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Question 1

Why be wary of CYP2D6 variations when it comes to codeine, Tramadol, Oxycodone, and Dihydrocodeine?

Answer 1

Genetic variation in the CYP2D6 liver enzymes can either result in morphine toxicity in the case of ultra rapid metabolisers (in which case reduce consciousness, somnolence, constipation, respiratory depression, pinpoint pupils and nausea and vomiting should be monitored for).

At the other end, poor metabolisers will have reduced therapeutic effect. However it’s worth mentioning that Dihydrocodeine parent compound has analgesic effect too and Tramadol parent compound is theorised to affect pain via increased inhibition in the spinal cord by acting as a neurotransmitter reuptake inhibitor)

Question 2

What are the symptoms of opioid overdose for patients on tramadol, codeine, morphine?

Answer 2

Circulatory / Respiratory depression
Coma
Pinpoint pupils
Reduced consciousness
Somnolence
Nausea and vomiting

Question 3

How does mu opioid binding affect respiratory rate?

Answer 3

It causes CO2 sensing chemoreceptors to lose their sensitivity resulting in a slower rate of respiration.

Question 4

Why might Remifentanil be of benefit over Fentanyl and Alfentanyl?

Answer 4

Remi has a unique method of metabolism, in that it is more lipid soluble than morphine and yet is metabolised by non-specific enterases extra-hepatically in blood / tissues, resulting in a faster clearance and consequently if of more use in cases where faster recovery is required.

Question 5

Why should you avoid Opioids in respiratory depression?

Answer 5

Due to reduced CO2 sensitivity it will further depression the breathing rate.

Question 6

What are the contra indications of opioids?

Answer 6

Risk of paralytic ileus
Acute respiratory depression
Head injury / raise intercranial pressure ( can reduce the pupillary response needed for neurological assessment).

Question 7

When would you reduce the dose of opioids?

Answer 7

Adrenalcorticoid insufficiency 
Debilitated
Elderly
Hypothyroidism
Hepatic impairment (as it may cause a coma).

Question 8

Why can increasing the dose of Buprenorphine result in reduced pain relief?

Answer 8

Buprenorphine is a partial agonist - Low doses results in interaction with MOP receptor to give pain relief however as doses increases it binds to both NOP and KOP receptors causes anti-analgesic effects.

Question 9

How does Tramadol act other than via MOP binding? How does this affect drug-drug interactions?

Answer 9

Modulates reuptake of serotonin and noradrenaline.

Increasing serotonin levels can increase the risk of serotonin syndrome when given with SSRI’s, SNRI’s, MAOIs, TCAs, Lithium, Methadone, Triptans, Pethidine, Pentazocine, Amphetamines. Serotonin syndromes presents with neuromuscular hyperactivity,, autonomic dysfunction, altered mental state. So be wary of patients who are potentially on these medications for; anxiety, depression, migraines, addiction, bipolar disorder, parkinsons, chronic pain or ADHD

Can increase the risk of seizures in those prone or with history of epilepsy.

Question 10

A patient on Tramadol comes back with creatinine clearance of 28ml/min, what is your recommendation?

Does this differ in hepatic impairment?

Answer 10

Increase dosing interval to 12 hours as renal elimination may be impaired.

With hepatic impairment the dosing interval can be increased to 12 hours OR halve dose. C/I in severe.

Question 11

Our previous patient on Tramadol lab results show creatinine clearance of 9ml / min, how do we proceed?

Answer 11

It is not recommended to be used in this patient.

Question 12

What are the very common and common side effects of Tramadol?

Answer 12

Very common; Nausea

Common; Vomiting,

Question 13

Why might you prefer Tapentadol as a strong painkiller?

Answer 13

Due to MOP and noradrenaline reuptake modulation it can result less opioid side effects such as constipation, nausea and vomiting.

Question 14

Why do patients on methotrexate (for non malignant indications, e.g. Crohns, RA) take folic acid?

