18/9/21 Flashcards

KFP Summit

1
Q

Risk Factors of Dupuytren’s Contracture (6 points)

A
  1. Diabetes Mellitus
  2. Vibratory Trauma + Repetitive Hand Use
  3. Cigarette Smoking
  4. Alcohol Consumption
  5. Presence of other localised fibrosing conditions
  6. Genetic Predisposition
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2
Q

Clinical Findings of Dupuytren’s Contracture (3 points)

A
  1. Nodules forming in palmar fascia
  2. Decrease flexibility of finger
  3. Contractures that draw one or more of the fingers into flexion at the MCP or PIP joint
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3
Q

Diagnosis of Dupuytren’s Contracture

A

Clinical diagnosis based on painless stiffness of the fingers and presence of characteristic findings on physical examination

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4
Q

Difference between Dupuytren’s Contracture and Trigger Finger?

A

Trigger finger shows a dynamic flexion contracture where one or more fingers that corrects with a distinct snap or “trigger’, while DC cannot be corrected.

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5
Q

Treatment of Mild Symptoms associated with Dupuytren’s Contracture

A
  • modifying tools → e.g gloves with padding

- limited data for massage, splinting and exercises will prevent progression of the contracture.

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6
Q

Treatment of Persistent or Progressive Symptoms associated with Dupuytren’s Contracture (3 points)

A
  1. Intralesional Glucocorticoid Injections -> nodules not cords
  2. Open Fasciotomy, Percutaneous Fasciotomy, Needle Aponeurotomy
  3. Collagenase Injections
    POST TREATMENT: ROM Stretching exercises with or without night splinting.
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7
Q

Eligibility for Home Detox (?in ATSI) (5 points)

A
  • No previous severe withdrawal including no seizures or delirium tremens
  • No concurrent acute medical illness
  • No evidence of psychosis, suicidal thoughts or severe depression
  • No evidence of other drug use except cannabis
  • Supportive, stable and drug free, alcohol free home environment
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8
Q

Options for pharmacological management of alcohol dependence.

A
  1. Naltrexone
  2. Disulfiram
  3. Acamprosate
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9
Q

Disulfiram Dosing

A

100mg PO daily initially for 1-2 weeks and uptitrate to 300mg PO daily

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10
Q

Mechanism of Action of Disulfiram + Risks of Disulfiram

A

Interacts with alcohol and preventing its metabolism → ingestion of alcohol therefore increases blood concentration of acetylaldehyde → this leads to aldehyde reaction (intense flushing, sweating, palpitatins, tachycardia, dyspnoea, hyperventilation and pounding headache) → can also result in chest pains, restlessness and sense impending doom → Severe reactions can include cardiorespiratory failure and DEATH

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11
Q

Acamprosate Dosing

A

Acamprosate 666mg PO TDS (>66kg) OR 666mg PO mane, 333mg midi and nocte (<66kg)
THE DEVILS CHOICE

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12
Q

Mechanism of Action of Acamprosate + Risks

A

Reduces neuronal excitability characteristic of alcohol withdrawal → Reduces the symptoms of protracted alcohol withdrawal → anxiety, irritability, insomnia, craving → reduces the time to first drink, prolongs abstinence and reduces the number of drinking days

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13
Q

Naltrexone Dosing

A

Naltrexone 50mg PO daily

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14
Q

Mechanism of Action of Naltrexone

A

blocks effect of endogenous opioids released following alcohol intake → person who drinks alcohol reports less pleasurable effects even though the alcohol related impairment remains unaffected. some studies report fewer cravings.

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15
Q

Diagnosis of Multiple Myeloma

A

CRAB

Calcium, Renal Failure, Anaemia, Bone Pain and Fractures

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16
Q

Multiple Myeloma: C

A

Calcium

Hypercalcaemia -> presenting with abdominal pain, constipation, polyuria

17
Q

Multiple Myeloma: R

A

Renal Failure

Uraemic Symptoms, Fluid Overload

18
Q

Multiple Myeloma: A

A

A - Anaemia + Other Cytopenias

- Leukopenia/Neutropenia with increased risk of infections
- Thrombocytopenia with increased risk of bleeding
19
Q

Multiple Myeloma: B

A

Bone Pain and Fractures

20
Q

Multiple Myeloma - Investigations (6 points + 2 bonus)

