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Medicine finals Prithvi > PSA > Flashcards

PSA Flashcards

1
Q

components of pharmacokinetics

A

absorption, distribution, metabolism, elimination

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2
Q

give some examples of enzyme inducers

A

enzyme inducers - reduce effect of drugs

PC BRAS:
phenytoin
carbamazepine
barbituates
rifampicin
alcohol excess (chronic)
sulphonylureas

Also St John’s wort

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3
Q

what is 1FTU

A

1 finger tip unit - 1 FTU is the amount of medication needed to squeeze a line from the tip of an adult finger to the first crease of the finger, and provides enough to treat one side of both hands.

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4
Q

examples of enzyme inhibitors

A

enzyme inhibitors - increase effects of drugs and hence toxicity risk

AODEVICES
allopurinol
omepraozole
disulfiram
erythromycin
valproate
isoniazid
ciprofloxacin
ethanol (acute intoxication)
sulphonamides

Don’t forget grapefruit juice!!

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5
Q

what drugs must be continued during surgery?

A

CCBs, beta blockers

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6
Q

general rule with regards to stopping drugs during surgery

A

As a general rule for all surgery, most drugs should be continued during surgery (i.e. not stopped beforehand) because the risk of losing disease control outweighs the risk posed by drug continuation.

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7
Q

what are the drugs to stop before surgery and when to stop them?

A
  1. COCP and HRT - 4 weeks before surgery
  2. lithium - Lithium should be stopped 24 hours before major surgery but the normal dose can be continued for minor surgery (with careful monitoring of fluids and electrolytes)
  3. postassium sparing diuretics day of surgery (risk of hyperkalaemia)
  4. ACEi/ARB - 24 hrs before surgery (risk of severe hypotension)
  5. anticoagulants and antiplatelts - variable acc to local policy (occasionally continued eg In patients with stable angina, perioperative aspirin should be only continued where there is a high thrombotic risk (e.g. patients with a recent acute coronary syndrome, coronary artery stents, or an ischaemic stroke).)
  6. oral hypoglycaemics, metformin and insulin - variable acc to local policy - since pts NBM, if these are continued metformin will cause lactic acidosis and the others hypoglycaemia if contd. usually sliding scale insulin is started instead. sliding scale now called Variable Rate Intravenous Insulin Infusion (VRIII)
  7. MAY be stopped - MAOIs can have important interactions with some drugs used during surgery, such as pethidine hydrochloride. Tricyclic antidepressants need not be stopped, but there may be an increased risk of arrhythmias and hypotension (and dangerous interactions with vasopressor drugs); therefore, the anaesthetist should be informed if they are not stopped.

**there is a BNF pg in treatment summaries - Diabetes, surgery and medical illness AND Surgery and long-term medication**

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8
Q

drugs to change arnd surgery

A

Patients on long-term corticosteroids - to be given IV steroids at induction of anaesthesia in addition to usual dose and to be given more steroids in the post operative period

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9
Q

sections of PSA

A

over 2hrs

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10
Q

safe routine for prescribing

A

ensure correct patient
notice and record allergies
consider CIs for each drug
consider best route
consider need for IV fluids, VTE prophylaxis, pain relief and antiemetics
sign

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11
Q

CIs and interactions for anti platelets and anticoagulants

A

CIs - bleeding, suspected bleeding, at risk of bleeding (liver disease with prolonged PT) (prophylactic heparin generally not appropriate in acute ischaemic stroke due to risk of bleeding into the stroke)
Interactions - enzyme inhibitors can inc PT and INR and warfarin’s effect (eg erythromycin)

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12
Q

side effects and possible CIs for steroids

A

STEROIDS -
stomach ulcers
thin skin
edema
right and left heart failure
osteoporosis
infection (eg candida)
diabetes (hyperglyccaemia and diabetes)
syndrome (cushing’s)

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13
Q

CIs for NSAIDs

A

indigestion
asthma
heart failure
renal failure
clotting abnormality

**aspirin at low doses given for CVD and cerebrovascular disease is not subject to same level of caution as other NSAIDs

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14
Q

CIs and side effects of antihypertensives

A

hypotension (incl postural)
bradycarida - beta blockers and CCBs
electrolyte disturbances - ACEi/ARB and diuretics
dry cough - ACEi
asthma - b blockers
peripheral oedema and flushing - ccbs
renal failure - diuretics
gout - thiazide diurteics
gynaecomastia - k+ sparing diuretics

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15
Q

for pts NBM, what shd be done with regards to PO medications?

A

Prescribed regular oral medication and pre-medication, unless contraindicated and excepting oral hypoglycaemic medicines, should be administered pre-operatively. Adults can have up to 30ml of water.

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16
Q

general rules for choice of replacement IV fluids

A

generally give IV 0.9% saline unless -

  1. hypernatraemic or hypoglycaemic - give 5% dextrose
  2. ascites - human albumin solution
  3. shocked from bleeding - blood transfusion but crystalloid first if no blood immediately available
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17
Q

how to decide quantity and speed of replacement fluids?

A

assess HR, BP and UO.
if tachycardic or hypotensive - give 500mL bolus (250mL if hx/risk of heart failure). then re-assess.
if oliguric (<30mL/h) (not due to obstruction) - give 1 L over 2-4h then reassess.
in general -
- reduced UO - 500mL of fluid depletion
- reduced UO + tachycarida - 1L of fluid depletion
- reduced UO + tachycardia + hypotnesion - >2L of fluid depletion

** never prescribe more than 2L of fluid for a sick pt. always reassess and review subsequent fluid prescriptions.

**IV potassium should not be given at more than 10mmol/hr

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18
Q

maintenance fluid choice

A

general rule - adults require 3L in 24 hrs and elderly require 2L.
usually 1 salty and 2 sweet - 1L of normal saline and 2L of 5% dextrose
to provide potassium - always check U&E before deciding how much to give. bags of dextrose or saline containing KCl can be used. in someone with normal potassium lvls - roughly 40mmol KCl per day so 20mmol KCl in 2 bags.

**remember do not give KCl IV at more than 10mmol/hr
**Fluids may come with an additional 20 mmol or 40 mmol of potassium in a 1 litre bag. Potassium should not be added to fluids. The mixtures should come ready-made from the manufacturer.
***When prescribing routine maintenance fluids for obese patients you should adjust the prescription to their ideal body weight. You should use the lower range for volume per kg (e.g. 25 ml/kg rather than 30 ml/kg)
***For the following patient groups you should use a more cautious approach to fluid prescribing (e.g. 20-25 ml/kg/day):

Elderly patients
Patients with renal impairment or cardiac failure
Malnourished patients at risk of refeeding syndrome

The NICE guidelines give approximate requirements of maintenance IV fluids:
25 – 30 ml / kg / day of water
1 mmol / kg / day of sodium, potassium and chloride
50 – 100 g / day of glucose (this is to prevent ketosis, not to meet their nutritional needs)
The NICE guidelines suggest starting with 25-30 ml/kg/day of 0.18% sodium chloride in 4% glucose with 27 mmol/l of added potassium. This is available as a ready-made solution. They point out that more than 2.5 litres of this fluid increases the risk of hyponatraemia as it is hypotonic.

