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4TH YEAR > CPTP4 > Flashcards

CPTP4 Flashcards

1
Q

define adverse drug reaction

A

any response to a drug which is noxious, unintended and occurs at doses used for prophylaxis, diagnosis or therapy

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2
Q

define medication error

A

any preventable event that may cause or lead to inappropriate medication use or patient harm

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3
Q

how does the human medicines regulations categories medical substance?

A
  1. prescription- only medicines
    - registered medical practitioners can do all
    - midwives, nurses and pharmacists can do some
    - patient group directions
  2. pharmacy
    - pharmacists can give
  3. general sales list
    - anyone
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4
Q

how are pharmacy medicines released from the POM category?

A
  • must be appropriate to self diagnose
  • small chance of causing harm
  • no chance of dependence
  • cant be parental or eye admin
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5
Q

what does ‘controlled’ mean in the context of medicines?

A

controlled under the Misuse of Drugs Act. they are categorized into class (how harmful is it?) and schedules

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6
Q

what 3 criteria could mean a substance becomes controlled?

A

misuse may result in psychological, physical or social harm

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7
Q

in the misuse of drugs act, what does the schedule determine?

A

requirements for wholesale, storage, prescription etc.
schedule 1: no medical use
cant have/ use without a licence e.g. cannabis
schedule 2: medical use
controlled drug prescription and special arrangement for storage e.g. diamorphine

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8
Q

what is a named patient drug?

A

a drug that might have been discontinued from marketing regulations etc. but you can keep prescribing it for a person who’s been on it for a long time

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9
Q

what extra information must you put when prescribing a controlled substance?

A

total quantity in both words and figures

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10
Q

define tolerance

A

high dose required to achieve same response

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11
Q

physical dependence

A

develops when neurons adapt to repeated drug exposure and only function normally in the presence of the drug. therefore withdrawal precipitates unpleasant physiological effects

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12
Q

psychological dependence

A

emotional need for a drug that has no underlying physical need

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13
Q

what is the %UK lifetime prevalence of drug misuse?

A

35%

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14
Q

how many deaths are there in the UK per year as a result of drug misuse? population distribution?

A

~2000
males >females
highest in 35-44 yo
NE england highest

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15
Q

which illegal drugs are responsible for the most deaths in the UK?

A

opioids

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16
Q

define therapeutic drug monitoring

A

individualisation of dosage by maintaining plasma/ blood drug concentration within a target range

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17
Q

3 ways therapeutic drug monitoring is carried out and examples.

A
  1. monitoring plasma/ blood drug conc.
  2. measuring clinical response (e.g. how much angina)
  3. measuring the pharmacodynamic effect (e.g. effect of insulin on blood glucose)
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18
Q

why should gentamicin be closely monitored?

A

narrow therapeutic window : ototoxicity and nephrotoxicity

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19
Q

three examples of drugs that indicate monitoring of plasma drug conc.?

A

digoxin
phenytoin (anti-epileptic)
gentamicin

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20
Q

what is the most common cause of iatrogenic disease?

A

adverse drug reactions (occur in 20% of hospital admissions)

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21
Q

3 adverse reactions to prednisolone?

A

hyperglycaemia
GI complications
OP

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22
Q

three example of augmented drug reactions?

A

insulin -> hypos
warfarin -> bleeding
nitrates -> headaches (vasodilation)

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23
Q

which drug is antagonistic to salbutamol?

A

B-blockers

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24
Q

how can antacids interact with other drugs?

A

decrease stomach acidity so more drug ionisation
this means it cannot be absorbed as fast
(the opposite is true for drugs that increase stomach acidity

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25
Q

muscarinic agents will have what effect on drug absorption? e.g.

A

decrease it due to increasing GI motility

bethanecol for urinary retention

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26
Q

what are the two types of allorecognition in transplants?

A

direct- donor APC migrates to regional lymph node and activates host t cells -> direct cytotoxic T cell response. seen in acute rejection
indirect- recipient APC processes peptides from dead cells from transplant organ. host t cells migrate to attack graft. fewer t cells are activated. seen in chronic

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27
Q

what does the suffix -mab mean in a drug?

A

that its a monoclonal antibody drug

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28
Q

define pharmacogenomics

A

use of genetic information to guide the choice of drug and dose on an individual

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29
Q

what is the effect of fast or slow acetylation on the metabolism of isoniazide?

A

fast- get lots of the hepatotoxic metabolite

slow- get a build of the drug which is neurotoxic

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30
Q

pathophysiology of PD

A

loss of dopaminergic cells in substantia nigra leads to degeneration of projections to other areas of basal ganglia

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31
Q

ways to intervene with dopamine levels

A
  1. give L-dopa (MOST EFFECTIVE)
  2. MAO-B
  3. block degradation of D in synaptic cleft- COMT inhibitors
  4. dopamine agonist
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32
Q

what must be given with l-dopa and why?

A

DDI- dopamine decarboxylase inhibitor

reduced sfx by stopping conversion of L-dopa into dopamine

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33
Q

long term side fx of l-dopa? which other drug does this?

