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
muscarinic agents will have what effect on drug absorption? e.g.
decrease it due to increasing GI motility | bethanecol for urinary retention
26
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
27
what does the suffix -mab mean in a drug?
that its a monoclonal antibody drug
28
define pharmacogenomics
use of genetic information to guide the choice of drug and dose on an individual
29
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
30
pathophysiology of PD
loss of dopaminergic cells in substantia nigra leads to degeneration of projections to other areas of basal ganglia
31
ways to intervene with dopamine levels
1. give L-dopa (MOST EFFECTIVE) 2. MAO-B 3. block degradation of D in synaptic cleft- COMT inhibitors 4. dopamine agonist
32
what must be given with l-dopa and why?
DDI- dopamine decarboxylase inhibitor | reduced sfx by stopping conversion of L-dopa into dopamine
33
long term side fx of l-dopa? which other drug does this?
dyskinesia- occurs in 50% of patients after 6 years COMT inhibitors
34
which parkinsons medication can cause loss of impulse control?
dopamine agonists
35
which PD drug can cause seretonin syndrome?
MOA-B
36
which neurotransmitter dysregulation can cause epilepsy?
glutamate
37
epilepsy drugs i should know?
``` carbamazapine sodium valproate levetiracetam phenytoin lamotrigine ```
38
what are absence seizures treated with?
ethosuximdie (or sodium valproate)
39
tx for status epilepticus
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
40
what is the risk of giving IV phenytoin?
can cause hypotenision
41
what are the features of a parkinsons tremor?
5Hz pill rolling asymmetrical
42
what drug class is apomorphine?
dopamine agonist
43
what effect does the carbamazapine have on metabolism?
enzyme inducer therefore speeds metabolism
44
carbamazapine side fx
``` blurred vision back and forth eye movement drowsiness nausea rash etc ```
45
drugs that induce parkinsons
dopamine antagnoinsts- neuroleptics and anti-emetics
46
when is a DAT scan helpful?
determine if there was pre-existing PD in someone with drug induced parkinsons
47
best initial Tx for drug induced PD?
co-benoldopa (l-dopa with decarboxylase inhibitor)
48
mechanism of metformin?
inhibits hepatic gluconeogenesis
49
sulphonylurease mechanism? and example
increase insulin secretion | gliclazide
50
sfx of sulphonylurease
hypos, weight gain
51
how do thiazolidinediones work?
increase lipogenesis decrease lipolysis (NOT USED MUCH NOW)
52
why is more insulin produced if sugar is ingested vs injected?
gut plays a role in hormone regulation
53
how do DPP-4 inhibitors decrease glucose?
prolong t1/2 of GLP-1 (which increases insulin secretion and decreases glucagon)
54
statins mechanism?
decrease cholesterol synthesis | increase uptake of cholesterol from blood to liver
55
two methods for calculating the anion gap?
Na + K - (HCO3 + CL) normal is 16+/-4 | Na - (HCO3 + Cl) normal is 12+/-4
56
causes for high anion gap?
``` MUDPILES methanol / metformin ureamia DKA Paracetamol Iron / isoniazide Lactic acidosis Ethanol salicylate ```
57
why is there raised blood glucose in DKA / HHS?
absolute or relative insulin deficiency stimulates hepatic glucose production this cannot get into the cells
58
criteria for diagnosing DKA?
ketones- in urine or blood glucose > 11mmol/L (or known diabetic) bicarb <15mmol/L OR acidosis
59
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
60
potassium levels in DKA and why?
serum potassium high as trying to get rid of H+ ions in the urine (potassium / hydrogen pump)
61
in what way is acidosis good in DKA?
improves O2 delivery to tissue by shifting saturation curve to the right
62
insulin therapy in DKA? what to do if this is delayed?
fixed rate IV insulin infusion | IM infusion
63
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
64
after DKA what is the most reliable way of measuring ketone level?
blood ketones | urine ketones will still be present for a while
65
in DKA, what should the overlap be in previous insulin regime and infusion?
infusion maintained until 30 mins after SC insulin
66
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
67
what should a diabetic woman trying for a child take?
5mg folic acid unitl 12 wks
68
during delivery, what should a diabetic woman be given?
GKI infusion
69
two side effects of statins?
rhabdomyalisis / myositis | raised transaminases
70
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 ```
71
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.
72
3 factors that determine drug elimination by the liver
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.
73
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.
74
if the extraction ratio of a drug is 0.4, what is the bioavailability?
