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GP Academy > 10. KFP: Aboriginal and Torres Strait Islander/Rheumatology > Flashcards

10. KFP: Aboriginal and Torres Strait Islander/Rheumatology Flashcards

1
Q

Potential complications from rheumatoid arthritis?

A
  • Atherosclerosis
  • Osteoporosis
  • Depression
  • Vasculitis
  • Peptic ulcer disease
  • Lung disease
  • Neuropathy
  • Atlanto-axial involvement
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2
Q

What is the definition of remission in rheumatoid arthritis?

A
  • Symptom relief
  • Normalisation of inflammatory markers
  • Absence of joint swelling
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3
Q

What is typically the drug of choice for conventional synthesis disease-modifying antirheumatic drug for rheumatoid arthritis?

A
  • Methotrexate 10mg weekly on one specified day PLUS
  • Folid acid 5 to 10mg weekly (on a different day)
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4
Q

What features on history and examiantion would make you suspect rheumatoid arthritis?

A

History:
- Joint pain and swelling +/- fever
- Morning stiffness > 30 minutes
- Family history RA
- Systemic flu-like features and fatigue

Exam:
- 3 or more tender and swollen joint areas
- Symmetrical joint involvement in hands and/or feet
- Positive squeeze at MCP/MTP

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5
Q

Initial therapy for rheumatoid arthritis?

A

Pharmacological:
- Simple analgesics
- Higher doses of omega-3 fatty acid
- NSAIDs/COX-2 inhibitors
- DMARDs
- Corticosteroids

Non-pharmacological:
- Weight control
- Patient education
- Occupational therapy
- Exercise (dynamic, aerobic, taichi)
- Psychosocial support
- Sleep promotion

Referral to rheumatologist

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6
Q

Risk factors for gout?

A
  • Dehydration
  • Diet: purine rich substances e.g. meat, seafood, alcohol, fructose-sweetened drinks
  • Disorders of high cell turnover e.g. haematological malignancies, severe psoriasis
  • Drugs that inhibit renal excretion of uric acid: thiazide diuretics, loop diuretics, cyclosporin
  • Comorbidities: hypertension, chronic kidney disease, dyslipidaemia, type 2 diabetes, obesity
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7
Q

What options are there for long term urate lowering therapy in the management of gout?

A
  1. Allopurinol
  2. Febuxostat
  3. Probenecid
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8
Q

What are the options for gout flare prophylaxis when initiating or titrating urate lowering therapy and how long are they usually required?

A
  1. Colchicine 500microg daily or BD PO
  2. NSAID orally on lower dosing end
  3. Prednisone 5mg daily PO

Colchicine can be used in conjunction with either NSAID or prednisone. Do not use NSAID and prednisone. Prednisone should be used in consultation with rheumatologist due to side effects.

Duration: 3 to 6 months

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9
Q

What is the hallmark of polymyalgia rheumatica?

A
  • Characterised by bilateral aching and stiffness of the shoulders and hip girdle area caused by low grade synovitis
  • Hallmark of the disease: Morning stiffness
  • Stiffness tends to improve after a hot shower and with activity
  • Occurs almost exclusively in people older than 50 years
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10
Q

Suggestive features for the diagnosis of polymyalgia rheumatica?

A

Features usually present:
- Age >50yo
- Bilateral shoulder aching
- Elevated ESR +/- CRP

Supportive features:
- Absence of RF and anti-CCP
- Morning stiffness lasting longer than 45 minutes
- Hip-girdle discomfort or limited range of motion
- Absence of involvement of joints other than the hip and shoulder

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11
Q

Management of polymyalgia rheumatica?

A
  • Prednisone 15mg daily PO for 4 weeks then reduce gradually
  • Usually needs 12 months of treatment
  • Do not reduce dose if there is active disease
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12
Q

Features suggestive of statin-related muscle symptoms?

A
  • Bilateral pain
  • Aching or stiffness
  • Pain located in large muscle groups
  • Onset 4 to 6 weeks after starting or increasing dose of statin
  • High dose or high potency statin therapy
  • Elevated serum CK that decreases with statin withdrawal
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13
Q

ANA staining pattern - what do they mean/what’s the significance?:
- Homogenous
- Speckled

A

Nonspecific

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14
Q

ANA staining pattern - what do they mean/what’s the significance?:
- Centromere
- Nucleolar

A

Systemic sclerosis

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15
Q

Diagnostic criteria for systemic lupus erythematosus?

A

Four of the eleven criteria are required for classifying a patient as having SLE.

  1. Malar rash: malar erythema, flat or raised
  2. Discoid rash: erythematous rasied patches with keratotic scaling and follicular plugging
  3. Photosensitivity: rash as an unusual reaction to sunlight
  4. Oral ulcers: oral or nasopharyngeal ulcers, usually painless
  5. Arthritis: nonerosive arthritis involving two or more peripheral joints with tenderness, swelling or effusion
  6. Serositis: pleurisy or pericarditis
  7. Renal features: proteinuria or cellular casts
  8. Neurological and neuropsychiatric features: seizures or psychosis
  9. Haematological features: haemolytic anaemia, leucopenia, lymphopenia or thrombocytopenia
  10. Presence of anti-double stranded DNA antibody, anti-Smith antibody, or antiphospholipid antibodies
  11. Antinuclear antibody positive: ANA positive in the absence of drugs known to cause drug-induced lupus
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16
Q

Differentials for non-inflammatory causes of arthralgia and myalgia

A
  • Fibromyalgia
  • Benign hypermobility syndrome
  • Osteoarthritis
  • Hypothyroidism
  • Osteomalacia
  • Multiple myeloma
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17
Q

Differentials for inflammatory causes of arthralgia and myalgia

A
  • Polymyalgia rheumatica
  • Giant cell arteritis
  • Systemic lupus erythematosus
  • Sjogren syndrome
  • Polymyositis
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18
Q

What is Sjogren’s syndrome?

A
  • Chronic autoimmune disease associated with lymphoid infiltration of the exocrine glands, particularly the salivary and lacrimal glands, leading to secretory gland dysfunction and usually severe sicca symptoms
  • In severe cases, dryness can cause salivary gland enlargement and calculus formation, and can affect the trachea causing dry cough and/or hoarse voice
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19
Q

Features of Sjogren’s syndrome?

A
  • Can be primary or secondary (when in association with rheumatoid arthritis or another connective tissue disease e.g. SLE or systemic sclerosis)
  • Glandular hypofunction
  • Fatigue
  • Arthralgia
  • Nonerosive arthritis
  • Raynaud phenomenon
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20
Q

Diagnosis of Sjogren’s syndrome?