Answer 14

Methotrexate inhibits dihydrofolate reductase the enzyme responsible for reducing dihydrofolate to tetrahydrate folate (co factor in thymidylate synthesis - purines) this can result in various side effects (ab pain, diarrhoea, GI bleeding, malaise, nausea, visual disturbances are a few of many) due to affecting DNA synthesis.
Folic acid reduces the incidence of these.

Question 15

Why would you refer a patient on Methotrexate experiencing:
Sore throat, mouth ulcers, bruising

N+V, ab discomfort, dark urine

Breath shortness, dyspnoea, cough, fever

Answer 15

Respiratory effects including shortness of breath could be signs of pulmonary toxicity, referral needed if above and if pneumonitis suspected - discontinue

Liver issues such as cirrhosis

Could be signs of infection due to reduced immune response

Question 16

Why can Trimethroprin and proguanil/ pyrimethamine increase risk of side effects when taken with methotrexate?

Answer 16

Act via a similar mechanism - dihydrofolate reductase inhibition.

Question 17

Why is it important to continually confirm a patients methotrexate dose, frequency, tablet strength and enquiry about health issues?

Answer 17

Due to risk of various toxicities, blood disorders presenting as sore throat, mouth ulcers, bruising. Liver toxicity presenting as NV, abdominal discomfort, dark urine. Respiratory toxicity presenting as SoB, dyspnoea, cough and fever.
GI toxicity first presenting as stomatitis
It is contraindicated in infection so signs of this require referral.

Question 18

Why monitor FBC on methotrexate?

Answer 18

To check for clinically significant bone marrow suppression, in which the risk increases with age / renal impairment and if on Trimethropin

Question 19

Why would a patient on methotrexate prescribed the following require possible intervention?
NSAIDs
PPIs
Retinoids
Trimethropin
Quinolones
Sulfamethoxazole/Sulfadiazine/Sulfadoxine

Others…

Answer 19

NSAIDs, retinoids Trimethropin, Penicillins, Quinolones all increase risk of toxicity so would be avoided (except NSAIDs in which dose monitoring and reduction appropriate)

PPIs reduce clearance so use with caution or avoid.

Sulfa’s increase exposure so use caution or avoid.

Caution in hepatotoxic, nephrotoxic, myelosuppressive or drugs that increase risk of thromboembolism.

Question 20

Why are opioids contraindicated in acute respiratory depression and cautioned in asthma?

Answer 20

The mew receptors mediate respiratory depression so when activated reduce sensitivity to plasma CO2 and inhibit respiratory rhythm generation. It should be avoided in acute asthma attack and COPD.

Opioids also cause histamine release leading to itching, bradycardia, hypotension and importantly BRONCHOCONSTRICTION.

Question 21

Why might you need 5HT3 antagonists, antihistamines, droperidrol or Prochlorperazine, especially initially, in opioid use?

Answer 21

Nausea and vomiting due to opioid action on chemoreceptor trigger zone in medulla.

Question 22

Why are opiates contraindicated in biliary disease?

Answer 22

Opioids cause biliary sphincter contraction and gall bladder contraction

increase risk of gallstones (increased amylase and lipase) in biliary colic so avoid

Question 23

Why does morphine need dose reduction in liver and renal impairment?

Answer 23

In liver metabolised primarily by glucoronide conjugation and impaired function may cause a coma.

In renal the 3/6 metabolites are excreted.

Question 24

Why would you be vigilant administrating Naloxone to buprenorphine, methadone and pentazocine?

Answer 24

Both Buprenorphine and Pentazocine are partial agonists so may not have full effect.

Both Buprenorphine and Methadone are long acting and repeated dosing of Naloxone May be required.

Question 25

Why would you stop Phenelzine before surgery?

