8) urinary, trauma + substance abuse Flashcards
Male urinary incontinence
- commonest type of incontinence in men? 1
- other type of incontinence that can occur if large prostate? 1
nb female is in GOSH notes
commonest = URGE (see gynae notes for symptoms etc)
nb men a lot less likely to get stress as better pelvic floors / no babuies stretching them…
can get OVERFLOW incontinence due to large prostate (BPH or Ca) - ie in retension but then a bit comes through
nb elderly men can also get functional incontinence - ie they just forget / can’t get to loo in time (eg dementia, difficulty mobilising) - pads best mx for this!
nb urinary incontinence prevelence: Up to 50% of women and up to 25% of men older than 65 years are affected.
MALE URINARY INCONTINENCE
- what examinations to consider? 2
- bedside tests to consider? 2
- abdo exam (looking for bladder distension)
- DRE
- MSU (could be a symptom of a UTI)
- bladder scan (too see if overflow secondary to retension)
nb if doing PSA as suspision of Ca - either take blood test before to DRE or take blood 1 week after DRE (as DRE will increase PSA!)
urge incontinence management:
- 1st line? 1
- 2nd line? 1
URGE INCONTINENCE
1st line) bladder retraining for at least 6 WEEKS!
2nd line) OXYBUTININ (is an anticholinergic so can increase falls risk in elderly!)
BENIGN PROSTATIC HYPERTROPHY (BPH)
- voiding / obstructive symptoms? 5
- storage / irritative symptoms?
- main complications? 3
VOIDING / OBSTRUCTIVE - hesitancy - weak or intermittent urinary flow - straining - terminal dribbling - incomplete emptying ^think of these in chronological order!
STORAGE / IRRITATIVE - urgency - frequency - urgency incontinence - nocturia (don't forget these ones, get from chronic stretching of bladder and muscles/nerves etc!)
COMPLICATIONS
- UTI
- urinary retention
- obstructive uropathy
Benign prostatic hypertrophy
- 1st line med? 1 (class and named example)
- 2nd line med? 1 (class and named example)
also mechanism of action AND side effects for both
- surgical management option?
1) ALPHA BLOCKER
= Tamsulosin, doxazosin
- decrease smooth muscle tone
- SE: dizzy, postural hypotension, dry mouth (block adrenaline etc so makes sense)
2) 5a-REDUCTASE INHIBITORS
= finasteride (takes 6 months to be effective)
- blocks conversion to testosterone to active form -> reduction in size of prostate
- SE: reduced libido, erectile dysfunction + ejaculation probs, gynaceomastia
SURGERY = transurethral resection of prostate (TURP)
nb can also use desmopressin if persistent and refractory nocturia
NEPHROTIC SYNDROME
- pathophysiology?
- biggest cause in children? 1
- other primary causes? 2
- secondary causes?
injury to the podocyte meaning that large proteins can be excreted by the kidneys (when can’t normally!)
kids = minimal change disease
PRIMARY (90%)
- minimal change disease
- membranous nephropathy/ glomerulonephritis
- focal segment glomerulosclerosis (FSGS)
SECONDARY
- diabetic nephropathy
- hep B or C
- SLE
- amyloidosis (incl from RA and myeloma)
- paraneoplastic
- drug-related (NSAIDs, anti-TNF
nb many of these can present as nephritic of nephrotic syndrome
NEPHROTIC SYNDROME
- main triad of features? 3
- describe urine (ie appearance + amount)
- other symptoms? 3
- Obs change? 1 (nb not commonly seen in minimal change disease)
- later signs / features? 2
1) OEDEMA
2) PROTEINURIA
3) HYPOALBUMINAEMIA
nb oedema norm starts periorbitally then peripheral
urine
- oligouric
- frothy (high protein)
- abdo pain
- anorexia
- diarrhoea
- norm or high BP (norm in MCD)
later
- pleural effusion
- ascites
nb may also have symptoms of underlying disease: eg malar rash in SLE
NEPHROTIC SYNDROME
- main 4 complications (+ how each presents)
also describe pathophysiology of each, briefly!
VTE (40%)
- renal vein trhombosis (flank pain + haematuria) and DVT/PE
- dt loss of antithrombin protein
INFECTION (20%)
- eg cellulitis, strep infections, spontaneous bacterial peritonitis
- dt loss of serum IgG + complements etc
HYPOCALCAEMIA
- presents as parasthesia, muscle spasms, tetany
- dt loss of vit D and binding protein
AKI (poss -> CKD)
- self explanatory
NEPHROTIC SYNDROME
- bedside tests? 2
- blood test need for diagnosis
^and what all of these show
- what investigation to find underlying cause? 1 (and who should NOT have this 1st line)
other possible findings on blood tests:
- urea + Cr?
- cholesterol?
- sodium?
- calcium?
- vit D?
- clotting?
- inflamm markers?
1) urine dip (protein+++)
2) protein:Cr ratio (PCR) VERY high
- nb can do 24hr protein urine instead
3) albumin blood test (low)
RENAL BIOPSY
- on ALL (except kids, unless don’t respond to treatment)
- urea + Cr = norm or raised
- cholesterol = raised
- sodium = low
- calcium = low
- vit D = low
- clotting = prolonged clotting time
- inflamm markers = ESR + CRP may be raised
nb can also do other tests to find cause based on clinica suspision (eg HbA1c if think DM, bez-jones proteins if think myeloma, ANA and Anti-DsDNA for SLE etc)
MANAGEMENT of NEPHROTIC SYNDROME
- management for children? 1
- mx to reduce oedema? 1
- mx to reduce proteinuria? 1
- mx to reduce infection risk? 2
- mx to reduce thrombotic risk? 1
- mx to reduce cholesterol? 1
STEROIDS for kids (90% will go away - although can remit - use cyclophosphamide is refractory)
reduce oedema
= furosemid (+ fluid restrict, daily weights)
reduce protein loss
= ACEi/ARBs
infeciton risk
= flu vaccine
= pneumococcal vaccine
(and treat any infections promptly)
thrombotic risk
= LMWH prophylactic dose
cholesterol
= statin
ALSO FIND OUT AND TREAT UNDERLYING CAUSE!
NB MAJORITY RELAPSE
BLADDER CANCER
- which type are majority in developed country?
