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Practice Exams > 10/10/21 > Flashcards

10/10/21 Flashcards

1
Q

How is uric acid eliminated from the body?

A

Uric acid is eliminated by the kidneys (2/3) and the gut (1/3).

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2
Q

What are the main risk factors for gout? (5 categories)

A
  • *Increased intake of Dietary Purines**
  • Purine-Rich foods → Meat and Seafood
  • Alcohol → Beer and Spirits
  • Fructose-sweetened Drinks
  • *Disorders involving high cell turnover**
  • haematological malignancies
  • severe psoriasis
  • *Drugs that inhibit the renal excretion of urine acid**
  • thiazide diuretics, loop diuretics, cyclosporin
  • *Co-morbidities**
  • HTN, CKD, Dyslipidaemia, T2DM, Obesity
  • *Catabolic State**
  • Sepsis
  • Dehydrated
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3
Q

Key Principles in the Management of Gout (5 points)

A
  1. Rapid symptom relief for acute attacks
  2. Life-long urate lowering therapy - treat to target approach
  3. Prophylaxis for gout flares when starting or increasing urate-lowering therapy
  4. Address modifiable risk factors for gout
  5. Patient Education re: risk factors + lifestyle changes that can be made
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4
Q

How would you prescribe urate-lowering therapy for gout? Be Specific

A

Allopurinol 50mg PO daily for 4/52, then increase by 50mg every 2-4 weeks to achieve target serum uric acid concentration, up to maintenance maximum of 900mg daily

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5
Q

Why do you need flare-prophylaxis in managing gout?Be specific in how you would prescribe this.

A
  • when starting or increasing urate-lowering therapy → as this is associated with a high risk of a gout flare
    1. colchicine 500 micrograms PO, once or twice daily
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6
Q

How do you classify non-severe PID?

A
  • No severe pain, no fever, no systemic features (tachycardia, vomiting), no sepsis or septic shock and no suspected tubo-ovarian abscess
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7
Q

How do you treat non-severe PID? Be Specific.

A
  1. Ceftriaxone 500mg in 2ml of 1% lidocaine intramuscularly AND Metronidazole 400mg PO BD for 14/7 AND EITHER
    • Doxycycline 100mg PO BD for 14/7
    • For patients who are pregnant, breast-feeding or likely to be non-adherent → Azithromycin 1g PO stat and repeated 1 week later
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8
Q

What are the clinical features of nail psoriasis? (6 clinical features - describe them)

A

Nail Pitting -> Superficial depressions in the nail plate

Leukonychia -> 1-2mm wide white bands that involve more than one nail and are due to the internal desquamation of the parakeratotic cells

Oil Spots or Salmon Patches -> Translucid and Discoloured red-yellow patches located on the nail plate

Onycholysis -> Separation of the nail plate from the nail bed

Subungal Hyperkeratosis -> Yellow and oily nails that result from raising the nail plate off the nail bed as a result of deposition of keratinocytes

Splinter Haemorrhages -> Small, linear structures, 2-3mm long, at the distal end of the nail plate

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9
Q

How do you treat nail psoriasis?

A
  • apply to nail matrix and hyponychium for months or years

1. calcipotriol solution BD

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10
Q

What condition is associated with nail psoriasis?

A

Psoriatic Arthritis - nail psoriasis is present in 80-90% of patients with psoriatic arthritis

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11
Q

What is and how common is Hypertrophic Cardiomyopathy? At what age is it commonly diagnosed and what is the mortality rate?

A

Relatively common, inherited cardiac disease with a prevalence 1/500

Presence of otherwise unexplained thickening (hypertrophy) of the muscular wall of the left ventricle

Onset fo HCM-induced LVH typically occurs during adolescence

Annual mortality rate of HCM is about 1% and it is the most common cause of sudden cardiac death in young athletes

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12
Q

What is the most common way patients with HCM present?

A

MOST COMMON SYMPTOM - EXERTIONAL DYSPNOEA

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13
Q

What are the risk factors for Hypertrophic Cardiomyopathy and what does this mean for the management of this patient?

