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RACP 2024 > Gen Med, ICU and Misc > Flashcards

Gen Med, ICU and Misc Flashcards

1
Q

What is a Measurand with regard to biochemical testing?

A

A specifically defined analyte (=constituent of interest)

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2
Q

How do ion selective electrodes work to assess electrolytes? What are their advantages and disadvantages?

A

Contain an electrode which measures the potential difference the electrolyte of interest and a reference

Advantage: cheap, quick

Disadvantage: Affected by pH, unable to detect interference

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3
Q

What is the basic principle of chemical assays?

A

Chemical reaction creates colour change which is detected by spectrophotometry

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4
Q

What is the principle of enzymatic assays?

A

Quantification of substrate or enzyme by measuring the rate of reaction via colour change

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5
Q

What are the serum indices?

A

Factors that cause interference on assays, typically lipaemia, haemolysis, icterus and antioxidants

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6
Q

What is the underlying principle of immunoassays?

A

Detection of antigen via specific antibodies, with labelling of antigen or antibody

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7
Q

What is the principle behind sandwich immunoassays?

A

Detection of an analyte through the capture antibody and a detection antibody, quantity correlates to intensity of signal

Good for larger analytes as requires 2 immunoreactive sites

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8
Q

What is the principle behind competitive immunoassay?

A

Samples competes with a labelled analyte for binding to a specific antibody, where quantity inversely correlates to intensity of signal

Good for smaller molecules

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9
Q

What is the principle behind a lateral flow assay?

A

Sandwich assay for specific antigen, with control line often containing antibody against capture antibody

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10
Q

What is the principle behind immunoturbidimetry/nephelometry?

A

Aggreagation of antibody labelled microbeads due to the presence of antigen increases the turbidity of a sample, which is detected by scatter of light (nephelometry) or penetrance of light (turbidimetry)

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11
Q

What are the main interferences for immunoassays?

A
  1. HAMA (human anti-mouse antibody) - result from “immunisation” due to exposure to animal antigen, administration of animal immunoglobulin
  2. Heterophile antibodies -non specific antibody interference (associated with RF)
  3. Biotin - used as binding in assay, outcompetes this
  4. Structurally similar compounds
  5. Hook effect - feature of rate of assay reaction, where signal decreases with increasing concentration beyond the maximal point, leading to a lower concentration result being inferred from standard curve
  6. Free hormone hypothesis - where biological activity of hormone is related to unbound proportion, which is difficult to estimate
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12
Q

Why is vitamin D level often falsely low in pregnancy?

A

Due to free hormone hypothesis, where stripping of vitamin D from protein in incomplete resulting in falsely low results

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13
Q

What is the principle underlying high performance liquid chromatography?

A

An analyte can be separated based on its physical characteristics
Used for vitamin A+E, -azole drugs

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14
Q

What is the principle underlying gas chromatography mass spectrometry?

A

Heating of a sample to form a gas (eluent) that is ionised and separated via magnets bending the path of eluent based on mass and charge

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15
Q

What is the principle behind liquid chromatography tandem mass spectrometry?

A

Analyte separated based on physical characteristics, the irrelevant compounds removed based on mass/charge ratio and then collided with an inert gas to form daughter ions which are run through a second magnet chamber and selected by ratio of mass to charge

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16
Q

What is harmonisation and standardisation with regard to biochemical testing?

A

Harmonisaton is the process of achieving uniformity of results so that results from different labs can be compared, whereas standardisation is more focussed on being close to the true value

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17
Q

What is the incidence of chronic wounds in Australia and New Zealand, and their common aetiologies?

A

At any one time 200,000 Aus and 30,000 NZ

Venous and arterial ulcers, diabetic foot ulcers, skin tears

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18
Q

Over what timeframe will most chronic wounds heal with correct diagnosis and mangement?

A

12 weeks

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19
Q

What are clinical features of venous leg ulcers?

A
  • champagne bottle appearance of lipodermatosclerosis
  • haemosiderosis of surrounding skin
  • irregular border, shallow, above malleoli but below knee
  • Oedema
  • Atrophie blanche: small white areas caused by skin ischaemia
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20
Q

How are venous leg ulcers treated?

A
  • rarely with antibiotics
  • Debridement: sharp or blunt, mechanical or with dressing
  • protect peri ulcer skin
  • Dressing: primary, absorbent layer, compression
  • Address factors for wound healing: nutrition, smoking, exercise, venous ablation
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21
Q

What are features of lymphoedema ulcer?