- main risk factor? 1
- age and gender at greatest risk?
- other risk factors? 4
TRANSITIONAL CELL (>90%)
= SMOKING
- increased age
- male (5:2)
- aromatic amines (rubber)
- radiotherapy
- chronic cystitis
- schistosomiasis
nb schistomiasis common in developing world and causes squamous cell cancer!
nb can also rarely get adenocarcinoma
BLADDER CANCER
- most common symptom? 1
- additional symptoms? 3
- finding on exam in advanced disease? 1
PAINLESS VISIBLE HAEMATURIA
irritiative voiding symptoms - dysuria - urinary frquency - urgency (ie can mimic a UTI)
palpable suprapubic mass (if advanced)
nb can rarely present in urinary retension (either due to direct pressure of tumour or clot retension)
BLADDER CANCER
- bedside tests? 2
- which two groups of people (based on age and symptom) get a 2WW? 2
- what’s the 1st and 2nd line investigations (once referred to renal)? 2
- urine dip (blood++ and no other findings - ie no WBCs or nitrites)
- MSU - negative for bacteria
2WW
- over 45 AND unexplained visible haematuria
- over 60 AND unexplained non-visible haematuria AND either dysuria or raised WCC on blood test
1) cystoscopy + biopsy
2) CT or MR urogram (for staging)
haematuria - main DDx for bladder Ca? 3
- haemorrhagic cystitis
- UTI
- renal cancer
or could be trauma eg from catheter or if on anticoagulants etc
Management of bladder cancer
- non-invasive (Tis/Ta/T1)? 1 for all (3 to consider)
- muscle invasive (T2-3)? 1 is 1st line (2 to consider)
- metastatic? 1
NON-INVASIVE (Tis/Ta/T1)
1) TURBT (trans-urethral resection of bladder tumour
consider:
- post-op chemo (if intermediate risk)
- intravesical immunotherapy (BCG) (if high risk)
- radical cystectomy (if high risk)
MUSCLE INVASIVE (T2-3) 1st) radical cystectomy (with urinary stoma or continent urinary diversion)
consider
- neoadjuvant chemo before surgery (cisplatin)
- radiotherapy (if not fit for surgery)
METASTATIC
- palliative chemo (cisplatin + gemcitabine)
nb can have pallitive radiotherapy as well
HYDRONEPHROSIS
- causes of UNI-lateral? 4 (incl acronym)
- causes of BI-lateral? 5 (incl acronym)
UNILATERAL = PACT
- Pelvic-ureteric obstruction (congenital or acquired)
- Aberrant renal vessels
- Calculi
- Tumours of renal pelvis
BILATERAL = SUPER
- Stenosis of urethra
- Urethral valve
- Prostatic enlargement
- Extensive bladder tumour
- Retro-peritoneal fibrosis
“have a PACT with the body to only mess up one of the kidneys, oh SUPER (sarcastic) they’ve failed on their pact!”
also makes sense - higher up the urin ary tract - more likely to cause unilateral!
nb Women with gynecological malignancies may present with hydronephrosis. Cervical, uterine, and ovarian cancers should therefore always be considered in nonpregnant women with new-onset hydronephrosis!
HYDRONEPHROSIS
- how normally present?
- main finding on exam?
- main two complications?
depends on cause
- isolated hydronephrosis often asymptomatic
- LUTS if prostate
- flank pain if secondary to stones
enlarged kidneys (one or both)
COMPLICATIONS
- chronic kidney disease (esp if bilateral)
- super-imposed infection (often bad!!)
HYDRONEPHROSIS
- main investigation to diagnose? 1
- 2nd line investigaiton to find cause? 1
- other bedisde tests to do? 2
- blood to always do? 1
1st) USS KUB - to diagnose
2nd) CT KUB - to find cause
- urine dip
- MSU
(to exclude infection)
U+Es
- if renal function impaired, more likely to be bilateral pathology!
Management of HYDRONEPHROSIS
- options for acute upper tract obstruction? 2
- what can be given to reduce pain associated with these? 1
- immediate options for lower tract obstruction? 2
- definitive management?
UPPER tract (ACUTE)
- nephrostomy tube
- ureteric stent
= a-blocker (tamsulosin) to reduce stent-related pain
LOWER tract (ACUTE)
- urethral catheter
- suprapubic catheter
TREAT UNDERLYING CAUSE
- get stone out
- TURP if prostate causing
- pyeloplasty
- debulking if large gynae tumour
CAUSES of URINARY TRACT OBSTRUCTION
- luminal? 3
- mural? 4
- extra-mural? 4
nb this is just another way of classifying
LUMINAL
- stones
- blood clots
- intra-luminal tumour
MURAL
- congenital
- acquired stricture
- neuromuscular dysfunction
- schistosomiasis
EXTRA-MURAL
- abdo/pelvic tumour
- retroperitoneal fibrosis
- iatrogenic (post-op)
- prostatic enlargement (BPH, Ca)
RENAL CANCER
- type of cancer most commonly seen in adults? 1
- name and type of cancer seen in children? 1
Clear cell carcinoma = adults (80%)
wilms tumour (nephroblastoma) = children (see paeds notes)
nb Transitional cell/urothelial carcinoma of the renal pelvis is the second most common renal malignancy and accounts for ∼ 8% of renal cancers in adults.
RENAL CANCER
- age and gender most at risk?
- lifestyle risk factors? 2
- renal risk factors? 2
- other medical risk factors? 4
- hereditary cancer syndromes that increase risk? 4
nb exclude wilms tumour from this - see paeds notes
- male
- age >40
- smoking
- obesity
- polycystic kidney disease as a result of end-stage kidney failure (nb not hereditary PKD)
- renal pelvic stones
- HTN
- immunosuppression
- chronic hep C infection
- sickle cell disease (get renal medullary carcinoma, diff to clear cell)
CANCER SYNDROMES
- Von Hippel-Lindau syndrome
- Hereditary papillary renal cell carcinoma (HPRCC)
- Tuberous sclerosis
Hereditary - leiomyomatosis and renal cancer syndrome (HLRCC, Reed’s syndrome)
^all of these are autosomal dominant (also affect at a younger age than sporadic cancers)
KIDNEY CANCER:
- classic triad of symptoms?