Nasogastric fluids or enteral feeding is preferable when maintenance needs are more than 3 days.

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19
Q

how fast to give maintenance fluids?

A

If giving 3 L per day = 8-hourly bags (24 ÷ 3).
If giving 2 L per day = 12-hourly bags (24 ÷ 2).

every time you prescribe fluids in real life, you must assess the pt.
Check the patient’s U&E to confirm what to give them.
Check that the patient is not fluid overloaded (e.g. increased jugular venous pressure (JVP), peripheral and pulmonary oedema).
Ensure that the patient’s bladder is not palpable (signifying urinary obstruction) if giving replacement fluids because of ‘reduced urine output’.

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20
Q

CIs for blood clot prophylaxis

A

bleeding, risk of bleeding (incl recent ischaemic stroke) - CIs for anticoagulants
peripheral arterial disease - absent foot pulses - CI for compression stockings

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21
Q

main indications for IV fluids

A

resuscitation eg sepsis or hypotension
replacement eg vomiting and diarrhoea
maintenance eg NBM due to bowel obstruction

Generally, IV fluids should be avoided if the patient can adequately meet their fluid requirements with oral fluids.

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22
Q

examples of crystalloid fluids

A

0.9% sodium chloride (“normal saline”)
5% dextrose
0.18% sodium chloride in 4% glucose
Hartmann’s solution
Plasma-Lyte 148

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23
Q

contents of Hartmann’s solution

A

water
sodium
chloride
potassium
calcium
lactate (helps to buffer the solution – reducing the risk of acidosis)

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24
Q

plasmalyte contents

A

water
na
cl
K
Mg
acetate (helps to buffer the solution – reducing the risk of acidosis)
gluconate (helps to buffer the solution – reducing the risk of acidosis)

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25
Q

give examples of isotonic, hypotonic and hypertonic solutions

A

Isotonic solutions (e.g., 0.9% saline, Hartmann’s and Plasma-Lyte) match the concentration of solutes (osmolality) in the plasma.

Hypotonic solutions (e.g., 5% dextrose and 0.18% sodium chloride) have a lower concentration of solutes than the plasma.

Hypertonic solutions (e.g., 3% saline) have a higher concentration of solutes than the plasma.

**Theoretically, if you dilute the blood with a hypotonic solution, water will flow out of the blood into the interstitial space. This is why hypotonic solutions (e.g., 5% dextrose) are not used for fluid resuscitation. Hypotonic solutions also carry a risk of hyponatraemia (low sodium) by diluting the sodium content of the blood.

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26
Q

signs of hypovolaemia

A

Hypotension (systolic < 100 mmHg)
Tachycardia (heart rate > 90)
Capillary refill time > 2 seconds
Cold peripheries
Raised respiratory rate
Dry mucous membranes
Reduced skin turgor
Reduced urine output
Sunken eyes
Reduced body weight from baseline
Feeling thirsty

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27
Q

IV fluid resuscitation general guideline -

A

The NICE guidelines suggest:

An initial 500 ml (250mL if elderly/HF) fluid bolus over 15 minutes (“stat”), followed by reassessment with an ABCDE approach
Repeat boluses of 250 – 500 mls of fluid if required, each time followed by a reassessment
Seek expert help if the patient is not responding, particularly after 2 litres of fluid

*generally IV normal saline is used

a more cautious approach to fluid resuscitation used in pts with HF, RF, elderly

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28
Q

adverse effects of overprescribing IV fluids

A

Too much fluid can lead to dilution of important components of the blood:

Sodium (with hypotonic solutions)
Potassium (if potassium is not included)
Other electrolytes, e.g., calcium or magnesium
Haemoglobin and haematocrit (red blood cells in the blood) causing anaemia
Clotting factors, platelets and fibrinogen causing coagulopathy (clotting problems)

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29
Q

which pts need additional caution and senior guidance ini order to avoid fluid overload

A

Elderly or frail patients
Significant oedema
Sodium imbalance (hyponatraemia or hypernatraemia)
Heart failure
Renal impairment
Liver impairment

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30
Q

practicality of prescribing maintenance fluid during normal working day

A

When prescribing maintenance fluids during a normal working day, try to ensure enough bags of fluid are prescribed to last through to the next working day (unless you want the fluids to stop). If the bag of fluid runs out at 2 AM and no further bags are prescribed, the on-call junior doctor will get a bleep to attend the ward and prescribe more fluids. Not only does this interrupt whatever that doctor is doing at the time, but they have to work out what to prescribe for a patient that they don’t know. This might involve waking the patient up, disturbing important rest. If the fluids are being stopped out of hours, remember to give clear instructions to the nurses and in the notes.

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31
Q

eg of loop diuretics

A

furosemide and bumetanide

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32
Q

nephron diagram

A
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33
Q

what is countercurrent multiplier in the nephrons? how do loop diuretics work?

A

the system of secreting solutes (Na+, K+ and Cl-) from the thick ascending loop (impermeable to water movement) to draw water out of the thin descending loop is called countercurrent multiplier. the loop of Henle is responsible for reabsorbing abt 20% of filtered sodium and 15% of filtered water.

loop diuretics work by blocking the function of the membrane Na-K-2Cl (NKCC2) cotransporter at the apical membrane of the thick ascending limb of the loop of Henle.

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34
Q

onset of action and duration of action for loop diuretics

A

start working within 1 hr if given PO and within 5 mins if given IV
effects last abt 6 hrs
best to give them earlier in the day and giving at night disrupts sleep, inc risk of falls.

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35
Q

adverse effects of loop diuretics

A

hypokalaemia
hypotension
AKI
urinary retention (where there is outflow restriction)
can worsen diabetic control and cause hyerglycaemia (hyperglycaemia is less likely than with thiazides)
exacerbate gout
ototoxicity

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36
Q

cautions/CIs for loop diuretics

A

hepatic encephalopathy
hypokalaemia
dehydrated/hypovolaemic pts
hyponatraemia
lithium treatment - can increase lithium lvls

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37
Q

eg of thiazide diuretics

A

bendroflumethiazide
indapamide

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38
Q

target of action of thiazide diuretics?

A

thiazide sensitive sodium chloride cotransporter on the luminal side of the epithelial cells in the distal convoluted tubules.

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39
Q

adverse effects of thiazide diuretics

A

dehydration and AKI
postural hypotension (esp in older, frail multimorbid pts)
hyponatraemia
hypocholraemia
hypokalaemia
hyperglycaemia - esp in diabetic pts
hypercalcaemia
raised urea - gout

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40
Q

thiazide diuretics to be used with caution in which pts?

A

frail pts
gout
diabetes
hypercalcaemia

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41
Q

onset of action and duration of action of thiazide diuretics

A

They act within 1 to 2 hours of oral administration and most have a duration of action of 12 to 24 hours; they are usually administered early in the day so that the diuresis does not interfere with sleep.

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42
Q

which diuretic can interact with which antihypertensive to cause severe hyperkalaemia

A

Administration of a potassium sparing diuretic to a patient receiving an ACE inhibitor or an angiotensin-II receptor antagonist can cause severe hyperkalaemia.

