CPTP4 Flashcards
define adverse drug reaction
any response to a drug which is noxious, unintended and occurs at doses used for prophylaxis, diagnosis or therapy
define medication error
any preventable event that may cause or lead to inappropriate medication use or patient harm
how does the human medicines regulations categories medical substance?
- prescription- only medicines
- registered medical practitioners can do all
- midwives, nurses and pharmacists can do some
- patient group directions - pharmacy
- pharmacists can give - general sales list
- anyone
how are pharmacy medicines released from the POM category?
- must be appropriate to self diagnose
- small chance of causing harm
- no chance of dependence
- cant be parental or eye admin
what does ‘controlled’ mean in the context of medicines?
controlled under the Misuse of Drugs Act. they are categorized into class (how harmful is it?) and schedules
what 3 criteria could mean a substance becomes controlled?
misuse may result in psychological, physical or social harm
in the misuse of drugs act, what does the schedule determine?
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
what is a named patient drug?
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
what extra information must you put when prescribing a controlled substance?
total quantity in both words and figures
define tolerance
high dose required to achieve same response
physical dependence
develops when neurons adapt to repeated drug exposure and only function normally in the presence of the drug. therefore withdrawal precipitates unpleasant physiological effects
psychological dependence
emotional need for a drug that has no underlying physical need
what is the %UK lifetime prevalence of drug misuse?
35%
how many deaths are there in the UK per year as a result of drug misuse? population distribution?
~2000
males >females
highest in 35-44 yo
NE england highest
which illegal drugs are responsible for the most deaths in the UK?
opioids
define therapeutic drug monitoring
individualisation of dosage by maintaining plasma/ blood drug concentration within a target range
3 ways therapeutic drug monitoring is carried out and examples.
- monitoring plasma/ blood drug conc.
- measuring clinical response (e.g. how much angina)
- measuring the pharmacodynamic effect (e.g. effect of insulin on blood glucose)
why should gentamicin be closely monitored?
narrow therapeutic window : ototoxicity and nephrotoxicity
three examples of drugs that indicate monitoring of plasma drug conc.?
digoxin
phenytoin (anti-epileptic)
gentamicin
what is the most common cause of iatrogenic disease?
adverse drug reactions (occur in 20% of hospital admissions)
3 adverse reactions to prednisolone?
hyperglycaemia
GI complications
OP
three example of augmented drug reactions?
insulin -> hypos
warfarin -> bleeding
nitrates -> headaches (vasodilation)
which drug is antagonistic to salbutamol?
B-blockers
how can antacids interact with other drugs?
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
muscarinic agents will have what effect on drug absorption? e.g.
decrease it due to increasing GI motility
bethanecol for urinary retention
what are the two types of allorecognition in transplants?
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
what does the suffix -mab mean in a drug?
that its a monoclonal antibody drug
define pharmacogenomics
use of genetic information to guide the choice of drug and dose on an individual
what is the effect of fast or slow acetylation on the metabolism of isoniazide?
fast- get lots of the hepatotoxic metabolite
slow- get a build of the drug which is neurotoxic
pathophysiology of PD
loss of dopaminergic cells in substantia nigra leads to degeneration of projections to other areas of basal ganglia
ways to intervene with dopamine levels
- give L-dopa (MOST EFFECTIVE)
- MAO-B
- block degradation of D in synaptic cleft- COMT inhibitors
- dopamine agonist
what must be given with l-dopa and why?
DDI- dopamine decarboxylase inhibitor
reduced sfx by stopping conversion of L-dopa into dopamine
long term side fx of l-dopa? which other drug does this?
dyskinesia- occurs in 50% of patients after 6 years
COMT inhibitors
which parkinsons medication can cause loss of impulse control?
dopamine agonists
which PD drug can cause seretonin syndrome?
MOA-B
which neurotransmitter dysregulation can cause epilepsy?
glutamate
epilepsy drugs i should know?
carbamazapine sodium valproate levetiracetam phenytoin lamotrigine
what are absence seizures treated with?
ethosuximdie (or sodium valproate)
tx for status epilepticus
- 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 - PR diazapam or buccal midazolam -> IV lorazapam -> phenytoin
- if they don’t respond to this then give IV phenytoin
what is the risk of giving IV phenytoin?
can cause hypotenision
what are the features of a parkinsons tremor?
