2013 OSCE
Booklet
Lia Stepan
Fe Menz
Lachy Stranks
Table of Contents
13. HISTORIES
- General Medicine & Geriatrics: 8. MMSE/Cognitive assessment 13. Fall in the elderly
19. Headache 1 21. Headache 2
26. Febrile illness (HIV) 29. Obesity 32. Painful rash 36. Polycythaemia 65. SOB 1 74. SOB 2 - Surgery: 10. Difficult swallowing 40. Prostate disease
46. Peripheral vascular disease 53. Back pain (renal colic) 58. Retinal detachment - Orthopaedics:
4. Joint Pain
61. Scaphoid fracture + exam - Obstetrics & Gynaecology:
81. Abdo pain (ectopic pregnancy) 85. Menopause 93. Pre-term labour 100. Pregnancy dating 104. Salpingitis - Paediatrics: 111. Respiratory (Croup) 114. Febrile seizure 119. Anaphylaxis - Psychiatry: 124. Anxiety 1 129. Dementia vs. Depression 134. Anxiety 2 137. Schizophrenic patient 140. Psychosis 145. PTSD 150. Suicidal ideation 158. Suicide attempt
164. PHYSICAL EXAMS
165. Acute abdo 1 (cholecystitis) 168. Acute abdo 2 (appendicitis) 172. Driving assessment
174. Breast
177. Cardiovascular 182. Carpal Tunnel Exam 187. Cranial nerve
189. Diabetic lower limb 193. Groin lump
197. Scrotal exam
200. Hearing assessment 204. Knee exam
207. Parkinson’s exam
210. Peripheral vascular exam 213. Respiratory 216. Resuscitation (BLS, ALS) 220. Rheumatological hand 224. Shoulder 1 (impingement) 228. Shoulder 2 (dislocation) 230. Thyroid/neck
233. Trauma & Primary survey
236. COUNSELLING
237. SPIKES
238. ACEi commencement 240. Angry patient
243. Breaking bad news (CRC) 246. Childhood obesity
250. Genetic counseling
255. Cardiovascular risk factors 258. Pre-operative counseling 261. Skin lesion (melanoma) 265. Dementia
266. Oesophageal cancer 266. Breast cancer
267. Pap smears & HPV 270. Cervical cancer
271. DATA STATIONS
272. ABG interpretation 274. Acute renal failure 280. Assess foetal growth 284. Assess early child growth 288. Asthma management plan 291. Prescribing – Asthma 294. Prescribing – Statin 298. Prescribing – Diabetes 302. Prescribing – Analgesia 305. Prescribing – Incontinence 307. Blood dipstick 311-18. ECGs 319. Pathology 2
HISTORIES
JOINT PAIN
Ben Smith is a 68-year-old retired man who lives with his wife. Ben has
noticed pain in his left knee for the past day and has come to the ED as
he is concerned about this.
Description of task:
Take a focused history to formulate differential diagnoses and
explain them to the patient
Explain to the patient what investigations are needed
Patient Profile:
- Ben Smith - 68 year old
- Lives with wife, retired lawyer
PC: Pain in left knee for past day HPC:
- Knee pain;
Onset earlier this morning about 5 hours ago, gradually worsening Severity 8/10
Burning deep pain in left knee Nil radiation
Worse on movement, cannot move leg anymore - Additional;
Knee is red and swollen, feels hot Associated fever and malaise
Had been to ED 4 days previously for pain in same leg – was found to have Staph aureus cellulitis; was given antibiotics but didn’t take them
Nil injury to the joint Nil pain in any other joint
Nil family history, PMH, social history
DIFFERENTIALS FOR ACUTE ARTHRALGIA:
- Septic arthritis
- Crystal arthropathy – gout, pseudogout - Osteomyelitis
- Trauma – fracture, haemarthrosis, dislocation
INVESTIGATIONS & MANAGEMENT:
- Urgent joint aspiration for synovial fluid microscopy and culture - Empirical antibiotics – flucloxacillin 2g IV to cover staph
- Blood cultures
- Bloods – CBE, ESR, CRP - Joint X-ray
- Further mgmt dependent on aspirate
- Consult with orthopaedics and microbiology
SEPTIC ARTHRITIS
- Infection of one or more joints by pathogenic inoculation of microbes
- 10x more common in people with underlying joint disease or with prosthetic joints Aetiology & Pathophysiology:
- Most common organisms are Staph and Strep Together account for 91% of cases
- Other organisms;
Gonorrhoea – consider in sexually active patients Gram –ve – elderly, immunocompromised
Anaerobes – rare except in penetrating trauma - Risk factors;
Underlying joint disease – OA, RA Joint prostheses
IVDU
DM, immunosuppression, alcoholism
Previous intra-articular corticosteroid injection Cutaneous ulcers
- Inoculation either by direct inoculation or haematogenous spread
- Septic arthritis can destroy a joint in <24 hours, therefore urgent mgmt essential Clinical features:
- Hallmark is hot, swollen, tender, restricted joint - 60% have fever
- May have clinical features of primary focus of infection (if haematogenous spread) e.g. pneumonia
Investigations:
- Urgent joint aspiration for synovial fluid MCS;
Perform gram stain and culture prior to commencing ABs - +ve in 70% A –ve result does not exclude septic arthritis
Exclude crystal arthropathies
- Blood culture – prior to commencing ABs, +ve in 25% - Bloods;
CBE – raised WCC ESR, CRP elevated
- Plain X-ray – no diagnostic benefit but may reveal underlying joint disease Management:
- All patients suspected for septic arthritis should be commenced on empirical ABs, but only after joint aspiration and blood cultures (unless major delays)
- Usual ABs to cover common organisms; Flucloxacillin (or vancomycin if MRSA) Cefotaxime (from gram –ve organisms) - Consultations;
Microbiology for AB duration Orthopaedics
Complications: - Osteomyelitis - Joint destruction Prognosis:
- Irreversible joint destruction if Tx delayed - 11% mortality
MMSE/COGNITIVE ASSESSMENT
7STEM
Perform an MMSE and interpret the results
EXAM FINDINGS (FOR SP TO FAKE)
Orientation – season correct (1/5) 8
Orientation (location) – correct state, country, town (3/5) Registration – 3/3
Attention + calculation – 1/5 Recall – 0/3
Language – 1/3 for 3 stage command but otherwise good (7/9)
WHAT STUDENT MUST DO
Introduce self
Explain task to patient Do MMSE
Identify cognitive impairment o Score 15/30
o Dementia cut off (according to QEH geris): 15-21 = early
9-15 = moderate <9 = severe Differentials
o Delirium – UTI, pneumonia
o Dementia – Alzheimers, Vascular, Lewy Body, B12/folate deficiency, hypothryoid
o Depression
o Medications – e.g. sedated from benzos Investigations
o Take full history first, with collateral from family
o Physical exam – fluctuating consciousness, signs of infection, CVS, neurological etc
o Urinalysis o Bloods
CBE, ESR, CRP - anaemia, infection (e.g. UTI)
Electrolytes (hypercalacaemia), blood glucose, LFTs (hepatitis, alcoholism), renal function (renal failure)
Vitamin B12 + folate
Thyroid function (hyper and hypothyroidism)
Syphilis serology - rare, only present in those > 55
HIV antibodies - HIV is the most common cause of dementia in young people
o Neuroimaging
All should at least get a CT head
CT – atrophy, SOL, normal pressure hydrocephalus, subdural haematoma, vascular disease
MRI – Generalised atrophy with temporoparietal predominance (AD), infarction + SOLs
Other PET, SPECT
o Further geriatric assessments – nutrition, continence, falls screen, depression screen, ADLs, iADLS
11
Interteaching OSCE Generated by TY Kang MBBS V
OSCE Station History: (6 minutes)
You are a GP working at a practice you just joined yesterday, and so far it’s been pleasant. A 72 year old fe/ male presents with difficulty swallowing for the last few months.