A
  • cobble stone cracks
  • Stemmer sign: attempt to pinch and lift skin fold at base of second toe, positive = unable to pinch
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22
Q

How is lymphoedema treated?

A
  • compression
  • massage
  • weight loss
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23
Q

What are features of arterial ulcers?

A
  • sharp, punched out (deep) ulcers
  • distal to ankle
  • poor perfusion: poor capillary return, shiny hairless skin
  • ABPI < 0.7
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24
Q

When is compression safe for mixed arterial/venous ulcers?

A

ABPI >0.7

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25
Q

What are the treatments for arterial ulcers?

A
  • antibioitcs
  • debridement
  • dressings
  • compression if ABPI > 0.7
  • analgesia
  • revascularisation
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26
Q

What are clinical features of diabetic foot ulcers?

A
  • usually distal or planatar foot/toes, or distal ankle where footwear rubs
  • charcots foot
  • prone to infection
  • callus
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27
Q

How are diabetic neuroischaemic ulcers treated?

A
  • debridement except for dry gangrenous
  • dressings
  • offload
  • podiatry
  • BSL control
  • Agressive treatment of infection and high suspicion for osteomyelitis
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28
Q

What are the categories of skin tears?

A

Category 1: linear with no tissue loss OR flap with 10% approximation

Category 2: larger but flap present

Category 3: flap completely missing

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29
Q

How are skin tears prevented and managed?

A
  • prevention: moisturisation, avoid trauma, minimise steroid
  • treatment: oppose edges, non-adhesive dressing, remove dressings from base of flap
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30
Q

What are features of zoster rash?

A
  • Vesicular rash clustered on erythematous base
  • unilateral in sensory dermatome distribution, most common thoracic, also cervical and ophthalmic
  • vesicles crust over 7-10 days, full healing over 1 month
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31
Q

How are Zoster rashes treated?

A
  • antivrial
  • treat secondary infection
  • hydrogel, non adhesive dressing
  • vaccination for prevention
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32
Q

What are features of vasculitic ulcers?

A
  • associated with underlying autoimmune condition
  • associated rash (palpable purpurae)
  • red edge
  • non diagnostic biopsy
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33
Q

How are vasculitic ulcers treated?

A
  • immunosuppresion: steroids incl. topical, tacrolimus, anti-TNF mAbs (adalimumab, infliximab)
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34
Q

What are common features of pyoderma gangrenosum?

A
  • peripheral necrotic tissue
  • purplish edge
  • no rash
  • occur anywhere on body
  • biopsy non diagnostic
  • DO NOT GRAFT: get pathergy = new disease at site of graft
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35
Q

What are treatments of calciphylaxis ulcers?

A
  • sodium thiosulfate to treat nephrocalcinosis
  • 10 g IV 3x/week for 12 weeks
  • can also be given topically
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36
Q

How is mycobacterium ulcerans managed?

A
  • biopsy with PCR to confirm diagnosis
  • Rifampicin/clarithromycin
  • initially deteriorates over first 2-4 weeks due to release of lactoferin and inflammatory response
  • simple dressing
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37
Q

What is the definition of a pressure injury?

A

Any lesion caused by unrelieved pressure resulting in damage of underlying tissue

Includes pressure, friction and shear forces

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38
Q

Pressure over what size will cause a pressure injury?

A

> 30 mmHg over a bony prominence

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39
Q

How are pressure injuries classified?

A

Stage 1: no blanching hyperaemia

Stage 2: partial thickness ulcer, extending into epidermis and/or dermis = superficial ulcer/abrasion

Stage 3 = tissue loss down to fascia = deep ulcer

Stage 4: tissue loss through muscle, bone or supporting structures such as tendons. May also have sinus tracts

Unstageable = full thickness loss but base is not visible due to slough (needs to be removed UNLESS if dry)

Suspected deep tissue injury: purple/maroon discoloured skin with blistering

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40
Q

How are pressure injuries managed?

A
  • prevention through frequent turning, if bed bound at least every 2 hours
  • if chair bound reposition every hour
  • padding with pillows or foam wedges
  • cleaning (no soap, reduce friction)
  • moisturisers
  • lifting devices to lift
  • pressure relieving devices
  • treat at first sign of redness
  • nutrition (some evidence for 4.5 -9g arginine per day)
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41
Q

What are the 4 factors of wound bed preparation with regard to wound healing?