0.6
75
why avoid sedative, diuretics and drugs that cause constipation in LD?
precipitates encephalopathy
76
what regulates the secretion of H+ in the stomach?
gastrin
77
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. ```
78
epigastric pain relation to meals?
GU – worse with / shortly after meals | DU – relieved during meals, worse 2-3h after meals or at night
79
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
80
sfx of ant acids
constipation- the Al ones | diarrhoea - the Mg ones
81
first line treatment of peptic ulcer disease and GORD
H2r antagonists
82
how do PPIs work? 2 examples
PPIs cause irreversible inhibition of H+/K+ ATPase responsible for H+ secretion from parietal cells omeprazole, lansoprazole
83
H2r antagonists mech of action
H2 receptor antagonists competitively block the action of histamine on the parietal cell by antagonising the H2 receptor
84
what is triple therapy for H. pylori?
PPI, amoxicillin and clarithromycin OR | PPI, amoxicillin and metronidazole
85
4 types of laxatives and their mech?
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
86
contraincations for bran / hisk / methylcellulose?
dysphagia obstruction faecal impaction clonic atony
87
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
88
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
89
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
90
what counts as a high extraction ratio?
>_0.7
91
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
92
which abx for H pylori?
amoxicillin + (clarithromycin OR metronidazole)
93
diagnosis of a perforated PUD?
adbo x-ray : can see air under the diaphragm
94
what drug class is loperamide hydrochloride?
anti-motility | acts on opioid receptor
95
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
96
if H pylori positive, how long do you continue the PPI for in eradication therapy ?
2 months
97
problems with PPIs?
low mg risk of C diff actue intertial nephritis (rare but this is a common cause of it) microscopic colitis
98
why doesnt loperamide cause euphoria?
cant cross BBB
99
how does loperamide reduce diarrhoea?
binds to opioid receptors to decrease peristalisis
100
constipation red flags
Weight loss Unexplained microcytic anaemia New onset constipation in an elderly patient
101
in dyspepsia who should be referred for urgent endoscopy?
new onset AND over 55
102
Mx for dyspepsia in the U55s
'test and treat' test for H pylori : urea breath test or stool antigen 4 weeks full dose PPI
103
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
104
Mx for symptoms of an upper gastrointestinal bleed?
ABC urgent endoscopy + therapy inform ITU and surgeons
105
what is the endoscopic therapy for UGIB? and what else do you give?
``` adrenaline injections haemospray clips heat probe argon- plasma coagulation ``` IV PPIs
106
when to give PPIs in UGIB?
only after confirmation by endoscopy
107
two reasons to do another endoscopy 8 weeks after UGIB?
check healing | ?cancer
108
effect of NSAIDS on the kidneys?
cause afferent renal arteriol vasoconstriction
109
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)
110
indications for opioid anti-motility drugs
- mild infective diarrhoea - irritable bowel syndrome - chronic IBD diarrhoea - high output stomas
111
which types of laxatives are avoided if there is suspected obstruction?
stimulant | bilk forming
112
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
113
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
114
electrolyte abnormality caused by B2 agonists?
hypOkalaemia they are sometimes used to treat hypERkalaemia
115
what drug class is ipatropium?
SAMA
116
what drug class is tiotropium?
LAMA
117
which patients cant tolerate adrenergic agonists e.g. B2 agonists?
ischaemic heart disease or tachycardia
118
Theophylline use and mech of action?
second line therapy in asthma Inhibits phosphodiesterase to cause an increase in cAMP in smooth muscle cells
119
use of leukotriene receptor antagonists and example
prohylaxsis for asthma NOT symptom relief | montelukast
120
two main adverse effects of corticosteroids in asthma
horse voice | oral candidiasis
121
what oral corticosteroid is used in asthma?
prednisalone
122
what is the first line regular preventer?
low dose ICS
123
if low dose ICS is not controlling asthma what is added next?
LABA
124
drugs that can exacerbate asthma?
B-blockers -> bronchospasm (esp. non-selective e.g. propranolol) NSAIDS -> bronchospams (aspirin sensitivity affects 20%
125
how much of an inhaled drug ends up in the lungs?
10%
126
why are there systemic side effects when drugs are inhaled?
90% is swallowed
127
Mx of acute asthma
``` O2 steroids B2 agonists IV mg sulphate ipatropium bromide ```
128
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)
129
what increase in peak flow post SABA indicates asthma?