5Hz
pill rolling
asymmetrical
what drug class is apomorphine?
dopamine agonist
what effect does the carbamazapine have on metabolism?
enzyme inducer therefore speeds metabolism
carbamazapine side fx
blurred vision back and forth eye movement drowsiness nausea rash etc
drugs that induce parkinsons
dopamine antagnoinsts- neuroleptics and anti-emetics
when is a DAT scan helpful?
determine if there was pre-existing PD in someone with drug induced parkinsons
best initial Tx for drug induced PD?
co-benoldopa (l-dopa with decarboxylase inhibitor)
mechanism of metformin?
inhibits hepatic gluconeogenesis
sulphonylurease mechanism? and example
increase insulin secretion
gliclazide
sfx of sulphonylurease
hypos, weight gain
how do thiazolidinediones work?
increase lipogenesis
decrease lipolysis
(NOT USED MUCH NOW)
why is more insulin produced if sugar is ingested vs injected?
gut plays a role in hormone regulation
how do DPP-4 inhibitors decrease glucose?
prolong t1/2 of GLP-1 (which increases insulin secretion and decreases glucagon)
statins mechanism?
decrease cholesterol synthesis
increase uptake of cholesterol from blood to liver
two methods for calculating the anion gap?
Na + K - (HCO3 + CL) normal is 16+/-4
Na - (HCO3 + Cl) normal is 12+/-4
causes for high anion gap?
MUDPILES methanol / metformin ureamia DKA Paracetamol Iron / isoniazide Lactic acidosis Ethanol salicylate
why is there raised blood glucose in DKA / HHS?
absolute or relative insulin deficiency stimulates hepatic glucose production
this cannot get into the cells
criteria for diagnosing DKA?
ketones- in urine or blood
glucose > 11mmol/L (or known diabetic)
bicarb <15mmol/L OR acidosis
what initial fluid do you give in DKA?
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
potassium levels in DKA and why?
serum potassium high as trying to get rid of H+ ions in the urine (potassium / hydrogen pump)
in what way is acidosis good in DKA?
improves O2 delivery to tissue by shifting saturation curve to the right
insulin therapy in DKA? what to do if this is delayed?
fixed rate IV insulin infusion
IM infusion
in DKA what should be monitored continuously?
- 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
after DKA what is the most reliable way of measuring ketone level?
blood ketones
urine ketones will still be present for a while
in DKA, what should the overlap be in previous insulin regime and infusion?
infusion maintained until 30 mins after SC insulin
initial response to hypos
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
what should a diabetic woman trying for a child take?
5mg folic acid unitl 12 wks
during delivery, what should a diabetic woman be given?
GKI infusion
two side effects of statins?
rhabdomyalisis / myositis
raised transaminases
whys that liver disease alters response to drug?
Impaired drug metabolism - more will be in circulation Hypoproteinemia Reduced clotting Hepatic encephalopathy Fluid overload - abnormal Na handling Hepatotoxic drugs
how can hepatic disease effect pharmacokinetic?
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.
3 factors that determine drug elimination by the liver
- blood flow (Q) throught the liver
- The fraction of drug (f) in the blood that is free or unbound to plasma proteins and capable of interacting with hepatic enzymes
- 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.
what is the extraction ratio?
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.
if the extraction ratio of a drug is 0.4, what is the bioavailability?
0.6
why avoid sedative, diuretics and drugs that cause constipation in LD?
precipitates encephalopathy
what regulates the secretion of H+ in the stomach?
gastrin
drug induced dyspepsia
NSAIDs – gastritis and peptic ulcers Steroids – gastritis and peptic ulcers Calcium antagonists - gastritis Nitrates - Reflux Theophyllines - gastritis Bisphosphonates – oesphageal erosion and ulceration.
epigastric pain relation to meals?