A
  • Significant and persistent picca symptoms (e.g. severe dry eyes needing ocular lubricants several times a day)
  • Associated polyclonal hypergammaglobulinaemia
  • Positive antinuclear antibody
  • Presence of antibodies to Ro (SS-A) and La (SS-B)
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21
Q

Management of common clinical features of inflammatory connective tissue diseases?:
- Sicca symptoms

A
  • Wear sunglasses outdoors to avoid wind-drying effects on the eyes
  • Avoid dry and heated air, cigarette smoke, anticholinergic drugs (e.g. TCAs, antiparkinsonian drugs)
  • Ensure adequate oral hydration and good dental hygiene to prevent dental caries
  • Dry eyes: lubricant drops, gels, ciclosporin drops to improve tear flow
  • Dry mouth: hydration, good dental hygiene and regular exams, topical remineralising agents to prevent tooth decay, artificial oral lubricants, products that stimulate saliva e.g. lozenges or gum
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22
Q

What’s the diagnosis?
urethritis + conjunctivitis +/- iritis + arthritis?

A

Reactive arthritis

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23
Q

When does reactive arthritis tend to appear?

A

1-3 weeks after the initial infection

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24
Q

What infections can cause reactive arthritis?

A
  • Genitourinary: chlamydia trachomatis
  • GI: Salmonella, shigella, yersinia, campylobacter
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25
Q

Clinical features of reactive arthritis?

A
  • Inflammatory peripheral arthropathy with an asymmetrical oligoarticular distribution, predominantly affecting the lower limbs
  • Common: dactylitis, enthesitis
  • Articular symptoms develop after atleast 1 week after an infective illness

Extra-articular features:
- Conjunctivitis, anterior uveitis
- Genitourinary inflammation: urethritis, prostatitis, balanitis
- Keratoderma blennorhagica: pustular hyperkeratotic rash typically affecting the palms and soles of the feet

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26
Q

Management of reactive arthritis?

A
  • Treat active infection if present

Joint Pain - options:
- NSAID OR
- Intra-articular corticosteroid injections OR
- Prednisone 10-50mg daily PO

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27
Q

Who is more likely to be affected by systemic lupus erythematosus?

A
  • F > M
  • AgeL 15 - 45yo (child bearing years)
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28
Q

Management of systemic lupus erythematosus?

A
  • Hydroxychloroquine - can reduce risk of flares and improve lipid levels
  • Moderate or severe: systemic corticosteroids
  • Belimumab - immunomodulatory drugs can take several months to become effective
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29
Q

Clinical features of fibromyaglia?

A

History:
- Chronic widespread musculoskeletal pain (hallmark)
- Cognitive clouding
- Fatigue
- Impaired concentration
- Sleep dysfunction
- Depression
- GI dysfunction and discomfort (irritable bowel)
- Urogenital dysfunction and discomfort (irritable bladder)

Exam:
- Soft-tissue tenderness to pressure is typically diffuse
- Tender in the majority of patients: lateral epicondyles, trapezius muscles, anserine bursae
- Allodynia

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30
Q

Management of fibromyalgia?

A

Patient education:
- Pain is real but not caused by tissue damage
- Not a progressive or deforming disease
- Fluctuating symptoms
- Goal is to manage pain

Lifestyle & Non-pharm management:
- Regular graded aerobic exercise - graded by duration of time exercising, rather than pain experienced
- Cognitive behavioural therapy
- Good sleep practices

Pharm management:
1. Low dose TCAs: amitriptyline
2. Gabapentinoid
3. Serotonin-noradrenaline reuptake inhibitor

Analgesia: paracetamol, NSAIDs

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31
Q

Features of streptococcal throat infection?

A
  • Abrupt onset of symptoms
  • Fever > 38C
  • Tender cervical lymphadenopathy
  • Tonsillar exudate
  • Scarlet fever-type rash: bright, red, bumpy rash
  • Absence of cough, rhinorrhoea or nasal congestion
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32
Q

Clinical features associated with airway obstruction or deep neck infection?

A
  • Muffled voice
  • Stridor
  • Trismus: muscle spasms in your temporomandibular joint
  • Drooling
  • Unilateral throat pain
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33
Q

Conditions associated with airway obstruction or deep neck infection?

A
  • Acute epiglottitis
  • Peritonsillar abscess (quinsy) and peritonsillar cellulitis
  • Severe Epstein-Barr virus infection
  • Severe croup or bacterial tracheitis
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34
Q

Antibiotic therapy for streptococcal pharyngitis and tonsillitis?

A

Phenoxymethylpenicillin 500mg Q12hourly PO for 10 days

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35
Q

Why is adhering to Phenoxymethylpenicillin 500mg Q12hourly PO for 10 days important for patients at high risk of acute rheumatic fever?

A
  • To eradicate strep pyogenes from the pharynx and prevent the development of acute rheumatic fever
  • IM benzathine benzylpenicillin can be used in those who may experience difficulties adhering to the 10 day oral regimen OR if oral therapy is not tolerated OR a single dose is preferred
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36
Q

Can children with grommets swim?

A

Yes, if they wear ear plugs and swimming caps

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37
Q

Management of tympanostomy tube otorrhoea?

A
  • Cleaning (dry mopping or syringing with dilute betadine 1:20)
  • Topical ciprofloxacin 5 drops BD for 7 days
  • Review weekly for 4 weeks
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38
Q

How long should swimming be avoided for after grommet insertion surgery?

A

One week

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39
Q

What is trichiasis and what is its significance?

A
  • Trichiasis is defined as normal lashes growing inward. In trichiasis, the lash follicle is normal, but the direction of lash growth is abnormal. In the presence of inflammation, there may be a misdirection of the follicle with the lash growing inwards towards the cornea
  • Where trachoma is endemic, trichiasis of any degree indicates trachoma until proven otherwise
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40
Q

Management of trachoma?

A
  • Antibiotics: azithromycin 1g STAT PO
  • Treat contacts
  • Preventative measures for patient and contacts: face washing
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41
Q

When to check for donovanosis?

A

Anyone with an ano-genital ulcer in remote areas

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42
Q

Acute rheumatic fever: major manifestations and minor manifestations?

A

Major:
- Carditis
- Mono/Polyarthritis
- Sydenham chorea
- Erythema marginatum
- Subcutaneous nodules

Minor:
- Fever > 28C
- Monoarthralgia
- ESR >/= 30 or CRP >/= 30
- Prolonged PR interval on ECG

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43
Q

Which areas in Australia are endemic with acute rheumatic fever?

A
  • Far North Queensland and North Queensland
  • Northern territory
  • Pilbara and Kimberley regions of Western Australia
  • Other remote areas
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44
Q

Risk factors for chronic kidney disease?

A
  • Smoking
  • Obesity
  • Hypertension
  • Diabetes
  • Severe socioeconomic disadvantage
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45
Q

What is the uric acid level goal when managing gout?

A
  • No tophi: < 0.36mmol/L
  • Tophi: < 0.30mmol/L
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46
Q

Differentials for dyspnoea?

