
  • ischaemic heart disease - angina & ACS
  • chronic heart failure & post MI - improve tone
  • AF, SVT
  • hypertension when other meds are inapp or insuff
151
Q

Why should you be cautious about giving beta blockers to asthmatic patients?

A

most will already be on beta 2 agonists → block = life threatening!

152
Q

What is beta blocker poisoning and what is the antidote?

A
  • if overdose - heart relaxes - emergency
  • antidote is glucagon as it increases MI contractility irrespective of presence of beta blockers (bypass beta adrenergic site)
153
Q

beta blockers, non selective - examples?

A

propanolol - beta 1 and beta 2

carvedilol - non selective beta & alpha 1 antagonist

154
Q

Propanolol - indications?

A
  • thyrotoxicosis (adjunct), thyrotoxic crisis
  • angina, hypertension, stops tremor! others
  • CI bronchospasm! total beta blocker!
155
Q

Carvedilol - effect and indications?

A
  • Affects the heart and cause vasodilation too
  • hypertension, angina
  • chronic heart failure but adjunct with others
  • CI bronchospasm! total beta blocker!
156
Q

beta blockers - CI?

A

caution - myasthenia gravis

ci - asthma, hypotension, metabolic acidosis // heart block 2&3, heart failure, p’s angina

157
Q

effects of beta 2 agonists?

A

DILATE

  • bronchi: bronchodilation (smooth muscle relaxation)
  • uterus: inhibition of labour, delay = tocolysis

CONSTRICT (less important?)

  • skeletal muscle: increases contraction speed → induce tremor
  • pancreas: insulin & glucagon secretion
  • bladder wall: inhibits micturition
158
Q

pharmacological application of beta 2 agonists?

A
  • asthma & COPD, both long & short term therapy
  • hyperkalaemia (along with insulin, glucose and calcium gluconate)
159
Q

examples and types of beta 2 agonists?

A

Short acting - salbutamol, terbutaline

Long acting - salmeterol, formoterol

160
Q

SE beta agonists?

A

tremor hyperglycaemia (glucagon release) & tachyarrythmia

161
Q

Nature of adrenaline

A

non selective! works at any alpha or beta adrenoreceptor

162
Q

Possible targets and effects of adrenaline and receptors?

A

alpha 1 - blood vessels - vasoconstriction (BP +, but only at large dose)

beta 1 - heart - positive inotropic

beta 2 - lungs - bronchodilation
(at lower doses its mostly beta effects)

163
Q

Possible uses of adrenaline?

A

anaphylaxis - reduce BP, bronchodilate

cardiac arrest

acute hypotension - large dose

164
Q

What neurotransmitters can be found in the parasympathetic system?

A

Acetylcholine only

165
Q

Which neurotransmitter is used in the pre-ganglionic segment of the parasympathetic pathway?

A

ACh

166
Q

Which receptor is used in the pre-ganglionic segment of the parasympathetic pathway?

A

nicotinic receptors

167
Q

Which neurotransmitter is used in the post-ganglionic segment of the parasympathetic pathway?

A

ACh

168
Q

What receptors are used in the post-ganglionic segment of the parasympathetic pathway?

A

Muscarinic receptors

169
Q

What are cholinergic receptors?

A

receptors which can receive acetylcholine = both nicotinic and muscarinic receptors!

170
Q

Function and types of muscarinic receptors?

A

= mediates effect of ACh in parasympathetic system, receptive to drug targeting!

= all receptors are found outside the cell & activates intracellular processes through G proteins

= M 1-5 but focus is on M2-3

171
Q

M1, 4 & 5 muscarinic receptors?

A

M1 brain

M4 & M5 CNS

172
Q

Effects of activating the M2 receptors?

A

effects mainly on the heart

  • on SA node: decrease heart rate
  • on AV node: decrease conduction velocity, induce AV node block (PR interval +)
173
Q

Effects of activating the M3 receptors?