A

dyskinesia- occurs in 50% of patients after 6 years

COMT inhibitors

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34
Q

which parkinsons medication can cause loss of impulse control?

A

dopamine agonists

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35
Q

which PD drug can cause seretonin syndrome?

A

MOA-B

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36
Q

which neurotransmitter dysregulation can cause epilepsy?

A

glutamate

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37
Q

epilepsy drugs i should know?

A 
carbamazapine
sodium valproate
levetiracetam
phenytoin
lamotrigine
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38
Q

what are absence seizures treated with?

A

ethosuximdie (or sodium valproate)

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39
Q

tx for status epilepticus

A
  1. Secure airway and give O2 – airway or intubate, cardiac monitoring, oximetry
    IV access + bloods
    Glucose ( rule out hypo) , thiamine ( alcohol is often a cause) , maintain AEDs
  2. PR diazapam or buccal midazolam -> IV lorazapam -> phenytoin
  3. if they don’t respond to this then give IV phenytoin
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40
Q

what is the risk of giving IV phenytoin?

A

can cause hypotenision

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41
Q

what are the features of a parkinsons tremor?

A

5Hz
pill rolling
asymmetrical

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42
Q

what drug class is apomorphine?

A

dopamine agonist

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43
Q

what effect does the carbamazapine have on metabolism?

A

enzyme inducer therefore speeds metabolism

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44
Q

carbamazapine side fx

A 
blurred vision
back and forth eye movement
drowsiness
nausea
rash
etc
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45
Q

drugs that induce parkinsons

A

dopamine antagnoinsts- neuroleptics and anti-emetics

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46
Q

when is a DAT scan helpful?

A

determine if there was pre-existing PD in someone with drug induced parkinsons

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47
Q

best initial Tx for drug induced PD?

A

co-benoldopa (l-dopa with decarboxylase inhibitor)

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48
Q

mechanism of metformin?

A

inhibits hepatic gluconeogenesis

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49
Q

sulphonylurease mechanism? and example

A

increase insulin secretion

gliclazide

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50
Q

sfx of sulphonylurease

A

hypos, weight gain

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51
Q

how do thiazolidinediones work?

A

increase lipogenesis
decrease lipolysis

(NOT USED MUCH NOW)

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52
Q

why is more insulin produced if sugar is ingested vs injected?

A

gut plays a role in hormone regulation

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53
Q

how do DPP-4 inhibitors decrease glucose?

A

prolong t1/2 of GLP-1 (which increases insulin secretion and decreases glucagon)

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54
Q

statins mechanism?

A

decrease cholesterol synthesis

increase uptake of cholesterol from blood to liver

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55
Q

two methods for calculating the anion gap?

A

Na + K - (HCO3 + CL) normal is 16+/-4

Na - (HCO3 + Cl) normal is 12+/-4

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56
Q

causes for high anion gap?

A 
MUDPILES
methanol / metformin
ureamia
DKA
Paracetamol
Iron / isoniazide
Lactic acidosis
Ethanol 
salicylate
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57
Q

why is there raised blood glucose in DKA / HHS?

A

absolute or relative insulin deficiency stimulates hepatic glucose production
this cannot get into the cells

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58
Q

criteria for diagnosing DKA?

A

ketones- in urine or blood
glucose > 11mmol/L (or known diabetic)
bicarb <15mmol/L OR acidosis

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59
Q

what initial fluid do you give in DKA?

A

0.9% saline
w/o K+ at first then give it after the first bolus
the first one needs to be given very quickly so isn’t safe to give K

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60
Q

potassium levels in DKA and why?

A

serum potassium high as trying to get rid of H+ ions in the urine (potassium / hydrogen pump)

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61
Q

in what way is acidosis good in DKA?

A

improves O2 delivery to tissue by shifting saturation curve to the right

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62
Q

insulin therapy in DKA? what to do if this is delayed?

A

fixed rate IV insulin infusion

IM infusion

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63
Q

in DKA what should be monitored continuously?

A
  • Hourly capillary blood glucose
  • Hourly capillary ketone measurement
  • Venous bicarbonate and potassium at 60 minutes, 2 hours and 2 hourly thereafter
  • 4 hourly plasma electrolytes
  • Continuous cardiac monitoring if required
  • Continuous pulse oximetry if required
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64
Q

after DKA what is the most reliable way of measuring ketone level?

A

blood ketones

urine ketones will still be present for a while

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65
Q

in DKA, what should the overlap be in previous insulin regime and infusion?

A

infusion maintained until 30 mins after SC insulin

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66
Q

initial response to hypos

A

ABC
give 80ml 20% glucose IV
1mg of glucagon IM (to mobiles glucose from the liver)
repeat BM:
-if < 4 then repeat glucose
-if >4 then give long acting CHO once recovered

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67
Q

what should a diabetic woman trying for a child take?

A

5mg folic acid unitl 12 wks

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68
Q

during delivery, what should a diabetic woman be given?

A

GKI infusion

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69
Q

two side effects of statins?

A

rhabdomyalisis / myositis

raised transaminases

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70
Q

whys that liver disease alters response to drug?