A

Indications for insertion of an implantable cardioverter defibrillator (ICD) for primary prophylaxis

  • Family History of SCD
  • Unexplained Syncope
  • Documented non-sustained ventricular tachycardia
  • Maximal left ventricular wall thickness ≥ 30mm
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14
Q

Discuss management of Hypertrophic Cardiomyopathy. (5 points)

A
  1. Lifestyle Modification
    • adolescents with HCM → cease competitive sport as this can prevent SCD
    • in most adolescents → benefits of regular non-competitive exercise outweigh the risks
  2. Pharmacotherapy
    • beta-blockers (metoprolol, atenolol) and verapamil are indicated in SYMPTOMATIC patients
  3. Endocarditis Prophylaxis
    • NO evidence for routine ABx prophylaxis
  4. Septal Reduction Therapy
    • surgical septal myomectomy is considered in adolescent with disabling symptoms because of LV outflow tract obstruction
  5. Implantable Cardioverter-Defibrillator Insertion
    • as above → if ≥ 1 risk factor → consider ICD implantation
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15
Q

After an infection, when does reactive arthritis present? Also what kind of infections are common for reactive arthritis to develop?

A

Form of arthropathy → non-septic arthritis and often sacroiliitis develop after a urogenital infection (usually chlamydia) or an enteric infection (Salmonella or Shigella)

  • usually presents 1-3 weeks after the infection
  • usually presents in males (20-40yo) after a urogenital infection
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16
Q

What is the diagnostic triad associated with reactive arthritis?

A

Can’t See - conjunctivitis
Can’t Pee - genitourinary inflammation (Urethritis)
Can’t Climb a Tree - arthritis
C..Rash - keratoderma blennorrhagica

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17
Q

How doe the arthritis component of reacticve arthritis present? When, where and common specifically.

A
  • inflammatory peripheral arthropathy with an asymmetrical oligoarticular distribution, predominantly affecting the lower limbs
    • Dactylitis → inflammation of the whole finger or toe is a common features
    • Enthesitis → inflammation at the site of tendon or ligament attachment to bone
  • Develop at least 1 week after an illness
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18
Q

How do you manage reactive arthritis? (infection, mild vs severe)

A

Treat active infection as indicated
- if chlamydia → treat with doxycycline 100mg PO BD for 7/7

Depends on the severity and extent of joint involvement

  1. For Mild to Moderate → an NSAID PO
  2. For Severe:
    1. Intra-articular corticosteroid injection (if a small number of accessible joints are involved)
    2. Prednisolone 10-50mg PO, daily until symptoms improve, then taper dose to stop
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19
Q

History of Rheumatoid Arthritis? (5 points)

A
  • Joint Pain + Swelling and/or Fever
  • Morning Stiffness >30mins
  • Previous Episodes
  • Family History of RA
  • Systemic Flu-Like Features and Fatigue
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20
Q

Examination Findings in Rheumatoid Arthritis (3 points)

A
  • ≥3 tender and swollen joint areas
  • symmetrical joint involvement in hands and/or feet
  • Positive squeeze at MCP or MTP joints
21
Q

Joint distribution of RA in the hands - which joints are involved?

A

MCP + PIP joints, DIP joints spared

22
Q

How do you classify Acute Kidney Injury? What are some causes of each category? (specifically 5 intrarenal causes)

A 
### Pre-Renal → Renal Hypoperfusion
- Hypovolaemia, - Sepsis, - Reduced effective arterial volume → heart failure, decompensated liver failure

Intra-renal

  • Acute Glomerulonephritis
  • Acute Interstitial Nephritis
  • Acute Tubular Necrosis (due to prolonged renal hypoperfusion)
  • Vasculitis
  • Nephrotoxins
### Post-Renal → Obstruction of the Urinary Tract
- Kidney stones, - Urethral stricture, - Prostatic hypertrophy, - Malignancy
23
Q

History questions associated with Acute Renal Failure. (5 points - be specific about medications)

A
  • Symptoms of acute illness - vomiting, diarrhoea and infection
  • Systemic symptoms - rash or arthralgia (suggestive of vasculitis or rheumatological condition)
  • Recent change in medications in particular NSAIDs, PPI and ABx: can be exacerbated by antihypertensive (ACEi, ARB), diuretics or NSAIDs. PPI → can cause interstitial nephritis
  • Flank Pain - kidney stones
  • Obstructive Lower Urinary Tract Symptoms
24
Q

Clinical Features of Blue Toe Syndrome (3 points)

A
  • Blanching occurs in first stages of blue toe syndrome → sluggish flow of desaturated blood results in the temporary obstruction of blood flow
  • Pain in the affected blue toe or toes is acute onset and usually occurs at rest
  • Affected toes are cold compared to unaffected parts of the foot. Foot pulses may be normal and rest of foot and other toes will be warm.
25
Q

Complications of Blue Toe Syndrome. Usual prognosis if mild. If untreated?