A

Respiratory: mucus production, bronchoconstriction

GI tract: increase saliva production, gut motility, stimulate biliary secretion

Sweating! from ACh sympathetic

Urinary: contract detrusor, relax internal urethral sphincter

Eye: myosis, + drainage of aqueous humour, secretion of tears

174
Q

Useful M3 agonist?

A

Pilocarpine

  • contract iris muscle = increase aqueous humour drainage, reduces ocular pressure → tx acute glaucoma
  • stimulate saliva production → tx dry mouth
  • for Sjogren, or post radio
  • SE slow heart
175
Q

Adverse effect of muscarinic agonists?

A

DUMBELSS

Diarrhoea

Urination

Miosis → excessive pupil constrict

Bradycardia

Emesis → vomitting

Lacrimation → tears

Salivation / Sweating

176
Q

Antimuscarinics / Muscarinic antagonists: 4 main uses & mechanism?

A

as bronchodilators (resp), on the heart, GI, and GU

through competitive inhibition with acetylcholine

177
Q

Antimuscarinic - general side effects?

A

inhibit parasympathetic M receptors in other area = dry mouth (GI tract blocked so secrete - saliva), urinary retention, worsen glaucoma

178
Q

How are antimuscarinics indicated in the respiratory system?

A

relieving acute exacerbations short term, and prevention in long term

COPD & asthma

CI type 2 resp failure, CA arrhythmias & urinary

179
Q

Inhaled antimuscarinics: mechanism, ex?

A

mechanism: local antimuscarinic delivery to airway → dilation of airway

ex tiotropium, glycopyrronium, umeclidinium, aclidinium

180
Q

Antimuscarinics:
Atropine - benefits & adverse effects?

A

1st line bradycardia

Benefits: increase heart rate, treat bradyarrthmias & AV node block

Adverse: dilated pupils, hallucinations, palpitations, blindness and death

181
Q

Antimuscarinics:
hyoscine & mebeverine - benefit?

A

1st line IBS, as an antispasmodic

SE (hyoscine) reduces respiratory secretions so also in palliative care, also for nausea as ACh in somatic too

182
Q

How are antimuscarinics indicated for genitourinary uses?

A

for overactive bladder, blocks M3 so
promotes bladder relaxation & increase bladder capacity

→ reduce urinary frequency, urgency & urge incontinence

183
Q

GU antimuscarinic: examples, use & CI?

A

oxybutynin, tolterodine, solifenacin

1st line for urge incontinence to reduce urgency & urinary frequency if bladder training ineffective

CI UTI, CA elderly, dementia, angle closure glaucoma, arrhy, uri retention

184
Q

Where else in the neuro system is ACh found?

A

also in somatic system! receptors known as N1 receptors (autonomic is N2)

185
Q

Effect of ACh in the somatic system?

A
  • implicated in memory - anticholinergics SE memory problems
  • target tx for nausea
  • muscle relaxant in surgery (-onium ending meds)
186
Q

Diseases related to ACh in the somatic system?

A

clostridium botulinum as botulinum toxin is anti-ACh

myasthenia gravis - blocks normal transmission by inhibiting N1 receptors producing skeletal muscle weakness

187
Q

tx myasthenia gravis (just for fun)

A

reverse ACh blocking
= anti-cholinesterase

→ increase ACh availability at neuromuscular junction

ex pyridostigmine

→ avoid beta blockers (not ci just ca)

188
Q

Anti-drug to opioids?

A

Naloxone

189
Q

What is in opium?

A

Morphine & codeine

190
Q

How does opium work (3)?

A
  • modulate pain perception in higher centres euphoria to change the emotional perception of pain
  • inhibit pain transmission to brain (the release of pain transmitters at spinal cord and midbrain)
  • reduce pain by acting on descending pain modulatory system (inhibition of pain signalling in spinal cord)
191
Q

How does opium work chemically?