A

Cardiac:
- Increased left sided intracavity filling pressure: HFrEF, HFpEF, left sided valvular dysfunction (aortic or mitral stenosis or regurgitation)
- Myocardial ischaemia
- Arrhythmia (tachyarrhythmia, bradyarrhythmia, ectopy, AF, atrioventricular dissociation)
- Low cardiac output (left sided): pulmonary hypertension, hypovolaemia, cardiac shunt, cardiac compression (pericardial constriction, cardiac tamponade, tension pneumothorax)

Respiratory:
- Hypoxia: pulmonary parenchymal abnormality (pneumonia, fibrosis, emphysema, pulmonary oedema, alveolar haemorrhage, pleural effusion, pneumothorax), airway obstruction (asthma, bronchitis, upper airway), ventilation perfusion mismatch (pulmonary embolus, pulmonary shunt)
- Central respiratory drive abnormality (pharmacologic, metabolic)
- Musculoskeletal respiration abnormality: skeletal myopathy, respiratory muscle fatigue, chest wall abnormality (kyphoscoliosis, thoracic skeletal pain, obesity)

Peripheral muscle oxygen extraction abnormality or inefficiency:
- Poor physical fitness
- Myopathy

Anxiety: panic attack, chronic anxiety state

Anaemia, iron deficiency

Hyperventilation:
- Acidosis (renal failure, ketoacidosis, shock)
- Pharmacological cause
- Thyrotoxicosis

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47
Q

Drug classes and examples that improve outcomes in HFrEF?

A

Renin-angiotensin system inhibitors:
- ACEi - e.g. perindipril
- Angiotensin-receptor neprilysin inhibitor (ARNI) - sacubitril + valsartan [contraindicated in hypotension]
- ARBs (only if above not tolerated)

Heart failure-specific beta blockers e.g. metoprolol XR, bisoprolol - defer starting if there are clinical signs of congestion

Mineralocorticoid receptor antagonists e.g. spironolactone

Sodium-glucose co-transporter 2 (SGLT2) inhibitors e.g. empagliflozin

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48
Q

How would you classify heart failure?

A
  • Left ventricular ejection fraction 40% or less: HFrEF
  • Left ventricular ejection fraction 41 - 49%: mild HFrEF
  • Left ventricular ejection fraction 50% or more: HFpEF
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49
Q

What is a possible complication from the combination of a mineralocorticoid receptor antagonist and a renin-angiotensin system inhibitor?

A

In renal impairment, life-threatening hyperkalaemia

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50
Q

Non-pharmacological management strategies for heart failure?

A
  • Develop heart failure action plan
  • Fluid restriction of 1.5L/day
  • Daily weight monitoring (watching 2kg increase over 2 days)
  • Advise no-added-salt diet OR limit salt intake to <2g/day OR refer to dietitian for nutritional assessment
  • Arrange review in 48-72 hours for assessment of response to treatment
  • Refer to cardiac rehabilitation OR refer to multidisciplinary heart failure management program
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51
Q

Examination findings expected for systemic sclerosis?

A
  • Calcinosis - calcium deposits in the skin
  • Sclerodactyly - thickening and tightening of digit skin
  • Telangiectasia - dilation of capillaries
  • Decreased oral aperture OR perioral skin tightening OR microstomia
  • Digital ulcers OR pitted scars
  • Wrist crepitus OR tendon friction rub
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52
Q

What is systemic sclerosis, how is it classified and what are its key features?

A

Systemic sclerosis is an autoimmune inflammatory condition that results in widespread fibrosis and vascular abnormalities

It is subdivided according to the distribution of skin involvement
- Diffuse cutaneous systemic sclerosis
- Limited cutaneous systemic sclerosis (previously CREST syndrome) —- confined to the fingers, distal portion of the extremities, and the face

Limited cutaneous systemic sclerosis (CREST syndrome):
- Calcinosis
- Raynaud’s phenomenon
- Oesophageal dysmotility
- Sclerodactyly
- Telangiectasias

Key features:
- Skin thickening of the fingers and toes (sclerodactyly)
- Specific autoantibodies (anti-Scl70 or anti-centromere)
- Abnormal nail fold capillaries
- Internal organ fibrosis and/or vascular damage

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53
Q

Pulmonary manifestations of systemic sclerosis?

A
  • Interstitial lung disease (common)
  • Pulmonary hypertension (common - more associated with limited cutaneous systemic sclerosis)
  • Pulmonary embolism
  • Pleural effusion
  • Spontaneous pneumothorax
  • Airways disease
  • Aspiration pneumonia
  • Lung cancer
  • Drug-induced pneumonitis
  • Respiratory muscle weakness
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54
Q

What should all patients with systemic sclerosis be screened for regularly?

A
  • Interstitial lung disease - High resolution CT chest, pulmonary function tests
  • Pulmonary arterial hypertension - Transthoracic echocardiogram, ?NT proBNP

Annual screening

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55
Q

What is watermelon stomach and which autoimmune disease can it be a complication of?

A
  • Watermelon stomach: vascular ectasia (angiodysplasia) in the antrum of the stomach
  • Systemic sclerosis
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56
Q

Questions to ask when assessing patchy hair loss/alopecia areata and differentials?

A
  • Family history of alopecia areata
  • Cold/heat intolerance OR unintentional weight change (thyroid disorder)
  • [Past history of vitiligo OR autoimmune disease] or [Arthralgia OR other rashes] (symptoms of possible autoimmune disease)
  • Past history of dermatitis OR alopecia areata
  • Localised tingling OR itching in the preceding weeks (trichodynia)
  • Any new nail changes (pitting or ridging most common in alopecia areata) OR any hair loss noted in other areas (e.g. eyebrows, lashes - alopecia areata)
  • Excessive OR irresistible urge for hair pulling OR obsessive compulsive disorder (trichotillomania)
  • Significant stressors OR anxiety (telogen effluvium)
  • Preceding redness OR scaliness of scalp OR pet dogs or cats - Tinea capitis
  • Hair grooming behaviour - Traction alopecia
  • Use of hair chemicals/dye
  • Painless hair loss
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57
Q

What is alopecia areata and who gets affected?

A

Alopecia areata: autoimmune condition affecting hair follicles causing hair loss and typically presents with discrete bald patches on the scalp but can cause hair loss from all hair-bearing areas on the body

Peak incidence occurs in second and third decades and most patients experience onset before the fourth decade

Groups at increased risk of alopecia areata:
- Other autoimmune conditions such as vitiligo and thyroid disease
- A family history of alopecia areata

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58
Q

Differential diagnoses for alopecia areata?

A
  • Trichotillomania
  • Tinea capitis
  • Telogen effluvium
  • Androgenetic alopecia
  • Discoid lupus erythematosus
  • Secondary syphilis
  • Lichen planopilaris
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59
Q

Clinical features of alopecia areata?

A
  • Discrete oval/round patchy hair loss
  • Scalp is most affecte but can occur in: beard, eyebrows, eyelashes, other hair-bearing areas
  • “Exclamation point hairs” at periphery of bald patches: thick distally and thin proximally due to anagen arrest
  • Trichodynia (localised tingling or itching preceding hair loss)
  • Nail changes: pitting and ridging
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60
Q

What is trichotillomania and its causes?

A

Trichotillomania is a disorder characterised by an irresistible urge to remove or pull one’s own hair.