- additional systemic symptoms? 4
- what paraneoplastic syndromes can be seen? 6
- symptoms if local involvement of IVC? 3
- symptoms if local spread to left testicular vein? 1
1) HAEMATURIA (non-visible and intermittent initially)
2) loin pain (only get if tumour >10cm)
3) loin/abdo mass
^haematuria is commonest
- weight loss
- fatigue
- night sweats
- fever (may present as fever of unknown origin!!)
PARANEOPLASTIC SYNDROMES
- HTN (^renin)
- HYPERCALCAEMIA (PTHrP parathyroid hormone-related protein from tumour - or bone mets!)
- POLYCYTHAEMIA (epo) or leukemoid reaction
- CUSHING’S syndrome (^ACTH)
- STAUFFER’S syndrome (non-metastatic derangement in LFTs and clotting - pathology unknown)
- LIMBIC ENCEPHALITIS (memory loss, psychosis, depression)
IVC (budd-chiari syndrome)
- lower limb oedema
- ascites
- hepatic dysfunction
LEFT TESTICULAR VEINS
- a rapidly developing VARICOCELE in men (doesn’t empty when pt lies down)
- a rare but classic symptom of RCC in the left kidney (nb doesn’t happen on R as R testicular vein drains directly in IVC)
nb also lumg symptoms if mets to lung and same with bone!
nb also often anaemic!
nb probs don’t need to know all of these - I just found it interesting…
RENAL CANCER
- gold standard investigation? 1
- what to consider to rule out bladder Ca? 1
- what two imaging to do to look for mets? 2 (classic sign on one of these?)
1st) CONTRAST CT
- if poor renal function, flush with lots of saline (but need contrast!)
consider cytoscopy to rule out bladder Ca
nb can do USS as first line but will end up needing CT
looking for mets:
- CXR (canonball mets = classic!)
- skeletal survey or bione scan
RENAL CANCER
- 1st line management?
- additional management option? 1
- what therpaies DON’T work? 2
1) RADICAL NEPHRECTOMY
biologics in addition (or instead if mets!)
RCC tend to be radio and chemo-resistant!
URINARY STONES
- risk factors for calcium oxalate stones? 3
- risk factors for uric acid stones? 4
- risk factor for struvite stones? 1
- risk factor for calcium phosphate stone? 1
- main risk factor for cystine stones? 1
- main risk factors for xanthine stones? 1
- which of these types is (by far) the commonest? 1
- which causes staghorn calculi? 1
- other risk factors for all? (one lifestyle, one FHx, one med condition)
nb see other flashcards for meds risk factors
aka urolithiasis/nephrolithiasis
CALCIUM OXALATE (75%)
= HIGH calcium (incl high PTH)
= HIGH oxalate (nuts, peanuts + other foods)
= LOW citric acid (ie citrus fruits)
(- also high uric acid!)
(nb can also get if drink antifreeze, and also in IBD dt malabsorption)
(vit C supplements -> oxalate - so increase risk)
URIC ACID (aka urate) (10%) anything that increases uric acid!
= gout
= ileostomy/colostomy (loss of bicarb + fluid -> acidic urine -> precipitation of uric acid
= extensive tissue breakdown (eg cancer)
= kids with inborn errors of metabolism
STRUVITE (10%)
= chronic/repeated UTIs from urease producing bacteria (Proteus mirabilis, S. saprophyticus, Klebsiella)
- causes STAGHORN CALCULI
CALCIUM PHOSPHATE (<5%) = renal tubular acidosis (type 1 + 3) (also in high PTH)
CYSTINE (<5%)
= cystinuria (inherited recessive)
XANTHINE (<5%)
= Xanthinuria (hereditary)
RISK FACTORS FOR ALL
- dehydration
- FHx kidney stones
- polycystic kidney disease or medullary sponge kidney
(also urinary stasis is risk factor for bladder stones!)
Medications and urinary stones
- diuretic which increases risk? 1
- other meds that increase risk? 3
- diuretic which reduces risk?
INCREASE RISK = loop diuretics - steroids - acetazolamide (glaucoma med) - theophylline
DECREASE RISK
= thiazides (they increase distal tubular calcium resorption)
nb these are generally risks for calcium oxalate stones
nb see amboss for crystal appearance, urine pH and radiopacity of each
CLINICAL PRESENTATION of urinary tract stones:
- classic renal colic pain?
- systemic symptoms? 2
- possible findings if bladder stones? 3
- what sign on examination for hydronephrosis? 1
- what sign indicates concurrent infection? 1
Severe unilateral and colicky flank pain (renal colic)
- loin to groin
- Paroxysmal or progressively worsening
- Area around kidneys may be tender on percussion (costovertebral angle tenderness)
nb can get visible haematuria (but is often non-visible)
- nausea + vomiting
- diaphoresis
- if FEVER or RIGOR - think infection added on! = bad!
bladder stones - Dysuria - frequency - urgency (may get complete urinary retention!!)
if palpable kidney - think hydronephrosis!
nb Renal colic is a misnomer as the pain does usually not wax and wane like in intestinal colic - but people do writh around - like in other colic!
nb can also get reduced bowel sounds - dt partial illeus dt pain
URINARY STONES
- bedside tests? 2
- important bloods? 2 (why?)
- diagnostic test? 1
- three places in urinary tract where most comon to find a stone? 3
- dipstick (blood!! - leuco or nitrite mean added infection!)
- MSU (check for infection)
- FBC (high WCC means infection)
- U+Es (if kidney function off = bad/bilateral!)
NON-CONTRAST CT KUB for diagnosis (ultrasound should not be used!)