A

TIME

Tissue: debridement to develop a viable wound base
Infection: bacterial balance to control chronic inflammation
Moisture: exudate management (specifically to minimise proteases which delay wound healing)
Edge: promote re-epithelialisation via debridement, skin grafts, biologics

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42
Q

What are the aims for different tissue types when choosing a wound dressing?

A

Eschar: to remove it unless dry without erythema
Slough: aid autolyic debridement
Granulation tissue: protect + provide moisture management
Epithelium: protect

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43
Q

What is the role in compression in wound management?

A

Reduces fluid escape from the venous/capillary system to reduce oedema, including through supporting incompetent venous valves and venous return

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44
Q

What are the indications for Ga68-PSMA PET/CT in prostate cancer?

A
  • Elevated PSA without tumour detection
  • Initial staging
  • detection of recurrence after initial therapy in the setting of rising PSA
  • therapy monitoring
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45
Q

What is the significance of PET for cardiac amyloid?

A
  • can identify TTR cardiac amyloid (in conjunction with negative urine and serum amyloid light chains), which informs ability to use tafamidis (presents amyloidogenesis)
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46
Q

What is theranostics with regard to nuclear medicine?

A

The ability to diagnose a condition and then treat it with high dose radionucleotide

e.g. prostate cancer identified with Ga68-PSMA uptake, the treated with Lu177-PSMA

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47
Q

What is the incidence and common causes of secondary hypertension?

A
  • 5-10% people with elevated BP
  • young = renal parenchymal disease, coarctation of the aorta
  • > 65 = atherosclerotic renal artery stenosis, CKD, hypothyroidism8
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48
Q

What clinical features suggest a diagnosis of secondary hypertension?

A

Age < 30
On 3 or more agents
Acute worsening control

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49
Q

What are indicators of a renovascular cause for secondary hypertension?

A
  • increase in serum Cr >50% occurring in 1/52 of initiating ACEi/ARB
  • severe hypertension with unilateral smaller kidney or size discrepancy > 1.5 cm
  • recurrent flash pulmonary oedema
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50
Q

What is the triad of hyperaldosteronism?

A

Hypertension, unexplained hypokalaemia, metabolic alkalosis
(note 50-70% patients have normal potassium)

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51
Q

What proportion of patients with phaeochromocytoma have paroxysmal hypertension?

A

50%

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52
Q

What is the definition of hypertensive urgency and what is recommended management?

A

SBP >180 or DBP > 110, with symptoms such as headache, moderate non acute end organ damage

Managed with oral medications (small doses of short acting medications, or usual if missed dosed)

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53
Q

What is the definition of a hypertensive emergency and how is it managed?

A

SBP > 220 or DBP > 140, severe end organ damage such as APO, encephalopathy, neurological symptoms, AKI, aortic dissection, eclampsia

Lower MAP by 20-25% within first 2 hours with rapid acting meds (may need to be faster in haemorrhagic stroke or aortic dissection)

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54
Q

When is pharmacological management indicated for elevated BP?

A
  • if high absolute risk (>15%)
  • High BP >160/100
  • CKD, TIA/CVA, diabetes, MI, CCF, PAD, elderly
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54
Q

What are lifestyle modifications that can help to manage elevated BP?

A
  • weight
  • physical activity
  • salt reduction
  • diet
  • alcohol intake
  • smoking cessation
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54
Q

What are recommended first line anti-hypertensives?

A

ACEi or ARB, CCBs or thiazides

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54
Q

From the REASON study, what factors and complications were associated with increased mortality?

A

FACTORS:
- increasing age
- higher ASA status
- pre op albumin < 30
- unplanned surgery

COMPLICATIONS:
- renal impairment
- unplanned ICU admissions
- systemic inflammation

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55
Q

What are features of a bundle of care in perioperative medicine?

A
  • clinical pathways
  • multi disciplinary involvement
  • dedicated ward
  • early recognisation of complications
  • dedicated champions
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56
Q

What is the definition of high risk surgery?

A

> 5% risk of mortality

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57
Q

What are the ASA classifications?

A

Stratification of patients based on disease status, does correlate with outcomes

1- normal healthy patient
2- mild systemic disease (no functional limitation)
3- severe systemic disease (functional limitation)
4- severe systemic disease that is constant threat to life
5- moribound patient who is not expected to survive without an operation
6- declared brain dead for organ removal

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58
Q

What cardiac conditions are high risk and pose as contraindications to non-cardiac surgery?