Task:
1. Please take a history from him and
FALLS IN THE ELDERLY
You have 6 minutes at this station Description of task:
Fred Johnson is a 70-year old man who has been admitted to the ward for
investigation of falls.
He has fallen several times over the past two weeks and has severe
bruising over his buttocks and shoulders.
Take an appropriate focused history, with the intention of clarifying the
possible causes of his falls. Tell the examiner which diagnosis you think is
more likely
.
Patient profile:
- Fred Johnson - 70 years old - Retired carpenter - Widower, lives alone
PC: I’ve fallen a few times over the past couple of weeks, and now I’m pretty battered
and bruised
HPC:
- Fallen 4 times in the past 2 weeks;
All occurred at home, none witnessed
3 falls occurred inside after getting out of chair; o Feeling fine beforehand
o Felt dizzy when getting out of chair and subsequently fell over o Never lost consciousness
o Was on ground for no more than 20 minutes each time
o Did not hit head, but was quite painful where he landed (buttocks, shoulder)
o Able to mobilise comfortable afterwards 1 fall occurred outside whilst gardening;
o Hot day, had not been drinking much water o Got up from weeding, felt faint and then fell o No LOC, no head injury, no fractures
o Wasn’t able to get up straight away – neighbor heard him calling for help, spent an hour on the ground
o Subsequently admitted to hospital
- Able to move shoulders arms freely but significant pain, also in buttocks - No palpitations
- No LOC
- No weakness
- No visual/hearing problems
- Did not trip, no obvious environmental cause
- Recently commenced on new antihypertensive medication; Beta-blocker commenced 3 weeks ago
Already on ACEi and diuretic Has been taking it as prescribed
- Has never fallen before, no previous fractures
PMH:
- HT, previous MI, CABG 10 years ago
- ‘Stiff joints’ – OA in knees but mobilises independently - No memory problems, no depression
- Meds;
Antihypertensives – ACEi, diruteic, B-blocker (started 3 weeks ago) Aspirin
‘Sleeping tablet’ - Smoker – 10 cigs per day
- Alcohol – only drinks on Thursdays at the bowls club
Social:
- Lives alone at home
- Wife died of breast cancer 15 years ago - 3 adult children, sees them regularly
- Plays bowls once a week, otherwise not much physical activity
LIKELY DIAGNOSIS:
- Multifactorial, but likely cause of fall is orthostatic hypotension, occurring secondary to;
Recent commencement of new, 3rd antihypertensive medication (beta-blocker)
PLUS Dehydration, hypovolaemia when he fell outside - Contributing factors;
Osteoarthritis, impaired mobility Polypharmacy
Deconditioning (little physical activity)
- Antiplatelet therapy likely contributing to significant bruising - Given his PMHx, must also consider;
Arrhythmias TIA
(although history is not suggestive of these causes)
Falls in the Elderly
- Common occurrence in elderly population, and are major factors threatening the independence of older individuals
- Usually occur when impairments in multiple domains compromise compensatory ability of the individual
A number of environmental and physical conditions that predispose to falls are modifiable, and can be prevented to some extent
- Related to significant morbidity and mortality 16
Epidemiology:
- Increases with increasing age, and varies according to living status - Community-dwelling;
30-40% of people >65 years fall each year 50% of people >80 years fall each year - Long-term care setting;
50% of individuals in care fall each year 60% with Hx of previous fall will fall again - Equal prevalence in men and women
- Account for majority of nonfatal injuries in adults >65 years, 5% will result in hospitalization
Risk factors:
- Past history of a fall
- Lower extremity weakness - Increasing age
- Cognitive impairment - Balance problems - Psychotropic drug use
- Fear of falling - Arthritis - History of stroke - Orthostatic hypotension - Dizziness - Anaemia Aetiology & Pathophysiology:
- Usually multifactorial in origin and reflect failure/demise of compensatory mechanisms
- Can be broadly divided into intrinsic/medical and environmental causes - Sensory impairment; Poor vision Poor hearing Peripheral neuropathy - Neuropsychiatric; Vestibular dysfunction
Gait and balance disturbance – Parkinson’s, previous stroke Cognitive/mood impairment – dementia, depression, delirium Seizure disorder
Subdural haematoma CVA or TIA
- Cardiovascular;
Syncope – arrhythmias, bradycardia, vasovagal syncope Orthostatic hypotension
Carotid sinus syndrome Post-prandial hypotension Anaemia
- Musculoskeletal;
Joint bucking/instability
Mechanical mobility/gait abnormality – previous fracture, arthritis De-conditioning - Medications; Benzodiazepines Antidepressants Antipsychotics Sleeping medications Antihypertensives Diuretics NSAIDs Marijuana 17
- Others;
Polypharmacy – use of 5 or more medications increases risk by 30% Substance abuse
Environmental – poor lighting, uneven surfaces, loose rugs, ill-fitting shoes, slippery floors
Clinical assessment: - History of most recent fall;
Conscious or unconscious collapse/fall – syncope, amnesia etc. Was the fall witnessed?
Intrinsic or environmental?
o Palpitations, syncope, visual disturbance, neuropathy, weakness etc. o Poor lighting, uneven surface etc.
Were they able to get up after the fall? How long were they on the ground? Complications – fractures, bruising, bleeding, head injury etc.