Commonest places
PUJ, pelvic brim and VUJ
also: clotting if percutaneous intervention planned and blood cultures if pyrexial or other signs of sepsis
nb can also do calcium and urate to look for causes!
nb CRP and ESR are norm psotive too
MANAGEMENT of URINARY STONES
- best analgesic mx for all? 1
- when do you manage expectantly? 1 (med can give to help pass? 1)
- when do you do schock-wave lithotripsy? 1
- when do you do ureteroscopy? 1
- when do you do a percutaneous nephrolithotomy? 1
- when would you do a nephrostomy tube / stent? 3
IM or PR diclofenac = best analgesic (not in pregnancy, severe heart disease or renal impariment though!)
manage expectantly
= <0.5cm (will pass on it’s own within 4 wks)
(nb manage actively if single kidney, prev transplant, any structural kidney abnormality)
- TAMSULOSIN can help pass!
external shock-wave lithotripsy
= stone 0.5-2cm (aggregate)
ureteroscopy
= stone 0.5-2cm (aggregate) in PREGNANCY
Percutaneous nephrolithotomy
- >2cm stone burden or staghorn calculi
neophrostomy tube / stent (ie urgent decompression)
- hydronephrosis
- complete blockage form one kidney (or AKI)
- concurrent pyelonephritis
nb Percutaneous nephrolithotomy
- In this procedure, access is gained to the renal collecting system. Once access is achieved, intra corporeal lithotripsy or stone fragmentation is performed and stone fragments removed.
prevention of urinary stones:
- dietary advice for calcium stones? 3
- med for calcium stones? 1
- med options for oxalate stones? 2
- med options for uric acid stones? 2
Prevention of renal stones
Calcium stones - high fluid intake - low animal protein - low salt diet = thiazide diuretics
(a low calcium diet has not been shown to be superior to a normocalcaemic diet)
Oxalate stones
- cholestyramine
- pyridoxine
Uric acid stones
- allopurinol
- urinary alkalinization e.g. oral bicarbonate
POLYCYSTIC KIDNEY DISEASE
- inheritance pattern?
- main presenting symptom?
- other common way to present?
- change to obs that often seen?
- who to screen for in?
- investigation to diagnose/screen? 1
- prognosis?
dominant (nb can rarely get recessive form)
abdo pain (60%) dt increased formation of stones, haemorrhage into cyst
LARGE PALPABLE KIDNEYS ON EXAM!
recurrent UTIs
get HYPERTENSION
screen everyone with positive family history
- there is a diagnostic criteria used (ie no. of cysts and age)
abdo USS for diagnosis and screening
prognosis depends on type - end-stage renal failure by 50 or slower one that is by 70years
POLYCYSTIC KIDNEY DISEASE:
- most common extra-renal complication? 1
- other extra-renal complications? 6
LIVER CYSTS (70%) - get mild hepatomegaly
- berry aneurysms (8%)
- mitral valve prolapse
- aortic dissection
- pancreatic cysts
- spleen cysts
- ovarian / testicular cysts
nb shouldn’t do contact sports as risk of haermorrhage
nb also higher risk of VTE
CAUSES of URETHRAL STICTURE
- commonest? 2
- rare? 3
= iatrogenic (norm traumatic catheter insertion) 45%
= STI 20%
nb can also be idiopathic! 30%
- hypospadias (or other congeintal)
- lichen sclerosis
- cancer (very rare!)
nb is uncommon in both sexes - but more common in men!
URETHRAL STRICTURE
- symptoms?
- decreased urine flow (1st symp)
- hesitancy / straining
- spraying or double stream
- dribbling
- ejaculatory dysfunction
+/- urinery freq or infections
- pain
may be asymptomatic until get urinary retension!
nb investigation is fancy test to assess flow
mx is internal urethrotomy or orethroplasty
VESICOURETERIC REFLUX
- describe pathology?
- what often present with? 1
- what % of children presenting with this will have VUR?
- investigation to diagnose? 1 (additional investigation to assess severity? 1)
- main long-term complication if undiagnosed?
- management?
Ureters are displaced laterally → abnormal backflow of urine from bladder into ureter and kidney when pass urine → RECURRENT UTIs → Renal scarring
30% of children with UTIs will have this!!
diagnosis = Micturating cystourethrogram
for severity: DMSA scan – looks for renal scarring (use grades to describe severity)
can -> CKD!
mx = surgical repair of valves!
GLOMERULONEPHRITIS:
- three features / mechanism of damage?
- three possible clinical presentations / syndormes? 3
nb these are regardless of cause! (see other flashcard)
inflammation of glomerulus or small renal vasculature of the kidney causing characteristic features:
A) Damage to vasculature: restricts blood flow to kidney → ↑Renin → compensatory ↑BP (mild → malignant)
B) Damage to filtration: ↑Protein ↑Blood to enter urine (mild → severe)
C) Loss of filtration capacity → AKI → CKD (ALL have potential to do this!!)
PRESENTATIONS
- asymptomatic
- nephritic syndrome
- nephrotic syndrome
depends on cause as to presentation - although some causes can present in multiple different ways
difference between nephritic and nephrotic syndrome in:
- main symptom?
- BP?
- finding on urine dip?
- U+Es?
- serum albumin?
NEPHRITIC
- haematuria (visible or not)
- mod-severe HTN
- blood++ protein+ (if severe can have nephrotic range protein!)
- mod-severe drop in eGFR
- norm/slightly reduced serum albumin
NEPHROTIC
- oedema (peri-orbital 1st)
- norm-mild HTN
- no blood or +, protein++++
- eGFR can be normal
- very low albumin!
BOTH have oliguria!
also both have sterile urine (unless have infection as well!)
nb see other flashcards for causes of nephrotic syndrome and other features etc
Causes of nephritic syndrome:
- triggered by URTIs?
- vasculitises? 3
- other autoimmune? 2
- basement membrane probs? 2
- other? 1
- Poststreptococcal glomerulonephritis
- IgA nephropathy (Berger disease)
- Granulomatosis with polyangiitis (Wegener’s)
- Microscopic polyangiitis
- Churg-Strauss syndrome
- Goodpasture syndrome (anti-GBM disease)
- Lupus nephritis
- Alport syndrome (hereditary nephritis)
- Thin basement membrane disease
- Rapidly progressive glomerulonephritis (RPGN) (CAN BE ANY CAUSE!)
nb SLE can cause nephritic or nephrotic, as can:
- Membranoproliferative glomerulonephritis
- Diffuse proliferative glomerulonephritis
nb see amboss for description of each of these
one day I will properly learn these - but not today…
Causes of GLOMERULONEPHRITIS
- IgA nephropathy (Beurgers)
- post-streptococcal
- age group affected?
- trigger/cause (same for both) and timescale (diff)?
- main presenting symptom?