A 
Impaired drug metabolism - more will be in circulation
Hypoproteinemia
Reduced clotting
Hepatic encephalopathy
Fluid overload - abnormal Na handling 
Hepatotoxic drugs
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71
Q

how can hepatic disease effect pharmacokinetic?

A

either causes drug accumulation or failure to form an active / inactive metabolite
Increased bioavailability after oral administration
Alteration in drug protein binding, and kidney function.

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72
Q

3 factors that determine drug elimination by the liver

A
  1. blood flow (Q) throught the liver
  2. The fraction of drug (f) in the blood that is free or unbound to plasma proteins and capable of interacting with hepatic enzymes
  3. Intrinsic clearance (Clint) is the intrinsic ability of the liver to metabolize drug in the absence of flow limitations and binding to cells or proteins in the blood.
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73
Q

what is the extraction ratio?

A

The fraction of the drug removed from the perfusing blood during its passage through the organ
i.e. Drugs with high hepatic ER have a large first-pass effect, therefore low oral bioavailability.

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74
Q

if the extraction ratio of a drug is 0.4, what is the bioavailability?

A

0.6

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75
Q

why avoid sedative, diuretics and drugs that cause constipation in LD?

A

precipitates encephalopathy

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76
Q

what regulates the secretion of H+ in the stomach?

A

gastrin

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77
Q

drug induced dyspepsia

A 
NSAIDs – gastritis and peptic ulcers
Steroids – gastritis and peptic ulcers
Calcium antagonists - gastritis
Nitrates - Reflux
Theophyllines - gastritis
Bisphosphonates – oesphageal erosion and ulceration.
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78
Q

epigastric pain relation to meals?

A

GU – worse with / shortly after meals

DU – relieved during meals, worse 2-3h after meals or at night

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79
Q

ways to test for H pylori

A

Faecal antigen test
Carbon 13 urea breath test
Serum H.pylori antibody test
Endoscopic biopsy samples – rapid urease test

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80
Q

sfx of ant acids

A

constipation- the Al ones

diarrhoea - the Mg ones

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81
Q

first line treatment of peptic ulcer disease and GORD

A

H2r antagonists

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82
Q

how do PPIs work? 2 examples

A

PPIs cause irreversible inhibition of H+/K+ ATPase responsible for H+ secretion from parietal cells

omeprazole, lansoprazole

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83
Q

H2r antagonists mech of action

A

H2 receptor antagonists competitively block the action of histamine on the parietal cell by antagonising the H2 receptor

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84
Q

what is triple therapy for H. pylori?

A

PPI, amoxicillin and clarithromycin OR

PPI, amoxicillin and metronidazole

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85
Q

4 types of laxatives and their mech?

A
  1. Bulk forming - Increase volume of non- absorbable material in the gut therefore distending the colon and increasing peristalsis
  2. Osmotic - Increase water content in the bowl via osmosis therefore distending the colon and increasing peristalsis
  3. Stimulant - Increase gastrointestinal peristalsis
  4. Faecal softeners - Promote defecation by softening /or lubricating the stool
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86
Q

contraincations for bran / hisk / methylcellulose?

A

dysphagia
obstruction
faecal impaction
clonic atony

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87
Q

in liver disease, how should the dose of an oral drug with a high extraction be changed?

A

reduced initial dose
reduced maintenance dose

all undergoing less first pass metabolism so will have higher bioavailablity

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88
Q

in liver disease, how should the dose of an IV drug with a high extraction be changed?

A

normal initial dose
reduced maintenance dose

the initial dose will not undergo first pass metabolism via the portal vein as it isnt in the GI system
however eventually it will go through the liver and be metabolised so maintenance should be less

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89
Q

how to work out reduced dose for liver disease patients

A

Reduced dose = (normal dose X bioavailability)/100

normal dose is the dose in a patient without LD
bioavailability is drugs availability in a healthy person

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90
Q

what counts as a high extraction ratio?

A

> _0.7

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91
Q

what is the CLO test for and how does it work?

A

diagnosing H. pylori AKA rapid urease test
biopsy of mucous from the lining of the stomach, h. pylori produces urease that converts urea to ammonia hence changing the pH of your solution

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92
Q

which abx for H pylori?

A

amoxicillin + (clarithromycin OR metronidazole)

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93
Q

diagnosis of a perforated PUD?

A

adbo x-ray : can see air under the diaphragm

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94
Q

what drug class is loperamide hydrochloride?

A

anti-motility

acts on opioid receptor

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95
Q

what is the mx pathway for suspected gastric cancer?

A

lifestyle changes and URGENT endoscopy

must be off PPIs for at least 2 weeks for endoscopy

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96
Q

if H pylori positive, how long do you continue the PPI for in eradication therapy ?

A

2 months

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97
Q

problems with PPIs?

A

low mg
risk of C diff
actue intertial nephritis (rare but this is a common cause of it)
microscopic colitis

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98
Q

why doesnt loperamide cause euphoria?

A

cant cross BBB

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99
Q

how does loperamide reduce diarrhoea?