- History of previous falls/PMHx
Number of falls (>2 falls within a 12 month period is considered significant) Previous fragility fractures? If yes, patient must receive bone-strengthening
meds
Other complications
PMHx – previous stroke/TIA, CVD, osteoporosis, DM etc. - Medications;
Polypharmacy (>5 meds) is a risk factor for falls Significant meds for falls;
o Benzodiazepines o Anticholinergics
o Psychotropics (antipsychotics, antidepressants, sedatives) o Diuretics
o Antihypertensives o Statins
Anticoagulants, antiplatelets – bleeding risk - Physical exam;
General wellbeing – level of self care, nutritional status, body habitus CV exam – arrhythmias, postural BP, bradycardia
Gait assessment Balance assessment;
o Timed up and go test;
Time taken to get out of chair, walk at a comfortable speed for 3 metres to a line on the floor, turn, return to chair and sit down Time taken >15 seconds suggests a high risk of falls
o Single leg stance test – observe patient standing on one leg with eyes open on firm surface for 10 seconds; repeat 2 more times
Lower limb strength Cognitive assessment
Visual acuity and hearing assessment Assessment of feet and footwear
Investigations:
- May be indicated based on Hx and exam, but no standard diagnostic evaluation exists for a person with a history of or at high risk for falls - Investigations are to rule out potential causes
- Serology; CBE – anaemia
Biochemistry – elevated urea and creatinine (dehydration) BSL, HbA1c
Vitamin D - ECG, echo - Brain CT/MRI
- EEG (if seizures suspected) - Spine x-ray, MRI
- DEXA scan
Falls prevention:
- Exercise – gait and balance training, muscle strengthening, flexibility, endurance
- Medication assessment and modification – especially benzos/psychoactive drugs
- Vitamin D supplementation;
High dose cholecalciferol especially if vitamin D low - OT assessment;
Hazard reduction in the home Proper footwear
Training and education Mobility devices
- Vision – glasses, cataract surgery etc. - Podiatry review
- Indications for referral to Geriatrician/falls clinic; >2 falls in 12 month period
Unexplained falls with syncope, dizziness or poor recall
Falls as part of downward physical, social or psychological spiral Falls occurring at low threshold (e.g. with basic ADLs)
Falls with head injury, low trauma fracture on floor >1 hour Gait disturbance or unsteadiness
Complications:
- Falls often result in injury of some type, usually minor soft tissue injuries (bruises etc.)
41% of falls result in minor injury
6% result in major injury (fractures, head trauma, lacerations etc.) - Fractures – NOF, pelvis, upper limb (fall on outstretched hand) - Head injury
- Bleeding, bruising, lacerations
- Downward physical/social spiral, reduced QOL - Loss of independence/ability to perform ADLs
- Rhabdomyolosis, acute renal failure – if immobile on floor for prolonged period - Hospitalisation (5% of falls result in hospitalization)
- Death
HEADACHE 1
Mary Smith is a 55 year old lady who has been experiencing
new-onset headaches for the last 5-6 weeks.
Please:
Take a history from Mrs Smith (4 minutes)
Ask the examiner for relevant results of the physical examination
that you would perform (1 min)
Discuss differential diagnoses and further investigations (1 min)
HISTORY Profile o 55 years old o Accountant
o Lives at home with her husband and teenaged children PC
o 5-6 weeks of headache Headache
o Non localised
o Worse in the morning, worse on lying down o Non responsive to analgesia
o Hasn’t noticed coughing making it worse o Never had this before
o Has not been unwell recently
Last week or so has had some double vision and been unable to look with her left eye to the left side
Nil seizures noticed, husband has been telling her that she has had short moments of unresponsiveness
Weird feelings of déjà vu lately
Slightly less propensity for concentration Otherwise well
No hx cancer
No melanomas previously diagnosed, gets skin checked regularly No recent trauma
Physical Findings
Papilloedema 6th nerve palsy
Right sided homonymous hemianopia Upbeat nystagmus
Diagnosis with differentials
Space occupying lesion – GBM
o Other tumour (30% are metastatic from breast, lung, melanoma) o Idiopathic intracranial hypertension
o Trauma Investigations CT head
HEADACHE 2
Charles / Charlotte Young (Fe)Male, age 30‐50, presents with a
history of headaches over the past month.
Tasks for the station:
1. Please take a history from this patient in relation to the
presentation. (4 minutes)
2. Tell the examiner what you consider is the relevant examination
and ask for the results of that clinical examination. (1 minute)
3. Inform the examiner of your likely diagnosis or diagnoses and
what would be the important investigations if any required. (1
minute)
Patient profile: Charles Young 45 year old man Works as lawyer
PC: Headache for the past few weeks
HPC:
- Headache;
Present for the past month
Worst at the back of head but hard to localise, not feeling pain anywhere else Worse when lying down, coughing, leaning forward
Worse in the mornings when getting out of bed
Never experienced anything like this before, never had migraines
- Visual changes – blurred vision a couple of times in R eye in the past week – ‘blacking/blurring’ of vision
- Sometimes feels nauseous when waking up in the morning, has vomited twice in the past couple of days on waking
- No dizziness - No weakness
- Slightly more tired than usual, but is doing long hours at work
- No migraine features – no photophobia, no phonophobia, no aura etc. - No tinnitus
- No obvious trigger – has not bumped head, no caffeine, drugs etc. PMH:
- Nil significant - Asthma as child - No operations
- Not on any medications, occasional Panadol for headache but with little effect - No history of malignancy
- Nil allergies
SMOKING/ALCOHOL:
- Smokes half a pack/day, has been smoking since age 12 - Drinks socially on weekends
FAM/SOCIAL:
- Nil significant family history
- Happily married, 3 children, all well
DIFFERENTIALS:
- Raised ICP of any cause Brain tumour
Intracranial haemorrhage - Migraine unlikely
- Other headache causes unlikely – tension, cluster
EXAMINATION:
- Vitals – pulse rate and rhythm, BP - Clinical features of raised ICP;
Fluctuating conscious level
Cushing’s triad – HT, abnormal breathing, bradycardia
- Visual function testing – peripheral vision, ocular movements (may have palsy of abducens nerve)
- Full neurological examination – any features of UMNL
INVESTIGATIONS:
- Bloods – CBE, biochemistry - CT/MRI head
- If SOL identified, further investigation and referral required
HEADACHE HISTORY
Introduction History of presenting complaint; Headache;
o Location of pain
o Onset of pain, duration o Character
o Radiation o Chronicity o Severity
o Aggravating/relieving factors inc. time of day o Ever had anything like this before?
