NPC Modules Flashcards

National Prescribing Curriculum notes. Including; NPC: Analgesia for Low Back Pain NPC: Child with Acute Otitis Media NPC: Chronic obstructive pulmonary disease (COPD) exacerbation NPC: Hypertension NPC: Polypharmacy NPC: Postoperative Pain and Vomiting NPC: Prevention of Venous Thromboembolism NPC: Type 2 diabetes: Initiating treatment NPC: Urinary Tract Infection

1
Q

What are the 4 stages of prescribing?

A

Information gathering, clinical decisionmaking, communication, monitoring & review

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2
Q

Why choose to work with a few select medicines (personal formulary)?

A

It will increase your knowledge & confidence in using them safely & effectively

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3
Q

What are SNAP risk factors?

A

Smoking, Nutrition, Alcohol, and Physical activity

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4
Q

What are common presenting symptoms of DM2? (4 classic, 4 additional)

A

Classically: polydipsia, polyuria, polyphagia, pruritis; also: frequent fungal or bacterial infections, blurred vision, loss of sensation, poor wound healing

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5
Q

When do you assess vision in DM2?

A

Can’t be properly assessed until later; organize a followup.

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6
Q

What initial Ix do you do in DM2?

A

Lipids; HbA1c; Albumin-creatinine ratio (monitor kidney disease); electrolyes, urea, & creatinine; LFTs

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7
Q

What medicines are high-risk?

A
Anti-infectives
Potassium and electrolytes
Insulin
Narcotics and sedatives
Chemotherapy agents
Heparin and anticoagulants
Systems
Mnemonic: A PINCHS
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8
Q

What risk is there in using beta blockers in a pt with DM?

A

Beta-blockers blunt adrenergic response to hypoglycaemia (increased HR, palpitations); benefit of beta blocker is still substantial

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9
Q

What risk factors increase the likelihood of postop nausea and vomiting? Name 5

A

female sex
<50 years old
non–smoker
history of motion sickness
prior history of postoperative nausea and vomiting
type of anaesthetic medicines used (opioids, volatile anaesthetics and nitrous oxide)
dehydration
longer duration of surgery and type of surgery

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10
Q

Why is it important to assess a pt who has increasing pain after surgery, instead of just increasing pain medication?

A

Rule out severe complications (compartment syndrome, bleeding, infection)

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11
Q

What is the benefit of treating postop pain & nausea (beyond pt comfort)?

A

Facilitate nursing care
Encourage early mobilisation
Reduce postop complications
Enable timely discharge

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12
Q

What should be used to monitor patient response to analgesia?

A

Unidimensional pain scale

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13
Q

What should be used to monitor patient response to opioids?

A

Sedation scale

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14
Q

What should always be given with, before, or instead of opioids, to lower dose of opioids required?

A

Regular acetaminophen (e.g. q6h)

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15
Q

What are other options for post-op pain management? (in addition to acetaminophen and opioids)

A

NSAIDs, local anesthesia

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16
Q

What 3 classes of antiemetic are good options for postop N&V?

A

5HT3 receptor antagonists
dexamethasone
droperidol

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17
Q

You prescribed IV because your patient couldn’t tolerate PO, but now they can. Is it better to stay with IV or switch to PO?

A

Switch: Use PO whenever possible

and if e.g. writing and order for an antiemetic, notify the team they may want to switch to PO in 12h

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18
Q

Why is hydromorphone a high-risk medicine?

A

It is 5x more powerful than morphine, but the names are similar so they get mistaken.

Hydromorphone is not the same as morphine.

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19
Q

If you’ve tried one antiemetic and it hasn’t worked (including for pre-op prophylaxis), what is the next step?

A

Antiemetic from a different class

5HT3 receptor antagonists
dexamethasone
droperidol

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20
Q

When presenting with symptoms of UTI, who should have their urine sample sent for culture?

A
  • pregnant women
  • male patients
  • residents of aged care facilities
  • patients with recurrent infection
  • patients who have travelled internationally in the last 6mo
  • patients who have used Abx in the last 6 months
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21
Q

What are the 5 questions to ask when deciding about any test, treatment, or procedure?

A

Is the test, treatment or procedure really necessary?
What are the risks?
Are there simpler, safer options?
What will happen if we don’t do anything?
What are the costs?

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22
Q

What is the most common organism causing UTI?

A

E. coli

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23
Q

What is the difference in the antibiotic course for male vs female patients?

A

Longer (e.g. 7 days vs 3 days)

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24
Q

What does reaction to a penicillin imply for prescribing a cephalosporin?

A

Proceed with caution / avoid if sensible: 10% of patients with allergic reaction to penicillin will also react to a cephalosporin

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25
Q

What does spinal tenderness indicate on exam?