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43
Q

eg of situations where pt might need acute fluid resuscitation?

A

hypovolaemia -
eg
haemorrhage
severe D&V
burns
sepsis

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44
Q

eg of situations where pts may need maintenance fluids

A

reduced oral intake
eg bowel obstruction
perioperatively

AND
Patient unable to meet their fluid and/or electrolyte needs orally/enterally

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45
Q

what are the IV fluids available on the PSA database?

A
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46
Q

what are the diff blood products that can be used?

A

packed red cells
platelets
FFP

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47
Q

classic signs of hypovolaemia

A

tachycardia
low UO
low BP

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48
Q

initial fluid choice for fluid resus?

A

normal saline

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49
Q

what are the monitoring req when prescribing fluids?

A

fluid status
FBC and U&Es
BP, HR and UO

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50
Q

the 5Rs of prescribing IV fluids

A

Resuscitation
Routine maintenance
Replacement
Redistribution
Reassessment

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51
Q

wht pts will require fluid replacement and/or redistribution rather than fluid maintenance

A

Complex fluid issues - existing fluid/electrolyte deficits/excess
Electrolyte replacement issues
Abnormal fluid distribution issues (seek senior input)

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52
Q

ongoing abnormal fluid or electrolyte losses - how to prescribe fluids in these cases

A

Estimate amount of ongoing fluid or electrolyte losses
Add or subtract these estimates from the standard routine maintenance fluid regimen discussed in the last section to provide a more tailored fluid prescription.

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53
Q

what signs on clinical examination may suggest hypovolaemia

A

cool peripheries
prolonged CRT>2s
tachycardia
hypotension (incl postural)
dry mouth
reduced UO (but could be from hx rather than clinical exam unless pt has active fluid monitring)

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54
Q

metoclopramide to be avoided in -

A

CI: 3–4 days after gastrointestinal surgery; epilepsy; gastro-intestinal haemorrhage; gastro-intestinal obstruction; gastro-intestinal perforation; phaeochromocytoma

caution:

  • pts with parkinson’s disease - due to risk of exacerbating symptoms as metoclopramide is a
    dopamine antagonist
  • young women due to risk of dyskinesia, ie, unwanted movements especially acute dystonia
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55
Q

antiemetic choices?

A

check bnf before prescribing

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56
Q

pain relief options

A

An NSAID may be introduced at any stage regularly or ‘as required’ if not contraindicated. With neuropathic pain the first line treatment is amitriptyline (10 mg oral nightly) or pregabalin (75 mg oral 12 hourly); duloxetine is indicated in painful diabetic neuropathy.

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57
Q

practicalities of prescribing morphine sulphate

A

In order of increasing effectiveness, morphine sulphate may be given orally (as Oramorph®), subcutaneously or intravenously. Oramorph® is a liquid and comes in two strengths thus the strength must be specified and is usually 10 mg/5 mL. Remember, do not use trade names in prescriptions: if you wish to prescribe Oramorph you should still write MORPHINE SULPHATE 10mg/5ml.

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58
Q

rule with paracetamol prescribing

A

In ADULTS - ensure that no more than 4 g of paracetamol each day are given in total (look at co-codamol and paracetamol prescriptions)

NOTE in patients <50kg the MAXIMUM dose of Paracetamol is 500mg 6-hourly (2g in 24hrs).

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59
Q

why is domperidone safe to use in PD?

A

Metoclopramide and domperidone are both dopamine antagonists. Metoclopramide crosses the blood-brain barrier (BBB), and so exacerbates parkinsoninan symptoms by acting on central dopamine receptors. Domperidone does not cross the BBB, and so is safe to use in Parkinson’s disease.

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60
Q

why is combination of NSAIDs and ACEinhibitors threat to renal perfusion?

A

Ibuprofen inhibits prostaglandin synthesis which reduces renal artery diameter (and blood flow) and thereby reduces kidney perfusion and function. Ramipril, an ACE-inhibitor, reduces angiotensin-II production necessary for preserving glomerular filtration when the renal blood flow is reduced. In effect, NSAIDs combined with ACEi are a double threat to renal perfusion. The combination nips tight the afferent artery (the way in) and opens up the efferent artery (the way out).

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61
Q

typical presentation of antimuscarinic toxicity

A

Antimuscarinic drugs can cause confusion, particularly in the elderly. antimuscarinic agents commonly cause pupillary dilation, with loss of accommodation, dry mouth, and tachycardia (after a transient bradycardia)

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62
Q

drugs that can exacerbate/cause confusion (part in the elderly)?

A

oxybutynin (reduced doses are recommended in the elderly)
tramadol
cyclizine can cause drowsiness and confusion (reduced doses are recommended in the elderly)
BDZs

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63
Q

CIs and cautions for MTX

A

NSAIDs shd be used with caution in pts on MTX due to inc risk of nephrotoxicity
Methotrexate is contraindicated in active infection
Trimethoprim is a folate antagonist, and is a direct contraindication to patients taking methotrexate (another folate antagonist) due to the risk of bone marrow toxicity. This can lead to pancytopenia and neutropenic sepsis.

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64
Q

in prescription review section, what can be the problems with the medications?

A
  1. pt allergic to meds
  2. meds CI in pts conditions
  3. meds given wrong route, dose, freqeuncy
    1. meds interact with each other
      1. meds causing SEs/toxicity
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65
Q

what shd ppl with migraine with aura NOT take?

A

Patients who have migraine with aura should not take the COCP as it significantly increases their risk of stroke

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66
Q

general rule for route of administration for insulin

A

as a rule all insulin is s/c except for sliding scales using short-acting insulin (e.g. Actrapid® or NovoRapid®) given by IV infusion OR in hyperkalaemia where actrapid is used WITH glucose

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67
Q

how much time to spend on prescribing and prescription review sections?

A

can spend 60 mins on them as they carry 112/200 marks

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68
Q

most worrying SE of clozapine

A

agranulocytosis resulting in neutropaenia

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69
Q

if an asthmatic pt is currently on NSAIDs but doesn’t have a wheeze with it, shd it be continued or stopped?

A

the NSAID could be continued as it would suggest her asthma was not NSAID-sensitive.