Causes - largely unknown:
- Obsessive compulsive disorder - correlation
- May be a coping mechanism triggered by stress or anxiety
- Commonly associated with other body-focused repetitive behaviours

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61
Q

What is tinea capitis and its symptoms?

A

Tinea capitis is a fungal infection of the scalp, involving both skin and hair. It is contagious and spread through contact with infected persons/animals and contaminated objects (fomites).

Symptoms: hair loss, dry scaly areas, redness, itch

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62
Q

Management of alopecia areata?

A

First line: Topical steroid options - needs potent or very potent strength for response:
- Betamethasone diproprionate 0.05% (Diprosone OR diprosone OV OR Eleuphrat) topically
- Mometasone furoate 0.1% (Elocon OR Novasone) topically
- Methylprednisolone aceponate 0.1% (Advantan +/- fatty ointment)

Duration: 3-4 months

Second line: intralesional corticosteroid injections (e.g. triamcinolone 5mg/mL)

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63
Q

What is required for patients considering Q fever vaccination?

A
  • Q fever skin test
  • Serum Q fever antibody test

Rationale: to identify people who have been previously infected with the Q fever organism and not aware of it. These people are likely to have adverse reactions to the vaccine, based on hypersensitivity to the organism

Patients previously infected with Q fever should not be vaccinated

64
Q

Questions to ask when working up “tiredness/sleepiness”?

A
  • Does he have trouble falling OR initiating sleep?
  • Does he have trouble staying OR maintaining sleep?
  • Does he work night shift?
  • Any recent international air travel? (Jetlag)
  • How many hours does he try to sleep at night? - assess for chronic sleep restriction
  • What time does he usually go to sleep? - assess for delayed sleep phase disorder
  • Does he have a history of sleep walking OR night terrors OR unusual behaviours? - assess for parasomnia
  • Does he have restless limbs during sleep? - restless limb syndrome
  • Does he fall asleep during the daytime OR take naps in the daytime? - assess for disorder of excessive daytime sleepiness
  • Does he have low mood OR anhedonia OR anxiety? - depression/anxiety
  • Does he use screens OR have exposure to blue light before bedtime? - assess for poor sleep hygiene
  • Does he drink coffee after midday?
  • Duration of the sleep problem and if it was triggered by an event?
65
Q

Physical exam findings you’d search for when assessing sleepiness?

A
  • Hypertension
  • Waist circumference >/= 100cm OR BMI >/= 35 OR neck circumference > 40cm
  • Malampati score >/= 3 OR reduced nasal patency OR retrognathia (OSA)
  • Blunted/restricted affect OR dishevelled appearance OR psychomotor retardation (part of mental state assessment)

Less relevant for sleepiness but more for tiredness:
- Brittle nails OR dry hair OR delayed reflexes (hypothyroidism)
- Subconjunctival pallor OR tachycardia (anaemia)

66
Q

Non-pharmacological management of sleep disturbance?

A
  1. Restrict in bed activity to sleeping or sex only OR reduce bedroom stimuli (ensuring environment is quiet and dark)
  2. Optimise light exposure (natural light exposure in the daytime, limit evening blue-light exposure) OR cessation of screen use at least 2 hours before bed
  3. Get out of bed if unable to sleep for 20 minutes
  4. Progressive muscle relaxation OR other relaxation activity before bed (meditation, visualisation, deep breathing) OR develop a 30 minute wind down routine e.g. warm drink or warm bath
  5. Referral to a psychologist for cognitive behavioural therapy for insomnia (CBTi)
  6. 30 minutes moderate intensity exercise 5 days a week during daytime OR avoid vigorous exercise within a few hours of bedtime
  7. Adopt a regular sleep-wake schedule even when not working (strengthen circadian rhythm)
  8. Avoid napping in the daytime OR avoid oversleeping
  9. Avoid large meals late in the evening
  10. Avoid caffeine in the evening OR minimise or eliminate caffeine, nicotine and alcohol
67
Q

Questions to ask for when assessing for kidney dysfunction (either AKI or CKD)?

A
  • Duration of ibuprofen use if any
  • Past history of hypertension
  • Past history of recurrent UTIs/pyelonephritis OR dysuria OR urinary frequency
  • Past history of autoimmune disease (secondary glomerular disease)
  • Recent URTI symptoms (sore throat, coryza, cough) - post-infectious glomerulonephritis
  • Unintentional weight loss OR night sweats OR new character of back pain (multiple myeloma)
  • Loin to groin pain OR gross haematuria (calculi, obstructive malignancy)
  • Recent diarrhoea OR nausea OR vomiting OR gastroenteritis - pre-renal cause of AKI but urea is usually elevated too
68
Q

Differentials for subacute kidney injury?

A

Pre-renal:
- Overdiuresis
- Decreased oral intake
- Diarrhoea
- Unreplenished insensible losses

Intrinsinc glomerular disease:
- Primary (Acute proliferative glomerulonephritis, rapidly progressive glomerulonephritis, membranous glomerulopathy, minimal-change disease, focal segmental glomerulosclerosis, IgA nephropathy, membranoproliferative glomerulonephritis)
- Secondary (paraneoplastic, drug-induced, part of systemic rheumatologic disease

Intrinsic tubular and interstitial disease:
- Interstitial nephritis
- Cast nephropathy in multiple myeloma

Obstructive nephropathy - substantial eGFR decrease suggests bilateral obstruction:
- Prostatic disease
- Intra-abdominal cancer
- Kidney stones
- Acute obstruction causes pain and gradual, severe obstruction may cause kidney dysfunction without obvious symptoms

69
Q

What are the most common causes of end stage kidney disease in Australia?

A
  • Diabetes
  • Glomerulonephritis
  • Hypertension
  • Polycystic kidney disease
70
Q

Which is more sensitive/accurate in detecting haematuria?
- Urine dipstick
- Urine microscopy

A

Urine dipstick

71
Q

Risk factors for urological malignancy?

A
  • Male
  • Age >40
  • History of macroscopic haematuria
  • Smoking
  • Pelvic irritation
  • Exposure to occupational chemicals, dyes or cyclophosphamide
72
Q

What is the gold standard for imaging of the urinary tract for the assessment of malignancy?

A
  • CT IVP
  • In younger patients <50 years or those with significant renal impairment, renal tract ultrasonography is sufficient

CT IVP is the modality of choice for older patients, those with risk factors for malignancy, and those with persistent haematuria

73
Q

Non-pharmacological management for chronic kidney disease?

A
  • Refer to nephrologist for further investigation of haematuria with renal impairment OR possible glomerulonephritis
  • Refer to urologist to exclude urological cause of haematuria (macroscopic)
  • Aim for weight loss towards BMI < 25 OR waist circumference < 80cm OR referral to dietitian to assist in weight loss towards BMI < 25 (CKD)
  • Advise to follow Dietary Approaches to Stop Hypertension (DASH) diet OR limit salt intake to <6g a day (hypertension)
  • Muscle strengthening exercise on at least 2 days a week OR aim for 150-300min/week of physical activity (physical activity)
  • Aim for BP < 130/80
74
Q

Differentials for haematuria?