IgA NEPHROPPATHY (BEURGERS)
- young people (es male)
- 1-2 days after/during URTI
- intermittent macro/microscopic haematuria
POST-STREP GLOMERULONEPHRITIS
- children
- 1-2 weeks after URTI
- haematuria + proteinuria (rarely nephrotic range though)
both often have oliguria and HTN
nb big overlap with HSP for IgA nephropathy
ORTHOSTATIC PROTEINURIA
- what is it?
- age groups affected?
- how present?
- investigation?
- serious DDx to exclude? 1
normal urinary protein excretion during night, increased excretion during day a/w activity and upright posture = TOTALLY BENIGN!
Commonly children and young adult males
Asymptomatic (if sysmptoms, think of another cause!)
24 hr urinary collection of protein + creatinine clearance – overnight and daytime
- will be v low/zero overnight and lots in day/esp near end of day
if this is only feature then don’t worry! - worry if any blood, signs of infection, diabetes etc
serious DDx = nutcracker phenommenon
= Compression of Left Renal Vein between aorta and superior mesenteric artery
- also have proteinuria that goes away at night
BUT ALSO HAVE: - Haematuria (asymptomatic) + Orthostatic proteinuria
Flank or Abdo Pain
Variocele, Dyspareunia, Dysmenorrhoea
nb MRI for diagnosis
nb think this is super rare - just thought was quite interesting…
LOIN/FLANK PAIN DDx
- renal? 4
- cardiovascular? 2
- other? 4
- what else to consider on R side?
- pyelonephritis
- renal colic
- renal tumour
- renal cysts (incl PKD)
- AAA
- renal artery infarction (eg in AF)
- muscle strain
- radiculopathy
- varicella zoster (shingles)
- psoas abscess
- remember biliary if on right (biliary colic, cholecystitis, cholangitis) also hepatic! - eg hepatitis
also remember other stuff like pancreatitis, ectopic preg, appendicitis, bowel obstruction, even PE!
HAEMATURIA
- causes of transient / spurious non-visible haematuria? 4
- malignant causes of persistent non-visible haematuria? 3
- other causes of persistent non-visible haematuria? 5
TRANSIENT / SPURIOUS NON-VISIBLE
- urinary tract infection
- menstruation
- vigorous exercise (norm settles after 3 days)
- sexual intercourse
MALIGNANT CAUSES
- bladder Ca
- renal Ca
- prostate Ca
OTHER CAUSES
- urinary tract stones
- urethritis
- prostatitis
- BPH
- renal causes (eg IgA nephropathy, thin basement membrane disease, other causes of nephritic syndrome)
nb non-visible haematuria is present in 2.5% of pop! (same numbers as if on aspirin/blood thinners - so still need to, if relevant, investigate these people too!)
nb also Spurious causes - red/orange urine, where blood is not present on dipstick
foods: beetroot, rhubarb
drugs: rifampicin, doxorubicin
HAEMATURIA
- if find what investigations should you do:
- bedside? 2
- obs? 1
- bloods? 2
nb see flashcard on bladder Ca about 2WW rules
- urine dip
- albumin creatitne ration (ACR)
- BP
- U+Es
- FBC
COMPARTMENT SYNDROME
- pathophysiology? (INCL TIMESCALE)
- two main areas of body most at risk? 2
- which two bone fractures most at risk of producing it? 2
- other main causes / risk factors? 4
swelling of tissue in anatomical compartment → ↑compartment pressure → occludes vascular supply → hypoxia → acute ischaemia + oedema → necrosis (can happen within 4-6 hours!!)
- lower limbs
- upper limbs
(also less common in: hands, feet, gluteal regions, abdo)
HIGH RISK FRACTURES
= supracondylar
= tibial shaft
OTHER CAUSES
= OTHER TRAUMA (other fractures, crush injury)
= VASCULAR (reperfusion injury following ischaemic limb, haemorrhage)
- burns
- infection
COMPARTMENT SYNDROME
- main symptom? 1
- what may mask this symptom? 1
- initial signs on exam? 4 (1 of these is a clinical test)
- late signs? 2
- how diagnose?
EXCRUCIATING PAIN (despite immobilisation of injury)
- totally out of proportion to injury!
- may be masked by post-op analgesia (eg PCA, regional blocks etc)
- if someone keeps needing PRNS, consider this!!
1) PASSIVE STRETCH PAIN
- move distal joint with tendons passing through suspected compartment, will cause excruciating pain
2) MUSCLE SWELLING AND TENDERNESS
- Very tight, wood-like muscles that are extremely tender to touch
3) SENSORY DEFICITS
- may be as parasthesia (ie pins + needles)
4) INTACT PERIPHERAL PULSES
- if peripheral pulses not palpable then this is very LATE!!
late signs
- ischaemic limb (pale, pulseles, paralysis, cold etc)
- paralysis of muscle group
is a CLINICAL DIAGNOSIS!
COMPARTMENT SYNDORME
- who to call immediately? 1
- investigation to confirm diagnosis? 1
- important bloods? 2
call ORTHOPAEDIC SURGEONS!
1) INTRACOMPARTMENTAL PRESSURE MEASUREMENTS
- Pressures in excess of 20mmHg are abnormal and >40mmHg is diagnostic (wick catheter, needle manometry)
bloods
- CK
- U+Es
^to asses for rhabdo / AKI
nb Compartment syndrome will typically not show any pathology on an x-ray (although can see underlying fractures)
nb can use USS doppler to assess for cause if unclear!
COMPARTMENT SYNDROME
- conservative management? 4
- definitive mx? 1 (within what time frame)
- what additional management might be needed? 2
conservative is while waiting for definitive!! - everyone needs definitive fast!
CONSERVATIVE
1) remove any restrictive castss/dressing
2) cool limb and position limb at level of heart (not above!)
3) ANALGESIA!!
4) aggressive IV fluids (to prevent / treat AKI)
nb don’t elevate leg! - this may worsen ischaemia!
definitive = FASCIOTOMY! (within 6 hrs of onset - but ideally within 1 hr!!!)
may need
- fasciectomy (to remove necrotic tissue)
- amputation of limb - if too late!
?all pts need re-exploration at 48hrs? (check this!)
ACUTE COMPARTMENT SYNDROME
- main DDx? 3
- acute compartment syndrome
- rhabdomyolysis
- acute limb ischaemia (eg with AF or PVD)
- DVT
also could be cellulitis
CHRONIC COMPARTMENT SYNDROME
- who at risk?