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70
Q

causes of anaemia

A
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71
Q

causes of high and low WCC

A
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72
Q

causes of thrombocytosis and thrombocytopaenia

A

thrombocytosis -

  1. reactive: bleeding, postsplenectomy, tissue damage (infection, inflammation, malignancy)
  2. primary: myeloproliferative disorders

Thrombocytopaenia:

  1. reduced production:
  • infection (usually viral)
  • drugs (eg penicillamine used in RA)
  • myelodysplasia, myelofibrosis, myeloma
  1. increased destuction:
  • heprin
  • DIC
  • ITP
  • HUS/TTP
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73
Q

causes of hyponatraemia

A

assess fluid status

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74
Q

causes of hypernatraemia

A

causes all begin with ‘d’: dehydration; drips (i.e. too much IV saline); drugs (e.g. effervescent tablet preparations or intravenous preparations with a high sodium content); diabetes insipidus

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75
Q

causes of hypo and hyperkalaemia

A

hypokalaemia -

DIRE -

Drugs (loop and thiazide diuretics)

Intestinal loss (D&V) or inadequate intake

Renal tubular acidosis

Endocrine causes (cushing’s and conn’s syndromes)

hyperkalaemia -

DREAD

Drugs (aldosterone antagonsits and ACEi/ARBs)

Renal failure

Endocrine (addison’s)

Artefact

DKA (BUT K+ drops when insulin given to treat DKA so regular monitoring is req)

76
Q

causes of AKI

A

prerenal (70%):

  • Dehydration (or if severe, shock) of any cause, e.g. sepsis, blood loss.
  • Renal artery stenosis (RAS) - AKI in RAS is often triggered by drugs (ACEI or NSAIDs)
  • Urea rise >>creatinine rise

intrinsic renal (10%):

  • INTRINSIC: Ischaemia (due to prerenal AKI, causing acute tubular necrosis) Nephrotoxic antibiotics[esp - gentamicin, vancomycin and tetracyclines.]
    Tablets (ACEI, NSAIDs)
    Radiological contrast
    Injury (rhabdomyolysis)
    Negatively birefringent crystals (gout)
    Syndromes (glomerulonephridites)
    Inflammation (vasculitis)
    Cholesterol emboli
  • urearise<< creatinine rise. bladder and hydronephrosis not palpable.

postreanl (20%)(obstructive):

  • In lumen: stone or sloughed papilla
    In wall: tumour (renal cell, transitional cell), fibrosis External pressure: benign prostatic hyperplasia, prostate cancer, lymphadenopathy, aneurysm
  • urearise<< creatinine rise. bladder and hydronephrosis may be palpable.

Note: the creatinine can rise with severe prerenal AKI; to differentiate this from intrinsic and obstructive AKI, multiply the urea by 10; if it exceeds the creatinine (showing a relatively greater increase in urea compared to creatinine) then this suggests a prerenal aetiology.

**Raised urea indicates kidney injury or upper gastrointestinal (GI) haemorrhage. Thus, a raised urea with normal creatinine in a patient who is not dehydrated (i.e. does not have prerenal failure) should prompt a look at the haemoglobin; if this has dropped then the patient probably has an upper GI bleed.

77
Q

2 main causes of raised urea

A

Raised urea indicates kidney injury or upper gastrointestinal (GI) haemorrhage.

because it is a breakdown product of amino acids (such as globin chains in haemoglobin), it can also reflect an upper GI bleed where haemoglobin has been broken down by gastric acid into urea, which is subsequently absorbed into the blood. The same phenomenon occurs if you eat a big (and bloody) steak. Thus, a raised urea with normal creatinine in a patient who is not dehydrated (i.e. does not have prerenal failure) should prompt a look at the haemoglobin; if this has dropped then the patient probably has an upper GI bleed.

78
Q

what tests can be used to assess liver function

A

Hepatocyte injury or cholestasis such as:

▶

bilirubin
▶

alanine aminotransferase (ALT) and the less commonly measured aspartate aminotransferase (AST)
 ▶

alkaline phosphatase (alk phos or ALP).

•

Synthetic function (i.e. the proteins it makes):

▶

albumin
▶

vitamin K-dependent clotting factors (II, VII, IX and X) measured via prothrombin time (PT)/international normalized ratio (INR).

79
Q

causes of deranged LFTs

A

1.prehepatic -raised bilirubin

  • haemolysis
  • gilbert’s and criggler najjar syndromes
  1. hepatic - raised bilirubin and raised AST/ALT
  • fatty liver
  • hepatitis
  • cirrhosis
  • malignancy
  • metaboic: wilson’s disease/haemochromatosis
  • heart failure

Hepatitis and cirrhosis may be due to (1) alcohol, (2) viruses (Hepatitis A–E, CMV, and EBV), (3) drugs (paracetamol overdose, statins, rifampicin), and (4) autoimmune (primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis).

  1. posthepatic (obstructive): raised bilirubin and ALP
  • in lumen: gallstones and drugs causing cholestasis (Flucloxacillin, CO-AMOXICLAV, nitrofurantoin, steroids and sulphonylureas)
  • In wall: tumour (cholangiocarcinoma), primary biliary cirrhosis, sclerosing cholangitis
  • Extrinsic pressure: pancreatic or gastric cancer, lymph node
80
Q

causes of hepatitis and cirrhosis

A

Hepatitis and cirrhosis may be due to (1) alcohol, (2) viruses (Hepatitis A–E, CMV, and EBV), (3) drugs (paracetamol overdose, statins, rifampicin), and (4) autoimmune (primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis).

81
Q

drugs causing cholestasis

A

Flucloxacillin, CO-AMOXICLAV, nitrofurantoin, steroids and sulphonylureas.

82
Q

common causes of raised alk phos

A

ALKPHOS

Any fracture, Liver damage (posthepatic), K (for kancer), Paget’s disease of bone and Pregnancy, Hyperparathyroidism, Osteomalacia, and Surgery.

83
Q

target range for TSH in someone on levothyroxine for hypothyroidism

A

∼0.5–5 mIU/L

84
Q

How to interpret and change levothyroxine dose following TFT results

A

The trick to this is to use the TSH as a guide: target range ∼0.5–5 mIU/L and, unless grossly hypo/hyperthyroid, change by the smallest increment offered.

85
Q

causes of abnormal TFTs

A
86
Q

how to assess quality of CXR film?

A

PRIM

Projection (e.g. posterioanterior (PA) (normally) or anterioposterior (AP). If AP, the heart will appear larger. If no label, then it is PA).
•

Rotation (e.g. if distance between spinous process and clavicles is equal, then no rotation).
•

Inspiration (e.g. if the seventh anterior (down-sloping) rib transects the diaphragm, then adequate).
•

Markings (if additional markings, e.g. ‘red mark’, then the radiographer has spotted an abnormality).

87
Q

main structures to consider when looking at CXR

A

Heart, which should be less than 50% of the width of the lungs (in PA film); if more, then cardiomegaly should be considered.∗
•

Lungs, where, if a white area is present, then effusion (seen as unilateral and solid), pneumonia (seen as unilateral and fluffy), oedema (seen as bilateral and fluffy∗), or fibrosis (seen as bilateral and honeycomb) should be considered.
•

Trachea, which should be central and if not, consider collapse (i.e. towards affected side) or pneumothorax (i.e. away from affected side).
•

Mediastinum, which if widened, aortic dissection (without tracheal deviation) or hilar lymphadenopathy or mediastinal masses etc
•

Bones, where it is important to look for rib fractures or lytic lesions (i.e. usually suggesting metastases).

88
Q

if any signs of HF/pulmonary oedema are present, what to look for in a CXR?

A

ABCDE signs of pulmonary oedema:Alveolar oedema (bat wings)Kerley B lines (interstitial oedema)Cardiomegaly Diversion of blood to upper lobes (where vessels in upper zone are larger than in lower zone), andpleural Effusions.