A

binds to opioid receptors to decrease peristalisis

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100
Q

constipation red flags

A

Weight loss

Unexplained microcytic anaemia

New onset constipation in an elderly patient

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101
Q

in dyspepsia who should be referred for urgent endoscopy?

A

new onset AND over 55

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102
Q

Mx for dyspepsia in the U55s

A

‘test and treat’
test for H pylori : urea breath test or stool antigen
4 weeks full dose PPI

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103
Q

response to a meal in duodenal ulcers and why?

A

initially eases pain then gets bad again

the pyloric sphincter closes therefore the acid cannot reach the duodenum. about 2-3 hours later the sphincter opens

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104
Q

Mx for symptoms of an upper gastrointestinal bleed?

A

ABC
urgent endoscopy + therapy
inform ITU and surgeons

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105
Q

what is the endoscopic therapy for UGIB? and what else do you give?

A 
adrenaline injections
haemospray
clips
heat probe
argon- plasma coagulation

IV PPIs

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106
Q

when to give PPIs in UGIB?

A

only after confirmation by endoscopy

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107
Q

two reasons to do another endoscopy 8 weeks after UGIB?

A

check healing

?cancer

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108
Q

effect of NSAIDS on the kidneys?

A

cause afferent renal arteriol vasoconstriction

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109
Q

contraindications for opioid anti-motility drugs

A

Severe ulcerative colitis or C.diff – increases the risk of Toxic megacolon
Severe infective diarrhoea
Dysentery (bloody stool)
Liver disease (risk of accumulation)

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110
Q

indications for opioid anti-motility drugs

A
  • mild infective diarrhoea
  • irritable bowel syndrome
  • chronic IBD diarrhoea
  • high output stomas
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111
Q

which types of laxatives are avoided if there is suspected obstruction?

A

stimulant

bilk forming

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112
Q

indications for investigating constipation?

A 
>40yrs
Recent change in bowel habit
Iron deficiency anaemia
Assoc symptoms (weight loss, rectal bleeding, mucous discharge or tenesmus)

mostly it doesnt need investigating

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113
Q

difference between SABA and LABA?

A

LABAs are chemical analogues of salbutamol with a long lipophilic side chain anchors the drug in the lipid membrane therefore:
the active portion of the molecule to remain at the receptor site

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114
Q

electrolyte abnormality caused by B2 agonists?

A

hypOkalaemia

they are sometimes used to treat hypERkalaemia

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115
Q

what drug class is ipatropium?

A

SAMA

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116
Q

what drug class is tiotropium?

A

LAMA

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117
Q

which patients cant tolerate adrenergic agonists e.g. B2 agonists?

A

ischaemic heart disease or tachycardia

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118
Q

Theophylline use and mech of action?

A

second line therapy in asthma

Inhibits phosphodiesterase to cause an increase in cAMP in smooth muscle cells

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119
Q

use of leukotriene receptor antagonists and example

A

prohylaxsis for asthma NOT symptom relief

montelukast

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120
Q

two main adverse effects of corticosteroids in asthma

A

horse voice

oral candidiasis

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121
Q

what oral corticosteroid is used in asthma?

A

prednisalone

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122
Q

what is the first line regular preventer?

A

low dose ICS

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123
Q

if low dose ICS is not controlling asthma what is added next?

A

LABA

124
Q

drugs that can exacerbate asthma?

A

B-blockers -> bronchospasm (esp. non-selective e.g. propranolol)
NSAIDS -> bronchospams (aspirin sensitivity affects 20%

125
Q

how much of an inhaled drug ends up in the lungs?

A

10%

126
Q

why are there systemic side effects when drugs are inhaled?

A

90% is swallowed

127
Q

Mx of acute asthma

A 
O2
steroids
B2 agonists
IV mg sulphate
ipatropium bromide
128
Q

Mx of COPD exacernation

A

Oxygen (high flow O2 can be dangerous in type 2 resp. failure)

Oral Steroids (Short course)
Antibiotics (Simple (amox.) and Short)

Nebulised Bronchodilators
NIV (non-invasive ventilation)

129
Q

what increase in peak flow post SABA indicates asthma?

A

200ml

130
Q

theophylline mech and use?

A

raises intracellular cAMP which promotes smooth muscle relaxation

used in asthma

131
Q

alternative for B blockers in asthmatic patients?

A

prostaglandins

132
Q

abx for CAP?

A

amox
clarithromycin
doxycycline (this is used if someone with COPD is hospitalised as it covers the more obscure pathogens)

133
Q

Tx for exacerbation of COPD?

A

salbutamol and ipratropium NEB
?O2
prednisalone (oral)

134
Q

name a leukotriene receptor antagonist used in asthma

A

montekeukast

135
Q

3 ICS used in asthma?

A

beclamethosome
budensoide
fluticasone

136
Q

interaction between glaucoma and asthma tx?

A

topical b-blocker used in glaucoma can have systemic effects of bronchospasm

137
Q

define acute severe asthma and when should you admit?

A

PEF 33-50% best or predicted
respiratory rate ≥25/min
heart rate ≥110/min
inability to complete sentences in one breath

admit if symptoms persist after initial tx

138
Q

two drug classes that exacerbate asthma and alternatives?