A
  • Mild Forms have good prognosis and subside without sequelae
  • Patients with untreated blue toe syndrome from embolisation can suffer from further emboli in the subsequent weeks
26
Q

Definition of Unstable Angina (3 points)

A
  1. Rest Angina - generally lasting longer than 20 mins
  2. New Onset Angina that markedly limits physical activity
  3. Increasing Angina → frequent, lasts longer or occurs with less exertion than previous angina
27
Q

Absolute contraindications for Cardiac Stress Testing. (6 points)

A
  • Acute Myocardial Infarction → including new LBBB
  • High Risk Unstable Angina
  • Symptomatic Severe Aortic Stenosis
  • Uncontrolled Arrhythmia causing symptoms or haemodynamic instability
  • Unstable Heart Failure
  • Acute PE or Acute Aortic Dissection
28
Q

Otitis Externa: Clinical Features on History (6 points)

A
  • ear pain
  • conductive hearing loss
  • feeling of fullness (blockage) or pressure
  • itchiness
  • tenderness on manipulation of the tragus or auricle
  • +/- discharge
29
Q

Non-pharmacological management of otitis externa (2 points)

A
  1. External ear canal must be kept as dry as possible
  2. Discharge and debris must be removed from the ear canal by dry aural toilet not by syringing with water.
    • Dry Aural Toilet can be performed by patient or carer by dry mopping the ear with rolled tissue spears or similar, 6 hourly until the external canal is dry
30
Q

What is the pharmacological option of choice in treatment of otitis externa? Explain factors involved in choosing pharmacological management of otitis externa.

A

Combination Corticosteroid + Anti-Microbial Ear Drops

- The choice depends on whether the tympanic membrane has been perforated or not and if fungal infection if suspected

31
Q

If not concerned re: fungal infection, what are the options of treatment of otitis externa?

A
  • Sofradex: dexamethaxone + framycetin + gramicidin 0.05% + 0.5% + 0.005% ear drops, 3 drops instilled into the affected ear, 3 times daily for 7 days
  • OR Locorten Vioform: flumethasone + clioquinol 0.02% + 1% ear drops, 3 drops instilled into the affected ear, twice daily for 7 days
32
Q

if concerned re: fungal infection, what are the treatment options of otitis externa?

A
  • Locorten Vioform: flumethasone + clioquinol 0.02% + 1% ear drops, 3 drops instilled into the affected ear, twice daily for 7 days
  • OR Trimacolone + Neomycin + Gramicidin + Nystatin 0.1% + 0.25% + 0.025% + 100000 units/ml ear drops, 3 drops instilled into affected ear, 3 times daily for 3 to 7 days
33
Q

If the ear drops cannot be administered because the canal is occluded, what can be done?

A

If ear drops cannot be administered because the canal is occluded → insert a wick into the occluded ear as this can facillitate ear drop administration

34
Q

Following treatment of otitis externa, can the patient return to swimming? What advice do you need to give a patient with otitis externa?

A
  • Advise patient to keep ear dry during and for 2 weeks after treatment → use ear plugs + shower or bathing cap during showering and swimming.
35
Q

Clinical Diagnosis of Henoch-Schonlein Purpura.

A
  • Rash + ≥1 of:
    • Arthritis/Arthralgia (50-75%)
    • Abdominal Pain (50%)
    • Nephritis (25-50%)
36
Q

Describe the rash of Henoch-Schonlein Purpura.

A

Palpable purpura, petechiae and ecchymoses.
May be preceded by urticarial, erythematous, maculopapular or bullous skin lesions

Usually symmetrical
Located on gravity/pressure-dependent areas → buttocks and lower limbs in ambulatory children

37
Q

Common abdominal complication of Henoch Schonlein Purpura?

A

intussusception

38
Q

What complication needs to routinely reviewed in the context of Henoch-Schonlein Purpura? How does the follow-up schedule look for patients with HSP?