A

Non-specific finding.
Severe spinal tenderness may indicate vertebral compression fracture, spinal infection or malignancy
Tenderness over facet joints may be seen in arthritis or inflammation

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26
Q

What tests assess for L4 radiculopathy?

A

Knee strength and reflexes

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27
Q

What tests assess for L5 radiculopathy?

A

Great toe and foot dorsiflexion

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28
Q

What tests assess for S1 radiculopathy?

A

Foot plantarflexion and ankle reflexes

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29
Q

What is the non-pharmacological therapy for nonspecific low back pain?

A

Moderate exercise as tolerated
Heat
NOT bed rest

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30
Q

What is the treatment goal in nonspecific low back pain?

A

Reduce pain (not completely stop it) and restore function & activity

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31
Q

What class of medication is first line for well patients with inonspecific low back pain?

A

NSAIDs (after weighing CV, GI, and renal risk)

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32
Q

Should acetaminophen be used in nonspecific low back pain??

A

Not considered effective (for low back pain), but very safe, so can consider a trial

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33
Q

Are muscle relaxants used in nonspecific low back pain?

A

No: none show improvement over placebo

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34
Q

What are the presenting SSx of acute OM?

A

acute onset of signs and symptoms
middle ear effusion
red tympanic membrane indicating middle ear inflammation

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35
Q

Is middle ear effusion enough on its own to diagnose acute OM?

A

No: effusion can persist dor several weeks after an episode of OM

36
Q

Why is it important to examine a febrile child thoroughly when they present with OM?

A
  • child can have sepsis from acute OM

- could have other source of infection

37
Q

What are some age-appropriate non-pharmocological interventions and distractions for an 18mo child?

A

a warm room and calm atmosphere
a familiar toy
parental presence, hugging or stroking
music, storytelling, non–nutritive sucking (a dummy), blowing bubbles.

38
Q

What is the analgesic of choice in children with pain and high fever, with acute infection?

A

Acetaminophen

39
Q

When should ibuprofen not be used in a child?

A

SSx of dehydration, uncertain Dx

40
Q

For whom should Abx be considered for acute OM?

A

Children who are …

  • immunocompromised
  • systemically unwell (eg vomiting, fever)
  • < 6 months old
  • > 6 months old with symptoms that last more than 48 hours or worsen.
41
Q

What should be communicated to a patient’s GP on discharge from ED?

A
  • overview of presenting illness
  • documentation of past history, results of investigations and examinations
  • management plan including prescription (name, dose, frequency, length of treatment and route of administration), analgesia, non-pharm
  • response to treatment while in the ED
  • follow-up management, including when to seek further medical assessment
  • documentation that written information has been provided to patient
42
Q

Should Abx regularly be given for acute OM? Why/not?

A

No: most cases resolve spontaneously, and Abx only have small benefit in children with acute OM who are otherwise well. (Need to weigh risk of Abx against small benefit)

43
Q

What is an appropriate initial treatment course in most children with acute OM?

A

observe the natural course w/o Abx
treat Sx with simple analgesics (acetaminophen)
review the child w/in 24 to 48 hours

44
Q

What organisms cause most bacterial acute OM?

A

Streptococcus pneumoniae and Haemophilus influenzae

though Haemophilus influenzae has declined dramatically since immunisation

45
Q

How do you position a patient who is propping themselves forward to breathe?

A

You don’t: ensure pt is able to position themselves, and do not reposition them.

46
Q

How should patients with acute COPD exacerbation be treated?

A

Bronchodilator

SABAs and ipratropium bromide both work well acutely

47
Q

What is the recommendation around oral corticosteroids in acute COPD exacerbation?

A

5 day course of corticosteroids shortens recovery time and reduces the severity of acute exacerbations

48
Q

Should you use Abx in acute COPD exacerbation?

A

Patients with clinical signs of infection (increased volume and colour change of sputum and/or fever and leucocytosis) will benefit

49
Q

What Abx should be used in acute COPD exacerbation? How long?

A

Amoxicillin or doxycycline (5 days)

Remember only if SSx of infection

50
Q

What is the initial medical management of acute COPD exacerbation

A

O2 (.5-2L/min, to O2 sat of 88-92%)
SABA (eg salbutamol); adequate dose (eg 8-10 inh of 100mcg)
5d course of oral prednisolone 50mg

51
Q

If the patient does not respond to initial SABA, what is the next step?

A

Ipratropium

52
Q

What is good turbuhaler technique?

A
  • Hold upright when loading
  • Create a seal around the mouthpiece (with lips)
  • Lift chin to straighten path into lung
53
Q

Name 4 LABAs

A

Formoterol
Salmeterol

“ultra-long-acting”:
indacaterol
vilanterol

54
Q

Name 4 LAMAs

A

Tiotropium
Glycopyrronium
Aclindinium
Umeclidinium

55
Q

What common analgesic can elevate blood pressure?