89
Q

routine for interpreting ABG

A
  1. check inspired FiO2. approximately normal PaO2 for a pt on oxygen shd be above (FiO2 in kPa -10). if lower then pt is hypoxic. eg if pt on 60% oxygen if PaO2 is below 50, then hypoxic
  2. check for resp failure - type 1 vs type 2 (COPD, neuromuscular failure, restrictive chest wall abnormalities, near-fatal asthma attack)
  3. check acid-base status - look at pH. look at PaCO2 and HCO3 to determine resp or metabolic cause.
    1. only PaCO2 abnormal then resp cause
    2. only HCO3 abnormal then metabolic cause
    3. If both are increased or both decreased this indicates compensation; if the pH is normal then it is fully compensated; if pH remains abnormal then it is partially compensated.
    4. If both PaCO2 and HCO3 are abnormal but in opposite directions then there is coexistent metabolic and respiratory disease.
      1. Respiratory alkalosis caused by rapid breathing, whether due to disease or anxiety. Respiratory acidosis has the same causes as type 2 respiratory failure. Metabolic alkalosis caused by vomiting, diuretics, and Conn’s syndrome. Metabolic acidosis has multiple causes and the most frequent are lactic acidosis, DKA, renal failure, and ethanol/methanol/ethylene glycol intoxication. One can use the anion gap to narrow the cause
90
Q

QRS complex interpretation

A

1.Width: if QRS <3 small squares wide, then there is no bundle branch block (BBB); if QRS >3 small squares wide, then BBB is present; to determine which subtype assess QRS shape

if in V1 the first deflection of the QRS is ⇓ (w-shape) and in V6 the first deflection is ⇑ (m-shape), then this is left BBB

if in V1 the first deflection of the QRS is ⇑ (m-shape) and in V6 the first deflection is ⇓ (w-shape), then this is right BBB.

  1. Height: add the largest deflection of the QRS in V1 to that in V6 (in terms of large squares) and if the sum exceeds 3.5 large squares then left ventricular hypertrophy (LVH) is present. If there are small complexes throughout then consider a pericardial effusion
91
Q

interpret

A

Digoxin effect. There is widespread down-sloping ST depression and T-wave inversion, most obviously in leads V3-V6. Note that the rhythm is atrial fibrillation; the patient had been taking digoxin for several months.

92
Q

most common drugs with narrow therapeutic index

A

digoxin, theophylline, lithium, phenytoin, and certain antibiotics (gentamicin and vancomycin).

93
Q

what does drug monitoring require (esp for drugs with narrow therapeutic index)

A

Monitoring requires assessment of the clinical state (i.e. patient response to the drug and evidence of drug toxicity) plus measurement of serum drug levels.

**If adequate response to the drug and normal or low serum drug level, then no change to the dose is required, i.e. clinical response is more important. There is no point in increasing the dose just to get the patient into what is generally considered a ‘therapeutic’ range – it’s already therapeutic!

If adequate response to the drug and high serum drug level, then decrease the dose. If there is evidence of toxicity and clearly if the level is very high, then omitting the drug for a few days is appropriate. The only exception to this is gentamicin, where a high serum level (without signs of toxicity) should pre-empt a decrease in frequency by 12 h rather than reducing the dose, e.g. changing from every 24 h (daily) to every 36 h.

If evidence of toxicity, regardless of drug levels, then there are three treatments: (1) stop drug (+/−alternative if required); (2) supportive measures (usually IV fluids); (3) give antidote (if one is available).

94
Q

features of toxicity of digoxin

A

Confusion, nausea, visual halos, and arrhythmias

95
Q

features of toxicity of lithium

A

Early: tremor

Intermediate: tiredness

Late: arrhythmias, seizures, coma, renal failure, and diabetes insipidus

96
Q

features of toxicity of phenytoin

A

Gum hypertrophy, ataxia, nystagmus, peripheral neuropathy, and teratogenicity

97
Q

features of toxicity of gentamicin

A

Ototoxicity and nephrotoxicity

98
Q

features of toxicity of vancomycin

A

Ototoxicity and nephrotoxicity

99
Q

how is gentamicin dose calculated for a pt?

A

Gentamicin is an IV aminoglycoside antibiotic used for severe infections. Doses are calculated according to the patient’s weight and renal function. Most patients are treated with a high-dose regimen of 5–7 mg/kg once daily; patients with severe renal failure (creatinine clearance <20 mL/min) or endocarditis may receive a divided daily dosing (1 mg/kg) 12 hourly (in renal failure) or 8 hourly (in endocarditis) depending on individual hospital policy.

MONITORING REQ:

  1. serum concentration
  2. Renal function should be assessed before starting an aminoglycoside and during treatment.
  3. Auditory and vestibular function should also be monitored during treatment.
100
Q

Gentamicin: Once-Daily Regimen Monitoring

A

exact monitoring will be determined locally, but usually involves:

Measuring gentamicin levels at particular times such as 6–14 h after the last gentamicin infusion is started (i.e. the time of the sample must be recorded).

Using a nomogram (e.g. Hartford if 7 mg/kg dose (see Fig. 3.3) or Urban and Craig if 5 mg/kg dose (similar principles)) to determine whether the level is too high: plot the blood concentration (y-axis) against the time between starting last infusion and taking the blood (x-axis). If the resultant point on the graph falls within the 24 h area (q24h), then continue at the same dose; if it falls above the q24h area, then change the dosing interval as follows:

  • if point falls in the q36h area, change to 36-hourly dosing
  • if point falls in the q48h area, change to 48-hourly dosing
  • if point rests above the q48h area, repeat the gentamicin level and only re-dose when the concentration is <1 mg/L.
  • This adjustment of the frequency of the dose (rather than the dose itself) reflects the need for a sufficient dose to provide the required peak to hit the minimum inhibitory concentration of the organism.
101
Q

Gentamicin monitoring for divided daily dosing regimens

A

A nomogram exists for divided daily dosing although usually daily peak and trough levels are used instead.

102
Q

paracetamol overdose/poisoning pathophys

A

Paracetamol is normally metabolized by the liver in a process reliant on the antioxidant known as glutathione. In paracetamol overdose the limited hepatic stores of glutathione are quickly depleted, leading to accumulation of the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI). Accumulation of NAPQI is the cause of acute liver damage in paracetamol overdose. NAC replenishes the stores of glutathione, and so reduces the formation of NAPQI, therefore protecting against liver damage.

103
Q

how to use a paracetamol nomogram?

A

The paracetamol nomogram is simple to use: at least 4 h after ingestion, if the plasma paracetamol level is below the line, the patient does not require N-acetyl cysteine (NAC); if the plasma level is above the line, they do. If a staggered overdose was taken, or the time of ingestion is unknown, treatment with NAC is advised.

104
Q

usual target INRs for pts on warfarin and metal replacement heart valves

A

Target INRs for most patients on warfarin are 2.5 unless there is recurrent thromboembolism while on warfarin, where the INR target would be 3.5. In patients with metal replacement heart valves, target INR depends on the type and location of valve and on patient-related risk factors, but is also likely to be higher than 2.5.

105
Q

how to manage over anticoagulation with warfarin?