A

NSAIDS

  • only avoid if you know it worsens your asthma
  • aspirin sensitivity in 20%, use clopidogrel

B-blockers
-use prostaglandin analogue instead

139
Q

what does a rising PaCO2 tell you about a patient in an asthma attack?

A

they are getting exhausted and failing to blow off CO2- BAD

140
Q

Mx for acute severe asthma

A

O2
Neb : salbutamol and ipratropium
steroids

141
Q

what to consider in mx of pneumonia in asthmatic patient

A

are they on theophylline - this is INHIBITED by clarithromycin and ciprofloxacin

142
Q

theophylline mech?

A

Competitive nonselective phosphodiesterase inhibitor

  • reveres steroid insensitivity
  • reduces inflammation and innate immunity
143
Q

what is carbocistenine

A

mucolytic

144
Q

on an ABG which values tell you weather the problem is acute or chronic?

A

deranged pH means it’s a chronic problem - cant live with that for long
bicarb. - takes a while to change

145
Q

type 1 resp failure is due to what

A

V/Q mismatch i.e. the alveolar are well ventilated but O2 is not getting into the blood

e. g.
- O2 cant get to capillaries (seen in pneumonia)
- blood cant get to alveolar (seen in PE)

146
Q

type 2 resp failure is due to what

A

ventilatory failure
e.g.
obstructive disease
emphysema

147
Q

when to give LTOT?

A

PaO2 < 7.3
OR
PaO2 7.3 - 8 AND cor pulmonale

148
Q

what information is needed and how to calculate ‘no. needed to treat’

A

risk without treatment over 10 yrs
risk with treatment over 10 yrs

the difference between these two is the ABSOLUTE RSIK REDUCTION (ARR)

NNT = 100 / ARR

therefore you need to treat x number of people over 10 years to save 1 ‘event’

149
Q

what are ABPM and HBPM and whats the point in them?

A

ambulatory/ home BP monitoring
average BP over 24hrs.
HBPM- have to measure your own BP
ABPM- does it for you several times a day

to eliminate white coat hypertension

150
Q

define the stages of hypertension

A

stage 1

  • > 140 / 90 OR
  • > 135/85 AVERAGE if ABPM or HBPM

stage 2

  • > 160 / 100 OR
  • > 150 / 95 AVERAGE if ABPM or HBPM

severe
- >180 / 110

151
Q

when to treat hypertension?

A

stage 1 IF THEY HAVE A RAISED CV RISK (QRISK or other)

stage 2 always

152
Q

5 classes of drugs used in hypertension

A 
ACE inhibitors
CCBs
Diuretics
A2RB
cardiac glycosides
153
Q

Mx of hypertension in pregnancy?

A

use labetolol

154
Q

what QRISK score warrants a statin?

A

> 10% risk of CVD

155
Q

what U&E’s would be expected in someone not tolerating ARBs?

A

raised Na

low K

156
Q

acute heart failure Mx?

A

IV furosemide
O2
sit up right

157
Q

what is the ejection fraction and what is normal?

A

amount of blood squeezed out of ventricles

>55%

158
Q

what are the 4 steps of anti-hypertensive treatment?

A

step 1
A* (if under 55) or C (if over 55 or black)

step 2
add A or C in

step 3
add in thiazide like diuretic

step 4 (resistant hypertension)
further diuretic OR alpha blocker OR beta blocker

*ACE inhibitor OR A2RB

159
Q

two safe antihypertensive treatments in pregnancy

A

methyldopa

nifedipine

160
Q

how to calculate absolute risk reduction?

A

risk without treatment - risk with treatment

161
Q

first line tx for acute heart failure?

A

Sit patient up, give high flow oxygen, iv access
Furosemide 40-120mg i.v. (lower dose with diuretic naïve patient)
(do not offer diamorphine or nitrates)

162
Q

5 chronic heart failure drugs?

A 
ACE I
A2RB
B blockers
furosemide
digoxin
spironolactone
163
Q

adverse effects of HF treatment?

A

Loop diuretics
urinary frequency, hypokalaemia, volume depletion, renal impairment, gout, urinary retention
ACEI
cough, renal impairment, hyperkalaemia, hypotension, angioedema
Angiotensin antagonists
renal impairment, hyperkalaemia, hypotension
BBs
bradyarrhythmias, cold extremities, bronchospasm, fatigue, worsening HF, intermittent claudication
Spironolactone
hyperkalaemia, gynaecomastia
Digoxin
dig toxicity - nausea, vomiting, abdo pain, confusion, brady and tachyarrhythmias

164
Q

which HF drugs cause hypERkalaemia? and which hypO?

A

hyper:
ACE I
angiotensin antagonists
spironolactone

hypo:
furosemide

165
Q

what is metoclopramide?

A

increase smooth muscle activity

also used as anti emetic

166
Q

what is buscopan?

A

Hyoscine butylbromide- treats colicky abdo pain

167
Q

WHO analgaesia ladder

A

strong opioid + non-opoiod

                weak opioid

non-opioid

168
Q

3 examples of weak opioids

A

tramodol
codeine
dihydrocodeine

169
Q

what is the preferred method of delivery for pain relief and why?