A

NSAIDs

56
Q

What is AV nicking?

A

Compression of retinal vein by retinal artery. Indicates evidence of end-organ damage.

57
Q

What investigations should be done for initial presentation of hypertension?

A

ECG
Urinalysis
Serum lytes & Cr
Lipids

58
Q

Why do an ECG for HTN?

A

R/o outflow obstruction, check for LVH

59
Q

Why do urinalysis for HTN?

A

Check for renal cause

Check for renal complications

60
Q

Why do serum lytes & Cr for HTN?

A

Establish baseline, and monitor renal function

Important for monitoring disease progression, and may also indicate dosing adjustments required

61
Q

Why check lipids for HTN?

A

Metabolic syndrome

Also, independent risk factor for CV complications

62
Q

What does LVH indicate (in context of HTN)?

A

Chronic HTN

Elevated risk of further complications (stroke, heart failure, CKD)

63
Q

What change in Cr (after ACEi or ARB initiation) should prompt an investigation of renal impairment?

A

> 30% increase in serum Cr

64
Q

What is the basis for initiating treatment of HTN?

A

Overall CV risk (not HTN alone)

65
Q

For pharmacological management of HTN, most patients require…

A

More than one antihypertensive

Several months to attain target BP

66
Q

In otherwise uncomplicated HTN, begin pharmacological treatment with …

A
  • ACE inhibitors or angiotensin-II receptor blockers
  • dihydropyridine calcium channel blockers
  • for pt 65+: thiazide diuretics
67
Q

When should the patient’s electrolytes and renal function be checked?

A

Baseline, 1-2w after initiating treatment, and at increasing intervals afterward

68
Q

What diuretic should not be used for treatment of hypertension?

A

Furosemide: useful for edema, not for HTN

69
Q

Who should have VTE risk assessment on admission to hospital, and when?

A

All patients, within 24h

70
Q

What is the formula for calculating VTE risk?

A

There isn’t one, but more risk factors –> higher risk. Weigh risk of bleeidng vs risk of VTE.

71
Q

What non-pharm VTE prophylaxis options exist?

A

Mobilisation

Compression stockings: recommended until pt is mobilised to previous standard, regardless of pharm phrophylaxis

72
Q

What labs should be monitored when a patient is on VTE prophylaxis?

A
platelet count (? HITT) 
hemoglobin (? bleeding)
renal function (dosing)
73
Q

What clinical signs should be monitored when a patient is on VTE prophylaxis?

A

Monitor for signs of bleeding.
Vitals, operative site, review of drains
Nose bleeding, hematuria, melena

74
Q

How is minor bleeding controlled, if it happens while a patient is on VTE prophylaxis?

A

Withold the prophylaxis

75
Q

Why is it important to obtain an accurate medication history?

A
  • may be causing pt presentation

- pt may not be taking them as prescribed

76
Q

Name 3 classes of medication that should be held in the setting of acute cardiac and renal failure

A

ACE inhibitors, NSAIDs, metformin (Nephrotoxic)

77
Q

What should you always consider when a patient presents with a new symptom? (polypharmacy)

A

Possibility that symptom is a side effect of another medication

78
Q

Why should you be clear that you have intentionally ceased a medication, in your documentation?

A

Otherwise another provider might think you simply forgot to prescribe it

79
Q

When is digoxin indicated?

A

Heart failure with concomitant atrial fibrillation

Heart failure with inadequate response to ACEi, ARB, beta-blockers, loop diuretics, aldosterone antagonists

80
Q

When should metforming be held?

A

During illness (vomiting, fever, diarrhea), surgery, trauma, MI, renal impairment

81
Q

Why should you not simply cease a benzodiazepine on admission to hospital, even if you think it contributed to pt presentation?

A

If pt has developed tolerance, benzos need to be tapered

82
Q

What feature requires caution in use of IV ondansetron in the elderly?

A

Risk of prolonged CT interval. Use SL in the elderly

83
Q

Are serial digoxin levels required in digoxin toxicity?

A

No: one measurement indicates toxicity, and heart rate can be used as a proxy of digoxin clearance

84
Q

What is the prescribing cascade?

A

process of prescribing a patient a new medicine to alleviate symptoms that are in fact adverse effects of a medicine they are already prescribed

85
Q

What is the “triple whammy” (in context of renal function and medication)?

A

ACEi/ARB + NSAID + diuretic
Additive effect in reducing blood flow to the glomerulus, thus reducing renal perfusion and renal function.
(Aussie colloquialism)