A
  • ACS
  • Acute decompensated HF
  • Unstable arrhythmias
  • symptomatic severe AS
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59
Q

When is perioperative stress testing indicated?

A

For patients at elevated risk for non cardiac surgery with poor functional capacity (<4 METs) if the results of stress testing will change management

Stress testing performed as dobutamine stress echo

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60
Q

What are the guidelines for antiplatelets following cardiac stent for non cardiac surgery?

A
  • DAPT for minimum 1/12 after BMS (bare metal stent)
  • minimum 3-6 months after DES
  • minimum 12 months after ACS
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61
Q

What are the risk factors for post operative respiratory complications?

A
  • increased age
  • smoking
  • pre existing lung disease
  • OSA
  • pulmonary hypertension
  • heart failure
  • duration of anaesthesia
  • anaesthetic technique
  • neuromuscular blockade type

(not obesity)

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62
Q

What is the role of preoperative pulmonary function tests and CXR?

A

PFTs indicated for:
- cardiac surgery or lung resection
- investigation of undiagnosed SOB
- assess airways disease control

CXR indicated for undiagnosed dyspnoea, > 50 undergoing high risk surgery and known cardiopulmonary disease

63
Q

What is the definition of SIRS?

A

2 or more of:
T > 38 or < 36
HR > 90
RR > 20 or pCO2 < 32
WCC > 12 or > 10% immature band forms

64
Q

What is the definition of sepsis?

A

Life-threatening organ dysfunction caused by dysregulated host response to infection

qSOFA 2 or more of:
- SBP < 100
- GCS < 15
- RR > 22

65
Q

What is the definition of septic shock?

A

Sepsis despite adequate volume resuscitation and:
- persisting hypotension requiring vasopressors to maintain MAP > 65
- Lactate > 2

66
Q

How is procalcitonin used to guide antibiotics management?

A

Indicator of bacterial source of inflammatory response, > 0.5 indicates bacterial infection
If decreasing from baseline and still > 0.5 continue antibiotics
If increasing from baseline and > 0.5 switch antibiotics
If < 0.5 stop antibiotics

67
Q

How should patients with septic shock be resuscitated?

A
  • broad spectrum antibiotics
  • IV fluid at 30 mL/kg, balanced crystalloid initially (avoid albumin in head trauma)
  • aim MAP > 65 on arterial measurement
  • Blood if Hb < 70
  • corticosteroid (hydrocortisone 200 mg)
  • source control
68
Q

What is the 1st line and 2nd line vasopressors for shock with normal cardiac output?

A

1st line = Noradrenaline or adrenaline (note adrenaline can affect lactate levels)
May use metaraminol until central line established
2nd line = vasopressin

69
Q

What are the vasopressors used in shock with low cardiac output?

A

1st line: dobutamine or adrenaline

70
Q

What are the features of Anticholinergic toxidrome?

A

Hot = hyperthermia
Dry = sweating
Mad = delirium, psychosis, seizure, coma
Blind = blurred vision
Red = vasodilation
Other: urine retention, tachycardia

71
Q

What are the features of Cholinergic toxidrome?

A

CNS: agitation, confusion, seizures

Muscarinic:
Diarrhoea
Urination
Miosis
Bronchospasm
Bronchorrhoea (sputum)
Bradycardia
Emesis
Lacrimation
Salivation

Neuromuscular = fasiculations, muscle weakness, paralysis

72
Q

What are the features of neuroleptic malignant syndrome?

A

CNS: confusion, delirium, decreased LOC, coma

ANS: tachycardia, labile BP, dysrrhythmia, hyperthermia, diaphoresis

Neuromuscular: hypertonia, tremor, hyperreflexia

73
Q

What are the features of opioid intocxication toxidrome?

A

CNS: decreased mental status, miosis
CV: hypotension (histaminergic)
Resp: respiratory depression

74
Q

What are the features of serotonin syndrome?

A

CNS: agitation, delirium

ANS: hypertension, tachycardia, hyperthermia, diaphoresis, vomiting, diarrhoea

Neuromuscular excitation: rigidity LL > UL, hyperreflexia, clonus, mydriasis

75
Q

What are the features of sympathomimetic toxidrome?

A

CNS: agitation, hallucinations, paranoia, seizures

ANS: hypertesnion, tachycardia, dysrhythmias, hyperthermia, diaphoresis

Neuromuscular: hyperreflexia, tremor

76
Q

What are methods for decontamination and enhanced elimination in drug toxicity?