GU – worse with / shortly after meals
DU – relieved during meals, worse 2-3h after meals or at night
ways to test for H pylori
Faecal antigen test
Carbon 13 urea breath test
Serum H.pylori antibody test
Endoscopic biopsy samples – rapid urease test
sfx of ant acids
constipation- the Al ones
diarrhoea - the Mg ones
first line treatment of peptic ulcer disease and GORD
H2r antagonists
how do PPIs work? 2 examples
PPIs cause irreversible inhibition of H+/K+ ATPase responsible for H+ secretion from parietal cells
omeprazole, lansoprazole
H2r antagonists mech of action
H2 receptor antagonists competitively block the action of histamine on the parietal cell by antagonising the H2 receptor
what is triple therapy for H. pylori?
PPI, amoxicillin and clarithromycin OR
PPI, amoxicillin and metronidazole
4 types of laxatives and their mech?
- Bulk forming - Increase volume of non- absorbable material in the gut therefore distending the colon and increasing peristalsis
- Osmotic - Increase water content in the bowl via osmosis therefore distending the colon and increasing peristalsis
- Stimulant - Increase gastrointestinal peristalsis
- Faecal softeners - Promote defecation by softening /or lubricating the stool
contraincations for bran / hisk / methylcellulose?
dysphagia
obstruction
faecal impaction
clonic atony
in liver disease, how should the dose of an oral drug with a high extraction be changed?
reduced initial dose
reduced maintenance dose
all undergoing less first pass metabolism so will have higher bioavailablity
in liver disease, how should the dose of an IV drug with a high extraction be changed?
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
how to work out reduced dose for liver disease patients
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
what counts as a high extraction ratio?
> _0.7
what is the CLO test for and how does it work?
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
which abx for H pylori?
amoxicillin + (clarithromycin OR metronidazole)
diagnosis of a perforated PUD?
adbo x-ray : can see air under the diaphragm
what drug class is loperamide hydrochloride?
anti-motility
acts on opioid receptor
what is the mx pathway for suspected gastric cancer?
lifestyle changes and URGENT endoscopy
must be off PPIs for at least 2 weeks for endoscopy
if H pylori positive, how long do you continue the PPI for in eradication therapy ?
2 months
problems with PPIs?
low mg
risk of C diff
actue intertial nephritis (rare but this is a common cause of it)
microscopic colitis
why doesnt loperamide cause euphoria?
cant cross BBB
how does loperamide reduce diarrhoea?
binds to opioid receptors to decrease peristalisis
constipation red flags
Weight loss
Unexplained microcytic anaemia
New onset constipation in an elderly patient
in dyspepsia who should be referred for urgent endoscopy?
new onset AND over 55
Mx for dyspepsia in the U55s
‘test and treat’
test for H pylori : urea breath test or stool antigen
4 weeks full dose PPI
response to a meal in duodenal ulcers and why?
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
Mx for symptoms of an upper gastrointestinal bleed?
ABC
urgent endoscopy + therapy
inform ITU and surgeons
what is the endoscopic therapy for UGIB? and what else do you give?
adrenaline injections haemospray clips heat probe argon- plasma coagulation
IV PPIs
when to give PPIs in UGIB?
only after confirmation by endoscopy
two reasons to do another endoscopy 8 weeks after UGIB?
check healing
?cancer
effect of NSAIDS on the kidneys?
cause afferent renal arteriol vasoconstriction
contraindications for opioid anti-motility drugs
Severe ulcerative colitis or C.diff – increases the risk of Toxic megacolon
Severe infective diarrhoea
Dysentery (bloody stool)
Liver disease (risk of accumulation)
indications for opioid anti-motility drugs
- mild infective diarrhoea
- irritable bowel syndrome
- chronic IBD diarrhoea
- high output stomas
which types of laxatives are avoided if there is suspected obstruction?
stimulant
bilk forming
indications for investigating constipation?
>40yrs Recent change in bowel habit Iron deficiency anaemia Assoc symptoms (weight loss, rectal bleeding, mucous discharge or tenesmus)
mostly it doesnt need investigating
difference between SABA and LABA?
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
electrolyte abnormality caused by B2 agonists?
hypOkalaemia
they are sometimes used to treat hypERkalaemia
what drug class is ipatropium?