A
  1. If major bleed (causing hypotension or bleeding into confined space ie brain or eye) -
    1. stop warfarin
    2. give 5-10mg IV vitamin K (aka phytomenadione)
    3. give prothrombin complex
  2. INR 5-8:
    1. minor bleeding - omit warfarin and give 1-5mg IV vit K
    2. no bleeding - withhold 1 or 2 doses of warfarin sodium and reduce subsequent maintenance dose
  3. INR >8
    1. minor bleeding - omit warfarin and give 1-5mg IV vit K
    2. no bleeding - omit warfarin and give 1-5mg PO vit K
106
Q

USE THE BNF

A

DON’T TRY AND DO THE PSA WITHOUT USING THE BNF

107
Q

how is PRN morphine usually prescribed?

A

‘As required’ doses of morphine sulphate (in this case Oramorph®) are usually calculated as one sixth of the total daily dose (in this case one sixth of 30 mg, i.e. 5 mg) given up to every 4 to 6 hours. If a patient in chronic pain is requiring higher ‘as required’ doses, it follows that the regular dose requires adjustment.

108
Q

how do u manage an acutely unwell patient?

A

ABCDE

109
Q

quick summary of mx of STEMI, NSTEMI and acute LVF

A

acute LVF not so sure abt GTN spray/tablet. can be given IV for heart failure but not sure if I’ll be initiating

110
Q

mx of tachycardia >125 bpm

A

in PSA check arrhythmia treatment summary on BNF

111
Q

mx of anaphylaxis in ADULTS

A

remember - ABCDE and 500 micrograms, using adrenaline 1 in 1000 (1 mg/mL) injection, repeat dose after 5 minutes if no response; if life-threatening features persist, further doses can be given every 5 minutes until specialist critical care available, to be injected preferably into the anterolateral aspect of the middle third of the thigh.

112
Q

pneumothorax mx

A

ABCDE

If tension pneumothorax(i.e. clinical distinction but often tracheal deviation +/− shock), then emergency needle decompression required, and then will need chest drain quickly.

If secondary pneumothorax (i.e. patient has lung disease), then always needs treatment: chest drain if >2 cm or patient has shortness of breath (SOB) or if >50 years old; otherwise aspirate

Otherwise (i.e. if primary) determine whether the patient needs treatment:
if <2 cm rim and not SOB, then discharge with outpatient follow-up in 4 weeks.
if >2 cm rim on CXR or feels SOB, then aspirate and if unsuccessful aspirate again, and if still unsuccessful, then chest drain.

113
Q

pneumonia mx

A

ABCDE

calculate CURB65 score - 1 point each:

confusion (abbreviated Mental Test score 8 or less, or new disorientation in person, place or time)

raised blood urea nitrogen (over 7 mmol/litre)

raised respiratory rate (30 breaths per minute or more)

low blood pressure (diastolic 60 mmHg or less, or systolic less than 90 mmHg)

age 65 years or more.

Patients are stratified for risk of death as follows:

0 or 1: low risk (less than 3% mortality risk)

2: intermediate risk (3‑15% mortality risk)

3 to 5: high risk (more than 15% mortality risk).

For the patient with none or one of these then home treatment is possible; with two or more of these then hospital treatment with oral or IV antibiotics according to policy and severity is required; and with more than three of these then given IV abx and consider ITU admission.

114
Q

PE Mx

A

ABCDE

Offer anticoagulation treatment for at least 3 months to people with confirmed proximal DVT or PE (6 months in ppl with active cancer and consider continuing anticoaulation beyond 3 months for those with unprovoked DVT or PE based on balance bw person’s risk of VTE recurrence and bleeding)

Offer either apixaban or rivaroxaban to people with confirmed proximal DVT or PE.

If neither apixaban nor rivaroxaban is suitable offer:

LMWH for at least 5 days followed by dabigatran or edoxaban or

LMWH concurrently with a vitamin K antagonist (VKA) for at least 5 days, or until the INR is at least 2.0 in 2 consecutive readings, followed by a VKA on its own

115
Q

mx of GI bleeding

A
116
Q

mx of bac meningitis in hosp

A
117
Q

mx of seizures

A

any seizure -

ABC (make sure airway patent); put in recovery position with oxygen and perform bedside tests for provoking factors (e.g. plasma glucose, electrolytes, drugs, and sepsis)

If seizure lasts for more than 5 mins, then drugs are req -

118
Q

mx of stroke

A

If CT shows haemorrhage (of any type), discuss with neurosurgery unit immediately and do not give aspirin or thrombolysis.

119
Q

hypoglycaemia mX

A

check bnf

120
Q

AKI mx

A

inv - as a minimum request FBC, U&E, CRP, LFT, ABG, urinalysis, USS KUB, check drugs for nephrotoxic medications

complications of AKI are hyperkalaemia, acidosis and fluid overload

121
Q

acute poisoning mx

A
  1. ABCDE
  2. Hx,o/e,inv, diagnosis:acute poisoning
  3. cannula and catheter, strict fluid balance
  4. supportive measures - IV fluids
  5. correct electrolyte disturbances
  6. reduce absorption IF within 1 hr of ingestion by - gastric lavage (ie stomach pumping unless caustic/acid content), whole bowel irrigation (if Li/Fe), charcoal (dx-dependent)
    1. increase elimination by giving generous IV fluids plus: NAC (paracetamol lvl at 4hrs or more is above treatment nomogram); naloxone if opiates have been taken and there is now slow breathing or low GCS; flumazenil if BDZs have been taken
122
Q

pharmacological options for angina

A

GTN sublingual spray for symptomatic relief PRN

statins and aspirin for 2ndary prevention

anti-anginal drugs for long term management - beta blocker or CCB; then inc dose; then both; ineffective/CI - then - isosorbide mononitrate or nicorandil.

123
Q

SEs of ICS therapy

A

increased risk of pneumonia, candidiasis

124
Q

what conditions is pioglitazone associated with an increased risk of?

A

pioglitazone is associated with an increased risk of heart failure, bladder cancer and bone fractre

125
Q

egs of SGLT-2 inhibitors

A

canagliflozin, dapagliflozin

126
Q

pharmacological options for PD

A

co-beneldopa or co-careldopa (i.e. levodopa combined with a peripheral dopa decarboxylase inhibitor (benserazide or carbidopa, respectively)), unless the question presents a patient with very mild Parkinson’s disease who is particularly concerned about the finite period of benefit from levodopa. In this case a dopamine agonist (such as ropinirole) or monoamine oxidase (MAO)-inhibitor (such as rasagiline) may be more appropriate.

127
Q

1st line antiepileptics?

A

Myoclonic seizures: valproate (for males), levetiracetam (for females)
Tonic seizures: valproate (for males) or lamotrigine (for females)
All other focal seizures: carbamazepine or lamotrigine
Absence seizures: ethosuximide or valproate
Generalised tonic-clonic seizures: valproate (for males), lamotrigine (for females)

some common adverse effects -

valproate - teratogenic

lamotrigine - rash

128
Q

common SEs of anti epileptics

A
129
Q

alzheimer’s disease pharma options -

A

If mild/moderate dementia, then treat with acetylcholinesterase (AChE) inhibitors. However, note the following:
treatment may only be started by specialist doctors
there are three licenced drugs: donepezil, rivastigmine and galantamine.
If moderate/severe dementia, then treat with NMDA antagonist (memantine).