A

Activated charcoal is preferred method for decontamination, also used for elimination if given in multiple doses

Can eliminate through HD, plasmapheresis, exchange transfusion, urinary alkalinization

77
Q

What are the antidotes for each of these toxins?
1. Organophosphate
2. CCB, Beta blockers
3. Digoxin
4. Benzodiazepine
5. Cyanide
6. Local anaesthetic toxicity
7. Paracetamol
8. Opioids
9. Tricyclics, aspirin

A
  1. Atropine
  2. Calcium
  3. Digibind
  4. Flumenazil
  5. Hydroxycobalamin
  6. Intralipid
  7. Paracetamol
  8. naloxone
  9. sodium bicarbonate
78
Q

How is the relative risk calculated?

A

RR = Risk(treatment)/Risk(control)
Where risk = N(outcome)/total N of that trial arm

e.g RR = (a/(a+b))/(c/(c+d))

79
Q

How is the risk difference calculated?

A

RD = Risk(control) - Risk(treatment)
Where risk = N(outcome)/total N of that trial arm

e.g RD = (c/(c+d)) - (a/(a+b))

80
Q

How is the odds ratio calculated?

A

OR = Odds(treatment)/Odds(control)
Where Odds for a given arm = N(with outcome)/N(without outcome)

81
Q

What statistical tests are used for binary data?

A

Chi-square test to test for an association between event and group

Logistic regression for adjusted analyses

82
Q

How are continuous data summarised?

A

Mean and standard deviation
OR
Median and interquartile range

83
Q

How are continuous data compared?

A

Difference in mean or difference in medians

84
Q

How are differences in continuous data tested?

A

T-test (comparing population means between groups)
Adjusted analyses using linear regression

85
Q

What is time to event data, how is it summarised, compared and what are appropriate statistical tests?

A

Time from starting point, such as disease diagnosis or exposure, to the occurrence of an event of interest

Summarised for a group as median time to event (i.e. timepoint at which 50% of group have had event of interest)

Comparisons between groups made using hazard ratio

Statistical test = log-rank test, proportional hazards regression

86
Q

How is the hazard ratio calculated?

A

HR = treatment hazard rate/placebo hazard rate

87
Q

What are the four possible explanations for a difference to be observed between groups?

A

Bias
Error
Chance (random variation)
True difference

88
Q

How are bias and error controlled during a scientific study?

A

Through study design, randomisation, blinding, auditing, validating

89
Q

How is the effect of chance in a scientific study controlled for?

A

Statistical analyses

90
Q

What does a 95% confidence interval measure?

A

A range of plausible values for a summary measure in which 95% of repeated studies will cover the true value of a summary measure

91
Q

What is the null hypothesis?

A

The assumption that the rate of outcome is the same between groups

92
Q

What does a p-value indicate?

A

The strength of evidence in a study that a difference between two groups is not the result of chance
IS NOT the significance level

93
Q

What is Type I (alpha) error? What influences it?

A

A false positive conclusion
Alpha error = 0.05 (level of statistical significance you set = p-value), where <5% chance of null hypothesis being true

Influenced by chance
Type I error can be reduced by setting a lower statistical significance cut-off (p-value)

94
Q

What is type II (beta) error?

A

A false negative conclusion
Beta error = acceptable false negative conclusion
Statistical power = 1- beta, usually> 80% to detect a specified effect size

Influences:
- Inversely proportional to statistical power (determined by sample size)
- proportional to effect size
- Measurement error
- inversely proportional to statistical significance cut-off (p-value)

95
Q

Are statistically significant events always clinically significant?

A

No

96
Q

What is the sensitivity of a test and how is it calculated?

A

The proportion of true positives for a given test, low sensitivity indicates high false negatives

Sensitivity = true positives/total positive tests

97
Q

What is specificity and how is it calcualted?

A

The proportion of true negatives for a given test, low specificity indicates high false positives

Specificity = true negatives/total negative tests

98
Q

What is positive predictive value and how is it calculated?

A

The probability a person with a positive test has a disease

PPV = sensitivity x prevalence
———————————–
sens. x prevalence + (1-spec.) x (1 - prevalence)

99
Q

What is negative predictive value and how is it calculated?

A

The probability a person with a negative test does not have the disease

NPV = Specificity x (1 - prevalence)
—————————————–
(1 - sens.) x prevalence + spec. x (1 - prevalence)

100
Q

What influences the PPV and NPV?