Associated symptoms; o Aura, flashing lights o Nausea, vomiting o Photo/phonophobia
o Lacrimation, rhinorrhoea (cluster headache) o Neck stiffness
o Weakness, paraesthesia o Fever
Possible causative factors; o Head injury
o Lack of sleep o Stress, exertion o Refractive errors o Caffeine, alcohol Past medical history;
History of headaches? Migraines? Medications – OCP
Alcohol, smoking, caffeine
Family history – cancer, headaches
Raised intracranial pressure:
- Headache worse in mornings and after lying flat - Associated with nausea and vomiting
- Often have transient unilateral or bilateral visual disturbances – blurring, blackening
- Signs;
Altered conscious level Papilloedema
Abnormal ocular movement, sluggish light reflexes Bradycardia Systemic HT - Causes; Tumours Subdural/extradural haematoma Brain abscess Hydrocephalus
Benign intracranial hypertension Aneurysms, AV malformations - Investigations – CT/MRI head
Migraine:
- Defined as recurrent headache that occurs with or without aura and lasts 2-48 hours
- Characteristic features;
May have preceding aura – flashing lights etc. Usually unilateral
Gradual onset (15-30 mins) Pulsating/throbbing in quality Moderate-severe intensity
Aggravated by routine physical activity
Commonly associated with nausea, vomiting, photo/phonophobia - Investigations – clinical diagnosis
- Management;
Identify any precipitating factors and remove them (e.g. dark chocolate, caffeine etc.)
Withdraw OCP if recurrent episodes Acute attack;
o First line = simple analgesia i.e. paracetamol, NSAID (2x aspirin + 1 maxalon +/- 3 panadol)
o If these fail, codeine can be used
o Others – antiemetics if vomiting, ergotamine Prophylaxis for recurrent episodes;
o Propranolol
o TCAs e.g. amitryptilline
o Flunarizine (Ca2+ channel blocker) Relaxation techniques
Tension headache:
- Most common cause of headache - Characteristic features;
Steady dull ache
Usually bilateral Episodic
- Can occur chronically
Cluster headache:
- Occur in ‘clusters’ i.e. periodically - Characteristic features;
Severe headache, typically steading boring sensation often behind one eye Tearing (lacrimation)
Red eye
Runny nose/nasal congestion (rhinorrhoea) Horner’s syndrome
Subarachnoid haemorrhage: - Medical emergency
- Due to rupture of intracranial Berry aneurysm - Characteristic features;
Severe, acute headache – ‘thunderclap’, worst pain ever felt Meningism
Decreased consciousness/LOC Focal neurological deficits
Features of raised ICP +/- herniation
Temporal arteritis:
- Unilateral throbbing headache
- May have associated visual disturbances and jaw claudication - Tender to palpation over temporal artery
- Associated with polymyalgia rheumatic
- Requires temporal artery biopsy for diagnosis with subsequent corticosteroid treatment
Station Name: HISTORY
1 minute reading time 6 minute question time
Instruction to Students
You have 6 minutes at this station. You will be warned at 5 minutes. If you finish early, you will be asked some questions for bonus marks.
Description of task:
You are the student in a local GP practice and have been asked to see Miss Carmen Sandiago, a 22 year old woman. She has had a fever, and been feeling unwell.
OBESITY
An obese patient (BMI 35) is concerned about their weight and its
effect on their health.
Please take a history focussed on the following two aspects of their
obesity:
1) factors leading to their obesity (4 minutes) AND
2) obesity-related complications (2 minutes)
This is a history station. DO NOT give management advice.
Patient profile: Barry Chubb 42 years old Works in IT, lives alone
PC: concerned about his weight and what it might be doing to my health
HPC:
- Has always been ‘big’ since he was a teenager, but is now at his heaviest (BMI 35)
- Has just gradually been putting on weight up to this point - Previous attempts at weight loss;
Tried a few diets he saw advertised on TV and bought an AbSwing Pro – none of these worked
Wasn’t exercising on the diet and would still snack on junk food, became frustrated with lack of results so gave up
Has never tried drug therapy Has never had gastric stapling - Reasons for gaining weight;
Does not exercise – sits behind desk for work, watches a couple of hours of TV per night
Diet – lots of meat, some vegetables, gets McDonalds for dinner a couple of times per week because he can’t be bothered cooking, lots of soft drink, icecream
Drinks socially on weekends - Family history;
Mother was obese and had high blood pressure – died from MI when she was 63 Father has DM
Brothers and sisters all on the bigger side
- Obesity related complications;
Occasionally gets reflux – uses antacid, not a major problem
Has some back pain and knee pain – was told he probably has osteoarthritis Can walk 500m before getting puffed
Has never been told he has diabetes, but sugars were ‘borderline’ on his last test
Hypertensive – 150/100 High cholesterol
His weight does get him down – feels socially isolated and constantly judged, has no hope of finding a partner when he is this big – ‘I eat becomes I’m unhappy, but I’m unhappy because I eat’
Has never had chest pain, SOB
PAINFUL RASH
You have 6 minutes at this station
Description of task:
The patient had a painful rash which has cleared up 6 weeks ago.
She still has pain.
- Take a focussed history (4 minutes)
- In the last 2 minutes describe to the examiner the patient’s
symptoms, give the most likely diagnosis and its natural history and
suggest a management plan for this patient.
- You will receive a warning when 4 minutes have passed.
Profile Joan Colins 72 years old Widowed Lives alone Received pension PC
Painful area over chest HxPc
Had a rash over current area of pain about 6 weeks ago o Very painful – burning, stinging
o Red, bumpy, weepy o Lasted for about a week
o Located unilaterally over chest o Went away by itself
o Pain started a few days before the rash and is still there now o Skin where rash was is currently more sensitive than usual Nil cardiac symptoms
Nil SOB
Nil recent trauma Otherwise well MHx
No allergies
Had chickenpox when she was a child Hypertension – metoprolol
Osteoporosis – vitamin D and calcium
Has been taking panadol for pain but no relief Otherwise well
FHx
Grandchild has just caught the chicken pox o Sees him regularly
Father died of MI at 60 Mother died naturally No hx other diseases SHx
Smoker
o 10/day for 20 years Non-drinker
No illicit drugs MARKING SCHEME Introduction
History
o Pain history – finds out onset and relationship to rash o Excludes cardiac/resp/traumatic causes
o Asks about history of chicken pox
HERPES ZOSTER
This is a sporadic disease that results from reactivation of latent VZV in the dorsal root ganglion.
It can occur at all ages, but has the highest incidence in individuals in their sixth decade of life and beyond.
Presentation
Characterised by a unilateral vesicular eruption within a dermatome Often there is severe pain
Dermatomes T3-L2 are most commonly involved Distribution:
o 50% thoracic o 10-20% trigeminal o 10-20% cervical o Disseminated in HIV
The factors leading to reactivation are unknown. In children the disease can be relatively benign, but in adults it can be debilitating.