200ml
130
theophylline mech and use?
raises intracellular cAMP which promotes smooth muscle relaxation used in asthma
131
alternative for B blockers in asthmatic patients?
prostaglandins
132
abx for CAP?
amox clarithromycin doxycycline (this is used if someone with COPD is hospitalised as it covers the more obscure pathogens)
133
Tx for exacerbation of COPD?
salbutamol and ipratropium NEB ?O2 prednisalone (oral)
134
name a leukotriene receptor antagonist used in asthma
montekeukast
135
3 ICS used in asthma?
beclamethosome budensoide fluticasone
136
interaction between glaucoma and asthma tx?
topical b-blocker used in glaucoma can have systemic effects of bronchospasm
137
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
138
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
139
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
140
Mx for acute severe asthma
O2 Neb : salbutamol and ipratropium steroids
141
what to consider in mx of pneumonia in asthmatic patient
are they on theophylline - this is INHIBITED by clarithromycin and ciprofloxacin
142
theophylline mech?
Competitive nonselective phosphodiesterase inhibitor - reveres steroid insensitivity - reduces inflammation and innate immunity
143
what is carbocistenine
mucolytic
144
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
145
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)
146
type 2 resp failure is due to what
ventilatory failure e.g. obstructive disease emphysema
147
when to give LTOT?
PaO2 < 7.3 OR PaO2 7.3 - 8 AND cor pulmonale
148
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'
149
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
150
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
151
when to treat hypertension?
stage 1 IF THEY HAVE A RAISED CV RISK (QRISK or other) | stage 2 always
152
5 classes of drugs used in hypertension
``` ACE inhibitors CCBs Diuretics A2RB cardiac glycosides ```
153
Mx of hypertension in pregnancy?
use labetolol
154
what QRISK score warrants a statin?
>10% risk of CVD
155
what U&E's would be expected in someone not tolerating ARBs?
raised Na | low K
156
acute heart failure Mx?
IV furosemide O2 sit up right
157
what is the ejection fraction and what is normal?
amount of blood squeezed out of ventricles | >55%
158
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
159
two safe antihypertensive treatments in pregnancy
methyldopa | nifedipine
160
how to calculate absolute risk reduction?
risk without treatment - risk with treatment
161
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)
162
5 chronic heart failure drugs?
``` ACE I A2RB B blockers furosemide digoxin spironolactone ```
163
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
164
which HF drugs cause hypERkalaemia? and which hypO?
hyper: ACE I angiotensin antagonists spironolactone hypo: furosemide
165
what is metoclopramide?
increase smooth muscle activity | also used as anti emetic
166
what is buscopan?
Hyoscine butylbromide- treats colicky abdo pain
167
WHO analgaesia ladder
strong opioid + non-opoiod weak opioid non-opioid
168
3 examples of weak opioids
tramodol codeine dihydrocodeine
169
what is the preferred method of delivery for pain relief and why?
oral - can be done at home
170
if you doubt someones pain (suspect they are after drugs) what should you do?
treat them regardless at first
171
what is 'step 4'?
new (since the 80's) pain management : | epidural , nerve block, spinal stimulation
172
what is the max. paracetamol dose?
4g / day
173
can you give paracetamol to someone with liver failure?
can give 1 - 3 g per day without increased incident of decompensation
174
NSAIDS mech of action?
block COX -> decreased prostaglandin synthesis
175
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
176
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
177
NSAID contraindications
GI symptoms / peptic ulcer disease Liver or renal impairment Asthmatic with aspirin sensitivity Coagulation disorders/treatment
178
can you give NSAIDS in a patient with cardiac failure?
yes, with caution
179
mech of action of codeine?
Converted to morphine by CYP2D6
180
what must always be given with codeine?
regular laxatives
181
when is tramadol favoured over codeine and why?
bowel surgery - less constipating
182
adverse of effects of tramadol?
confusion in the elderly
183
contraindications of tramadol?
Severe renal / hepatic failure Raised intra-cranial pressure Severe respiratory depression
184
morphine mech of action?
Acts on µ-opioid receptors in the CNS
185
features of opioid toxicity?
``` myoclonic jerks, pin-point pupils, hallucinations, confusion, reduced RR. ```
186
when to give Naloxone in morphine OD?
difficult to rouse, RR<8 and/or saturations<90% (slow titration if on opiates for pain)
187
when are bisphosphonates used to manage pain?
bone pain - reduces turn over
188
when is buscopan used in pain management and how does it work?
reduce pain in constipation - anti muscarinic so less smooth muscle contraction
189
5 things we prescribe for at end of life
``` pain breathlessness N&V excess secretions agitation ```
190
what to give in renal impairment instead of morphine at end of life?
alfentanil if eGFR<30
191
drug to give in end of life care for N&V and an alternative for renally impaired?
cyclizine | haliperidol
192
drug for agitation at end of life?
midazolam
193
drug for excess secretions at end of life?