A

Sensitivity and specificity of a test
Prevalence of disease in the population the test is applied to

Higher prevalence = lower NPV but higher PPV and vice versa

101
Q

What is the traditional hierachy of epidemiological study designs from highest quality data to lowest?

A

Systematic review (secondary research)
RCT (primary research: interventional)
Cohort study (primary research: observational)
Case-control study (primary research: observational)
Cross sectional study (primary research: observational)
Case report or series (anecdotal)
Commentary (anecdotal)

102
Q

What are the study design, strengths and weaknesses of a cross-sectional study?

A

Survey of participants at a single point in time to assess exposure and outcome

Strength: convenience

Weaknesses:
- taken at single point in time so cannot establish temporal association
- risk of confounding due to lack of control of other participant characteristics

103
Q

What are the study design, strengths and limitations of case-control studies?

A

Participants selected on outcome and exposure assessed retrospectively

Strengths:
- longitudinal information (can verify temporal association)
- inexpensive
- efficient for rare outcomes

Weaknesses:
- assumes well-defined study base (cases and controls from same source population)
- risk of recall bias = measurement bias where cases more likely to recall exposure than controls

104
Q

What are the study design, strengths and limitations of cohort studies?

A

Patients are selected based on exposure and then outcome assessed
Either retrospective or prospective

Strengths:
- longitudinal information to inform temporality
- efficient for rare exposures

Limitations:
- expensive
- risk of selection bias due to characteristics of participants who choose to participate, or variation between exposed and unexposed groups
- vulnerable to loss to follow up

105
Q

What are the study design, strengths and limitations of randomised control trials?

A

Participants selected and randomly assigned to an exposure and outcome assessed
Variables are controlled so exposure is only difference between groups

Strengths:
- randomisation controls for known and unknown confounders
- allows assessment of causality

Weaknesses:
- expensive
- needs clinical equipoise
- unfeasible for rare disease

106
Q

What are the study design, strengths and limitations of ecology studies?

A

Study of a group rather than an individual

Strengths: convenience

Weaknesses: cannot determine if individuals with exposure are the same individuals with the outcome

107
Q

What are the phases of clinical trial design?

A
  • preclinical: laboratory based
  • Phase I: assessment of safety and dosing
  • Phase II: assessment of drug activity and safety
  • Phase III: assessment of efficacy and safety
  • Phase IV: assessment in real world population (pharmacovigilence)
108
Q

What are strengths and limitations of the cross over clinical trial design?

A

Strength: efficiency as each participant acts as their own control

Weaknesses:
- risk of carryover effect from late onset drug effects
- risk of period effects such as underlying disease trajectory over time

109
Q

What is a factorial clinical trial design?

A

Where participants are randomised twice for. total of four treatment arms
Allows two questions to be answered simultaneously, but may be subject to biases from interaction between questions

110
Q

What are platform trials?

A

Trials with a master protocol with adaptive elements e.g. discontinuing an arm due to lack of treatment effect

111
Q

What are features of umbrella design, basket design and seamless trials?

A

Umbrella design: study multiple biomarkers and drugs in a common disease

Basket design: study common biomarkers and drugs in multiple diseases

Seamless trials: combine two or more phases into one adaptive study based on pre-determined interim analyses

112
Q

What is the difference between blinding and concealment?

A

Allocation concealment = what happens at time of randomisation to avoid selective enrolment of participants e.g. computer randomisation, sealed envelopes

Blinding = what happens after randomisation to avoid bias in measurement of outcome

113
Q

What is stratified randomisation?

A

Randomisation between groups as well as in within key strata e.g. age or country

114
Q

What are intention to treat analyses and what effect do they have on analysis outcome?

A

Data analysed according to treatment participant was randomised to regardless of adherence
Preserves the balance of confounders

Underestimates effect of treatment

115
Q

What are per protocol analyses and what effect do they have on analysis outcome?

A

Data analysis based on treatment participant actually receives
Can introduce confounders and result in under or over estimation of an outcome
Purpose is to validate findings of intention-to treat analysis

116
Q

What is a confounder?

A

A factor that is unevenly distributed between treatment groups that independently affects outcome

117
Q

What is selection bias and how can it be controlled?

A

A systematic difference between treatment groups. Informed by comparing group characteristics and loss to follow up

Controlled through randomisation

118
Q

What is measurement bias and how can it be controlled?

A

A systematic difference in the measurement of endpoints.

Blinding, standardisation of measurement

119
Q

What is the difference between precision (reliability) and accuracy (validity)?