A
  • promote potassium conductance: neuron less likely to fire an action potential
  • inhibit calcium conductance: neuron less likely to release neurotransmitters
  • bind to periaquiductal grey
192
Q

Examples of opioid receptors and their mechanism?

A
  • MOP, KOP, DOP & NOP
  • lock and key mechanism with morphine
  • located in midbrain, spine, GI tract, breathing center → hence extended use can cause respiratory depression
193
Q

Effective duration of a single dose of morphine?

A

3-4 hours

never designed for sustained activation: leads to tolerance & addiction

194
Q

Side effects of opioid drugs?

A
  • potential for respiratory depression → opioid receptors exist here
  • Sedation, Nausea & Vomiting, Constipation, Itching, Immune suppression, Endocrine effects
  • titrate up, everyone responds diff!
195
Q

How would you treat an opioid overdose?

A
  • ABC - airways breathing circulation!
  • IM before IV - beware drug addict overdose
    • don’t repeat prescriptions without seeing the patient
  • naloxone = antagonist!
    • admit IV → fastest → 400 micrograms per ml
    • titrate dose to suit the patient: 1ml in 10ml saline
    • short half life: give depot: some IV some subcutaneous → depot will maintain levels
196
Q

What is potency and relative potency of opioid forms?

A

binding affinity of a drug, how well does it bind to the receptor - whether it is strong or weak

  • diamorphine 5mg
  • morphine 10mg
  • pethidine 100 mg
197
Q

Define tolerance

A
  • down regulation of receptors with prolonged use
  • need higher doses to achieve the same effect
198
Q

Define dependence

A
  • psychological: craving, euphoria
  • physical
199
Q

Define addiction

A
  • very big issue in US → careful in using in non-cancer pains!
  • don’t issue repeat prescriptions without seeing patient
200
Q

When would opioid withdrawal occur and how can you help

A
  • starts within 24 hours, lasts about 72 hours
  • can give methadone to slow down → safer
201
Q

How is codeine metabolised by the body?

A

= a prodrug

  • needs to be metabolised by cytochrome CYP2D6 to morphine to work
    • 10% absent, 10% activity decreased for Causasian population = reduced effect
    • 5% overactive = increased risk of respiratory depression
202
Q

How is morphine metabolised in the body

A

metabolised to morphine 6 glucuronide → more potent than morphine & renally excreted, clears up quickly

203
Q

Most common intolerant condition to morphine?

A
  • renal failure: will build up & cause respiratory depression
    • < 30% renal function patients (creatinine clearance < 30) → reduce dose & timing interval
    • use oxycodone instead! or look at acute pain guidance
204
Q

How is tramadol metabolised by the body?

A

prodrug & weak opioid agonist, slightly stronger than codeine

  • needs to be metabolised by cytochrome CYP2D6 to o-desmethyl tramadol to work
    • ineffective in 10% of patients
  • secondary effect as serotonin & nor-epinephrine reuptake inhibitor
    • ! take care in prescribing it to patients on antidepressants → serotonin syndrome
205
Q

Alternative for morphine if patient has renal failure

A

oxycodone

206
Q

Commonest! SE of opioid analgesics

A

respiratory depression

207
Q

Prodrug forms, opioid analgesics?

A

Codeine, Tramadol

208
Q

Opioid analgesics - if prodrug then metabolised by which P450?

A

CYP2D6

209
Q

How does naloxone work as a antidote?

A

via competitive receptor binding

210
Q

What are stereoisomers

A

have the same molecule formula and sequence of bonded atoms, but differ in the 3D orientations of their atoms in space

211
Q

What is an adverse reaction?

A

= unwanted or harmful reaction following administration of drug

not side effects - never beneficial, but side effects can be adverse reactions

212
Q

What is a side effect?

A

unintended effect of a drug related to its pharmacological properties & can include unexpected benefits of treatment

  • can be beneficial: PDE5 inhibitors improve urinary flow
213
Q

Types of ADR’s?