- part of body affected?
- how present?
- management options? 2
- main DDx? 2
young, fit athletes
norm bilateral legs
similar presentation to acute but a lot less severe
- pain/swelling rigidity
- worsens upon exercise + passive stretching, resolves with rest
- may get parasthesia + numbness
diagnosis is by intra-compartmental pressure monitoring (same as acute)
Mx
- conservative (limit or stop activity causing pain)
- fasciotomy (if conservative doesn’t work / want to continue doing activity)
DDx
- shin splints
- stress fractures
FEMORAL FRACTURES
- three types? (according to location)
- hip
- shaft
- supracondylar (distal)
FEMORAL SHAFT FRACTURE:
- two different mechanisms of cause? 2
- findings on examination? (2 look, 2 feel, 1 move)
- what should you always check on exam? 1
CAUSE:
- High-impact trauma (RTAs, crush injury, hard falls)
- Low-impact injuries associated with pathological fractures (eg fall from standing, also on bisphosphonates)
nb has a bimodal age distribution: early adult and old age!
- Painfully swollen, tense thigh
- Signs of fracture (e.g., shortening, deformity)
- Crepitus and distal neurovascular deficits could be present
- Restricted range of motion
always check NEUROVASCULAR intact!
FEMORAL SHAFT FRACTURES
- conservative management while waiting for imaging / definitive management? 1
- best analgesia to give? 1
- imaging? 1
- bloods to always do? 2
THOMAS SPLINT to prevent deformity and reduce bleeding
femoral nerve block for analgesia
x-ray leg (at least 2 views!)
- also x-ray hip and knee!!
- GROUP + SAVE! (can loose a lot of blood)
- clotting screen (going for surgery!)
nb definitive management on next flashcard
FEMORAL SHAFT FRACTURES
- commonest form of surgery done? 1
- what to do after surgery? 3
- prognosis / how long until completely healed?
INTRAMEDULLARY NAIL
= most common
can also do external fixation and other methods too
after surgery:
- immobilise (backslab initially so can swell!)
- re-xray! - to check alignment!
- physio (nb do with ALL long bone fractures!)
4-6 months until completely healed (check this!!)
FEMORAL SHAFT FRACTURES
- local complications at high risk of? 3
- additional complication if open? 1
- distal complications at high risk of? 2
- acute compartment syndrome
- large haematoma
- neurovascular damage
- infection (if open - give Abx to prevent - ALSO TETANUS VACCINE)
- fat emboli
- DVT/PE
also can have non-union of bones etc
FAT EMBOLI:
- biggest risk factors / causes? 2
- timeframe from cause to emboli?
- classic triad of symptoms? (+ order in which they happen)
- management?
95% are traumatic fat emboli
- long bone fractures
- orthopaedic surgery
(- also post bone marrow transplant)
nb can get rarely get from pancreatitis, osteomyelitis, sickle cell crisis
get symptoms 12hrs-2weeks after trigger (norm about 72hrs)
1) HYPOXIA
- most common symptom (appears like resp distress syndfrome: high RR, cyanosis, diffuse crackles in chest)
- also FEVER
2) NEURO SYMPTOMS
- confusion
- lethargy
- seizures
- focal neuro deficits
- coma
3) PETECHIAL RASH
- seen in up to 50% of pts
- mainly in axilla, chest wall, head, neck, conjunctiva, buccal mucosa
is a CLINICAL DIAGNOSIS
nb may have anaemia and thrombocytopenia
x-ray often normal, may have bilateral infultrates
mx = supportive care (norm in ICU)
15% mortality
nb Petechial rash in combination with the other symptoms is diagnostic of fat embolism. In patients who do not develop the rash, fat embolism is a diagnosis of exclusion (rule out other causes of hypoxia and neurological symptoms).
SUPRACONDYLAR FEMUR FRACTURES
- where are they?
- two main causes? 2
- three main categorisations? 3
Fracture of the distal 1/3rd of femur (typically weaker metaphyseal bone)
- Direct violent trauma in adolescent and young adults
- Osteoporosis with low energy trauma in elderly
Categorise as
- extra-articular
- partial articular
- complete articular
really important to get 2 x-ray views of knee and 2 of femur!
SUPRACOPNDYLAR FEMORAL FRACTURES
- what two structures are often damaged? 2 (ie complications)
- normal management? 1
Commonly COMMINUTED and intra-articular → DAMAGE TO KNEE JOINT
Distal fragment of femur pulls backward → POPLITEAL ARTERY DAMAGE
same as femoral shaft - incl nerve vlock, splinting beforehand etc
- norm do intermedullary nail!
HUMERUS FRACTURES
- who gets proximal? 1
- who gets distal? 1
- other type? 1
- most common mechanism of cause for all?
- other mechanisms? 4
proximal = norm in older people
distal = children
mid-shaft is other type
FOOSH is most cmmon cause of all types!
other causes
- RTAs
- violent seizures
- direct blow to back of humurus (norm mid-shaft)
- pathological fractures (less common)
PROXIMAL HUMERUS FRACTURE
- specific classification system to describe fracture?
- what other pathology can also happen?
- commonest neurovascular injuries? 2
- what % are treated non-operatively? type of sling given?
- indications for surgery? 4
- commonest type of surgery done?
NEER CLASSIFICATION
- proximal humerus has four major segments: the anatomical neck, the humeral shaft, the greater tuberosity, and the lesser tuberosity (the surgical neck is distal to the lesser and greater tuberosity)
- NEER = commonly used classification that is based on whether one or more of these four segments have been displaced
can get posterior shoulder dislocation (nb 95% of shoulder dislocations are anterior!)
neurovascular injuries
= AXILLARY NERVE (check regimental patch)
= AVASCULAR NECROSIS of femoral head (common if lots of fragments)
85% treated non-operatively
- collar + cuff sling (provides ownwards tration)
indications for surgery:
- displaced
- communited
- open
- neurovascular compromise
surgery norm = MUA (manipulation under anaesthetic) and internal fixation
Definition of displaced fracture? ie by what angle and what distnace?
displaced if
- >10mm movement
OR
- angulation > 45 degrees
HUMERAL SHAFT FRACTURE
- which neurovascular structure most at risk? 1 (how does this present?)