The pain is called zoster-associated pain:
Disease onset is marked by pain within a dermatome o This may precede rash by 24-72 hours
An erythematous maculopapular rash evolves rapidly into vesicular lesions (and bullae, pustules
In the normal host, these lesions tend to continue to form for 3-5 days and the disease generally resolves within 7-10 days, however it may take as long as 2-4 weeks for the skin to return to normal.
If located over the trigeminal nerve distribution, this is called ‘Ramsay Hunt Syndrome’
Taste lost at anterior 2/3 of tongue EAC pain
Ipsilateral facial palsy
Patients with herpes zoster can transmit infection to seronegative individuals chickenpox
Risk Factors
Immunosuppression Old age
Occasionally associated with haematological malignancy Complications
The most debilitating outcomes are: Acute neuritis
Postherpetic neuralgia
Postherpetic neuralgia is uncommon in a young population, but at least 50% of patients aged >50 report at least some pain for months after resolution of the cutaneous disease. This pain must have been present for AT LEAST 3 MONTHS. Changes in sensation of the dermatome (hyper or hypoalgesia) are common. Differentials
Consider other causes of chest pain if there is no rash Rash:
o Contact dermatitis
o Localised bacterial infection Management
Gabapentin 300-600mg PO TDS for post herpetic neuralgia, or TCA, or anticonvulsants
If active rash:
o Compress with normal saline or betadine solution o NSAIDs, amytriptiline
o If over 50 years with severe acute pain or ophthalmic involvment, or
immunocompromised, vancyclovir Non pharmacological o Acupuncture o Relaxation techniques o Heat/cold packs o TENS Outcome
In the majority of cases, there is gradual resolution of the pain over around 5 years. Some patients may have this for life
Manage with TCAs or gabapentin
POLYCYTHAEMIA
Description of the task:
A 65-year-old man has presented to the GP to receive his results
from the blood test that you performed a week ago due to his 3
month history of shortness of breath and cough. The CBE results are
shown below.
1. Take an appropriate history to determine the cause of this problem
2. Tell the examiner your differentials and what investigations are
required to distinguish them
3. Tell the examiner how you would manage this patient
Hb:
196
(135-175)
RBCs:
9.0 10
12/L (4.5-6)
PCV:
0.49 L/L (0.4-0.5)
MCV:
90 fL
(80-98)
WBCs:
8.6
(4-11)
Platelets:
260
(150-400)
Haematocrit:
Increased
This blood profile indicates polycythaemia.
Patient profile:
John Smith
65 year old man Retired carpenter
PC: Told to return for blood test results that were taken as he has been SOB and
coughing HPC:
Has been feeling increasingly SOB over the past few months which is getting worse
Used to be able to walk for 20+ mins without feeling SOB, now struggling to walk 5 minutes on the flat
Persistent cough for few months to year o Worse in mornings
o Usually clear, occasionally discoloured (brown/green) o No blood
Frequently gets chest infections – 1-2 a year, requiring antibiotics Not feeling unwell at the moment, has not lost weight, a little tired
Currently smoking; o Pack a day o Started age 17 PMH:
Generally well, rarely sees doctors
Has never been told about lung problems Surgical – cholecystectomy at age 50
Meds – friend suggested Ventolin but hasn’t been helping Nil allergies
Smokes
Drinks alcohol on weekends Nil illicit drugs
SOC:
Retired carpenter Lives with wife – well FAM:
Father died of lung cancer at age 65 – heavy smoker Mother died of stroke age 80
Diagnosis: Likely COPD causing secondary polycythaemia (due to chronic
hypoxia)
Polycythaemia
- A haematological abnormality characterized by increased number of circulating RBCs (erythrocytosis) – i.e. increased RBC mass
Also commonly associated with thrombocytosis and leukocytosis - Classification;
Relative (raised RBCs as a result of reduced plasma volume, normal RBC mass) Absolute (raised RBC mass)
o Primary – polycythaemia rubra vera
o Secondary – caused by hypoxia or inappropriate increase in EPO - CBE findings;
Raised RBCs Raised Hb
Raised haematocrit Raised PCV
May also have elevated WCC and platelets (depending on cause)
Relative polycythaemia:
- An apparent rise in circulating RBCs secondary to a decrease in plasma volume - RBC mass is normal, however Hb, haematocrit and RBC count are elevated - Typically an acute change secondary to;
Dehydration – diuretics, reduced fluid intake, alcohol Stress
Burns
Male gender more common
Hypertension (which produces reduced plasma vol) Obesity
High alcohol and tobacco intake
Absolute polycythaemia:
- The overproduction of RBCs with either a primary or secondary cause; Primary – myeloproliferative disorder caused by an acquired or inherited
mutation abnormality with RBC precursors (Polycythaemia rubra vera) Secondary – as a result of chronic hypoxia or increased EPO
Polycythaemia rubra vera:
- Myeloproliferative disorder characterized by neoplastic proliferation of cells derived from the pluripotent marrow stem cell
- Results in; Erythrocytosis Leucocytosis Thrombocytosis
- >90% of cases are related to a mutation in JAK2 (JAK2 V617F)
- Associated with thrombotic complications as a result of blood hyperviscosity - Clinical features;
May be asymptomatic and detected on routine CBE
Alternatively may present with vague S+S related to hyperviscosity; o Headaches
o Dizziness o Tinnitus
o Visual disturbance
o Itch after hot bath/shower
o Erythromelalgia – sudden, severe burning pain in hands and feet Signs;
o Facial plethora
o Splenomegaly (60%)
o Gout (increased urate due to increased RBC turnover) o Arterial or venous thrombosis
- Investigations; CBE as above
Marrow aspirate – hypercellularity with erythroid hyperplasia Reduced serum EPO
- Treatment;
Young patients – venesection Old patients – hydroxycarbamide - Complications;
Thrombosis – venous or arterial Transition to; o Myelofibrosis (30%) o Acute leukaemia (5%) Secondary polycythaemia:
Chronic hypoxia (increased O2 carrying capacity required erythrocytosis) Increased EPO production
- Chronic hypoxia; COPD
Cyanotic congenital heart disease High altitudes
Heavy smoking
- Increased EPO production; (AKA tumour polycythaemia) Renal carcinoma
Hepatocellular carcinoma Phaeochromocytoma haemangioblastoma
- May also be secondary to EPO doping in athletes
PROSTATE DISEASE
Mr McClean is a 68 year old man who has been having trouble with
his ‘waterworks’ and has been having some back pain.