A

oral - can be done at home

170
Q

if you doubt someones pain (suspect they are after drugs) what should you do?

A

treat them regardless at first

171
Q

what is ‘step 4’?

A

new (since the 80’s) pain management :

epidural , nerve block, spinal stimulation

172
Q

what is the max. paracetamol dose?

A

4g / day

173
Q

can you give paracetamol to someone with liver failure?

A

can give 1 - 3 g per day without increased incident of decompensation

174
Q

NSAIDS mech of action?

A

block COX -> decreased prostaglandin synthesis

175
Q

what do COX 1 and 2 do?

A

COX 1 is involved in normal physiological function e.g. protecting gastric mucosa , platelet aggregation

COX2 involved in pain and inflammation

176
Q

why do we not use COX 2 selective NSAIDS so much as ones more selective for COX1?

A

even though COX 2 are better for pain / inflammation they have been shown to increase CV events

177
Q

NSAID contraindications

A

GI symptoms / peptic ulcer disease

Liver or renal impairment

Asthmatic with aspirin sensitivity

Coagulation disorders/treatment

178
Q

can you give NSAIDS in a patient with cardiac failure?

A

yes, with caution

179
Q

mech of action of codeine?

A

Converted to morphine by CYP2D6

180
Q

what must always be given with codeine?

A

regular laxatives

181
Q

when is tramadol favoured over codeine and why?

A

bowel surgery - less constipating

182
Q

adverse of effects of tramadol?

A

confusion in the elderly

183
Q

contraindications of tramadol?

A

Severe renal / hepatic failure
Raised intra-cranial pressure
Severe respiratory depression

184
Q

morphine mech of action?

A

Acts on µ-opioid receptors in the CNS

185
Q

features of opioid toxicity?

A 
myoclonic jerks, 
pin-point pupils, 
hallucinations,
confusion,
 reduced RR.
186
Q

when to give Naloxone in morphine OD?

A

difficult to rouse,
RR<8 and/or saturations<90%
(slow titration if on opiates for pain)

187
Q

when are bisphosphonates used to manage pain?

A

bone pain - reduces turn over

188
Q

when is buscopan used in pain management and how does it work?

A

reduce pain in constipation - anti muscarinic so less smooth muscle contraction

189
Q

5 things we prescribe for at end of life

A 
pain 
breathlessness
N&amp;V
excess secretions
agitation
190
Q

what to give in renal impairment instead of morphine at end of life?

A

alfentanil if eGFR<30

191
Q

drug to give in end of life care for N&V and an alternative for renally impaired?

A

cyclizine

haliperidol

192
Q

drug for agitation at end of life?

A

midazolam

193
Q

drug for excess secretions at end of life?

A

Hyoscine Hydrobromide - normally used as motion sickness drug

194
Q

what is hyoscine butylbromide and when is it used? advantages?

A

anti motility used to reduce secretions in end of life care.
used when eGFR < 30
doesnt cross BBB therefore no drowsiness

195
Q

disadvantage of hyosine hydrobromide?

A

if it builds up it crosses the BBB and causes drowsiness

196
Q

what analgesia is provided for post op hip fracture

A

morphine and paracetamol

197
Q

what is a PCA machine?

A

patient controlled analgesia

198
Q

define dyasthesia

A

unpleasant sensation when touched due to peripheral nerve damage

199
Q

tx for neuropathic pain

A

amitryptaline, duloxatine, gabapentin/ pregabalin

200
Q

why avoid oral drugs in hip fractures?

A

want them to be nil by mouth for surgery

201
Q

define allodynia

A

pain in response to a non-painful stimuli

202
Q

how long do TCAs take to reduce neuropathic pain?

A

2 weeks

203
Q

when to take TCAs and why?

A

at night due to sedating effect

204
Q

difference between TCAs and SSRIs/SNRIs for pain?

A

TCAs work faster and is MORE effective

205
Q

what is the most you should increase a dose of morphine in 24 hours?

A

50%

206
Q

what is the ratio of oral to s/c morphine?

A

2:1

207
Q

if someone is on 100 mg of oral morphine and you want to switch it to s/c, how much do you give?

A

50 mg

208
Q

define bacteriostatic

A

stops bacteria multiplying

209
Q

5 areas to kill a bacterium

A

cell membrane

cell wall

210
Q

what is fluclox effective against?

A

gram + only

best thing for staph. aureus

211
Q

what is amoxicillin effective against?

A

some gram + and some gram -

212
Q

what is cefalexin good at penetrating?

A

skin and urine

213
Q

what is metronidazole good against?

A

Anaerobic organisms, protozoa

214
Q

how does metronidazole work?

A

Destroys bacterial DNA by forming toxic metabolites

215
Q

S/E of metronidazole?

A

disulfiram reaction with ethanol

CANNOT DRINK ON THIS

216
Q

how do macrolides work?

A

Inhibit protein synthesis by inhibiting binding at 50S ribosomal subunit

217
Q

which -mycin is NOT a macrolide?