A
  • hypersusceptibility
  • collateral effect
  • toxic effects
214
Q

What is a hypersusceptibility ADR & ex?

A
  • below therapeutic range
    • sub therapeutic dose
    • e.g. anaphylaxis from penicillin
215
Q

What is a collateral effect ADR?

A
  • drug issue is in therapeutic range
    • reaction from using a standard dose
216
Q

What is a toxic effect ADR?

A

can occur if dose is too high or drug secretion is reduced by impaired renal or hepatic function or by interaction with other drugs

217
Q

By the Rawlins Thompson classification, what are the different types of ADR’s

A

Augmented, Bizarre, Chronic, Delayed, End of treatment, Failure of therapy

218
Q

What is an Augmented ADR by the Rawlins Thompson classification

A
  • predictable, common, dose dependent; extension of primary pharmaceutical effect
  • the more you give the bigger the reaction
  • high morbidity low mortality
  • risk - renal or hepatic impairment - older, etc
219
Q

What is a Bizzare ADR by the Rawlins Thompson classification

A

unpredictable, not dose dependent; can’t be readily reversed

can be life threatening, can be idiosyncrasy, allergy or hypersensitivity

  • idiosyncrasy: inherent abnormal response to a drug
    • may be due to genetic abnormality, enzyme deficiency, or abnormal receptor activity
    • rare but serious

Low morbidity, high mortality

e.g. anaphylaxis - penicillin

220
Q

What is a Chronic ADR by the Rawlins Thompson classification

A

occurs after long term therapy

uncommon, related to cumulative dose & time

steroids and osteoporosis

e.g. analgesic nephropathy, colonic dysfunction due to laxatives

221
Q

What is a delayed ADR by the Rawlins Thompson classification

A

after immunosuppresion

uncommon, dose related, shows after a while of taking the medication

e.g. teratogenesis (congenital malformation) - thalidomide, carcinogenesis - cyclophophamide

222
Q

What is an end of treatment ADR by the Rawlins Thompson classification

A

when the drug is stopped, withdrawal

e.g. opiate withdrawal, glucocoticoid abrupt withdrawal: adrenocortical infusfficiency, anticonvulsant stopped: withdrawal seizures

223
Q

What is a failure of therapy ADR by the Rawlins Thompson classification

A

often caused by drug interactions

e.g. failure of the pill with enzyme inducers, failure of therapeutic effect in patients taking warfarin leading to CVA

224
Q

What are a few factors to think of in order to help you determine what kind of reaction it is

A

Dose related

Timing

Patient Susceptibility

225
Q

What is non-immune anaphylaxis?

A
  • due to direct mast cell degranulation
  • some drugs recognised to cause this
  • no prior exposure & clinically identical
226
Q

When should you suspect an ADR?

A

Symptoms that start …

  • soon after a new drug is started
  • after a dosage increase

Symptoms that disappear when drug is stopped & reappear when it is restarted

227
Q

What does it mean if a medication has a black triangle on them

A

medicine is undergoing additional monitoring! watch out for ADR’s

228
Q

When should you report an ADR?

A

all suspected reactions for herbal meds, black triangle meds

all serious suspected reactions (death / life threaten / disability / results prolong hospitalise) for well established drugs and interactions

229
Q

How to report an ADR?

A

Yellow card - download or at back of BNF

to the MHRA - Medicines and Healthcare products Regulatory Agency

230
Q

Are you obligated to report?

A

No - a voluntary scheme

but it is your duty to report - important for patient safety!!

Patients can report too

231
Q

Mechanism of action - amlodipine?

A

Calcium channel antagonist

= block calcium entry in response to depolarisation in blood vessels = vasodilation, lowers peripheral resistance

= lowers systemic blood pressure

232
Q

Most common SE for CCBs?

A

ankle swelling

233
Q

Ramipril - mechanism of action?