Hyoscine Hydrobromide - normally used as motion sickness drug
194
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
195
disadvantage of hyosine hydrobromide?
if it builds up it crosses the BBB and causes drowsiness
196
what analgesia is provided for post op hip fracture
morphine and paracetamol
197
what is a PCA machine?
patient controlled analgesia
198
define dyasthesia
unpleasant sensation when touched due to peripheral nerve damage
199
tx for neuropathic pain
amitryptaline, duloxatine, gabapentin/ pregabalin
200
why avoid oral drugs in hip fractures?
want them to be nil by mouth for surgery
201
define allodynia
pain in response to a non-painful stimuli
202
how long do TCAs take to reduce neuropathic pain?
2 weeks
203
when to take TCAs and why?
at night due to sedating effect
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difference between TCAs and SSRIs/SNRIs for pain?
TCAs work faster and is MORE effective
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what is the most you should increase a dose of morphine in 24 hours?
50%
206
what is the ratio of oral to s/c morphine?
2:1
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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
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define bacteriostatic
stops bacteria multiplying
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5 areas to kill a bacterium
cell membrane | cell wall
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what is fluclox effective against?
gram + only best thing for staph. aureus
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what is amoxicillin effective against?
some gram + and some gram -
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what is cefalexin good at penetrating?
skin and urine
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what is metronidazole good against?
Anaerobic organisms, protozoa
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how does metronidazole work?
Destroys bacterial DNA by forming toxic metabolites
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S/E of metronidazole?
disulfiram reaction with ethanol CANNOT DRINK ON THIS
216
how do macrolides work?
Inhibit protein synthesis by inhibiting binding at 50S ribosomal subunit
217
which -mycin is NOT a macrolide?
clindamycin
218
how does clindamycin work?
Inhibit protein synthesis by same mechanism as macrolides
219
how do tetracyclines work?
Bacteriostatic : Inhibit protein synthesis by inhibiting binding of tRNA to 30S ribosomal subunit
220
who cant have tetracyclines?
children (stains teeth) | and pregnant women - same reason
221
three S/Es of tetracyclines
GI sun sensitivity hepatotoxic
222
how do aminoglycosides work and an example?
Inhibit protein synthesis by inhibiting binding at ribosome (both subunits) gentomicin
223
S/E of aminoglycosides
Nephrotoxic, ototoxic (tinnitus)
224
most important quinolone?
ciprofloxacin
225
how does ciprofloxacin work?
Inhibit DNA gyrase which coils DNA
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S/E of ciprofloxacin?
GI - associated with c. diff
227
how does trimethprim work?
Inhibit DNA synthesis by folate inhibition
228
why is nitrofurantoin only used for UTIs?
Active concentrations only in urine
229
why dont you use nitrofurantoin in renal failure?
wouldnt get high enough concentrations in urine
230
how long after initial tx should abx be reviewed?
48 hrs
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which abx are always monitored?
vancomycin | gentamycin (and other aminoglycosides)
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s/e of gentamycin
ototoxic and nephrotoxic
233
fever + new mummer diagnosis?
IE
234
most common pathogens for IE?
staph and strep
235
abx for IE?
fluclox and gentamycin
236
define paroxysmal AF
2 or more episodes less than 48 hours duration
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what pre disposes a young person to AF
``` WPWS hyperthyroidism alcohol / drugs congenital heart disease valvular disease ```
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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
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what Ix would you following AF
bloods - infection - TFTs - U&Es 24 hr ECG ECHO
240
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
241
what is the target inr for AF patient?
2-3
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which rugs MUST be avoided in warfarin patients
ibuprofen | aspirin
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which foods must be avoided in warfarin patients?
vit. K high foods e.g. grapefruits
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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
245
2 most common organisms to cause cellulitis?
staph A | beta haemolytic strep
246
what abx is used initially in cellulitis?
IV fluclox | consider oral switch after a few days
247
good alternative to fluclox in cellulitis?
clindamycin
248
which drug is most suitable for cardioverting acute onset AF?
flecainide | amiodarone
249
in structural heart disease which drug is most suitable for cardioverting acute onset AF?
amiodarone
250
what is the most common side effect of IV amiodarone?
hypotension also can cause thrombophlebitis if not given by central line
251
when do you need to anti-coagulate a patient before electrical cardioversion?
if they've been in AF for more than 48 hrs
252
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
253
when does a person in AF need rate control?
if >89bpm
254
first line rate control drug in paroxysmal AF? if there is a contraindication?