A

clindamycin

218
Q

how does clindamycin work?

A

Inhibit protein synthesis by same mechanism as macrolides

219
Q

how do tetracyclines work?

A

Bacteriostatic : Inhibit protein synthesis by inhibiting binding of tRNA to 30S ribosomal subunit

220
Q

who cant have tetracyclines?

A

children (stains teeth)

and pregnant women - same reason

221
Q

three S/Es of tetracyclines

A

GI
sun sensitivity
hepatotoxic

222
Q

how do aminoglycosides work and an example?

A

Inhibit protein synthesis by inhibiting binding at ribosome (both subunits)

gentomicin

223
Q

S/E of aminoglycosides

A

Nephrotoxic, ototoxic (tinnitus)

224
Q

most important quinolone?

A

ciprofloxacin

225
Q

how does ciprofloxacin work?

A

Inhibit DNA gyrase which coils DNA

226
Q

S/E of ciprofloxacin?

A

GI - associated with c. diff

227
Q

how does trimethprim work?

A

Inhibit DNA synthesis by folate inhibition

228
Q

why is nitrofurantoin only used for UTIs?

A

Active concentrations only in urine

229
Q

why dont you use nitrofurantoin in renal failure?

A

wouldnt get high enough concentrations in urine

230
Q

how long after initial tx should abx be reviewed?

A

48 hrs

231
Q

which abx are always monitored?

A

vancomycin

gentamycin (and other aminoglycosides)

232
Q

s/e of gentamycin

A

ototoxic and nephrotoxic

233
Q

fever + new mummer diagnosis?

A

IE

234
Q

most common pathogens for IE?

A

staph and strep

235
Q

abx for IE?

A

fluclox and gentamycin

236
Q

define paroxysmal AF

A

2 or more episodes less than 48 hours duration

237
Q

what pre disposes a young person to AF

A 
WPWS
hyperthyroidism
alcohol / drugs
congenital heart disease
valvular disease
238
Q

how does the duration of AF effect how you cardio vert them?

A

always try drugs first
if more than 48hrs you CANNOT shock them due to risk of emboli
must anti coagulate for 2-3 weeks then bring them back

239
Q

what Ix would you following AF

A

bloods

  • infection
  • TFTs
  • U&Es

24 hr ECG

ECHO

240
Q

what are the options for initiating warfarin? why?

A

RAPID loading - give tinsaparin

in the first 24 hours warfarin will make your blood more coagulable because it uses up protein C and protein F

SLOW loading

241
Q

what is the target inr for AF patient?

A

2-3

242
Q

which rugs MUST be avoided in warfarin patients

A

ibuprofen

aspirin

243
Q

which foods must be avoided in warfarin patients?

A

vit. K high foods e.g. grapefruits

244
Q

what is given to reverse warfarin?

A

if very high (over 5 / 6 ) give vit K
even higher give it IV

if just a little high just omit a dose

245
Q

2 most common organisms to cause cellulitis?

A

staph A

beta haemolytic strep

246
Q

what abx is used initially in cellulitis?

A

IV fluclox

consider oral switch after a few days

247
Q

good alternative to fluclox in cellulitis?

A

clindamycin

248
Q

which drug is most suitable for cardioverting acute onset AF?

A

flecainide

amiodarone

249
Q

in structural heart disease which drug is most suitable for cardioverting acute onset AF?

A

amiodarone

250
Q

what is the most common side effect of IV amiodarone?

A

hypotension

also can cause thrombophlebitis if not given by central line

251
Q

when do you need to anti-coagulate a patient before electrical cardioversion?

A

if they’ve been in AF for more than 48 hrs

252
Q

in paroxysmal AF which type of control do you need?

A

rhythm (B-blocker or amiodarone)

rate control is useless as mot of the time they are fine

253
Q

when does a person in AF need rate control?

A

if >89bpm

254
Q

first line rate control drug in paroxysmal AF? if there is a contraindication?

A

B blocker

amioderone

255
Q

what is the relative risk reduction of using warfarin?

A

2/3s

256
Q

what are the contraindications for electrical cardioversion?

A

anything that makes recurrence likely

257
Q

target for INR in AF?

A

2-3

258
Q

effect of grapefruit juice on drugs?

A

enzyme inhibitor

259
Q

in a serious / life threatening bleed in a warfarin user, what is the mx?

A

IV vit K
Beriplex (pro-thrombin complex)

could also use fresh frozen plasma as this has all the clotting factors in

260
Q

how does erythromycin interact with other drugs?

A

it is an enzyme inhibitor therefore enhances them

261
Q

first line rate control drug in persistent AF? if there is a contraindication?

A

blocker

CCB e.g. verapamil

262
Q

why is AF bad

A

get stasis in the L atria

decreased CO -> tiredness

263
Q

most common causes of AF?

A

cardiac:
IHD, RHD, htn

non- cardiac:
thyrotoxicosis, infection

264
Q

how is amiodarone used in the management of AF?

A

for rhythm control but only short term

265
Q

what are the chronic adverse effects of B blockers?