A

Transient:
- Exercise induced
- Trauma
- Sexual intercourse
- Pelvic organ prolapse
- Vaginal atrophy

Malignant:
- Urothelial cancer
- Prostate cancer
- Renal cell carcinoma

Infectious/Inflammatory:
- Pyelonephritis
- Lower urinary tract infection
- Radiation cystitis
- Foreign body
- Urethral caruncle

Renal medical disease:
- Immunoglubilin A nephropathy
- Thin basement membrane disease
- Hereditary nephritis

Obstructive:
- Urolithiasis
- Benign prostatic hyperplasia/prostatic regrowth

75
Q

Definition of CKD?

A

Two options:
1. eGFR <60 for 3 months or more with or without evidence of kidney damage
2. Kidney damage with or without decreased eGFR for 3 months or more as evidenced by the following:
- Albuminuria
- Haematuria after exclusion of urological causes
- Structural abnormalities (e.g. kidney imaging)
- Pathological abnormalities e.g. renal biopsy

76
Q

Management of Chronic Kidney Disease?

A
  • Smoking: stop
  • Nutrition: DASH diet (dietary approaches to stop hypertension) - 4-5 vegetable servings/day, 2 or fewer servings of lean meats, poultry and fish, lots of grains [there’s more details]; limit salt <6g salt per day
  • Alcohol: limit 2 standards per day or less
  • Physical activity: 150 to 300 minutes of moderate physical activity; do muscle strengthening activities on at least 2 days each week
  • Obesity: ideal BMI < 25
77
Q

Management options for removal of a benign skin lesion?

A
  1. Shave excisional biopsy of lesion
  2. Curettage OR electrocautery of lesion
  3. Cryotherapy (only for thinner lesions)
78
Q

Differentials for unilateral nipple pain in the context of breastfeeding?

A
  • Suboptimal fit and hold/poor latch/nipple trauma
  • Nipple thrush
  • Strong infant sucking vacuum/infant biting nipple
  • Inappropriate use of breast pump (assess for inappropriate shield size or high suction)
  • Nipple bacterial infection
  • Nipple contact dermatitis OR eczema OR psoriasis
  • Blocked OR plugged milk duct OR milk blister
  • Nipple vasospasm
  • Mastitis
79
Q

Causes of nipple and breast pain in infant feeding?

A

Most common cause: poor positioning

Mechanical:
- Poor positioning and attachment
- Blocked duct
- Nipple variations e.g. flatness, retraction, inversion
- Inappropriate use of breast pump
- Infant with very strong sucking vacuum
- Infant biting nipple
- Anatomical variations in infant: e.g. high arched, flattened or bubble palate, disorganised sucking action, tongue-tie (ankyloglossia)

Physiological:
- Breast engorgement
- Nipple vasospasm
- Hormonal sensitivity e.g. during new pregnancy, ovulation, menstruation

Dermatological:
- White spot (blocked nipple pore)
- Eczema/dermatitis

Infective:
- Mastitis
- Bacterial infection
- Candida infection
- Herpes simplex

80
Q

Important elements on history for evaluation of breast pain during breastfeeding?

A
  • Onset of breast pain
  • Description of clinical setting
  • Feeding history
  • Previous yeast infections
  • Maternal breast surgeries e.g. breast reduction, piercings, implants, inverted nipples
  • Raynaud syndrome or autoimmune disease (associated with nipple vasoconstriction)
81
Q

Management of nipple thrush?

A

Baby:
- Miconazole 2% gel QID PO for 1 week then daily for 1-2 week (apply to cheeks and tongue with cotton bud or finger) OR
- Nystatin liquid QID PO for 7-14 days

Mum:
- Fluconazole 150mg every 2nd day for 3 doses THEN (nystatin 2 x 500,000 units TDS PO AND miconazole oral gel to nipples QID TOP)

82
Q

Signs and symptoms of thrush in:
- Nipple/areola?
- Breast?
- Baby?

A

Nipple/areola:
- Burning, stinging nipple pain which continues during and after the feed
- Nipples are often very tender to touch and even light clothing can cause pain
- Nipples appear pink and/or shiny and areola may be reddened, dry or slightly flaky
- Consider dermatitis if significant itching and/or rash
- Consider nipple vasospasm if exacerbated by cold and/or nipples blanch

Breast:
- Shooting, stabbing or deep aching breast pain
- Breast pain typically occurs after feeding or expressing. The let-down reflex may be more painful than normal
- Breasts will appear normal. If inflamed, consider mastitis

Baby:
- White oral plaques
- Assume baby is colonised with thrush if mother has evidence of nipple thrush

83
Q

Questions to consider with an infant vomiting after feeds and green frothy stool?

A
  • Frequency of vomit/vomiting at other times?
  • Volume of vomit OR projectile nature of vomit?
  • Blood in vomit OR bile in vomit?
  • Number of wet nappies per day?
  • Feeding duration OR feeding frequency OR feeding difficulties?
  • Malodorous urine OR cloudy urine OR cough? - infective symptoms
  • Fever
  • Blood in stool OR frequency of bowel motions?
  • Presence of rash
  • Timing of crying OR length/duration of crying
  • Social supports for mother OR mother’s mood OR how mother feels when infant is crying
  • Loss of weight OR stagnated weight gain
  • Perianal excoriation OR perianal ulceration
84
Q

Clinical characteristics of normal crying in babies?

A
  • Increases in the early weeks of life and peaks around 6-8 weeks of age and usually improves by 3-4 months of age
  • At 6-8 weeks of age, a baby cries on average 2-3 hours per 24 hours
  • Usually worse in late afternoon or evening but may occur at any time
  • Infant may draw up legs as if in pain, but there is no good evidence that this is due to intestinal problems

RED FLAGS:
- Sudden onset of irritability and crying
- Parental post-natal depression

Common non-pathological causes of crying:
- Excessive tiredness
- Hunger - more likely if there is poor weight gain

85
Q

Average sleep requirements for baby at:
- birth?
- 2-3 months?

A

At birth: 16 hours
At 2-3 months: 15 hours

86
Q

Differentials for unsettled or crying babies?

A
  • PURPLE crying
  • Non-IgE cow milk/soy protein allergy
  • Lactose overload/malabsorption: consider if infant has very frequent breastfeeds and frothy, watery diarrhoea with perianal excoriation
  • Gastro-oesophageal reflux disease (rare)
87
Q

When should you suspect non-IgE cow milk/soy protein allergy in infants?

A
  • Significant feeding problems that persist day and night
  • Frequent vomiting
  • Diarrhoea with blood or mucous
  • Poor weight gain
  • Wide-spread eczema
88
Q

Important differentials/causes to consider in an acute history of crying in a baby?

A
  • Raised ICP
  • Injury e.g. fracture
  • Incarcerated inguinal hernia
  • UTI
  • Hair tourniquet
  • Corneal abrasion
89
Q

What is PURPLE crying?