A

Angiotensin converting enzyme inhibitor (ACEi)

Blocks action of renin-angiotensin system = indirectly acting vasodilator

234
Q

Mose common SE for ACEi?

A

dry cough

235
Q

Other common SE for ACEi?

A

vasodilation, potassium retention & inhibition of salt & water excretion

→ hyperkalaemia = comp!!

236
Q

How is ACEi excreted? Complication?

A

Renal function

if preexisting impairment = hyperkalaemia can occur

237
Q

Why do Afro-Caribbean patients respond less well to ACEi?

A

they commonly have low renin essential hypertension, where renin angiotensin system is contributing little to their hypertension

238
Q

Mechanism of NSAIDs?

A

inhibiting cyclo-oxygenase, specifically COX2, which is induced by inflammatory cells

ratio of inhibition COX-1 to COX-2 = determine side effects

239
Q

Contraindications of NSAIDs?

A

active or recurrent GI bleeding, ulceration

severe heart failure

allergy to aspirin

avoid in renal failure & dehydration

240
Q

Why should NSAIDs be avoided in patients with asthma?

A

→ use NSAID with caution in any allergic disorders

8-20% asthmatics experience bronchospasm following ingestion of aspirin & other NSAID drugs

241
Q

SE NSAIDs (major)?

A

Renal dysfunction, esp in at risk
= acute interstitial nephritis

→ inhibition of prostaglandins are involved in maintenance of renal medullary blood flow

242
Q

How is metformin excreted?

A

Cleared by active tubular secretion

→ unchanged in urine

243
Q

Define half life in relation to elimination?

A

elimination half life
= time required for serum concentration of the drug to be decreased by 50%

244
Q

Precautions for patients on metformin requiring a radiological investigation?

A

measure serum creatinine in the preeceding month

  • *> 100ml contrast required** OR
  • *serum creatinine raised**,

withhold metformin 48 hours before contrast

raised creatinine = also withhold 28 hours post contrast

245
Q

How can you alter a prescription to mitigate the effects of reduced renal function?

A

for drugs that are excreted unchanged, adjust the dose in renal impairment

→ reduce the dose
→ lengthen dose interval
or both!

alt = substitute the drug

246
Q

What is St John’s wort & what is it used for?

A

herbal medicine = complementary!

used for symptoms of mild & moderate depression

247
Q

Significance of St John’s Wort & interactions (7)?

A

CYP450 inductor = increases metabolism of medications = makes them less effective.

SSRI, oral contraceptive, warfarin, digoxin, cyclosporin, HIV meds, statins

248
Q

1st line tx for depression?

A

Selective Serotonin Reuptake Inhibitor

249
Q

Mechanism for SSRi’s?

A

Inhibit neuronal reuptake of 5-HT from synaptic cleft → increases availability for neurotransmission

minimum 6 months, don’t stop!

250
Q

Examples of SSRIs?

A

sertraline, citalopram, fluoxetine

251
Q

SE of SSRIs?

A

Long QT, seizures

Increased suicidal thoughts at the beginning of therapy

serotonin syndrome

252
Q

2nd line tx for depression? what else is it used for?

A

Tricyclic Antidepressants (TCA)

neuropathic pain!

253
Q

Examples of tricyclic antidepressants?

A

amitriptyline, lofepramine

254
Q

Mechanism of TCA’s?

A

Inhibit neuronal reuptake of 5-HT and noradrenaline

also blocks a range of receptors e.g. muscarinic, histamine, adrenergic, dopaminergic → SE’s

255
Q

Last line depression?

A

Mirtazapine

256
Q

Advice to those on the oral contraceptive pill and have had several episodes of severe diarrhoea?

A

If severe diarrhoea = missed pill on those days

→ take additional contraceptive precautions for following 7 days

257
Q

Name a few contraceptive options?

A

the pill!

