Pharm Flashcards

1
Q

What are the symptoms of digoxin toxicity?

A

Clinical features of digoxin toxicity:

  • GIT: nausea, vomiting, anorexia, diarrhoea
  • Visual: blurred vision, yellow/green discolouration, haloes
  • CVS: palpitations, syncope, dyspnoea
  • CNS: confusion, dizziness, delirium, fatigue
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2
Q

How is digoxin toxicity treated?

A

Digoxin-specific antibody fab fragments (Digibind) is a recognised antidote for severe digoxin toxicity.

Management:

  • Digibind
  • correct arrhythmias
  • monitor potassium
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3
Q

What is the MoA of sildenafil?

A

Sildenafil is a phosphodiesterase type V inhibitor.

PDE5 inhibitors cause vasodilation through an increase in cGMP leading to smooth muscle relaxation in blood vessels supplying the corpus cavernosum.

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4
Q

What are the target O2 sats in a patient suffering form CO poisoning?

A

100% as they can be falsely elevated du to the CO - therefore the ususal 94-98 is not sufficient.

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5
Q

What anti-cancer drug causes peripheral neuropathy?

A

Vincristine

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6
Q

Name the side effects of the TB medications.

A
  • R: Hepatotoxicity, orange secretions, CYP450 inducer
  • I: Peripheral neuropathy. Give pyridoxine prophylactically to prevent. Liver enzyme inhibitor
  • P: Hepatotoxic; Gout
  • E: Optic neuritis and blindness
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7
Q

How does alcohol lead to polydipsia?

A

Ethanol reduces the calcium-dependent secretion of ADH by blocking channels in the neurohypophyseal nerve terminal.

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8
Q

If a patient complains of GI symptoms with metformin, what is the next-line drug for diabetes control?

A

If metformin is not tolerated due to GI side-effects, try a modified-release formulation before switching to a second-line agent.

2nd line options are e.g:

  • Sulphonylurea
  • Pioglitazone
  • Sitagliptin
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9
Q

What are side effects of thiozoladinediones?

A

Classical side effects of this PPAR-gama agonist are:

  • weight gain (rather than loss)
  • fluid retention (therefore contraindicated in cardiac failure)
  • liver dysfunction
  • associated fractures
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10
Q

What is the first-line investigation you should carry out in someone with a TCA overdose?

A

ECG - this is because TCAs can lead to sinus tachycardia, widening of the QRS and prolongation of the QT interval.

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11
Q

What is the effect of phenytoin on liver enzymes?

A

Phenytoin = Liver enzyme inducer

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12
Q

How can heparin cause a prothrombotic state?

A

Heparin is associated with heparin induced thrombocytopenia.

Despite the lower platelet number, this is a prothrombotic condition:

Molecules of the cytokine Platelet factor 4 (PF4) bind to heparin to form an antigen. This antigen is then recognised by antibodies which in turn activate platelets through their Fc receptors, and thereby initiate a pro-thrombotic cascade.

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13
Q

What vision defect can sildenafil cause?

A

Blue-tinted vision.

Remember by the tablet being blue.

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14
Q

What are the indications for N-acetylcystein in paracetamol overdose?

A

Give immediately if:

  • There is uncertainty about the time of overdose, but it is potentially toxic
  • The overdose was staggered over a time period longer than an hour
  • Plasma-paracetamol (taken >4 hours after OD) is over the treatment line. on the graph
  • Overdose was taken 8-36 hours before presenting

If presenting within 1 hour then give activated charcoal.

(BNF says htat 150mg/kg within 24 hours can be fatal)

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15
Q

What are the side effects of amiodarone?

A

The most common side effect is hypothyroidism (mediated via Wolff-Chaikoff effect as amiodarone contains iodine; or via destructive thyroiditis)

Others include:

  • Pulmonary fibrosis
  • Corneal deposits
  • Photosensitivity + grey skin
  • LFT derangement
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16
Q

Which opioid can cause serotonin syndrome - and how?

A

Serotonin syndrome - i.e. a disorder characterised by serotonin excess, manifests with changes in mental status, neuromuscular changes and autonomic overactivity. Clinically, this can be observed as hypertension, tachycardia, flushing and sweating, hyperflexia, clonus and muscle rigidity. Other potential signs include fever and changes in mental status, including agitation.

Tramodol has both opioid and serotonergic activity and can therefore cause serotonin syndrome.

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17
Q

How is serotonin syndrome treated?

A
  • Supportive with IV fluids
  • Benzodiazepines
  • Serotonin antagonists (chlorpromazine)
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18
Q

What drug class is indapamide?

A

A thiazide-like diuretic.

19
Q

How long do you need to wait after and acute gout attack before you can start allopurinol?

A

2 weeks.

Note that if the patient already is on allopurinol this should be continued and not stopped.

20
Q

What is the maximum speed that hyponatraemia should be corrected by?

A

Hyponatraemia should maximum be corrected by 6-12 mmol/L in the first 24 hours.

Otherwise the patient is at risk of cerebral pontine myelinolysis.

21
Q

What is the effect that St. John’s Wart may have on liver enzymes?