A
  • FBE with differential and blood film
  • UEC
  • Calcium
  • Serum Protein Electrophoresis, immunofixation
  • Routine Urinalysis
  • 24-hour urine collection for proteinuria, electrophoresis and immunofixation

Additional Tests

  • Bone Marrow Aspirate
  • Imaging of the Skeleton → Whole Body CT, MRI or PET Scan to detect lytic lesions and fractures
21
Q

Counselling points for PSA Informed Consent

A
  1. PSA can be raised secondary to other causes
  2. Overtreatment secondary to elevated PSA
  3. Normal PSA does not rule out prostate Ca
  4. Further invasive tests followng elevated PSA has its own risks
  5. If prostate Ca, many are low risk and would not have caused harm to man if gone undetected
  6. Prostate testing does not save lives
  7. If testing was wanted, every 2 years from 50-69
22
Q

Risk Factors for CKD (9 points)

A
  1. Age -> >60yo
  2. Established CVD
  3. Diabetes
  4. Hypertension
  5. FHx of Renal Failure
  6. History of AKI
  7. Smoker
  8. Obesity -> BMI >30
  9. ATSI
23
Q

Clinical Presentation of Acute or Acute-on-Chronic Lithium Toxicity

A

Begins with gastrointestinal symptoms (vomiting and diarrhoea) and progresses late to neurological symptoms (sluggishness → neuromuscular excitability → seizures)

24
Q

Risk Factors for Chronic Lithium Toxicity (9 points)

A
  1. Impaired Kidney Function
  2. Dehydration
  3. Age >50years → lower GFR + decreased volume of distribution
  4. Previous lithium toxicity
  5. Drug interactions → ACE inhibitors, ARBs, NSAIDs, Loop and Thiazide Diuretics
  6. Lithium-induced nephrogenic diabetes insipidus
  7. Intercurrent Illness
  8. Thyroid Dysfunction
25
Q

Treatment of Acute Lithium Toxicity

A
  • ingestion of <25g rarely causes major toxicity
  • No specific treatment is required except serial measurement of lithium concentration - to ensure lithium is being eliminated
26
Q

Long-Term Lithium Therapy → Chronic Toxicity if: (4 points)

A
  • Usual dose is increased
  • Prescribed additional medications
  • Elimination of lithium is reduced to due to kidney impairment
  • Lithium-induced nephrogenic diabetes insipidus → subsequent irreversible kidney injury
27
Q

Chronic Lithium Toxicity initially presents with _______ signs.

A

Neurological

28
Q

Clinical Presentation of Lithium Toxicity: 3 systems (4, 3,2 points)

A

CNS: tremor, hyperreflexia, ataxia, rigidity, drowsiness, confusion, coma, seizures, myoclonus

CV: QT prolongation (uncommon), bradycardia, hypotension

GIT: Nausea/Vomiting

29
Q

Can I use an ACEi or ARB in CKD?

A

Yes. Unless eGFR drops by >25% then refer to nephrologist

30
Q

Metformin Dose in CKD (eGFR 30-60)

A

500mg PO Daily if eGFR 30-60 -> can increase up to 1g daily according to response

31
Q

History of Paediatric Cough (11 points - give me 5)

A
  1. Onset → if sudden, consider foreign body inhalation
  2. Associated with Feeds
  3. Type
    • Paroxysmal Cough → pertussis, chlamydia or foreign body
    • Honking or Bizzare Disruptive Cough → psychogenic
    • Barking Cough → Croup
  4. Pattern
    • if absent during sleep - consider habit cough
  5. Recurrent Episodes vs Continuous Cough
  6. Symptoms of asthma, chronic rhinitis, sinusitis or other atopic conditions + FHx of the same
  7. Exercise Tolerance
  8. Poor Growth
  9. Associated Medical Concerns - pneumonia, fever, rash, wheeze, stridor, post-tussive vomiting
  10. Exposure to Passive Smoking
  11. Sick Contacts + Overseas Travel
32
Q

Common Causes of Paediatric Chronic Cough (5 points)

A
  1. Recurrent Post-Infective Cough
  2. Prolonged Post-Infective Cough (Pertussis, Mycoplasma)
  3. Cough as part of the asthma symptom complex
  4. Protracted Bronchitis
  5. Habit Cough