130
Q

pharma mx of crohn’s

A

inducing remission - Treat a mild flare with prednisolone 20–40 mg (as per BNF) daily orally, and treat a severe flare with hydrocortisone 100–500 mg three to four times daily or as required (as per BNF) IV and supportive care (e.g. IV fluid, nil by mouth, and antibiotics). In either case, if the patient has rectal disease, use rectal hydrocortisone too.

maintaining remission - Azathioprine or 6-Mercaptopurine

Azathioprine is a pro-drug, metabolized by the liver to the active agent 6-mercaptopurine. In turn, 6-mercaptopurine is metabolized to inactive components by the enzyme thiopurine S-methyl transferase (TPMT). In 10% of the population there is congenitally low activity of TPMT, which would lead to abnormal accumulation of 6-mercaptopurine when azathioprine is given in normal doses. This would increase the risk of liver and bone marrow toxicity. It is therefore important to check TPMT levels before starting either drug. If TPMT is found to be low (but not deficient/absent), start lower dose azathioprine. If TPMT levels are deficient/absent offer methotrexate.

131
Q

RA pharma

A

Treatment commenced by specialists typically using methotrexate, followed by additional disease-modifying antirheumatic drugs (DMARDs).
During a flare the following treatments are appropriate:

short-term glucocorticoids, e.g. IM methylprednisolone 80 mg
short-term NSAIDs, e.g. ibuprofen 400 mg 8 hourly with gastro-protection (e.g. lansoprazole)
re-instate DMARDs if dose previously reduced.

After failure to respond to two DMARDs, severely active rheumatoid arthritis may be managed with TNF-α inhibitors, e.g. infliximab.

132
Q

absolute CI for any laxative

A

evidence/strong clinical suspicion of bowel obstruction

133
Q

laxative options

A
134
Q

mx of diarrhoea

A

The commonest cause of diarrhoea is gastrointestinal infection (including norovirus and Clostridium difficilegastroenteritis). The quick removal of such infectious agents (via diarrhoea) should not be intentionally inhibited by drugs. However, chronic diarrhoea (that has been proven to be non infectious with negative stool cultures and microscopy) may be treated with loperamide 2 mg oral up to 3 hourly or codeine 30 mg oral up to 6 hourly (which will also provide relief of pain).

135
Q

insomnia mx

A

Many patients will complain of poor sleep in hospital: it is an unfamiliar, noisy, and often unpleasant environment. They may be on drugs that prevent sleep (for example corticosteroids, which should be given in the morning to prevent this), and they may nap during the day. These aspects should be dealt with where possible before reaching for a hypnotic, despite requests from nurses. Patients not used to such drugs, particularly the elderly, may become very drowsy and their risk of falling if visiting the toilet, for example, is high. For the purposes of the exam, if you do give a hypnotic, start with zopiclone 7.5 mg oral nightly in adults (and 3.75 mg nightly in the elderly).

136
Q

1% means

A

Usually -

1 g in 100 mL (or 10 mg in 1 mL) for weight/volume (w/v) calculations; or

1 g in 100 g for weight/weight (w/w) calculations.

BUT

Different concentrations exist for different indications. A ‘1 in 1000’ (1 g in 1000 mL) preparation is available for the treatment of anaphylaxis. A ‘1 in 10 000’ (1 g in 10 000 mL) preparation is available for use in the setting of cardiopulmonary resuscitation.

137
Q

how to write ‘units’ when prescribing insulin or LMWH?

A

UNITS

Protect your patients and always take the time to write out the word ‘units’ in full

Remember too, you must write out the word ‘micrograms’ in full for a similar reason to that above.

138
Q

drugs for which formulations may differ in terms of the so-called ‘salt-factor’, ie, a different preparation of the drug has a diff concentration

A

phenytoin, digoxin, sodium fusidate.

Use caution when switching patients from one formulation to another.

139
Q

diff available routes that can be prescribed?

A

oral

subcutaneous

intramuscular

intravenous

inhaled

nebulized

sublingual

rectal

NEBULIZED is different from INHALED for eg in acute asthma give NEBULIZED salbutamol!

topical

140
Q

common drugs SEs what to learn?

A

listing the five most common drugs for each body system and learning the common side effects.

141
Q

a side effect of Any antibiotic (but most commonly the broad-spectrum antibiotics like cephalosporins or ciprofloxacin)

A

Clostridium difficile colitis

142
Q

ACE-inhibitors, e.g. lisinopril SEs

A

Hypotension, electrolyte abnormalities, acute kidney injury, dry cough

143
Q

Beta-blockers, e.g. bisoprolol SEs

A

Hypotension, bradycardia, wheeze in asthmatics, worsens acute heart failure (but helps chronic heart failure)

144
Q

Calcium-channel blockers, e.g. diltiazem SEs

A

Hypotension, bradycardia, peripheral oedema, flushing

145
Q

Diuretics, e.g. furosemide, bendroflumethiazide, spironolactone SEs

A

hypotension, AKI, electrolyte disturbances (most commonly hyponatraemia and hypokalaemia except in spironolactone which can contribute to hyperkalaemia)

spironolactone can also cause gynaecomasita

146
Q

Heparins SEs

A

Haemorrhage (especially if renal failure or <50 kg), heparin-induced thrombocytopaenia

147
Q

Warfarin SEs

A

Haemorrhage (note that ironically warfarin has a procoagulant effect initially, as well as taking a few days to become an anticoagulant; thus heparin should be prescribed alongside warfarin and continued until the INR exceeds 2.

148
Q

Aspirin SEs

A

Haemorrhage, peptic ulcers and gastritis, tinnitus in large doses

reye’s syndrome in children

149
Q

digoxin SEs and K+ lvl relevance

A

Nausea, vomiting and diarrhoea, blurred vision, confusion and drowsiness, xanthopsia (disturbed yellow/green visual perception including ‘halo’ vision)

changes in serum K+ at the receptor can compete with digoxin; low K+ augments digoxin effect. High levels limit the effect

150
Q

amiodarone SEs

A

Interstitial lung disease (pulmonary fibrosis), thyroid disease (both hypo- and hyperthyroidism are reported; it is structurally related to iodine, hence its name amIODarone), skin greying, corneal deposits

151
Q

lithium SEs

A

Early – tremor

Intermediate – tiredness

Late – arrhythmias, seizures, coma, renal failure, diabetes insipidus

152
Q

haloperidol SEs

A

Dyskinesias, e.g. acute dystonic reactions, drowsiness

153
Q

clozapine SEs

A

agranulocytosis ((requires intensive monitoring of full blood count))

154
Q

Dexamethasone and prednisolone

A

Cushing’s syndrome

peptic ulcers

increased risk of infections

hyperglycaemia

osteoporosis

oedema

heart failure

hypertension

155
Q

Fludrocortisone SEs

A

hypertension

sodium and water retention

156
Q

NSAIDs SEs

A

peptic ulcers and gastritis

AKI

heart failure

clotting abnormalities

can make asthma worse

157
Q

statins SEs

A

Myalgia, abdominal pain, increased ALT/AST (can be mild), rhabdomyolysis (can be just mildly increased creatine kinase though)

158
Q

management of statin induced myalgia

A

STOP statins and exclude rhabdomyolysis (with creatine kinase (CK) level and urine dip).