A

fatigue

peptic ulcer disease

266
Q

which CCBs can you NOT use in AF? why?

A

dihydropyridines e.g. amlodapine, nifedipine

these have more effect on relaxing blood vessels than on relaxing heart muscle

267
Q

who is digoxin NOT used in?

A

active people

268
Q

how does digoxin work?

A

increase intra cellular Ca++ and vagal tone

269
Q

what are the chronic effects of amiodarone ?

A

photo sensitivity

thyroid dysfunction

270
Q

what are the types of DOAC and how do they work?

A

factor Xa inhibitors e.g. rivaroxaban , apixaban

direct thrombin inhibitors e.g. dabigatran

271
Q

warfarin mech?

A

vit K antagonist

272
Q

what organism is most commonly implicated in fever + purpuric rash?

A

Neisseria meningitidis

273
Q

what abx is used for meningococcal septicaemia

A

IV ceftriaxone

274
Q

what is given as well as abx in meningitis ?

A

steroids to reduce complications

275
Q

how are contacts of menigococcal meningitis managed?

A

contact public health -> give rifampicin / ciprofloaxacin

276
Q

most common pathogen in bac. endocarditis?

A

native valve- strep viridans

prosthetic valve - staph aureus

277
Q

what combination of abx is used to treat bac endocarditis in a person with their own valves?

A

benzyl penicillin & gentamycin

278
Q

what combination of abx is used to treat bac endocarditis in a person with prosthetic valves?

A

fluclox & rifampicin

279
Q

when do ex bac. endocarditis patients get prophylaxis? what is it

A

only in invasive procedures

amox

280
Q

patient group most commonly involved with poisoning?

A

deliberate self harm with substances that are easy to get

decreases with age from adolescents

281
Q

which substance is associated with the highest mortality in terms of poising?

A

opioids

282
Q

contraindications for use of charcoal in poisoning?

A

Absent bowel sounds (ileus)
Impaired gag reflex
Unsafe swallow

283
Q

common things that charcoal is ineffective against?

A

alcohols
iron
cyanide
hydrocarbons

284
Q

antidote for paracetamol and mech?

A

acetylecystine

glutathione repleter

285
Q

antidote for opioids? and mech

A

naloxone- specific antagonist

286
Q

antidote for methanol / ethylene glycol? mech

A

ethanol

specific antagonist

287
Q

how much paracetamol is worrying?

A

12g

288
Q

what is the dangerous metabolite in paracetamol OD?

A

NAPQI

289
Q

complication of acetylecystine?

A

anaphylactoid reaction (not immune mediated)

290
Q

symptoms of salicylate poisoning?

A 
Dizziness
Sweating
Tinnitus
Vomiting
Hyperventilation
Agitation
Delirium
291
Q

metabolic abnormalities in aspirin OD?

A

metabolic acidosis - salicylate ACID
respiratory alkalosis - resp. centre stimulation
hypoglycaemia
hypokalaemia

292
Q

Ix for aspirin OD?

A

Ix the metabolic abnormalites (ABG, glucose, U&Es)

plasma salicylate conc

293
Q

clinical features of iron toxicity and how they progress

A 
•	Early (0-6 hours):
o	Nausea and vomiting
o	Abdo pain
o	Diarrhoea [bloody]
o	Massive GI fluid loss
•	Delayed (2-72 hours):
o	Black offensive stools
o	Drowsiness/coma
o	Fits
o	Circulatory collapse
•	Late (2-4 days):
o	Acute liver necrosis
o	Renal Failure
•	Very late (2-5 weeks):
o	Gastric strictures
294
Q

when must iron be measured to establish toxicity?

A

4 hrs after ingestion

295
Q

what is used to chelate iron?

A

Desferrioxamine

296
Q

why is charcoal NOT normally indicated in bnzo OD?

A

increased risk of aspiration

297
Q

what is the antidote for bnzos and when is it used?

A

Flumenazil

best in bnzo naïve patients
can precipitate withdrawal in regular users

298
Q

presentation and mech of action of organophosphates?

A

Muscarinic effects – bronchospasm – may lead to airway compromise
Nicotinic effects – weakness and paralysis of respiratory muscles
Cardiac rhythm abnormalities

inhibition of acetylcholinesterase -> build up of ACh -> overstimulation of nicotinic and muscarinic receptors

299
Q

in what time frame does activated charcoal need to be given in?

A

1 hr

300
Q

what is the antidote for benzos? mech of action

A

flumazinil

anti-cholenergic

301
Q

Mx of anapylactoid reaction?

A

stop infusion
give H2 antagonist
restart infusion

302
Q

what is in codydramol?

A

paracetamol

dihydrocodeine

303
Q

t1/2 of naloxone?

A

1hr - important thing is that this is SHORTER than opioids

304
Q

what will an abg look like in paracetamol OD?

A

metabolic acidosis

305
Q

what will an abg look like in opioid OD?

A

resp. acidosis

306
Q

severe aspirin poisoing ->?

A

vasodilation, hypoventilation, delirium

as well as the symptoms of less severe OD: tinnitus, dizzy, sweating

4TH YEAR (12 decks)

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