SAMA
what drug class is tiotropium?
LAMA
which patients cant tolerate adrenergic agonists e.g. B2 agonists?
ischaemic heart disease or tachycardia
Theophylline use and mech of action?
second line therapy in asthma
Inhibits phosphodiesterase to cause an increase in cAMP in smooth muscle cells
use of leukotriene receptor antagonists and example
prohylaxsis for asthma NOT symptom relief
montelukast
two main adverse effects of corticosteroids in asthma
horse voice
oral candidiasis
what oral corticosteroid is used in asthma?
prednisalone
what is the first line regular preventer?
low dose ICS
if low dose ICS is not controlling asthma what is added next?
LABA
drugs that can exacerbate asthma?
B-blockers -> bronchospasm (esp. non-selective e.g. propranolol)
NSAIDS -> bronchospams (aspirin sensitivity affects 20%
how much of an inhaled drug ends up in the lungs?
10%
why are there systemic side effects when drugs are inhaled?
90% is swallowed
Mx of acute asthma
O2 steroids B2 agonists IV mg sulphate ipatropium bromide
Mx of COPD exacernation
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)
what increase in peak flow post SABA indicates asthma?
200ml
theophylline mech and use?
raises intracellular cAMP which promotes smooth muscle relaxation
used in asthma
alternative for B blockers in asthmatic patients?
prostaglandins
abx for CAP?
amox
clarithromycin
doxycycline (this is used if someone with COPD is hospitalised as it covers the more obscure pathogens)
Tx for exacerbation of COPD?
salbutamol and ipratropium NEB
?O2
prednisalone (oral)
name a leukotriene receptor antagonist used in asthma
montekeukast
3 ICS used in asthma?
beclamethosome
budensoide
fluticasone
interaction between glaucoma and asthma tx?
topical b-blocker used in glaucoma can have systemic effects of bronchospasm
define acute severe asthma and when should you admit?
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
two drug classes that exacerbate asthma and alternatives?
NSAIDS
- only avoid if you know it worsens your asthma
- aspirin sensitivity in 20%, use clopidogrel
B-blockers
-use prostaglandin analogue instead
what does a rising PaCO2 tell you about a patient in an asthma attack?
they are getting exhausted and failing to blow off CO2- BAD
Mx for acute severe asthma
O2
Neb : salbutamol and ipratropium
steroids
what to consider in mx of pneumonia in asthmatic patient
are they on theophylline - this is INHIBITED by clarithromycin and ciprofloxacin
theophylline mech?
Competitive nonselective phosphodiesterase inhibitor
- reveres steroid insensitivity
- reduces inflammation and innate immunity
what is carbocistenine
mucolytic
on an ABG which values tell you weather the problem is acute or chronic?
deranged pH means it’s a chronic problem - cant live with that for long
bicarb. - takes a while to change
type 1 resp failure is due to what
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)
type 2 resp failure is due to what
ventilatory failure
e.g.
obstructive disease
emphysema
when to give LTOT?
PaO2 < 7.3
OR
PaO2 7.3 - 8 AND cor pulmonale
what information is needed and how to calculate ‘no. needed to treat’
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’
what are ABPM and HBPM and whats the point in them?
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
define the stages of hypertension
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
when to treat hypertension?
stage 1 IF THEY HAVE A RAISED CV RISK (QRISK or other)
stage 2 always
5 classes of drugs used in hypertension
ACE inhibitors CCBs Diuretics A2RB cardiac glycosides
Mx of hypertension in pregnancy?
use labetolol
what QRISK score warrants a statin?
> 10% risk of CVD
what U&E’s would be expected in someone not tolerating ARBs?
raised Na
low K
acute heart failure Mx?
IV furosemide
O2
sit up right
what is the ejection fraction and what is normal?
amount of blood squeezed out of ventricles
>55%
what are the 4 steps of anti-hypertensive treatment?
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
two safe antihypertensive treatments in pregnancy
methyldopa
nifedipine
how to calculate absolute risk reduction?
risk without treatment - risk with treatment
first line tx for acute heart failure?