If CK level is normal, consider changing to another member or restart at a lower dose with cautious monitoring. Presence of rhabdomyolysis will require termination of treatment, and management of rhabdomyolysis

159
Q

2 types of drug reactions to remember?

A

It is advisable to know the difference between a common reaction and a dangerous one. For example, a common reaction to statins is myalgia and a dangerous one is rhabdomyolysis.

Type A reaction – common, predictable, and dose related. Type B reactions (sometimes called idiosyncratic) are bizarre and unexpected reactions related to gene/host/environmental interactions.

160
Q

Drugs with a narrow therapeutic index

A

digoxin, phenytoin, vancomycin, gentamicin, warfarin, theophyllines

161
Q

Drugs which require careful dosage control

A

antihypertensives and antidiabetic medications

162
Q

what combination of 2 drugs can cause profound hypotension and asystole?

A

Beta-blockers and verapamil together may cause profound hypotension and asystole and the combination is therefore avoided (and strictly contraindicated if IV verapamil)

163
Q

most common enzyme inhibitors?

A

omeprazole, ketoconazole, ciprofloxacin, and erythromycin. Do not forget grapefruit juice

164
Q

in PSA, what are the categories in which the drugs which interact fall into?

A

Drugs that are known to interact usually fall into one of three categories. SPOT these in the adverse drug reactions questions:

  1. Drugs with a narrow therapeutic index, such as warfarin, digoxin, and phenytoin. Interactions resulting in increased or decreased levels of these drugs can result in subtherapeutic or toxic levels.
  2. Drugs that require careful titration of dose according to effect, such as antihypertensives and antidiabetic drugs (where over-treatment can lead to clinically significant consequences – hypotension or hypoglycaemia, respectively). Furthermore, the body’s handling of these drugs may be affected by the addition of other drugs. For example, iodinated contrast media can cause renal impairment, which increases the risk of metformin-induced lactic acidosis or ACE-inhibitor associated acute kidney injury. This might seem quite complicated, but will become clearer as you start to practise some questions of this type. A useful hint is that if the scenario presented refers to symptoms of low Glasgow Coma Score (GCS) or acidotic behaviour, look for metformin in the question!
  3. Drugs that affect (or are affected by) the cytochrome P450 enzyme system - look out for antiepileptics, anti-TB meds, macrolides, grapefruit juice, alcohol, sulphonylureas and sulphonamides, ketoconazole
165
Q

sites of cytochrome P450 enzyme activity

A

liver and duodenum

The liver is not the only site of cytochrome P450 enzyme activity. The duodenum also has a role. It acts almost as a ‘backstop’ for the stomach, modifying toxic foodstuffs/poisons before further absorption in the gut. Drug companies are aware of this and modify their doses accordingly, sometimes doubling the physiological requirement to combat losses sustained in the duodenum. One problem is that everyday foodstuffs can interfere with their action. For example, a single glass of grapefruit juice can inhibit the duodenal cytochrome P450 system for approximately 24 hours. This means excessive drug doses can pass through the duodenum, a particular problem for drugs with a narrow therapeutic index and others that require careful dosage control.

Enzyme induction takes days–weeks to establish but inhibition only takes hours–days. Keeping in mind that foodstuffs can also affect enzyme activity, doctors need to remain vigilant for ADRs because they can present weeks after medication changes or anytime patients change eating habits.

166
Q

what to advice pts on metronidazole

A

advice to avoid alcohol while taking metronidazole. drinking alcohol while on metronidazole can cause fulminant nausea and vomiting

167
Q

Gastrointestinal bleeding caused by

A

NSAIDs incl aspirin and ibuprofen

168
Q

Lactic acidosis caused by

A

metformin

169
Q

Increased anticoagulation caused by

A

warfarin (with acute alcohol due to enzyme inhibition); chronic alcohol causes enzyme induction and thus reduces anticoagulant effect

170
Q

Sweating, flushing, nausea and vomiting caused by

A

metronidazole and disulfiram

171
Q

Hypertensive crisis caused by

A

monoamine oxidase inhibitors

172
Q

Sedation caused by

A

barbiturates, opioids, sedating antihistamines and benzodiazepines

173
Q

•Prescribed medications are third most common cause of death after heart disease and cancer

A

•Prescribed medications are third most common cause of death after heart disease and cancer

174
Q

drugs which commonly have prescribing errors

A

anticoagulants

analgesics

abx

insulin

175
Q

Classification of medication errors

A

•Mistakes – knowledge or rule based errors•Lapse – memory based errors i.e. forgetting the patient is allergic to penicillin•Slip – action based error i.e. picking up digoxin instead of diltiazem

176
Q

Types of medication incidents

A

Omission
Wrong drug
Wrong dose
Wrong frequency
Wrong duration
Wrong route
Wrong patient
Inappropriate prescribing

careful when prescribing meds with ‘look a like’ names eg •Dipryridamole Disopyramide•Carbamazepine Carbimazole•Chlorpromazine Chlorpropamide

177
Q

High risk medications – WHO 2019

A
178
Q

general advice to avoid errors when you are prescribing?

A

Rewriting a drug chart – quiet place, take time
Amending a previous prescription – re-write it
Being distracted whilst prescribing – find a quiet corner or room
Writing up drugs with more than 1 drug card/set of notes in front of you – avoid this
Unfamiliar drugs – ask for help
Prescribing parenteral drugs – take time, ask for help
Time pressured – take time
High risk drugs – take time, ask for help
Calculating drug doses – ask for independent calculation
Look-alike drugs – take time and meticulous handwriting

179
Q

in fluids quesn, how to approach how much fluid to give if fluid input and output is given?

A

base which fluid to give on electrolytes

how much to give based on ongoing losses ie fluid balance eg if patient seems to be losing 6L in a day and is currenlty able to tolerate 500mL orally, then this pt needs IV fluid replacement. since losing abt 1 L every 4 hrs, intial replacement with 1L over 4 hrs is appropriate, then moitor and reassess.

180
Q

general rule to changing dosings of drugs

A

inc/dec dose with the minimum increment/decrement possible. esp with drugs with narrow therapeutic index

181
Q

statin facts

A

avoid grapefruit when on statins as inc toxicity

shd not be taken in acute liver failure

conventionally taken at ngiht

to be stopped while taking clarithromycin as inc toxicity and SEs

182
Q

what extra things do you need to mention when prescribing abx?

A

Indication and stop/review date are CRUCIAL

183
Q

when prescribing PRN meds, what info is crucial?

A

indication, frequency and maximum dose/frequemcy

184
Q

whats imp to mention when prescribing senna

A

presciribe it nightly ie to be taken at night time

185
Q
A

Medicine finals Prithvi (22 decks)

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