A

Precision = same result produced repeatedly, where results correlate and are in agreement

Accuracy = where result reflects true result

120
Q

What are the anatomical structures involved in the perception of pain?

A

Sensed by Adelta and C fibres which synapse in dorsal horn
Then carried by spinothalamic pathway
- dull in paleospinothalamic
- sharp in neospinothalamic
Then up to somatosensory core
Receive modualtion from thalamus

121
Q

What is the ration of background opioid to breakthrough?

A

PRN is 1/6th of background except for methadone

122
Q

What is the conversion ratio of oxycodone and hydromorphone to morphine?

A

Oxycodone is 1.5x potent than morphine
Hydromorphone is 5x more potent than morphine

123
Q

What are key considerations with methadone prescription?

A

Causes QTc prolongation
Metabolised by CYP450:
- inducers cause decreased drug levels (anticonvulsants, rifampicin)
- inhibitors cause increased drug levels (azoles, fluoxetine)

124
Q

How do you convert oral morphine to subcut morphine?

A

Divide by 3

125
Q

What is malignant SVCO syndrome and what cancers is it commonly associated with?

A

Direct invasion or external compression of the SVC by a tumour that leads to thrombosis within the SVC

50% seen in NSCLC
30% SCLC
15% Non-hodgkins lymphoma

60% SVCO are in patients prior to cancer diagnosis, 10% SCLC present with SVCO

126
Q

What are clinical features of SVCO and the grades?

A

Face, neck or arm swelling
Chest pain
Dyspnoea, stridor, cough or hoarse voice
Cerebral oedema - headache

Grade I: incidental
Grade II: symptomatic
Grade III: severe symptoms
Grade IV: life threatening
Grade V: death

127
Q

How should SVCO be managed?

A

Diagnosed on CT with contrast

Glucocorticoids (dex) to reduce swelling
Recanalisation and stenting
Radiation therapy (risk of complete SVC obstruction due to swelling, needs dex cover)
Chemotherapy for underlying malignancy

128
Q

What are common cause of malignant spinal cord compression?

A

Prostate cancer
Breast cancer
Lung cancer
Multiple myeloma

129
Q

What are key features of malignant spinal cord compression?

A
  • New progressive severe back pain esp thoracic, worse on coughing, straining or lying flat
  • New motor deficit
  • Bowel or bladder disturbance (late sign)
130
Q

How should malignant spinal cord compression be managed?

A

MRI whole spine, CT myelography if patient unable to under go MRI

High dose dexamethasone (16 mg OD) started when suspected
Pain control
IDC
Laxatives
Surgical decompression and spine stabilisation or external beam radiotherapy

131
Q

What cancers are the most common cause of catastrophic bleeding? What are other high risk cancers?

A

Head and neck advanced cancer (5% of cases)

Central lung cancers
Cancers with thrombocytopenia
Cancers with liver disease

132
Q

How are catastrophic bleeds managed?

A
  • reassurance for patient and family
  • positioning of patient for comfort
  • midazolam 10 mg for sedation (may need to be higher if already on benzos)
  • consider opioid
133
Q

What cancers are associated with major airway obstruction?

A
  • lung cancers
  • laryngeal and nasopharyngeal carcinoma
  • oesophageal carcinoma
  • mediastinal tumours
134
Q

How should major airway obstruction be managed?

A

CT chest once stabilised

Bronchoscopy and stenting if appropriate
External beam radiation as appropriate
Dexamethasone
Opioids and benzodiazepines for comfort

135
Q

What are common causes of malignant hypercalcaemia?

A

-80% caused by PTHrP (many cancers)
- Osteolysis (breast, MM, lymphoma, leukaemia)
-1,25DihydroxyVitD: lymphoma, ovarian germinomas
- Ectopic PTH: ovarian, lung, NET, thyroid papillary, pancreatic)

136
Q

How should malignant hypercalcaemia be managed?

A

Serial measurements of CCa
PTH, PTHrP, Vit D levels

Bisphosphonate IV
Normal saline +/- IV frusemide
Denosumab in patients who cannot have bisphosphonate esp renal impairment

137
Q

What is the association between pre pregnancy creatinine and adverse outcomes in pregnancy?

A

Higher the creatinine the greater the chance of adverse effects:
- pre eclampsia
- pre term delivery
- SGA
- NICU admission
- 25% reduction in eGFR post partum

138
Q

What is the association between CKD stage and likelihood of complicated pregnancy?