A

P - peak of crying: peaks at 2 months and then decreases over 3-5 months
U - unexpected: can come and go without reason
R - resists soothing: may not stop no matter what you try
P - pain-like face: may look like they’re in pain even when not
L - longlasting: can last 5 hours a day or more
E - evening: may cry more in the late afternoon or evening

90
Q

How do you treat cows milk allergy?

A
  • Remove cows milk and cows milk based products from maternal diet
  • 0-6 months: extensively hydrolysed formula
  • 6-12 months: soy formula
  • Note: lactose free products still contain cows milk protein. Lactose intolerance and cows milk allergy are different
  • Lactose intolerance: intolerance to the sugar lactose
  • Cows milk allergy: immune reaction triggered by protein in cows milk
91
Q

Management of lactose overload?

A
  • Block feeding (using one breast within a 4 hour period and then alternate to reduce the speed that the breast makes milk; usually only done for a few days) OR offering one breast at a time until empty: aim to down regulate milk production so infants receive more of the cream based milk at the end of the feed and stay fuller
  • Referral to lactation consultant
  • Refer to Australian Breastfeeding Association
  • Acknowledge impact of child’s crying on mother’s mental health
92
Q

When to suspect lactose overload?

A
  • Unsettled
  • Adequate to large weight gains
  • Usually pass urine more than 10 times per day
  • Many bowel motions in 24 hours
  • Faeces may be green and frothy or explosive with perianal excoriation
93
Q

Why does lactose overload occur?

A

Cream/fat that is usually found at the end of the breastmilk supply slows down the breastmilk transit through the gut to allow lactose to be broken down

94
Q

What questions should be asked when evaluating restricted eating?

A
  • Are animal products OR meat consumed? - higher risk of micronutrient deficiencies if not consuming animal products
  • Dislike foods with certain textures?
  • Previous allergic reaction to any foods / history of vomiting OR rash OR abdominal pain OR swelling of his face after meals? - food allergy
  • Does he have difficulty making friends OR socialising OR maintaining eye contact / does he have difficulty coping with change in routines / does he get easily upset by certain sounds OR from overstimulation - exploring possibility of underlying autism
  • Does he have constipation OR altered bowel habits OR blood/mucous in stool - gastrointestinal symptoms of possible underlying disorder
95
Q

Which groups of children may have restricted food eating patterns that may place them at risk of micronutrient deficiency?

Note: diet highly limited in variety e.g. missing food groups, less than 10 foods/food types regularly consumed, minimal meal to meal variability

A
  • Neurodevelopmental conditions including autism spectrum disorder
  • Avoidant restrictive food intake disorder (ARFID)
  • Multiple food allergies
  • Elective dietary restrictions due to cultural, religious or environmental reasons
96
Q

What are some risk factors for deficiency in Vitamin A (retinol) in children?

A
  • Malabsorption e.g. exocrine pancreatic insufficiency, chronic liver disease, short bowel syndrome, inflammatory bowel disease
  • Maternal deficiency
  • Some refugee populations
97
Q

What are some risk factors for deficiency in Vitamin B1 (thiamine) in children?

A
  • White rice-based diets
  • Malabsorption
  • Some refugee populations
98
Q

What are some risk factors for deficiency in Vitamin B3 (niacin) in children?

A
  • Corn based diets
  • Malabsorption
99
Q

What are some risk factors for deficiency in Vitamin B9 (folate) in children?

A
  • Lack of fresh food in diet
  • Malabsorption
  • Medications e.g. phenytoin, phenobarbital, methotrexate, long term NSAID use
100
Q

Clinical features of deficiency in Vitamin A (retinol)?

A
  • Xerophthalmia: night blindness, dry conjunctiva, corneal ulceration, blindness
  • Dry skin and pruritus
  • Increased susceptibility to infection
  • Poor growth
101
Q

Clinical features of deficiency in Vitamin B1 (thiamine)?

A
  • Fatigue, irritability, apathy, nausea, abdominal discomfort
  • Dry beriberi (symmetric peripheral neuropathy)
  • Wet beriberi (cardiac failure)
  • Wernicke encephalopathy: confusion, reduced consciousness, ataxia, ophthalmoplegia
  • Korsakoff syndrome: confusion, amnesia
102
Q

Clinical features of deficiency in Vitamin B3 (niacin)?

A
  • Anorexia, vomiting, abdominal pain
  • Glossitis, cheilitis
  • Pellagra: triad of dermatitis, diarrhoea and confusion
  • Late symptoms include apathy, weakness, headache, confusion, irritability, anxiety, tremor, depression
103
Q

Clinical features of deficiency in Vitamin B9 (folate)?

A
  • Clinical signs of anaemia
  • Macrocytia anaemia and hyper-segmented neutrophils on full blood count
  • Glossitis, oral ulcers
  • Fatigue, slow growth
104
Q

What are some risk factors for deficiency in Vitamin B12 (cobalamin) in children?

A
  • Vegan and vegetarian diet
  • Some refugee populations
  • Gastrointestinal disease
  • Exclusively breastfed infants of mothers with vitamin B12 deficiency
105
Q

What are some risk factors for deficiency in Vitamin C (ascorbic acid) in children?

A
  • Diets without fruit and vegetables
106
Q

What are some risk factors for deficiency in Vitamin D (calciferol) in children?

A
  • Lack of skin exposure to sun
  • Dark skin
  • Obesity
  • Liver/renal failure
  • Gastrointestinal disease
  • Exclusively breastfed infants of mothers with vitamin D deficiency
107
Q

What are some risk factors for deficiency in Vitamin E (alpha-tocopherol) in children?

A
  • Malabsorption
108
Q

What are some risk factors for deficiency in Vitamin K (phytomenadione) in children?

A
  • Malabsorption
109
Q

What are some risk factors for deficiency in copper in children?

A
  • Prolonged total parenteral nutrition
  • Malabsorption
110
Q

What are some risk factors for deficiency in iodine in children?

A
  • Extremely rare unless immigrated from high-risk areas e.g. inland Asia or Africa
111
Q

What are some risk factors for deficiency in iron in children?

A
  • Vegetarian or vegan diet
  • High milk intake
  • Gastrointestinal disease
  • Heavy menstrual loss
  • Maternal iron deficiency
  • Prematurity
  • Low birth weight
112
Q

What are some risk factors for deficiency in selenium in children?

A
  • Prolonged total parenteral nutrition
113
Q

What are some risk factors for deficiency in zinc in children?

A
  • Malabsorption
  • Total parenteral nutrition
  • Vegetarian-diet
114
Q

Clinical features of deficiency in Vitamin B12 (cobalamin)?

A
  • Clinical signs of anaemia
  • Macrocytic anaemia and hyper-segmented neutrophils on full blood count
  • Irritability, developmental delay, developmental regression, involuntary movements, peripheral neuropathy
  • Glossitis, oral ulcers
  • Skin changes e.g. hyperpigmentation, vitiligo
115
Q

Clinical features of deficiency in Vitamin C (ascorbic acid)?