B blocker | amioderone
255
what is the relative risk reduction of using warfarin?
2/3s
256
what are the contraindications for electrical cardioversion?
anything that makes recurrence likely
257
target for INR in AF?
2-3
258
effect of grapefruit juice on drugs?
enzyme inhibitor
259
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
260
how does erythromycin interact with other drugs?
it is an enzyme inhibitor therefore enhances them
261
first line rate control drug in persistent AF? if there is a contraindication?
blocker | CCB e.g. verapamil
262
why is AF bad
get stasis in the L atria | decreased CO -> tiredness
263
most common causes of AF?
cardiac: IHD, RHD, htn non- cardiac: thyrotoxicosis, infection
264
how is amiodarone used in the management of AF?
for rhythm control but only short term
265
what are the chronic adverse effects of B blockers?
fatigue | peptic ulcer disease
266
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
267
who is digoxin NOT used in?
active people
268
how does digoxin work?
increase intra cellular Ca++ and vagal tone
269
what are the chronic effects of amiodarone ?
photo sensitivity | thyroid dysfunction
270
what are the types of DOAC and how do they work?
factor Xa inhibitors e.g. rivaroxaban , apixaban | direct thrombin inhibitors e.g. dabigatran
271
warfarin mech?
vit K antagonist
272
what organism is most commonly implicated in fever + purpuric rash?
Neisseria meningitidis
273
what abx is used for meningococcal septicaemia
IV ceftriaxone
274
what is given as well as abx in meningitis ?
steroids to reduce complications
275
how are contacts of menigococcal meningitis managed?
contact public health -> give rifampicin / ciprofloaxacin
276
most common pathogen in bac. endocarditis?
native valve- strep viridans | prosthetic valve - staph aureus
277
what combination of abx is used to treat bac endocarditis in a person with their own valves?
benzyl penicillin & gentamycin
278
what combination of abx is used to treat bac endocarditis in a person with prosthetic valves?
fluclox & rifampicin
279
when do ex bac. endocarditis patients get prophylaxis? what is it
only in invasive procedures | amox
280
patient group most commonly involved with poisoning?
deliberate self harm with substances that are easy to get | decreases with age from adolescents
281
which substance is associated with the highest mortality in terms of poising?
opioids
282
contraindications for use of charcoal in poisoning?
Absent bowel sounds (ileus) Impaired gag reflex Unsafe swallow
283
common things that charcoal is ineffective against?
alcohols iron cyanide hydrocarbons
284
antidote for paracetamol and mech?
acetylecystine glutathione repleter
285
antidote for opioids? and mech
naloxone- specific antagonist
286
antidote for methanol / ethylene glycol? mech
ethanol specific antagonist
287
how much paracetamol is worrying?
12g
288
what is the dangerous metabolite in paracetamol OD?
NAPQI
289
complication of acetylecystine?
anaphylactoid reaction (not immune mediated)
290
symptoms of salicylate poisoning?
``` Dizziness Sweating Tinnitus Vomiting Hyperventilation Agitation Delirium ```
291
metabolic abnormalities in aspirin OD?
metabolic acidosis - salicylate ACID respiratory alkalosis - resp. centre stimulation hypoglycaemia hypokalaemia
292
Ix for aspirin OD?
Ix the metabolic abnormalites (ABG, glucose, U&Es) | plasma salicylate conc
293
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 ```
294
when must iron be measured to establish toxicity?
4 hrs after ingestion
295
what is used to chelate iron?
Desferrioxamine
296
why is charcoal NOT normally indicated in bnzo OD?
increased risk of aspiration
297
what is the antidote for bnzos and when is it used?
Flumenazil best in bnzo naïve patients can precipitate withdrawal in regular users
298
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
299
in what time frame does activated charcoal need to be given in?
1 hr
300
what is the antidote for benzos? mech of action
flumazinil | anti-cholenergic
301
Mx of anapylactoid reaction?
stop infusion give H2 antagonist restart infusion
302
what is in codydramol?
paracetamol | dihydrocodeine
303
t1/2 of naloxone?
1hr - important thing is that this is SHORTER than opioids
304
what will an abg look like in paracetamol OD?
metabolic acidosis
305
what will an abg look like in opioid OD?
resp. acidosis
306
severe aspirin poisoing ->?
vasodilation, hypoventilation, delirium as well as the symptoms of less severe OD: tinnitus, dizzy, sweating