Instructions for students:
Take a history and give most likely differentials (4 minutes)
List further investigations and justify why you are ordering them
EXAMINER QUESTIONS Four minutes has passed
o List differentials and what is the most likely Which investigations would you like to do and why?
What are your management options if this patient was shown to have prostate cancer?
How would you manage this patient?
HISTORY
Don McClean 68 years old
Lives at home with wife
She is well Pensioner PC
Trouble with waterworks and back pain HxPc
Difficulty passing urine for the last year or so Takes 20 minutes for him to be able to pass urine
o Stopping/starting stream o Passes small volumes
o Feels as though the void was incomplete o Dribbling
Has the sudden urge to empty his bladder Happens nearly all the time
Gradual onset, getting worse
Has to get up to use the bathroom during the night (3-4 times)
Nothing seems to make it better or worse, but has tried running the tap and using warm water to ‘get things going’
No blood in urine
No offensive smell of urine No pain No overflow incontinence No fever No loin pain No discharge No change in bowels
Still able to get an erection Back pain
o Started a few weeks ago o Lower back
o 7/10
o No radiation to legs
o Constant pain
o Nothing makes it better o Worse at night – difficulty
Has never had his prostate checked MHx
Nil allergies UTIs
o A few over the last few years Kidney stones
o Once, 10 years ago Otherwise well
No medications
Doesn’t like going to the dr FHx
Grandfather died of prostate cancer at 75 No other Hx
SHx
Non smoker
Drinks 1 beer/night 2 children – both well DIFFERENTIALS Prostate cancer o Most likely BPH Prostatitis
o No blood, no pain, less likely Renal colic UTI/pyelonephritis Urethral stricture/tumour INVESTIGATIONS PSA Ultrasound
o Size, shape of prostate PR
o Smooth – BPH
o Rough, stony hard – malignancy
Trans-rectal biopsy
Vertebral XRAY/bone scan o Mets
Cystoscopy
Urinalysis and culture o Rule out UTI Renal function If suspecting calculi
o Abdo XRAY
MANAGEMENT AND TREATMENT
The patient most likely to benefit from radical prostatectomy is one with a relatively long life expectancy (>10 years)
Who have a low PSA
Moderately differentiated tumour
Interstitial Radiotherapy:
Patient group most likely to benefit are those with high life expectancy and low volume, low grade disease
No Initial Treatment:
Those who have a preference for no intervention, long life expectancy, low volume disease, moderately differentiated disease
TURP:
A vasectoscope is inserted through the urethra and sections of the prostate are removed in order to increase the opening of the urethra
Complications can include:
o Incontinence
Permanent dilation of the urethra Effects on external sphincter
o Infection o Bleeding o Retrograde ejaculation BRACHYTHERAPY
In patients with METASTATIC DISEASE, the aim of treatment is to control
symptoms and to retard the disease progression. Most cancers are androgen-dependent, at least initially, and hormonal manipulation is the mainstay of treatment of advanced disease. Local radiotherapy is frequently effective for treating painful metastases.
HORMONAL THERAPY
There are three main treatment options:
REMOVAL OF BOTH TESTES BY SUBCAPSULAR ORCHIDECTOMY
o Quick and simple procedure that removes around 95% of the testosterone synthesised (the rest is from the adrenals), producing an immediate fall in plasma testosterone
MONTHLY INJECTIONS OF DEPOT LHRH AGONISTS
o Need to be administered at intervals ranging from 4-12 weeks
o Therapy causes initial stimulation of LH from the pituitary, which turns up testosterone secretion for up to 2 weeks, which is followed by inhibition of LH release by competitively blocking the receptors
o Many patients experience a ‘flare’ in symptoms in the first 2 weeks, aggravating bone pain or spinal compression
o For this reason, the first dose is usually covered by anti-androgen therapy ANTI-ANDROGEN DRUGS SUCH AS CYPROTERONE ACETATE OR FLUTAMIDE
o These block the binding of dihydrotestoerone to its receptor at a cellular level 5-ALPHA-REDUCTASE INHIBITORS Examples Include: Dutasteride Finasteride Mode of Action
They inhibit 5-alpha-reductase, which is the enzyme that converts testosterone into dihydrotestosterone, which is an androgen that stimulates prostatic growth decreased prostatic enlargement
Indications
BPH
Contraindications
Adverse Effects
Common
o Impotence, decreased libido, ejaculation disorder
Uncommon
o Breast tenderness or enlargement
Rare o Allergic reaction ALPHA-ADRENDERGIC BLOCKERS Examples: Alfusozin Mode of Action
These block alpha1 receptors smooth muscle relaxation in the bladder neck and prostate decreased resistance to urinary flow symptom relief in BPH/obstruction Indications Symptom relief in BPH Contraindications Hepatic impairment Adverse Effects
This is a new drug so adverse events are relatively unknown GNRH ANALOGUES Examples Include: Goserelin Leuopolide Mode of Action
Stimulates production of testosterone in a continuous manner (non-pulsatile) increased LH production feedback to pituitary gland down-regulation of GnRH receptor down regulation of testosterone production eventual cessation of hypothalamus-pituitatry-gonad axis
Indications
Prostate cancer (specifically Goserelin) Endometriosis Uterine fibroids Breast cancer Contraindications Pregnancy Breastfeeding
Unexplained vaginal bleeding Polycystic ovarian disease Pituitary Adenoma
Adverse Effects
o Transient changes in BP, hot flushes, sweats, sexual dysfunction, reduced libido
Uncommon
o Bronchospasm, rash Rare
o Depression, hypersensitivity reactions ANDROGEN-AGONIST
Examples
Bicalutamide Mode of Action
Competitively inhibits the binding of androgens (eg, testosterone) to androgen-receptors
Indications
Metastatic prostate cancer with GnRH agonist
o This prevents the initial surge of testosterone from the GnRH agonist prostatic growth prior to receptor downregulation
Prevention of GnRH-agonist associated initial tumour flare Locally advanced prostate cancer
Contraindications
Consider dose reduction in hepatic impairment Adverse Effects
Common
o Dizziness, dyspnoea, constipation, dry skin, rash, weakness Rare
o Thrombocytopaenia, CVS disorders (angina, heart failure, arrhythmias, ECG changes), pneumonitis, pulmonary fibrosis
MANAGEMENT OF THIS PATIENT
Await results and gleason score, staging, PSA Low risk: o T1 or T2a o Gleason score </= 6 o PSA </= 10ng/mL High Risk o T3 o Gleason score 8-10 o PSA >20
Intermediate – in between these values Low risk:
o Active surveillance
o Radical prostatectomy if young and healthy If high risk:
o Radical prostatectomy if young and healthy o RadiotherapY
PERIPHERAL VASCULAR DISEASE
Description of task:
Mr Brian Watson, a 73-year-old retired builder, has come to you (his
GP) as he has been experiencing pain in both legs when walking.