A

Scurvy
- Skeletal fractures and joint pain
- Poor wound healing
- Fatigue
- Weight loss
- Gingival inflammation with gum bleeding
- Petechiae
- Ecchymosis
- Purpura
- Dry eyes and mouth
- Corkscrew hair

116
Q

Clinical features of deficiency in Vitamin D (calciferol)?

A
  • Rickets: lower limb deformities, enlargement of wrists and ankles, protruding abdomen, delayed gross motor development, generalised musculoskeletal pain
  • Hypocalcaemia: may present with seizures and tetany
117
Q

Clinical features of deficiency in Vitamin E (alpha-tocopherol)?

A
  • Decreased muscle mass
  • Weakness, unsteady gait
118
Q

Clinical features of deficiency in Vitamin K (phytomenadione)?

A
  • Excessive bleeding/bruising
119
Q

Clinical features of deficiency in copper?

A
  • Anaemia
  • Peripheral neuropathy
120
Q

Clinical features of deficiency in iodine?

A
  • Goitre
  • Other signs and symptoms of hypothyroidism
121
Q

Clinical features of deficiency in iron?

A
  • Clinical signs of anaemia: pallor, irritability, anorexia, fatigue
  • Microcytic anaemia on full blood count
  • Behavioural disturbance, impaired cognitive function, decreased memory, impaired learning and concentration
  • Pica (eating non-food items)
122
Q

Clinical features of deficiency in selenium?

A
  • Cardiomyopathy
  • Myositis
  • Shortened fingers and toes
123
Q

Clinical features of deficiency in zinc?

A
  • Acrodermatitis enteropathica: periacral, periorificial dermatitis, diarrhoea, alopecia
  • Depressed mood, apathy, and emotional disturbance in older children
124
Q

First line blood investigations for suspected micronutrient deficiency (even if asymptomatic)?

A
  • FBC
  • EUC, LFT, CMP
  • Iron studies
  • Vitamin A (light sensitive, cover tube with foil)
  • Thiamine
  • Folate and Vitamin B12
  • Vitamin C
  • Vitamin D
  • Zinc
125
Q

Second line investigations for suspected micronutrient deficiency (risk factors or clinical features identified)?

A

Blood:
- Coagulation profile (marker of vitamin K deficiency)
- Thyroid function test (marker of iodine deficiency)
- Vitamin E
- Selenium
- Copper

Urine:
- Vitamin B3

126
Q

Investigations required for children with more than 1 risk factor for vitamin D deficiency but asymptomatic?

A
  • Vitamin D
  • Calcium
  • Phosphate
  • ALP
  • If low calcium intake, symptoms or multiple risk factors: PTH
127
Q

What education points are required when prescribing oral liquid iron supplements?

A
  • Drink through a straw OR brush teeth after administration (baking soda to remove stains) OR liquid iron may stain teeth
  • Take with vitamin C OR orange juice to increase absorption OR do not take with milk due to decreased absorption with dairy, calcium, antacids, tea and coffee
  • Side effects can include nausea, black stools and constipation
  • Iron supplementation should be taken for 3-6 months
128
Q

What is the recommended dose of iron to treat iron deficiency and iron deficiency anaemia?

A

3-6mg/kg/day

129
Q

When is oral iron best absorbed?

A

On an empty stomach either:
- 1 hour before food OR
- 2 hours after food

130
Q

What are some non-pharmacological management strategies for fussy eating?

A
  • Offer a variety of foods from the core food groups (fruits, vegetables, meats or alternatives, grains and dairy)
  • Offer the same meal that everyone else is eating
  • Offer nutritious meals and snacks 5-6 times per day
  • Allow 20-30 minutes OR adequate time for mealtimes
  • Provide small portions to avoid overwhelming child
  • Eat together as a family
  • Avoid screens OR toys OR distractions at meal times
  • Praise child during each meal OR use positive reinforcement
  • Keep meal times relaxed
  • If child refuses to eat a meal, avoid offering an alternative food
  • Try different foods often/repeatedly - children may need to be offered a new food more than 10 times before accepting it
  • Offer new foods alongside accepted foods
  • Avoid milk OR fruit juice OR soft drinks between meals
131
Q

List examination findings you’d search for when assessing for alcohol-associated fatty liver disease and liver cirrhosis?

A
  • Elevated wasit circumference OR elevated body mass index
  • Spider naevi/angiomata - dilated superficial blood vessels
  • Palmar erythema
  • Dupuytren’s contracture - finger contractions caused by thickening of the palmar fascia
  • Leukonychia OR clubbing (nail changes)
  • Gynaecomastia - enlarged breast tissue
  • Hepatomegaly
  • Splenomegaly
  • Caput medusae - engorged epigastric vessels
  • Ascites OR shifting dullness
  • Pleural effusion
  • Metabolic flap OR asterixis
  • Testicular atrophy
  • Jaundice OR scleral icterus - hyperbilirubinaemia
  • Confusion - sign of hepatic encephalopathy
  • Incoordination OR gait disturbance
  • Muscle twitching OR myoclonus
  • Slurred speech
132
Q

When interpreting Hepatitis B serology, what does this mean?
- HBsAg: negative
- Anti-HBc: negative
- Anti-HBs: negative

A

Susceptible (consider vaccination)

133
Q

When interpreting Hepatitis B serology, what does this mean?
- HBsAg: negative
- Anti-HBc: positive
- Anti-HBs: positive

A

resolved HBV infection

134
Q

When interpreting Hepatitis B serology, what does this mean?
- HBsAg: negative
- Anti-HBc: negative
- Anti-HBs: positive

A

Vaccinated

135
Q

When interpreting Hepatitis B serology, what does this mean?
- HBsAg: positive
- Anti-HBc: positive
- IgM anti-HBc (high titre): positive
- Anti-HBs: negative

A

acute HBV infection

136
Q

When interpreting Hepatitis B serology, what does this mean?
- HBsAg: positive
- Anti-HBc: positive
- IgM anti-HBc (high titre): negative
- Anti-HBs: negative

A

Chronic HBV infection

137
Q

How would you monitor for hepatocellular carcinoma in patients with Hepatitis B at high risk for development of HCC?

A

Q6monthly liver ultrasounds and serum alpha-fetoprotein

138
Q

Which Hepatitis B positive patients are at high risk of developing hepatocellular carcinoma?

A
  • Patients with cirrhosis
  • ATSI > 50 yo
  • Asian male > 40 yo
  • Asian female > 50 yo
  • Sub-Saharan African patients > 20 yo
  • Patients with a family history of hepatocellular carcinoma in a first degree relative
139
Q

What non-pharmacological management advice would you give for a patient with Hepatitis B?

A
  • Condoms should be used for all types of intercourse
  • Alcohol cessation
  • Smoking cessation
  • Confirm contact tracing of sexual partners has occurred / ensure sexual partners are immunised against Hepatitis B / Ensure household contacts are immunised against hepatitis B
140
Q

Questions on history for the evaluation of acute ear ache in children?