Answer 25

As a MAOI (other monoamine oxidase inhibitors include Isocarboxazid, Tranylcypromine, and Moclobemide, the latter a reversible type A antagonist) it has many interactions (could potentiate hypotension or hypertension) and so should be stopped 2 weeks before surgery, albeit and ideally in a tapered withdrawal of 4 weeks (can cause movement disorders, insomnia, agitation and even potentially hallucinations)

Question 26

Why would you stop Yasmin before surgery?

Answer 26

Yasmin is a COC combining ethinylestradiol and drosperidone, other Monophasic COCs include Gedarel, Cilest, Rigevidon, Loestrin, which all vary in their progesterone element. Some biphasic include Logynon, which vary amounts per week. Ideally COCs should be stopped 4 weeks before all major surgery/ leg surgery/ surgery resulting in prolonged immobilisation due to increases of venous thrombosis. A progesterone only contraceptive, such as Levonogestrel (Cerazette, Cerelle, Zelleta) should be started after a complete cycle (no break) in this case. COC can be restarted 2 weeks after the first menses after mobilisation.

Question 27

How would you deal with a patient unable to stop COC before major surgery, ie. in emergency trauma?

Answer 27

Recommend a low molecular weight heparin (Enoxaparin, Dalteparin, Tinzaparin) and graduated compression hosiery in order to reduce risk of thrombosis.

Question 28

Why would you stop Lithium 24 hours before major surgery? Is it different for minor?

Answer 28

Lithium should be stopped 24 hours before surgery due to fluid and electrolyte changes. In minor surgery, can continue with lithium if fluid and electrolytes are monitored (contraindicated in dehydration and low salt as can change lithium plasma concentration leading to overdose - GI issues, tremor, CNS and cardiac issues).

Question 29

Why give premedication to patients before surgery?

Answer 29

Use of benzodiazepines (Temazepam, Diazepam. Midazolam) will reduce anxiety/ sleep issues, augment anaesthesia, reduce extraneous movements from drugs like Propofol and Etomidate and potentially give amnesia. This can be given as dose night before and smaller one just before or just the first dose on day of surgery. The alpha adrenergic agonist Clonidine is also used when standard treatment does not give enough sedation.

Question 30

In what situations would the short recovery of Midazolam increase?

Answer 30

May have slower recovery if used repeatedly, if used in the elderly or in patients with low cardiac output. Increased dose and a large drug combination before surgery could cause profound sedation too.

Question 31

Why might you use oral Temazepam over IV Diazepam?

Answer 31

Temazepam is fast acting even when oral so less invasive and diazepam can be painful upon injection due to low water solubility (therefore preferable to use emulsion).

Question 32

Why might you avoid use of Ketamine in anaesthesia?

Answer 32

Psychotic effects can present, albeit transiently, giving rise to hallucinations, nightmares (though benzos can reduce this). Ketamine can also give a slow recovery and extraneous muscle movements.

Question 33

How would you prevent NO associated hypoxia?

Answer 33

Mixture to have at least 30% oxygen and run the oxygen for several minutes after stopping NO. Do not give longer than 24 hours and do not use more than once every 4 days without close supervision and haematological monitoring.

Question 34

Why might you avoid intramuscular injections of Diclofenac and Ketopofen post op?

Answer 34

Patients with cardiac impairments, heart disease/ failure, elderly or with Crohns / UC (may exacerbate)

Question 35

Why give IV infusion of Remifentanil over repeated IV Alfentanil dosing during surgery as opioid enhancement of anaesthesia?

Answer 35

Remifentanil has a short half life (metabolised by blood and tissue esterases not in the liver) allowing the infusion to be terminated and giving no respiratory depression affects making it far more preferable in cases where ventilation is needed, whereas Alfentanil can give rise to post op respiratory depression. Please note; all fentanils can lead to muscle rigidity requiring antimuscarinic management.

Question 36

Why might you switch to Atracuronium from the other non depolarising neuromuscular blockers?