He has a history of coronary artery disease and MI, which occurred
10 years ago.
Tasks for the student:
Take a focused history from the patient
Explain the likely diagnosis
Describe what you would look for on examination of this patient and
what investigations you would order.
ID: Brian Watson, 73-year-old retired builder, lives at home with wife
PC: I’ve been having pain in my legs when I walk doctor
HPC:
- Pain in legs;
Present for 2-3 months
Occurs on walking, relieved with rest
Pain located in calves, both sides but worse on the left
Can now walk about 50m on flat before pain develops, could previously walk a few kms
Gradually getting worse - No pain at rest
- Has not noticed any ulcers, lesions on legs/feet - No acute critical ischemia
- Associated symptoms;
Erectile dysfunction – present for the past year or so, getting worse
Has been having some minor chest pain when walking in past couple of weeks, relieved with GTN and rest
PMH:
- MI 10 years ago – doctors told me it was a ‘small heart attack’ - Hypertension for quite a few years
- High cholesterol - Not diabetic
- Meds – a few have been prescribed but I don’t always take them Aspirin GTN ACEi Statin - No operations - No allergies Smok/Alc:
- Smokes 10 cigs/day – has been smoking since his 30s - Drinks beer socially on weekends
- No illicit drugs
DIAGNOSIS:
- Intermittent claudication – transient, exercise-induced muscular pain that is relieved with rest
Suggests that there is a build up of plaques/fatty tissue in the large arteries of your legs – just like in your heart when you had your MI
- Only differential is spinal claudication - pain in the buttocks and legs brought on by exercise with the back in an extended position
PERIPHERAL VASCULAR EXAM
- Performed with patient supine - Always compare both sides
General inspection:
- Patient able to comfortably move onto bed? - Body habitus – overweight/obese
- Any obvious respiratory distress etc.
Inspection of legs:
- Colour of skin – pale/purple/black? - Trophic changes;
Distal hair loss
Temperature change Shiny, dry, scaly skin - Muscle atrophy, scars
- Ulcers, gangrene – check whole foot and ankle (inc. between toes, heel, sole) Arterial – punched out, painful lesions over pressure areas/bony prominences Venous – irregular, moderately painful lesions over ‘gaiter’ area
Neuropathic (diabetic) – deeply penetrating, painless lesions over pressure areas
- Venous changes;
Varicose veins (best seen with patient standing) Venous ulcers, thrombophlebitis
Haemosiderin deposition, venous eczema
Palpation of legs: - Temperature change;
Start distally and move up leg
- Capillary refill of nail bed – normal <2 seconds
- Palpate aorta and peripheral pulses – start distally and move up - +/- check for radio-femoral delay to exclude coarctation of aorta
Buerger’s test:
- Test for arterial insufficiency
- Raise leg allowing to 45 degrees, allowing blood to drain from leg
In a leg with normal circulation, the foot and toes will remain pink, even with leg rasied to 90 degrees
In a leg with arterial insufficiency, the foot/toes will become pale - Then ask patient to dangle leg over side of the bed
In presence of PVD, foot will become pink-red and painful (reactive hyperaemia)
Auscultation:
- Auscultate for renal and femoral bruits
Other tests:
- Trendelenburg’s test – to assess level of venous insufficiency in patients with varicose veins
Patient lies supine and leg is flexed at hip to allow emptying of veins
Tourniquet/hand pressure is then applied at the sapheno-femoral junction (2cm below and 2cm lateral to pubic tubercle)
Patient then asked to stand – rapid filling of varicosities with tourniquet still on suggests incompetence is below SFJ
Depending on result, tourniquet can be raised or lowered and test repeated to determine level of incompetence
- Sensory examination
Peripheral Vascular Disease
- PVD refers to a wide range of arterial syndromes, but particularly obstructive disease (i.e. atherosclerosis) of major lower limb arteries ischaemia
Also occurs in upper limbs, but much less common - Defined as ABI <0.9
Epidemiology:
- Prevalence increases with age, from age 40 50-59 years = 3-5%
60-69 years = 5%
80 years = >20% (>25% in men) - More common in men
Aetiology & Pathophysiology:
- Most commonly caused by atherosclerotic disease
- Risk factors thus the same as for other causes of atherosclerosis (DM, HT, hyperlipidaemia, obesity, increasing age)
- Atherosclerosis causes obstruction and narrowing of arterial lumen distal ischaemia
- Thus ischaemia produces the 3 cardinal symptoms of PVD (represents progression of disease);
Intermittent claudication – exercise-induced leg pain relieved with rest Pain at rest
Gangrene
- Over time, the disease also affects the neurologic and metabolic function of the lower limb
Muscle atrophy, functional decline Neuronal ischaemia sensory loss - Rarer causes of claudication inc.; Aortic coarctation Arterial dissection Thrombosis, embolism Trauma Vasospasm Arterial tumour Spinal claudication Clinical features:
- Majority of patients are asymptomatic and diagnosis is based on risk factors - Intermittent claudication;
Exercise-induced muscular pain in lower limb, relieved with rest Occurs with ABI between 0.5-0.9
Must determine how far patient can walk (on flat) before pain occurs, and how far they could previously walk
Often more obvious in one limb, producing a limp
Pain almost always in calf, but may extend up to thing and buttocks (depending on level of disease)
- Ischaemic rest pain (chronic severe ischaemia);
Occurs with more severe arterial occlusion – may be a sign of critical limb ischaemia
Occurs with ABI <0.5
Very severe burning pain that occurs at rest – occurs mostly at night (reduced effect of gravity, reduced CO, reactive dilation of skin vessels to warmth) Characteristically relieved to a degree by dangling leg over side of bed, and
completely relieved with analgesics
Often associated with trophic changes in the limb – hair distribution, skin changes, temperature
NB: in patients with diabetic neuropathy, severe ischaemia may be painless - May present with arterial ulcers/gangrene
- Acute critical ischaemia (or acute-on-chronic ischaemia); Severe pain Pallor Pulselessness Paralysis Paraesthesias Perishingly cold
- Erectile dysfunction is a common early symptom of PVD that should be asked about in men – may suggest narrowing of internal iliac arteries
- Physical examination as above - Other features to determine on Hx; Erectile dysfunction
CVD – CAD, MI
Cerebrovascular disease FHx
Investigations:
- Doppler US of lower limb;
Assess blood flow in lower limb, as well as location and degree of stenosis Normal pressure is slightly above brachial systolic