Contraceptive patch / implant / injection

intrauterine device, condoms, contraceptive cap

258
Q

How does the combined oral contraceptive pill prevent pregnancy?

A

suppress ovulation by interfering with the gonadotrophin release by the pituitary via negative feedback on the hypothalamus

makes endometrium thinner & cervical mucus thicker

259
Q

Mechanism of loperamide?

A

opioid receptor agonist

→ reduces GI tract motility
= increases time material stays in intestine = allow for more H2O absorption

260
Q

Treatment in acute Crohn’s disease?

A
  • *Steroids**
  • *mild** = corticosteroids = budesonide
  • *moderate** = glucocorticoids = prednisolone

severe = corticosteroids = IV hydrocortisone
if rectal disease = per rectum
if perianal abscess or perianal disease = metronidazole

last = anti-TNF = infliximab or adalimumab

261
Q

Mechanism of anti-TNF antibodies in Crohn’s disease?

A

= infliximab, adalimumab

= reduce disease activity by countering neutrophil accumulation, granuloma formation, and activating complement

262
Q

How might you maintain remission in Crohn’s disease?

A

1st = Azathioprine

2nd = Methotrexate (+ folic acid)

263
Q

Methotrexate: mechanism of action?

A

inhibit dihydrofolate reductase
= converts folic acid → FH4
= prevent cellular replication

antiinflammatory & immunosuppression effects against ILs & cytokines

264
Q

Why must folic acid be prescribed alongside methotrexate?

A

counteract folate-antagonist action of methotrexate
= reduce toxicity & improve compliance

= alt days to avoid reducing effectiveness of methotrexate

265
Q

How to monitor patients on methotrexate for adverse drug reactions?

A

FBC + renal & LFT before tx, every 2-3 weeks until stabilised & every 2-3 months after

266
Q

What receptors do doxazosin and tamulosin act on?

A

doxazosin = alpha 1 adrenergic receptor antagonist

tamsulosin = selective alpha 1A & alpha 1D adrenoceptor antagonist

267
Q

Important complication for those on alpha-blockers & about to have surgery?

A

Intraoperative Floppy Iris syndrome (IFIS)

→ don’t have to stop, just inform & surgeon should be ready to modify technique

268
Q

Main SE of alpha blockers? How might you modify it?

A

Postural hypotension

Try taking medications at night & if not then swap meds

269
Q

What is retrograde ejaculation?

A

occurs in 30% of men taking alpha blockers

seminal fluid flows into bladder instead of normal antegrade direction → due to bladder neck failing to close

270
Q

2nd line BPH treatment?

A

finasteride

271
Q

Mechanism of 5alpha reductase inhibitors?

A

inhibiting the intracellular enzyme 5 alpha reductase, which converts testosterone to dihydrotestosterone (stimulates prostatic growth)

→ reduces size of prostate gland

272
Q

Why should you review someone’s contraception if they’re on carbamazepine?

A

Combined oral contraceptive = reduced by drugs which induce hepatic enzyme activity e.g. carbamazepine!

273
Q

Contraceptive options if on carbamazepine / other inducer drugs?

A

Parenteral progesterone only or intra-uterine devices

274
Q

If someone is pregnant while on Carbamazepine - what should they do?

A

Keep taking carbamazepine as risk of seizure is high, high dose folic acid 5mg to be started immediately

275
Q

Mechanism of aledronic acid?

A

oral bisphosphonte & inhibits osteoclast mediated bone resorption

276
Q

Advice when taking aledronic acid (4)?

A

Take tablets with plenty of water while sitting / standing

take on empty stomach 30m before breakfast

stay upright at least 30m after

→ seek help if symptoms of dysphagia, achalasia, heartburn, retrosternal pain

277
Q

Indications of letrozole?

A

Post menopausal women with oestrogen receptor positive breast cancer

278
Q

What is a spacer?

A

Add on device used to increase ease of administering inhalers esp in babies & children

Phase 2A (12 decks)

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