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)
5 chronic heart failure drugs?
ACE I A2RB B blockers furosemide digoxin spironolactone
adverse effects of HF treatment?
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
which HF drugs cause hypERkalaemia? and which hypO?
hyper:
ACE I
angiotensin antagonists
spironolactone
hypo:
furosemide
what is metoclopramide?
increase smooth muscle activity
also used as anti emetic
what is buscopan?
Hyoscine butylbromide- treats colicky abdo pain
WHO analgaesia ladder
strong opioid + non-opoiod
weak opioid
non-opioid
3 examples of weak opioids
tramodol
codeine
dihydrocodeine
what is the preferred method of delivery for pain relief and why?
oral - can be done at home
if you doubt someones pain (suspect they are after drugs) what should you do?
treat them regardless at first
what is ‘step 4’?
new (since the 80’s) pain management :
epidural , nerve block, spinal stimulation
what is the max. paracetamol dose?
4g / day
can you give paracetamol to someone with liver failure?
can give 1 - 3 g per day without increased incident of decompensation
NSAIDS mech of action?
block COX -> decreased prostaglandin synthesis
what do COX 1 and 2 do?
COX 1 is involved in normal physiological function e.g. protecting gastric mucosa , platelet aggregation
COX2 involved in pain and inflammation
why do we not use COX 2 selective NSAIDS so much as ones more selective for COX1?
even though COX 2 are better for pain / inflammation they have been shown to increase CV events
NSAID contraindications
GI symptoms / peptic ulcer disease
Liver or renal impairment
Asthmatic with aspirin sensitivity
Coagulation disorders/treatment
can you give NSAIDS in a patient with cardiac failure?
yes, with caution
mech of action of codeine?
Converted to morphine by CYP2D6
what must always be given with codeine?
regular laxatives
when is tramadol favoured over codeine and why?
bowel surgery - less constipating
adverse of effects of tramadol?
confusion in the elderly
contraindications of tramadol?
Severe renal / hepatic failure
Raised intra-cranial pressure
Severe respiratory depression
morphine mech of action?
Acts on µ-opioid receptors in the CNS
features of opioid toxicity?
myoclonic jerks, pin-point pupils, hallucinations, confusion, reduced RR.
when to give Naloxone in morphine OD?
difficult to rouse,
RR<8 and/or saturations<90%
(slow titration if on opiates for pain)
when are bisphosphonates used to manage pain?
bone pain - reduces turn over
when is buscopan used in pain management and how does it work?
reduce pain in constipation - anti muscarinic so less smooth muscle contraction
5 things we prescribe for at end of life
pain breathlessness N&V excess secretions agitation
what to give in renal impairment instead of morphine at end of life?
alfentanil if eGFR<30
drug to give in end of life care for N&V and an alternative for renally impaired?
cyclizine
haliperidol
drug for agitation at end of life?
midazolam
drug for excess secretions at end of life?
Hyoscine Hydrobromide - normally used as motion sickness drug
what is hyoscine butylbromide and when is it used? advantages?
anti motility used to reduce secretions in end of life care.
used when eGFR < 30
doesnt cross BBB therefore no drowsiness
disadvantage of hyosine hydrobromide?
if it builds up it crosses the BBB and causes drowsiness
what analgesia is provided for post op hip fracture
morphine and paracetamol
what is a PCA machine?
patient controlled analgesia
define dyasthesia
unpleasant sensation when touched due to peripheral nerve damage
tx for neuropathic pain
amitryptaline, duloxatine, gabapentin/ pregabalin
why avoid oral drugs in hip fractures?
want them to be nil by mouth for surgery
define allodynia
pain in response to a non-painful stimuli
how long do TCAs take to reduce neuropathic pain?
2 weeks
when to take TCAs and why?
at night due to sedating effect
difference between TCAs and SSRIs/SNRIs for pain?
TCAs work faster and is MORE effective
what is the most you should increase a dose of morphine in 24 hours?
50%
what is the ratio of oral to s/c morphine?
2:1
if someone is on 100 mg of oral morphine and you want to switch it to s/c, how much do you give?