A

Inducer of P450 system, therefore decreased levels of drugs such as warfarin, ciclosporin. The effectiveness of the combined oral contraceptive pill may also be reduced.

22
Q

What effect do LMWHs have on potassium?

A

They cause hyperkalaemia, as they inhibit aldosterone synthesis.

All heparins do this.

23
Q

What drugs are associated with hyperkalaemia?

A
  • ACE inhibitors
  • ARBs
  • Heparins/LMWHs
  • Calcineurin inhibitors
  • NSAIDs
  • Potassium sparing diuretics (spironolactone, amiloride, eplenerone)
  • Potassium containing salts/
24
Q

How long before surgery is Aspirin stopped?

A

For minor surgeries (removing cataracts, tooth surery, near surface of skin) they don’t need to be stopped.

25
Q

How do you calculate the anion gap?

A

This can be calculated by: (Na+ + K+) - (Cl- + HCO-3).

This can leave us with either high or normal anion gap. It is useful in classifying the causes of acidosis.

26
Q

What are causes of high anion gap acidosis?

A
  • Lactate raised: shock, sepsis, hypoxia
  • Ketones: DKA, alcholo
  • Urate: renal failure
  • Acid posioning, salicylates, methanol, ethylene glycol
27
Q

What are causes of normal anion gap acidosis?

A
  • Gastrointestinal bicarb loss
  • Renal tubular acidosis
  • Addison’s Disease
28
Q

Which NOAC is best for patients with poor renal function?

A

Apixiban, as it has minimal renal drug clearance

29
Q

What is the effect of trimethoprim on renal function?

A

Trimethoprim can cause a transient rise in creatinine, which reverses on stopping the drug.

Trimethoprim also block the ENaC channes in the distal nephron, causeing a hyperkalaemic distal RTA.

30
Q

How does cyclizine work?

In what group of patients should you be cautious prescribing it?

A

Cyclizine is an H1-receptor antagonist, blocking histamine recptors in the chemoreceptor trigger zone.

As cyclizine can cause a drop in caridac output and incrase the heart rate, it should be avoided in heart failure patients.

31
Q

What are the ECG features of tricyclic overdose?

A
  • Sinus tachycardia
  • Widening of the QRS
  • Prolongation of QT
32
Q

What is “Red Man Syndrome”?

How is it treated?

A

Red man syndrome is associated with rapid intravenous infusion vancomycin. It is a common adverse reaction of intravenous vancomycin use and is a distinct entity from anaphylaxis due to vancomycin use.

Treatment:

  • Stop vancomycin infusion
  • Readminister once symptoms have stopped, at slower rate
  • In severe cases, antihistamines can be co-administered
33
Q

What are P450 inducers?

A
  • Antiepileptics (phenytoi, carbamezapine)
  • Barbiturates (phenobarbitone)
  • Rifampicin
  • St. John’s Wart
  • Chronic EtOH intake
  • Smoking
34
Q

What are P450 inhibitors?

A
  • Antibiotics: cipro, erythromycin
  • Isoniazid
  • Imidazoles (ketakonazole, fluconazole)
  • SSRIs
  • Sodium valproate
  • Amiodarone
  • Allopurinol
35
Q

Which drugs are associated with galactorrhoea?

A

Drug causes of raised prolactin

  • metoclopramide, domperidone, chlorpromazine (dopamine antagonists)
  • phenothiazines
  • haloperidol
  • very rare: SSRIs, opioids
36
Q

What dose as a proportion of the maintenance dose of morphines should be given for breakthrough pain?

A

1/6th of the daily dose of morphine.

37
Q

Which enzyme do you need to check for before starting azathiorine?

A

Thiopurine methyltransferase (TPMT).

This enzyme is involved in metabolism of azathioprine and mercaptopurine. If deficient, there is a build-up of AZA, leading to BM suppression.

If below normal but not deficient, start at lower does.

38
Q

Which medications are most commonly associated with C. diff?

A
  • Clindamycin (historically the most common)
  • 2nd and 3rd generation cephalosporins (now the most common)

However, all antibiotics (even metranodazole which is used to treat C. diff) are associated with C. diff.

39
Q

What is the dose of atorvastatin for primary, and what for secondary prevention?

A
  • Primary: 20mg (titrate up until non-HDL has fallen by ≥40%)
  • Secondary 80mg
40
Q

What blood test needs to be performed before starting terbinafine?

A

LFTs need to be checked before starting terbinafine, and 4-6 weeks into treatment.

Treatment should be ceased or not commenced if there is derangement.

41
Q
A
42
Q

What is the MoA of loperamide?

A

Loperamide is an anti-diarrhoeal - it increases gut transit time.

It is a µ-opioid receptor agonist (like opioids), but doesn’t cross the BBB, so doesn’t have the addictive effects.

43
Q

What interacts with levothyroxin absorption?

A
  • Iron
  • Calcium carbonate

These two should teregore be given >4 hours apart from levothyroxine.

44
Q

Which morphine is preferred in patients with renal failure?

A

Buprenorphine and fentanyl are preferred opioids in patients with CKD.