A
  • Regular GP review to identify subsequent renal involvement
  • If initial urinalysis is normal or only reveals microscopic haematuria → review clinically and check BP + urinalysis:
    • Weekly for the first month after disease onset
    • Fortnightly from weeks 5-12
    • Single reviews at 6 and 12 months
    • Return to weekly reviewed if clinical disease flare or additional signs of renal involvement
    • If NAD at 12 months - nil further follow-up required
39
Q

Timeline of Impetigo - clinical features

A

Start as blisters that burst and become weepy, before being covered with a crust

  • start with a blister or group of blisters → blister then bursts leaving a patch of red, wet, weepy skin
  • sore usually becomes coated with a tan or yellowish crust → looks like it was covered in honey
40
Q

Pathogen responsible for Impetigo - endemic vs non-endemic setting.

A

Non-Endemic Settings → S. Aureus

Endemic Settings → S. pyogenes (MRSA)

41
Q

What is the role of skin swabbing in impetigo? When do you need to swab?

A
  • Mild Impetigo → NO swab prior to empirical treatment but should have swab taken for susceptibility testing if no response to empirical treatment. However for more severe disease → require a skin swab for culture and susceptibility before empirical antibiotic therapy.
42
Q

Non-pharmacological Treatment of Impetigo? including prevention of impetigo and keeping child at home (3 points)

A
  • Daily 10 minute bleach bath → reduce amount of bacteria on the skin + reduce the risk of the impetigo spreading
  • Important to remove the crusts from the sores, to allow any oiintments treating the sores to reach the infection properly. Use a unused, wet disposable cloth to wipe the crusts away.
  • Keep child home from childcare, kindergarten or school until 24hours after starting medical treatment → can be around children at this stage but need to cover up their sores completely with dressings.
43
Q

Pharmacological Treatment of Impetigo - non-endemic setting. (2 points + 2 bonus for hypersensitivity to penicillin)

A

Non-Endemic + Localised Skin Sores

  • Mupirocin 2% ointment or cream topically to crusted areas, 8 hourly for 5 days
    Non-Endemic + Multiple Skin Sores or Recurrent Infection
  • Dicloxacillin 500mg (child 12.5mg/kg up to 500mg) PO, 6 hourly for 7/7
  • If delayed nonsevere hypersensitivity to penicillins → cefalexin 500mg (child 12.5mg/kg up to 500mg) 6hrly for 7/7
  • If immediate or delayed severe hypersensitivity to penicillins → trimethoprim + sulfamethoxazole 160+800mg BD for 3/7
44
Q

Pharmacological Treatment of Impetigo - endemic setting (1 point + bonus for dosing)

A
  • Benzathine Benzylpenicillin IM Stat
    • adult or child >20kg → 1.2million units
    • child <6kg → 0.3million units
    • child 6-12kg → 0.45million units
    • child 12-16kg → 0.6million units
    • child 16-20kg → 0.9 million units
45
Q

What are the types of rash associated with HFMD? (2 points)

A
  • Small, oval, white blisters on the palms, soles of the feet as well as in the mouth. Can have sore throat or mouth → dehydration + poor appetite
  • Red skin rash with a brown scale to it → outearms, hands, legs, feet and around the mouth and upper buttocks
46
Q

What is the time line for Hand Foot and Mouth Disease in regards to the rash? Also is most commonly affected?

A
  • 3-7 days after becoming infected and can last from 7-10 days
  • affects children <10y, with most being <5yo
47
Q

How is HFMD spread? (3 points)

A
  • Very Infections → Spread through:
    • contact with the fluid from inside the blisters
    • droplets spread from sneezing and coughing
    • can be present in bowel movements up to several weeks after recovery
48
Q

How do you prevent the spread of HFMD? (3 points)

A
  • Prevent Spread:
    • Wash your hands
    • Make sure child doesn’t share items
    • Keep children home from school, kindergarten or childcare until all the fluid in their blisters has dried up
49
Q

What virus most commonly causes HFMD? What are the class of viruses that are responsible for HFMD?

A
  • Commonly caused by cocksackie virus

- can also be cased by other enteroviruses → e.g enterovirus 71 → associated with severe nervous system infections

Practice Exams (45 decks)

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