- conservative management?
- who gets closed reduction?
- indications for open reduction + surgical fixation? 2
HUMERAL SHAFT
RADIAL NERVE = most at risk
- Wrist drop (test with elbow flexed, wrist pronated)
- Sensory loss to dorsal 3 ½ fingers
conservative
- hanging arm cast (basically cast PLUS collar + cuff)
also need physio!
closed reduction + long arm splint
- if mildly displaced
open reduction + surg fixation
- communited
- vascular compromise
nb 70% of radial nerve injuries will recover spontaneously with conservative mx
DISTAL HUMERAL FRACTURE
- two types? 2 (which group get each)
- norm mechanism? 1
- neurovascular structures at risk? 4
- if can’t see fracture, what other signs do you see which indicate an occult suppracondyl fracture? 2
- mx? 1
- Supracondylar (children, crepitus)
- Transcondylar (T or Y shaped fractures, elderly, shortened)
fall onto outstretched arm
nb a/w shoulder and wrist injuries
- brachial artery
- radial nerve
- median nerve
- ulnar nerve
(ie all the nerves plus brachial artery!)
- LARGE anterior fat pad (small is norm)
- ANY posterior fat pad
probably similar to others - NEED TO LOOK UP PROPERLY!***
findings if damage to:
- axillary nerve?
- radial nerve?
- median nerve?
- ulnar nerve?
describe motor and sensory deficits
and which type of humeral fracture is each associated with?
AXILLARY
- Flat deltoid
- ↓ Arm abduction at shoulder > 15 degrees
- ↓ Sensation over deltoid and lateral arm
= Proximal humerus
RADIAL
- Wrist drop (Loss of elbow, wrist, and finger extension)
- ↓ Grip strength
- ↓ Sensation over dorsal hand and posterior arm
= Humeral shaft
= Distal humerus
ULNAR
- Claw hand deformity
- Froment’s paper sign (on holding piece of paper between thumb and finger, there is flexion of thumbs distal phalanx trying to pull apart)
- Radial deviation when wrist is flexed
- ↓ Sensation over medial 1 ½ fingers (5th digit and half of the 4th digit) including hypothenar eminence
= Distal humerus
MEDIAN
- Anterior interosseous nerve syndrome: unable to oppose index finger and thumb of affected hand
- ↓ Wrist flexion
- ↓ Flexion of lateral fingers and ↓ thumb opposition
- ↓ Sensation over thenar eminence and over lateral 3½ fingers (first 3½ digits, beginning with the thumb)
= Distal humerus
HAND INFECTION
- two commonest groups of causes?
- common bacteria seen in each (2 for each)
PENETRATING INJURY (eg nail)
- staph aures (commoest)
- strep
BITE (human or animal)
- Eikenella corrodens (human)
- pasteurella spp (animal)
HAND INFECTIONS
- what is a ‘felon’?
- palmar space infection (what is? and how present?)
- signs of flexor sheath infection? what addiutional management does this need?
- main complications of all hand infections? 2
felon = finger pulp infection
PALMAR SPACE INFECTION
- infection of one of the 4 fascial compartments of the palm
- pain, swelling and reduced movement
- swelling is often more prominent on the dorsum of the hand
FLEXOR SHEATH INFECTION
- flexed posture of finger with pain on passive extension of fingers
- fusiform swelling
- pain along flexor sheath
= often requires continuous saline irrigation for 24-48hrs post-drainage
- cellulitis
- loss of function
HAND INFECTIONS:
- initial treatment? (3 conservative, 2 medical, 1 imaging)
- what to do if any pus? 2
- would closure?
- management to promote healing / comfort after inital treatment? 4
- irrigate (esp if bite)
- elevate
- splint
- IV co-amox (?or oral)
- tetanus shot (if not had in 10 years)
- plain x-ray (to exclude associated fractures, foreign bodies, osteomyelitis, evidence of gas-forming infection)
any pus
- drain and irrigate fully
- send for culture
leave wound OPEN for delayed primary wound closure
ONGOING MX
- continue levation
- daily saline soaks / irrigation of wound
- splint for comfort (wrist extended, MCPJs flexed, IPJs extended)
- physio (if needed)
PARONYCHIA
- what is it?
- two groups of causes?
- management for each?
paronychia = infection of nailfold
BACTERIAL
- mx as with all other hand infections (incl drain if pus)
OTHER
- candida (topical antifungals)
- herpes simplex
^soak digit in warm water several times a day for both
nb this is acute infection - can also get chronic probs (see derm net NZ)
CLAVICLE FRACTURES
- most common mechanism of injury?
- 3 locations? which most common? classification?
- neurovascular sturctures possibly at risk? 2
- other possible complicaiton? 1
Direct trauma (95%)
- Fall onto the shoulder (most common cause)
- Direct blow to the clavicle, e.g., from a football tackle
(Indirect trauma (5%): mainly FOOSH or birth trauma)
I = midshaft/middle 3rd (70%) II = lateral/ distal 3rd (25%) III = medial / proximal 3rd (5%)
- brachial plexus
- subclavicular artery
- pneumothorax!
CLAVICLE FRACTURES
- how is each type managed?
- indications for possible surgery? 4
I = midshaft/middle 3rd (70%)
- BROAD ARM SLING (NOT collar + cuff)
- treat conservatively even if displaced - has to be displaced a lot for them to do surgery!
II = lateral/ distal 3rd (25%)
- undisplaced broad arm sling
- may require fixation with plates and screws, esp if ligament damage
III = medial / proximal 3rd (5%)
- broad arm sling if not displaced
- if displaced, esp posteriorly, then may need surgery
indications for surgery
- open
- floating shoulder
- significant neurovascular compromise
- ‘tenting’
JERSEY FINGER and MALLET FINGER
- what tendon damaged?
- cause of each?
- how present?
JERSEY FINGER
= Flexor digitorum profundus tendon
- Sudden hyperextension of a flexed DIP (forced extension) - what Asha had!
- Pain, swelling of the DIP (palmar aspect)
- Loss of DIP flexion → the affected finger does not flex when making a fist
MALLET FINGER
= Extensor digitorum tendon
- Sudden hyperflexion of the DIP (forced flexion) → avulsion/rupture of the distal portion of the ED tendon from the distal phalanx (eg when a ball hits finger tip!)