Patients with claudication range from 50-120 mmHg Peak systolic velocity >2 = stenosis >50%
- Ankle brachial index (ABI);
Ratio of BP in lower limbs compared to BP in upper limbs i.e. ABI = systolic BP of dorsalis pedis (or posterior tibial)/systolic BP of brachial artery
Assessed via Doppler US Results;
o 0.9-1.2 = normal
o 0.5-0.9 = moderate arterial disease intermittent claudication o <0.5 = severe arterial disease ischaemic rest pain, gangrene
o >1.2 = abnormal/artificially elevated result due to arterial calcification in PVD causing artificial patency of vessels
- Toe pressure test;
Performed if ABI normal but patient is clinically abnormal, or if ABI >1.2
If toe pressure is <30mmHg in a non-diabetic with an ulcer, it suggests this will not heal
- Arteriography (CT or MRI);
Reserved for patients thought to require intervention in the form of angioplasty or reconstructive surgery
Provides map or arterial system, showing sites and severity of stenosis Does not measure rate of blood flow
- CBE – to exclude polycythaemia or thrmocythaemia (hypercoagulability disorders)
Management:
- Intermittent claudication (mild-moderate disease); Lifestyle modification;
o Walking/exercise plan o Smoking cessation
o Weight loss
o Foot care and appropriate foot wear
Medical;
o Antihypertensives
o Statins (even if cholesterol levels normal) o Aspirin
Most patients do not require revascularisation - Disabling claudication;
Lifestyle modification as above (first line) Medical therapy as above
If there is no improvement, patient should be referred to vascular surgeon for assessment for revascularisation
Methods of revascularisation;
o Balloon angioplasty – most widely used method o Arterial reconstructive surgery with bypass grafting
o Lifestyle-limiting claudication without improvement with conservative therapies
o Critical limb ischaemia symptoms (rest pain, gangrene, non-healing wounds)
o Acute limb ischaemia - Acute limb ischaemia;
Emergency vascular study with ABI or Doppler US
If PVD found, should be immediately treated with antiplatelet (aspirin,
clopidogrel) and assessed for aetiology of ischaemia (embolism, progressive PVD with thrombus, popliteal cyst, trauma etc.)
Non-viable limb;
o Tissue loss, nerve damage, sensory loss o Requires amputation
Viable limb;
o None of the above features
o Urgent arteriography and revascularisation
o Localized intra-arterial infusion of thrombolytics (urokinase) - Chronic severe limb ischaemia (critical ischaemia);
IV drug therapies e.g. prostacyclin Lumbar sympathectomy
Revascularisation
Amputation if revascularisation not viable Terminal pain relief
Complications: - Gangrene
- Functional deficit, sensory loss - Permanent limb pain
- Amputation
- Complications of arterial surgery; Haemorrhage
Thrombosis of reconstructed vessels/graft acute limb ischaemia
Embolism to limb or renal vessels Infection
False aneurysm formation
Prognosis: - Asymptomatic;
All patients with PVD have increased risk of CV ischaemic events
20-60% increased risk of MI, 2-6x increased risk of death due to CAD, 40% increased risk of stroke
- Intermittent claudication;
Usually remains stable and does not rapidly worsen
Increased risk of chronic limb ischaemia with DM or significantly reduced ABI - Critical limb ischaemia;
1-year mortality = 25-45%
Poor prognosis unless revascularisation is performed
- Acute limb ischaemia – prognosis depends on speed and completeness of revascularisation
RENAL COLIC
Ross Bob is a 22 year old male who presents with a 4 hour history of
excruciating lower back pain. You are the intern at the RAH ED.
Take a history from Ross
Provide differentials
Suggest management for the most likely differential
Profile Ross Bob 22 years old Student
Lives at home with parents PC
Severe back pain starting a few hours ago HxPC
Was eating dinner after football training and had sudden onset of lower back pain
o Loin pain o Dull ache
o Constant pain that becomes more severe in waves o Radiates to groin
o Rates it at 8/10
o Worse on movement, better when lying still o Never had this before
o Hasn’t taken any pain relief
No haematuria
Has been feeling nauseous since pain onset and vomiting just before coming to the RAH
No fever
No difficulty urinating, no urgency, frequency, nocturia, dysuria No offensive smell of urine
No urethral discharge
No recent sore throat/flu like illness
Probably doesn’t drink enough water, diet is good, exercises often MHx No allergies No medications Previously well No hospitalisations FHx No renal disease
No significant family history Mum: 54, healthy
Dad 60, healthy SHx
Social smoker
Binge drinks on weekends and after footy matches Uni student, studying human movement
Doesn’t work, gets centrelink
RENAL STONE DISEASE
Renal stones consist of crystal aggregates. Stones form in collecting ducts and may be deposited anywhere from the urethra to the pelvis.
The four narrowest points of the urinary tract, and hence the likely places for stones to lodge are:
Pelviureteric Junction Pelvic Brim
Under the vas deferens/broad ligament Vesicoureteric junction
Incidence
2-3% prevalence (Toronto), oxford says 15% lifetime incidence Peak age 20-40 years
Male: female = 3:`1 Type of Stones
Magnesium ammonium phosphate (10-20%) Urate (5-10%)
Hydroxyapatite (5%) Pathogenesis
Supersaturation of stone constituents Stasis, low urine flow (dehydration)
These lead to crystal formation/stone nidus Risk Factors
Herediatry
o G6PD, Cystinuria Dietary Excess
o Vitmain C, oxalate, purine, hypercalcaemia/hypercalciuiria Renal tubular acidosis
Dehydration
Sedentary lifestyle UTI
o With urea splitting organism o Recurrent UTI
Urinary tract abnormalities
o Eg hydronephrosis, PUJ obstruction, horseshoe kidney, VUR, ureteral stricture Myeloproliferative disorders IBD Hypercalcaemia disroders o Hyperparathyroidism o Sarcoidosis Clinical Features Can be asymptomatic
Urinary obstruction upstream distension pain
o Flank pain from renal capsular distension (non-colicky)
o Severe waxing and waning pain radiating from flank to groin, testes, or tip of penis (colicky)
o “loin to groin” pain
o Obstruction of mid ureter may mimic appendicitis/diverticulitis
o Obstruction in urethra pelvic pain, dysuria, desire but inability to void Other
o Writhing on the bed during history/examinaitoin
o Never comfortable
o Better on lying still, worse on moving o Nausea o Vomiting o Haematuria (90% microscopic) o Diaphoresis o Tachycardia o Tachypnoea
There are occasionally symptoms of bladder irritation (frequency, urgency) Can have co-existing UTI or pyelonephritis
o Fevers, rigors, loin pain, nausea, vomiting Haematuria
Proteinuria Sterile pyuria Anuria