A

CKD 1-2: likely uncomplicated

CKD 3: likely complicated by CKD progression, pre term delivery at 34-36 weeks, 50% have pre-eclampsia

CKD 4: very likely to be complicated with CKD progression, pre term delivery at 34 weeks, 70-80% pre-eclampsia

139
Q

What is the most dangerous glomerulonephritis in pregnancy?

A

SLE

140
Q

What is the significance of maternal SSA/SSB (Ro/La) in pregnancy?

A

Fetal heart block (need to be on hydroxychloroquine)

141
Q

When is the best time to plan a pregnancy in CKD?

A

Stable kidney function
BP well-controlled
On pregnancy safe medications
Underlying disease (SLE) well-controlled

142
Q

What happens to serum creatinine in pregnancy?

A

Reduces EXCEPT in 3rd trimester when begins to rise

143
Q

What findings in pregnancy suggest an underlying kidney disease?

A
  • impaired renal function including “AKI”
  • new proteinuria with PCR > 30 (proteinuria > 300 mg/day) before 20/40
  • nephrotic syndrome
  • synpharyngitic macroscopic haematuria = IgA nephropathy
144
Q

Is RAAS blockade contraindicated in pregnancy?

A

Yes - is teratogenic

145
Q

What is the target BP in pregnancy and what medications are safe for hypertension?

A

Target BP < 140/90 and continue unless BP < 110/70

Nifedipine, methyldopa, labetalol, hydralazine

146
Q

When should aspirin be given in pregnancy?

A

For prevention of pre-eclampsia in women who are high risk

100-150 mg OD from 10-14/40 until 10 days before delivery

147
Q

How can pre eclampsia be diagnosed in women with CKD?

A

Worsening renal function, proteinuria and hypertension can be signs of disease progression

Need to assess platelets, LDH, LFTs, placenta and fetal growth
Role of biomarkers: sFLT1 = anti-aniogenic ratio to PlGF = pro-angiogenic, pre-eclampsia associated with ratio > 38

148
Q

What is the diagnostic criteria of pre-eclampsia?

A

Hypertension (BP > 140/90) arising after 20/40 accompanied by:
- Thrombocytopenia < 100
- Cr >88 or doubled from baseline
- elevated transaminases
- headache, confusion or visual symptoms
- haemolysis
- foetal growth restriction
- Proteinuria (NOT essenital)

149
Q

How is proteinuria in pregnancy defined and what is its significance?

A

> 300 mg protein in 24 hour urine
OR
Urine Protien:Cr ratio >30
OR
Urine albumin:CR ratio >8

Before 20 weeks = underlying renal disease
After 20 weeks and hypertensive = at risk of pre-eclampsia
After 20 weeks and normotensive = new onset renal disease including autoimmune disease

150
Q

What is the only definitive treatment of pre-eclampsia?

A

Delivery of the placenta

151
Q

What changes to thyroid hormone occur in pregnancy?

A

50% increase in thyroid hormone synthesis (only T4 can cross placenta)

152
Q

What are the most common thyroid pathologies in pregnancy?

A

Subclinical hypothyroidism
Subclinical hyperthyroidism
HCG-mediated hyperthyroidism
Thyroid nodules

153
Q

What changes happen to TSH in pregnancy?

A
  • decreases in 1st trimester as HCG stimulates thyroid hormone synthesis
  • the same in trimester 2 and 3
154
Q

How should hypothyroidism be managed in pregnancy?

A
  • iodine supplement 150 micrograms OD
  • TSH > 10 with decreased T4 should receive replacement
  • there is no role in treating or screening for anti-TPO antibodies in pregnancy
155
Q

How should Graves disease be managed in pregnancy?

A

PTU = 1st line
The can continue throughout or switch to carbimazole at 16/40 noting PU risk of maternal hepatotoxicity and carbimazole risk of maternal and foetal hypothyroidism

156
Q

What physiological changes occur in the liver in pregnancy?

A
  • increased liver metabolism
  • reduced serum albumin
  • Increased ALP (placental produced)
157
Q

What are characteristics of pregnancy-associated liver disease?

A

Arise in 3rd trimester and resolves post partum

158
Q

What are causes of liver disease in pregnancy?

A
  • hyperemesis gravidarum
  • intrahepatic cholestasis of pregnancy
  • acute fatty liver of pregnancy
  • Pre eclampsia/HELLP

RACP 2024 (15 decks)

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