A
  • Fever
  • Otorrhoea
  • Nausea OR vomiting
  • Headache / neck stiffness / altered mental state / photophobia - symptoms of meningitis
  • Coryzal symptoms / Sore throat
  • ATSI descent
  • Recent swimming history - otitis externa
  • Recent air travel - barotrauma
  • History of direct ear trauma OR foreign body insertion into ear
141
Q

What is the difference between acute otitis media and otitis media with effusion?

A

Acute otitis media - acute onset of either:
- Bulging of the tympanic membrane AND/OR
- Otorrhoea (provided acute diffuse otitis externa is excluded)

Acute otitis media: infected effusion
Otitis media with effusion: non-infected effusion

Signs and symptoms that support AOM instead of OMWE include:
- acute onset of pain: tugging, holding or rubbing the ear
- fever
- irritability
- poor feeding
- bulging tympanic membrane

142
Q

Management of acute otitis media in average risk children?

A
  • Paracetamol PO OR ibuprofen PO
  • Review in 48 hours to check if symptoms are improving
  • Advise that antibiotics are not currently indicated
  • Review in 3 months time for resolution of middle ear effusion
143
Q

When treating acute otitis media, what are the red flags or groups who should be treated with antibiotics earlier?

A
  • < 6 months old
  • Children younger than 2 years with bilateral infection
  • Immunocompromised
  • ATSI
  • Systemically unwell (e.g. lethargic, pale, very irritable)
  • Single hearing ear
  • Child has a cocklear implant
  • Possible suppurative complication
144
Q

How would you manage inappropriate request for antibiotics in acute otitis media?

A
  • Reassurance that acute otitis media is a self-limiting condition OR reassurance that severe complications are rare with or without antibiotics
  • Advise that the symptoms of acute otitis media usually last 2 to 3 days regardless of if antibiotiucs are used
  • Antibiotics do not improve pain at 24 hours
  • Antibiotics only shorten the duration of symptoms by about 12 hours total
  • For every 100 children treated with antibiotics, 7 will experience adverse effects OR adverse effects may include diarrhoea OR rash OR clostridium difficle OR antibiotic resistance
  • If there is no improvement in 48 hours then antibiotics can be trialled
145
Q

What questions would you ask on evaluation of hearing loss?

A
  • Otorrhoea?
  • Otalgia?
  • Vertigo OR dizziness OR dysequilibrium?
  • Nature of tinnitus - pulsatile or constant, pitch?
  • Previous exposure to loud noises
  • Previous head trauma?
  • Previous ear surgery?
  • Previous cerumen OR ear wax compaction OR ear syringing?
  • Past recurrent ear infections?
  • Family history of hearing disorders?
  • Facial numbness - acoustic neuroma
  • Aural fullness - Meniere’s disease
  • Associated headache OR aura - vestibular migraine?
146
Q

What would you look for on examination for a patient with hearing loss - aside from Rinne and Weber testing?

A
  • Otoscopy or pneumatic otoscopy - for impacted cerumen, tympanic membrane perforation, middle ear effusion/infection
  • Reduced sensation over face trigeminal nerve distribution OR temporalis/masseter muscle wasting OR impaired corneal reflex - CN V examination
  • Facial asymmetry OR facial droop - CN VII examination
  • Abnormal head thrust test OR vestibulo-ocular test - CN VIII vestibular component
147
Q

Differentials for sensorineural hearing loss?

A
  • Presbycusis OR age-related sensorineural heairng loss
  • Noise-induced hearing loss
  • Hereditary sensorineural hearing loss
  • Meniere’s disease
  • Acoustic neuroma OR meningioma
  • Cerebrovascular ischaemia/accident
148
Q

Which diagnostic investigations are always indicated when investigating CKD?

A
  • Renal tract ultrasound
  • Repeat (within 1 week) serum EUC and albumin
  • FBC, CRP, ESR
  • Urine ACR
  • Fasting lipids and glucose
  • Urine microscopy (for dysmorphic red cells, red cell casts or crystals)
149
Q

What investigations are required when investigating CKD and signs of systemic disease (e.g. rash, arthritis, features of connective tissue disease, pulmonary symptoms or deteriorating kidney function)?

A
  • Anti-glomerular basement membrane antibody
  • Anti-neutrophil cytoplasmic antibody
  • Anti-nuclear antibodies
  • Extractable nuclear antigens
  • Complement studies
150
Q

What investigations are required when investigating CKD and risk factors for HBV, HCV, HIV (these conditions are associated with an increased risk of glomerular disease)?

A

HBV, HCV, HIV serology

151
Q

What investigations are required when investigating CKD and age >40 years and possible myeloma

A

serum and urine protein electrophoresis

152
Q

Differentials for proteinuria?

A
  • Diabetic nephropathy
  • Hypertensive nephropathy
  • Multiple myeloma
  • Nephrotic syndrome / membranous nephropathy / minimal change disease / focal segmental glomerulosclerosis
  • Polycystic kidney disease
  • Amyloidosis
  • Congestive heart failure
153
Q

What are some factors other than CKD known to increase urine albumin excretion?

A
  • Urinary tract infection
  • High dietary protein intake
  • Congestive cardiac failure
  • Acute febrile illness
  • Heavy exercise within 24 hours
  • Menstruation
  • Genital discharge or infection
  • Drugs (especially NSAIDs)
154
Q

What questions would you ask on history when evaluating recurrent epistaxis and easy bruising?

A
  • Bleeding from mouth OR gums / bleeding from rectum OR malaena OR haematemesis / Haematuria
  • History of menorrhagia OR number/frequency of pad/tampon changes a day
  • Previous post procedural (e.g. dental) bleeding complications OR need for blood transfusions
  • Family history of bleeding disorders
  • Over the counter NSAID use OR intranasal spray use OR supplements
  • Weight loss OR night sweats - haematological malignancy
  • Alcohol use history
  • Cold intolerance OR weight gain OR hair thinning - acquired Von Willebrand’s disease from hypothyroidism
  • Cocaine use
  • Nose-picking OR previous trauma to nose
155
Q

What physical exam findings would you search for when evaluating easy bleeding?

A
  • Petechiae OR purpura OR ecchymoses
  • Telangiectasias - hereditary haemorrhagic telangiectasia
  • Oropharyngeal exam for mucocutaneous bleeding
  • Splenomegaly
  • Lymphadenopathy - haematological malignancy
  • Spider naevi OR jaundice OR hepatomegaly OR asterixis - stigmata of liver disease
  • Palmar crease pallor OR conjunctival pallor
156
Q

Differentials for prolonged prothrombin time (PT) and/or a prolonged activated partial thromboplastin time (aPTT)?

A

Von Willebrand disease
Haemophilia (inherited OR acquired)
- Haemophilia A = factor VIII deficiency
- Haemophilia B = factor IX deficiency
- Haemophilia C = factor XI deficiency (very rare)

157
Q
A

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