50 mg
define bacteriostatic
stops bacteria multiplying
5 areas to kill a bacterium
cell membrane
cell wall
what is fluclox effective against?
gram + only
best thing for staph. aureus
what is amoxicillin effective against?
some gram + and some gram -
what is cefalexin good at penetrating?
skin and urine
what is metronidazole good against?
Anaerobic organisms, protozoa
how does metronidazole work?
Destroys bacterial DNA by forming toxic metabolites
S/E of metronidazole?
disulfiram reaction with ethanol
CANNOT DRINK ON THIS
how do macrolides work?
Inhibit protein synthesis by inhibiting binding at 50S ribosomal subunit
which -mycin is NOT a macrolide?
clindamycin
how does clindamycin work?
Inhibit protein synthesis by same mechanism as macrolides
how do tetracyclines work?
Bacteriostatic : Inhibit protein synthesis by inhibiting binding of tRNA to 30S ribosomal subunit
who cant have tetracyclines?
children (stains teeth)
and pregnant women - same reason
three S/Es of tetracyclines
GI
sun sensitivity
hepatotoxic
how do aminoglycosides work and an example?
Inhibit protein synthesis by inhibiting binding at ribosome (both subunits)
gentomicin
S/E of aminoglycosides
Nephrotoxic, ototoxic (tinnitus)
most important quinolone?
ciprofloxacin
how does ciprofloxacin work?
Inhibit DNA gyrase which coils DNA
S/E of ciprofloxacin?
GI - associated with c. diff
how does trimethprim work?
Inhibit DNA synthesis by folate inhibition
why is nitrofurantoin only used for UTIs?
Active concentrations only in urine
why dont you use nitrofurantoin in renal failure?
wouldnt get high enough concentrations in urine
how long after initial tx should abx be reviewed?
48 hrs
which abx are always monitored?
vancomycin
gentamycin (and other aminoglycosides)
s/e of gentamycin
ototoxic and nephrotoxic
fever + new mummer diagnosis?
IE
most common pathogens for IE?
staph and strep
abx for IE?
fluclox and gentamycin
define paroxysmal AF
2 or more episodes less than 48 hours duration
what pre disposes a young person to AF
WPWS hyperthyroidism alcohol / drugs congenital heart disease valvular disease
how does the duration of AF effect how you cardio vert them?
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
what Ix would you following AF
bloods
- infection
- TFTs
- U&Es
24 hr ECG
ECHO
what are the options for initiating warfarin? why?
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
what is the target inr for AF patient?
2-3
which rugs MUST be avoided in warfarin patients
ibuprofen
aspirin
which foods must be avoided in warfarin patients?
vit. K high foods e.g. grapefruits
what is given to reverse warfarin?
if very high (over 5 / 6 ) give vit K
even higher give it IV
if just a little high just omit a dose
2 most common organisms to cause cellulitis?
staph A
beta haemolytic strep
what abx is used initially in cellulitis?
IV fluclox
consider oral switch after a few days
good alternative to fluclox in cellulitis?
clindamycin
which drug is most suitable for cardioverting acute onset AF?
flecainide
amiodarone
in structural heart disease which drug is most suitable for cardioverting acute onset AF?
amiodarone
what is the most common side effect of IV amiodarone?
hypotension
also can cause thrombophlebitis if not given by central line
when do you need to anti-coagulate a patient before electrical cardioversion?
if they’ve been in AF for more than 48 hrs
in paroxysmal AF which type of control do you need?
rhythm (B-blocker or amiodarone)
rate control is useless as mot of the time they are fine
when does a person in AF need rate control?
if >89bpm
first line rate control drug in paroxysmal AF? if there is a contraindication?
B blocker
amioderone
what is the relative risk reduction of using warfarin?
2/3s
what are the contraindications for electrical cardioversion?
anything that makes recurrence likely
target for INR in AF?
2-3
effect of grapefruit juice on drugs?
enzyme inhibitor
in a serious / life threatening bleed in a warfarin user, what is the mx?