Answer 36

All the others require caution, monitoring a dose changes in renal (impairment = increased duration) and liver impairment

Question 37

Why should the injection of combination of local anaesthetics + vasoconstrictors take special care not to be given into a vein. Ex. Lidocaine / Articaine / Bupivicaine and adrenaline

Answer 37

Vasoconstrictors stop the local anaesthetics being taken into the bloodstream therefore prolonging their effect by reducing absorption. If injected into a vein it may cause ischaemic necrosis, especially if an appendage, and systemic exposure in hypertensive / arrhythmic patients is dangerous.

Question 38

Why would you not use Neostigmine to reverse Suxamethoniun chloride?

Answer 38

Suxamethoniun works by acting as an acetylcholine mimics at the neuromuscular junction but with a slower hydrolysis, this increases depolarisation and gives neuromuscular blockade (leading to side effects like bradycardia, hypersalivation) Neostigmine is an anticholinesterase so will reverse competitive (non neuromuscular) blockage of drugs like Vecuronium (coupled with glycopyrroniun to control muscarinic sides) - will inhibit breakdown of acetylcholine and increase signalling however if given with Suxamethoniun it will prolong the depolarisation even more.`

Question 39

Why do you need caution in Flumazenil use?

Answer 39

Half life is shorter than benzos do repeated dosing may be required It may lead to anxiety conditions, N and V, agitation and tachcardia Should avoid breastfeeding for 24 hours.

Question 40

In which situation would you use Sugammadex in preference to Neostigmine (and Glycopyrronium)?

Answer 40

If rapid reversal is required for the non depolarising (competitive) aminosteroid blockers - Rocuronium and Vecuronium.

Question 41

Dantrolene is used for malignant hyperthermia arising from use of Suxamethonium and for chronic skeletal spasticity via oral route, in the latter, why do you need to monitor liver function?

Answer 41

Dantrolene is associated with hepatotoxicity - advise patients to look out for abdominal pain, jaundice, dark urine, pruritis, nausea and vomiting and fatigue and to see a doctor if they occur. This is increased in females, if in doses over 400 mg daily, if over 30.

Question 42

What is supine position?

Answer 42

Horizontal with face up

Question 43

What patient groups require dose adjustment in anaethesia?

Answer 43

Ill Hepatic impairment Shock patients Debilitated Robust (may require increased doses)

Question 44

How may you reduce the dose of an induction agent in anaesthesia?

Answer 44

Use of premedication such as sedative agents of opioids

Question 45

IV anaesthesia is used to induce or maintain anaesthesia. How long does it take for IV anaesthesia to work?

Answer 45

One arm-brain circulation

Question 46

In order to allow tracheal intubation, what is used?

Answer 46

A neuromuscular blocking drug such as non-depolarising (Pancuronium, Rocuronium, Verocuronium, Atracurium, Cisatracurium, Mivacurium) to relax vocal cords or Opioids

Question 47

What are the cautions for non-depolarising neuromuscular blocking drugs?

Answer 47

Fluid disturbances (sweating, fluid loss/ retention), electrolyte disturbances (hyper/hyponatraemia, hyper/hypokalaemia, ) and neuromuscular disorders can result in a unpredictable response (may increase of decrease dosage requirements) Hypothermia and myasthenia gravis can result in lower doses needed as it lasts longer and myasthenia gravis results in increased sensitivity to these agents. Hypersensitivity to other neuromuscular blockers and cross-allergy is possible. Burn patients may require higher doses and the action of the NMBD may be reduced. In cardiovascular disease the rate of administration may need to be reduced.

Question 48

Common side effects of non-depolarising neuromuscular blocking drugs?