- May be associated with an avulsion fracture of the distal phalanx
- Loss of extension of the DIP
all FLEXOR tendon injuries need to be repaired surgically! - extendor and some ligament injuries can be mamnaged conservatively
- but complete laceration or no response to conservative therapy are indications for surgical repair
nb fingers need THREE views on x-ray
ACL vs PCL
- anatomy (where to and from?)
- mechanism of injury?
- clinical test?
- imaging?
- conservative management?
- indications for surgery
ACL
= anterior tibial plateau -> postero-lateral aspect of intercondyl notch of femur
- sports injury: high twisting force applied to a bent knee
- presents w loud crack, pain and RAPID joint swelling (haemoarthrosis)
= anterior draw test
= MRI scan (x-ray not helpful)
- PRICER (rice + protect from further injury and rehab)
= most ACL tears managed SURGICALLY!
PCL
= posterior tibial plateau -> anteromedial aspect of intercondylar notch of femur
- rarer, norm high force RTA (or anything else that forces tibia posterior to bent knee)
= posterior draw test
- PRICER (see above)
= surgery if: avulsion fracture, associarted with other ligament injuries, failed conservative mx
nb triad of common injuries is: ACL, medial collateral and medial meniscus tear
LATERAL vs MEDIAL collateral ligament
- mechanism of injury for each?
- which may also present with nerve damage (which nerve)?
- clinical test for each?
- management for each?
- which more likely to need surgery?
LATERAL COLLATERAL
- excessive medial force to knee
- may damage common peroneal nerve -> foot drop
- VARUS stress test
- PRICER + non-weight bearing restriction, use crutches, knee brace in full extension for 4-6wks
- more likely to need surgery
MEDIAL COLLATERAL
- excessive lateral force to knee
- VALGUS stress test
- PRICER (incl physio)
- surgery rarely required for ISOLATED MCL tear (but may do MRI to look for associated mensical tear!)
both present with effusion and tnederness on damaged side of knee
KNEE MENISCAL TEARS:
- mechanism of injury?
- how present?
- clinical test? 1 (describe how to do it)
- imaging?
- management?
- indications for surgery? 2
mechanism norm a twisting sports injury
delayed effusion / swelling (2-36hrs) (if within a couple of hours suspect additional ligament injury)
Joint LOCKING (pt may develop skills to 'unlock' the knee) - may also just give way!
Recurrent episodes of pain and effusions are common, often following minor trauma
MCMURRAYS TEST
- knee flexed, apply stress and extend, +ve test is pain, popping or clicking
- Int rotation + varus = lateral
- Ext rotation + valgus = medial
MRI KNEE
- may also do an x-ray to look for associated fractures/avulsions
mx = PRICER
KNEE ARTHROSCOPY (essential)
surgery if 6-8wks of physio is not effective
also go to surgery straight if bad tear or associated ligament tears
OTTAWA RULES
- indication for FOOT x-ray? 4 (2 tender points, 1 other)
- indication for ANKLE x-ray? 4 (2 tender points, 1 other)
FOOT
- tender at: navicular bone (medial bone just distal to talus)
- tender at: base of 5th metatarsal
- inability to weight bear (4 steps) both immediately after injury AND in ED
ANKLE
- tender at: posterior edge/tip of medial malleolus
- tender at: posterior edge/tip of lateral malleolus
- inability to weight bear (4 steps) both immediately after injury AND in ED
if ANY ONE of these are found then x-ray!
FIBULAR / LATERAL MALLEOLAR FRACTURE:
- classification?
- which classification are stable? which not?
- what is a maisonneurve fracture?
WEBER CLASSIFICATION
weber A
- fracture below syndesmosis (deltoid ligament intact)
= usually stable
weber B
- fracture at level of syndesmosis (may be deltoid ligament injury)
= variable stability
weber C
- fracture above syndesmosis
- often deltoid ligament tear and/or medial malleoluys fracture
= unstable
^these are all FIBULAR / lateral malleolus fractures
MAISONNEURVE FRACTURE
= PROXIMAL weber C fracture (ie near the knee) with damage to ligaments at ankle -> talar shift
if see isolated talar shift - always do more imaging!!
ANKLE FRACTURES:
- how many x-ray views needed?
- conservative management?
- indications for surgery?
3 views
conservative = short leg cast 4-6wks
surgery if:
- unstable / displaced fractures
- open fractures (+abx +/- tetanus)
- neurovascular damage
nb bi and tri malleolar fractures are often unstable!
nb if ankle is very displaced do manual external reduction first - then backslab then surgery!
HAND INJURY
- conservative mx? 5
- who to refer to?
- imaging?
- meds to consider? 2
- analgesia
- remove rings ASAP
- clean wound site
- elevate hand
- cold compress
refer to PLASTICS
low threshold for x-ray - 3 views (AP, lateral, oblique)
open:
- consider tetanus
- antibiotics!
What is ilizarov frame surgery?
main 3 indications?
An ilizarov frame is an external frame surgeons use to lengthen or reshape bones or to treat complex mal-union or non-union fractures
- malunion fractures
- bone deformities (incl rickets and achondroplasia)
- following removal of bone (eg for ca or osteomyelitis)
can involve a live bone transplant - ie from one part of your body to the other
Smoking increases your risk of which cancers:
- squamous cell? 5
- others? 5
SQUAMOUS CELLS
- oropharynx
- larynx
- oesophagus
- lung
- cervix
OTHERS
- adenocarcinoma of oedeophagus
- small cell lung cancer
- pancreatic adenocarcinoma
- renal cell carcinoma (clear cell)
- transitional cell carcinoma of the bladder
LONG-TERM SOLVENT ABUSE:
- what areas of the body tend to be affected? describe briefly their effects
- management?
MAINLY NERVOUS SYSTEM
- dizziness / vertigo
- headache
- confusion
- behaviour changes
- sedation
- ataxia
- polyneuropathy
- nausea and vomiting
there are LOADS of different types of solvents which all have different effects
derm effects are also common!
- also damage liver, kidney + muscles
you can die from one episode!!!
management is mainly supportive and psychological - there are no antidotes / medications that are useful