IV vit K
Beriplex (pro-thrombin complex)
could also use fresh frozen plasma as this has all the clotting factors in
how does erythromycin interact with other drugs?
it is an enzyme inhibitor therefore enhances them
first line rate control drug in persistent AF? if there is a contraindication?
blocker
CCB e.g. verapamil
why is AF bad
get stasis in the L atria
decreased CO -> tiredness
most common causes of AF?
cardiac:
IHD, RHD, htn
non- cardiac:
thyrotoxicosis, infection
how is amiodarone used in the management of AF?
for rhythm control but only short term
what are the chronic adverse effects of B blockers?
fatigue
peptic ulcer disease
which CCBs can you NOT use in AF? why?
dihydropyridines e.g. amlodapine, nifedipine
these have more effect on relaxing blood vessels than on relaxing heart muscle
who is digoxin NOT used in?
active people
how does digoxin work?
increase intra cellular Ca++ and vagal tone
what are the chronic effects of amiodarone ?
photo sensitivity
thyroid dysfunction
what are the types of DOAC and how do they work?
factor Xa inhibitors e.g. rivaroxaban , apixaban
direct thrombin inhibitors e.g. dabigatran
warfarin mech?
vit K antagonist
what organism is most commonly implicated in fever + purpuric rash?
Neisseria meningitidis
what abx is used for meningococcal septicaemia
IV ceftriaxone
what is given as well as abx in meningitis ?
steroids to reduce complications
how are contacts of menigococcal meningitis managed?
contact public health -> give rifampicin / ciprofloaxacin
most common pathogen in bac. endocarditis?
native valve- strep viridans
prosthetic valve - staph aureus
what combination of abx is used to treat bac endocarditis in a person with their own valves?
benzyl penicillin & gentamycin
what combination of abx is used to treat bac endocarditis in a person with prosthetic valves?
fluclox & rifampicin
when do ex bac. endocarditis patients get prophylaxis? what is it
only in invasive procedures
amox
patient group most commonly involved with poisoning?
deliberate self harm with substances that are easy to get
decreases with age from adolescents
which substance is associated with the highest mortality in terms of poising?
opioids
contraindications for use of charcoal in poisoning?
Absent bowel sounds (ileus)
Impaired gag reflex
Unsafe swallow
common things that charcoal is ineffective against?
alcohols
iron
cyanide
hydrocarbons
antidote for paracetamol and mech?
acetylecystine
glutathione repleter
antidote for opioids? and mech
naloxone- specific antagonist
antidote for methanol / ethylene glycol? mech
ethanol
specific antagonist
how much paracetamol is worrying?
12g
what is the dangerous metabolite in paracetamol OD?
NAPQI
complication of acetylecystine?
anaphylactoid reaction (not immune mediated)
symptoms of salicylate poisoning?
Dizziness Sweating Tinnitus Vomiting Hyperventilation Agitation Delirium
metabolic abnormalities in aspirin OD?
metabolic acidosis - salicylate ACID
respiratory alkalosis - resp. centre stimulation
hypoglycaemia
hypokalaemia
Ix for aspirin OD?
Ix the metabolic abnormalites (ABG, glucose, U&Es)
plasma salicylate conc
clinical features of iron toxicity and how they progress
• 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
when must iron be measured to establish toxicity?
4 hrs after ingestion
what is used to chelate iron?
Desferrioxamine
why is charcoal NOT normally indicated in bnzo OD?
increased risk of aspiration
what is the antidote for bnzos and when is it used?
Flumenazil
best in bnzo naïve patients
can precipitate withdrawal in regular users
presentation and mech of action of organophosphates?
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
in what time frame does activated charcoal need to be given in?
1 hr
what is the antidote for benzos? mech of action
flumazinil
anti-cholenergic
Mx of anapylactoid reaction?
stop infusion
give H2 antagonist
restart infusion
what is in codydramol?
paracetamol
dihydrocodeine
t1/2 of naloxone?
1hr - important thing is that this is SHORTER than opioids
what will an abg look like in paracetamol OD?
metabolic acidosis
what will an abg look like in opioid OD?
resp. acidosis
severe aspirin poisoing ->?
vasodilation, hypoventilation, delirium
as well as the symptoms of less severe OD: tinnitus, dizzy, sweating