Answer 48

``` Bradycardia Hypotension Flushing Rash Bronchospasm less common ```

Question 49

How to reduce the effects of histamine release when using Atracurium in CVD patients and hypotensive sensitive patients ?

Answer 49

By administering over 1 minute it can reduce the hypotension, flushing and bronchospasm associated with Atracurium.

Question 50

What pharmacodynamic property allows non-depolarising neuromuscular blocking drugs to be used in pregnancy and breast feeding?

Answer 50

These drugs are ionised at physiological pH and therefore unlikely to cross placenta in significant amounts and to enter breast milk in significant amounts. Although manufacturers will recommend avoidance for 24 hours in terms of breast feeding and to avoid in pregnancy.

Question 51

How would we avoid excessive doses of competitive neuromuscular blocking drugs in obese patients?

Answer 51

Use ideal body weight. Ideal body weight (kilograms) = Constant + 0.91 (Height - 152.4) Where: Constant = 50 for men; 45.5 for women Height in centimetres

Question 52

Malignant hyperthermia is associated with volatile inhalation anaesthetics and suxamethonium chloride, what are the symptoms?

Answer 52

Rapid temperature increase Muscle rigidity Tachycardia Acidosis

Question 53

What is used to treat malignant hyperthermia

Answer 53

Dantrolene

Question 54

What advantages dose Sevoflurane have over other inhalational anaesthetics?

Answer 54

Non-irritant of upper respiratory tract (unlike Desflurane) therefore appropriate for induction of anaethesia. It has a rapid recovery and emergence too. as well as little affect on heart rate.

Question 55

How does the dosing of Sevoflurane change from induction to maintenance?

Answer 55

To induce anaesthesia it can be increase from 0.5% to up to 8% using a calibrated vaporiser whereas for maintenance the maximum licensed dose is 3%.

Question 56

What would be a contra-indication of Sevoflurane?

Answer 56

Malignant hyperthermia susceptibility / history.

Question 57

What is the minimum oxygen content in a Sevoflurane mixture?

Answer 57

25%.

Question 58

What counselling would you give a patient post surgery following Sevoflurane anaesthesia?

Answer 58

Avoid driving and alcohol for 24 hours due to risk of impairment consciousnous.

Question 59

When would you recommend VTE prophylaxis in patients already taking anti-platelet agents for other conditions? What would you recommend if bleeding risk outweighs VTE?

Answer 59

If risk of VTE outweighs bleeding risk. Consider mechanical (graduated compression hosiery that is M/F to provide 15mmHg of calf pressue until no longer significantly reduced mobility unless CI) in this case.

Question 60

When would you advise to stop oestrogen containing oral contraceptives or hormones replacement therapy before surgery? What are the alternatives?

Answer 60

4 weeks. Use progesterone only contraceptive or barrier method. Can use Tinzaparin or other LMWH prophylaxis if unable to stop

Question 61

If we unable to provide Apixaban for elective hip replacement what other VTE options are there?

Answer 61

Rivaroxaban and Dabigatran within their marketing. LMWH for 10 days followed by aspirin for further 28 days. LMWH for 28 days with anti-embolism stockings (stockings until discharge) Anti-embolism stockings

Question 62

How does VTE prophylaxis differ from elective knee and hip replacement surgery?

Answer 62

Apixaban 2.5mg 10 - 14 days instead of 32 - 38 days. Rivaroxaban 10mg for 14 days instead of 35 days. Dabigatran goes from 9 days to 27 - 34 days LMWH for 14 days (and anti-embolism stockings until discharge) instead of 28. Knee can just use aspirin 75 mg for 14 days

Question 63

Lifestyle advice following hip and knee surgery in order to reduce VTE risk?

Answer 63

Hydration Mobilisation Compression hosiery

Question 64

How would you adjust Apixaban dosing in renal impairment?

Answer 64

No adjustment until under 30ml/min. If between 15 - 29 then caution required. If under 15 manufacturer advises avoid.

Question 65

What risk factors increase the risk QT prolongation and therefore torsade de points (a type of ventricular tachycardia)

Answer 65

Metabolic disturbances notably Hypokalaemia Female Increasing age Cardiac disease Drugs, ex. Escitalopram, thyllines, steroids, beta adrenergics,

Question 66

What is the definition of thrombocytopenia?

Answer 66

Platelet count <150 x 10^(9)

Question 67

What are the risk factors associated with long QT?

Answer 67

Bradycardia Drug induced (examples Dronedarone, Adenosine, Sotalol, macrolides such as Clarithromycin), class IA (e.g. quinidine, disopyramide) or class III (e.g. amiodarone, sotalol, dofetilide, ibutilide) antiarrhythmic medicinal products, methadone, moxifloxacin, antipsychotics Hypokalaemia Genetic predisposition

Question 68

Why are gonadorelin analogues used 3 - 4 months before hysterectomy / myomectomy?

Answer 68

These reduce uterine volume, fibroid size and associated bleeding making vaginal procedures more feasible.

Question 69

Examples of Gonadorelin analogues?

Answer 69

