10/10/21 Flashcards
How is uric acid eliminated from the body?
Uric acid is eliminated by the kidneys (2/3) and the gut (1/3).
What are the main risk factors for gout? (5 categories)
- *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
Key Principles in the Management of Gout (5 points)
- Rapid symptom relief for acute attacks
- Life-long urate lowering therapy - treat to target approach
- Prophylaxis for gout flares when starting or increasing urate-lowering therapy
- Address modifiable risk factors for gout
- Patient Education re: risk factors + lifestyle changes that can be made
How would you prescribe urate-lowering therapy for gout? Be Specific
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
Why do you need flare-prophylaxis in managing gout?Be specific in how you would prescribe this.
- 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
How do you classify non-severe PID?
- No severe pain, no fever, no systemic features (tachycardia, vomiting), no sepsis or septic shock and no suspected tubo-ovarian abscess
How do you treat non-severe PID? Be Specific.
- 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
What are the clinical features of nail psoriasis? (6 clinical features - describe them)
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
How do you treat nail psoriasis?
- apply to nail matrix and hyponychium for months or years
1. calcipotriol solution BD
What condition is associated with nail psoriasis?
Psoriatic Arthritis - nail psoriasis is present in 80-90% of patients with psoriatic arthritis
What is and how common is Hypertrophic Cardiomyopathy? At what age is it commonly diagnosed and what is the mortality rate?
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
What is the most common way patients with HCM present?
MOST COMMON SYMPTOM - EXERTIONAL DYSPNOEA
What are the risk factors for Hypertrophic Cardiomyopathy and what does this mean for the management of this patient?
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
Discuss management of Hypertrophic Cardiomyopathy. (5 points)
- 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
- Pharmacotherapy
- beta-blockers (metoprolol, atenolol) and verapamil are indicated in SYMPTOMATIC patients
- Endocarditis Prophylaxis
- NO evidence for routine ABx prophylaxis
- Septal Reduction Therapy
- surgical septal myomectomy is considered in adolescent with disabling symptoms because of LV outflow tract obstruction
- Implantable Cardioverter-Defibrillator Insertion
- as above → if ≥ 1 risk factor → consider ICD implantation
After an infection, when does reactive arthritis present? Also what kind of infections are common for reactive arthritis to develop?
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
What is the diagnostic triad associated with reactive arthritis?
Can’t See - conjunctivitis
Can’t Pee - genitourinary inflammation (Urethritis)
Can’t Climb a Tree - arthritis
C..Rash - keratoderma blennorrhagica
How doe the arthritis component of reacticve arthritis present? When, where and common specifically.
- 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
How do you manage reactive arthritis? (infection, mild vs severe)
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
- For Mild to Moderate → an NSAID PO
- For Severe:
- Intra-articular corticosteroid injection (if a small number of accessible joints are involved)
- Prednisolone 10-50mg PO, daily until symptoms improve, then taper dose to stop
History of Rheumatoid Arthritis? (5 points)
- Joint Pain + Swelling and/or Fever
- Morning Stiffness >30mins
- Previous Episodes
- Family History of RA
- Systemic Flu-Like Features and Fatigue
Examination Findings in Rheumatoid Arthritis (3 points)
- ≥3 tender and swollen joint areas
- symmetrical joint involvement in hands and/or feet
- Positive squeeze at MCP or MTP joints
Joint distribution of RA in the hands - which joints are involved?
MCP + PIP joints, DIP joints spared
How do you classify Acute Kidney Injury? What are some causes of each category? (specifically 5 intrarenal causes)
### 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
History questions associated with Acute Renal Failure. (5 points - be specific about medications)
- 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
Clinical Features of Blue Toe Syndrome (3 points)
- 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.
Complications of Blue Toe Syndrome. Usual prognosis if mild. If untreated?
- 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
Definition of Unstable Angina (3 points)
- Rest Angina - generally lasting longer than 20 mins
- New Onset Angina that markedly limits physical activity
- Increasing Angina → frequent, lasts longer or occurs with less exertion than previous angina
Absolute contraindications for Cardiac Stress Testing. (6 points)
- 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
Otitis Externa: Clinical Features on History (6 points)
- ear pain
- conductive hearing loss
- feeling of fullness (blockage) or pressure
- itchiness
- tenderness on manipulation of the tragus or auricle
- +/- discharge
Non-pharmacological management of otitis externa (2 points)
- External ear canal must be kept as dry as possible
- 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
What is the pharmacological option of choice in treatment of otitis externa? Explain factors involved in choosing pharmacological management of otitis externa.
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
If not concerned re: fungal infection, what are the options of treatment of otitis externa?
- 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
if concerned re: fungal infection, what are the treatment options of otitis externa?
- 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
If the ear drops cannot be administered because the canal is occluded, what can be done?
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
Following treatment of otitis externa, can the patient return to swimming? What advice do you need to give a patient with otitis externa?
- Advise patient to keep ear dry during and for 2 weeks after treatment → use ear plugs + shower or bathing cap during showering and swimming.
Clinical Diagnosis of Henoch-Schonlein Purpura.
-
Rash + ≥1 of:
- Arthritis/Arthralgia (50-75%)
- Abdominal Pain (50%)
- Nephritis (25-50%)
Describe the rash of Henoch-Schonlein Purpura.
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
Common abdominal complication of Henoch Schonlein Purpura?
intussusception
What complication needs to routinely reviewed in the context of Henoch-Schonlein Purpura? How does the follow-up schedule look for patients with HSP?
- 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
Timeline of Impetigo - clinical features
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
Pathogen responsible for Impetigo - endemic vs non-endemic setting.
Non-Endemic Settings → S. Aureus
Endemic Settings → S. pyogenes (MRSA)
What is the role of skin swabbing in impetigo? When do you need to swab?
- 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.
Non-pharmacological Treatment of Impetigo? including prevention of impetigo and keeping child at home (3 points)
- 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.
Pharmacological Treatment of Impetigo - non-endemic setting. (2 points + 2 bonus for hypersensitivity to penicillin)
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
Pharmacological Treatment of Impetigo - endemic setting (1 point + bonus for dosing)
- 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
What are the types of rash associated with HFMD? (2 points)
- 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
What is the time line for Hand Foot and Mouth Disease in regards to the rash? Also is most commonly affected?
- 3-7 days after becoming infected and can last from 7-10 days
- affects children <10y, with most being <5yo
How is HFMD spread? (3 points)
- 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
How do you prevent the spread of HFMD? (3 points)
- 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
What virus most commonly causes HFMD? What are the class of viruses that are responsible for HFMD?
- Commonly caused by cocksackie virus
- can also be cased by other enteroviruses → e.g enterovirus 71 → associated with severe nervous system infections