``` Goserelin Buserelin Leuprorelin acetate Nafarelin Triptorelin ```

Question 70

What is the pharmacological action of Gonadorelin analogues ("relins" - Goserelin, Buserelin, Leuprorelin acetate, Nafarelin, Triptorelin)?

Answer 70

Gonadrorelin analogues (luteinising hormone releasing hormone) causes inhibition of pituitary luteinising hormone leading to decreased testosterone in men and decreased oestrogen in women (after an initial jump in serum levels). These reach suppressed levels after 21 days and are consequently kept low by injection every 28 days.

Question 71

How are Gonadorelin analogues administered?

Answer 71

Zoladex (Goserelin) is adminstered via intra abdominal depot injection Leuprorelin (Prostap) via subcutaneous / intramuscular Buserelin via subcutaneous / intranasal Nafarelin - Intranasal Triptorelin - Intramuscular / intranasal

Question 72

Counselling points for Gonadorelin analogues?

Answer 72

Decreases hormones Takes 21 days to reach required levels (maintained via injection every 28 days) Injection site will be rotated to reduce nodule formation / atrophy Common s/e: Joint / bone pain, headache, hot flush, mood altered, sexual dysfunction, weight changes,

Question 73

Why might you need to conside biphosphonates with Zoladex (or other Gonadorelin analogues ) treatment?

Answer 73

These medications can cause a reduction in bone mineral density (so particular caution in those with risk factors - FH, alcohol abuse / smokers, long term anticonvulsants / corticosteroids). This in turn can lead to risk of spinal compression (in men)

Question 74

Why might you monitor glucose whilst on Gonadorelin analogues?

Answer 74

Associated with decreased glucose tolerance and therefore associated with diabetes and loss of blood glucose control.

Question 75

Why would hormone replacement be added to Zoladex treatment?

Answer 75

In endometriosis, use of hormone replacement will reduce bone mineral loss and vasomotor symptoms (hot flushes, night sweats)

Question 76

How would you adjust treatment for COPD if disease becomes more severe (breathlessness and reduced exercise tolerance) whilst using a SAMA / SABA?

Answer 76

If inhaler technique is ok and FEV1 is over 50% then LAMA (Tiotropium, Glycopyrronium, Aclidinium, Umeclidinium) or LABA (Salmeterol / Formeterol, Indacaterol, Olodaterol) should be added on top. If LAMA added in then SAMA should be discontinued (if SAMA qds then switch to LAMA). If FEV is under 50% LABA + ICS or LAMA on it's own. This can be progressed further to ICS and LABA in combined inhaler + LAMA (although triple therapy is arguably not cost effective). Can then added on aminophylline / theophylline. Can add on mucolytics (Carbocisteine / Acetylcisteine).

Question 77

What would you monitor for in asthmatic / COPD patients on theophylline, ICS and beta agonists

Answer 77

Hypokalaemia

Question 78

How does acute oral prednisolone dosing differ between asthma and COPD?

Answer 78

Asthma is 40mg od for at least 5 days whereas COPD is less for longer 30mg od for 7-14 days.

Question 79

What can affect Aminophylline and Theophylline pharmacokinetics?

Answer 79

MR Body weight (use ideal body weight Age (increased clearance in children under 12) Respiratory disease Increased plasma concentration (reduced clearance) in heart failure, hepatic impairment, viral infections, hypothyroidism, fever Decreases plasma concentration from smoking (adjust if start / stop during treatment), alcohol consumption, hyperthyroidism

Question 80

What is the definition of sepsis?

Answer 80

Characterised by life threatening organ dysfunction due to dysregulated host response to infection. Layperson - life threatening condition when body’s response to infection injured own tissues and organs.

Question 81

How does septic shock differ from sepsis?

Answer 81

Septic shock is a subset of sepsis wherein circulatory, cellular and metabolic abnormalities increase mortality.

Question 82

What are the characteristics of SIRS and how is it useful?

Answer 82

Allows identification of infection: ``` Temperature > 38.3 or <36 Pulse > 90/min RR > 20/ min New confusion / drowsiness WBC >12 or < 4 (x 10^9) Blood glucose > 7.7 (if not diabetic) ```

Question 83

Sepsis risk factors?

Answer 83

Age (under 1 or above 75) Impaired immune systems ( on chemo, long term immunosuppressants, surgery in past 6 weeks, IV drug misuse, catheters / indwelling lines Pregnancy (given birth/ termination/ miscarriage in past 6 weeks) - Especially If impaired immune systems, gestational diabetes, invasive procedures, prolonged membrane rupture, streptococcus A infection exposure, vaginal bleeding/ discharge. Neonates - preterm birth <37 weeks, Fever over 38, parenteral AB given to mother at birth and 24hrs either side, infection in another baby in multiple pregnancy, streptococcus B exposure

Question 84

What are the could this be sepsis screening factors?

Answer 84

Patient looks sick Patient / carer worried NEWS triggering Risk factors present (age over 75, recent surgery / trauma/ invasive procedure, immunosuppressive, indwelling device or skin integrity breached

Question 85

Most common cause of sepsis?

Answer 85

Pneumonia Urinary tract Abdomen Skin, soft tissue, bone and joint

Question 86

Red flag criteria for sepsis? | How should you respond?

Answer 86

Change in AVPU Acute confusion Respiratory rate Oxygen needed to keep SpO2 at or over 92% (88% in COPD) HR over 130 bpm SysBP at or under 90 (or 40 drop from normal) Not passed urine <18 hours, UO <0.5mL/kg/hr Non-blanching rash Mottled/ashen/cyanotic Recent chemo (<6 weeks) Ensure delivery of sepsis 6 / ring 999/ hospital referral.

Question 87

Risk factors for DVT / PE?

Answer 87

``` Immobility Travel Surgery Thrombophilia Cancer HF DVT Hx HRT / Contraceptive pill Pregnancy Obesity Age Smoking ```

Question 88

How to distinguish between DVT and PE?

Answer 88

DVT will present with pain, swelling, warm/ red skin and a heavy ache in one leg (usually the calf) which will increase when the foot is bent upwards in contrast with a pulmonary embolism which will present with breathlessness, chest pain, collapse, sweating and light headness.

Question 89

Normally the Apixaban dose for prevention of stroke / embolism in NVAF is 5mg bd, in which situations would you reduce it?

Answer 89

``` Two or more of the following; If the patient is over 80 If the patient is under 61kg If patient creatinine clearance between 15 - 29 ml / min If creatinine is over 133 micromol / L ```

Question 90

How does the dose of Apixaban change from thromboembolism treatment to prophylaxis?

Answer 90

Initially 10mg bd for 7 days to treat DVT / PE, this then drops down to 5mg bd after the initial 7 days. Following 6 months on the treatment (5mg bd) it drops down to 2.5mg bd for the recurrent prophylaxis dose.