Renal_Medicine & Surgery Flashcards
AKI - key things to do?
1) Check trend (compared to baseline creatinine)
2) Check drug chart (any nephrotoxic?) –> remove/replace
- CANDA: Contrast (keep very hydrated), Aminoglycosides (Gent), NSAIDs, Diuretics, ACEi
- NOTE: DO NOT GIVE Metformin if kidney issue/low GFR - increases risk of lactic acidosis but unlikely to cause AKI
3) Check fluids (pre-renal - dehydration) –> give fluids
What is the AKI checklist?
Check baseline creatinine
Check fluid status
Check drug chart
Different measures of kidney function?
Measures of kidney function:
-
Serum creatinine concentration
- Creatinine = breakdown product of protein metabolism (small amount produced constantly)
- Freely filtered through kindey (concentration in blood: urine is the same) for excretion
- Produced & excreted @constant rate SO reduced renal function –> reduced creatinine excretion –> raised serum creatinine concentration
- eGFR (serum creatinine, age, sex, ethnicity) - reflection of glomerular filtration rate
-
Creatinine clearance (CrCl) - eGFR factors + height/weight
- NOTE: Cockroft & Gault equation
-
Urea
- Nitrogenous waste product of protein metabolism (like creatinine) but some active reabsorption in kidneys (e.g. in dehydration)
- Causes of increase: DEHYDRATION, upper GI bleed, high protein diet
AKI - def? Severity stages? Breakdown by pathology? Key things to do? Ix? Mx?
Def: abrupt loss of kidney function resulting in dysregulation of fluid balance + electrolytes & retention of nitrogenous waste products
Severity defined based on creatinine/urine output:
- Stage 1: 1.5-1.9x baseline/UO <0.5mL/kg/hr for 6-12hrs
- Stage 2: 2-2.9x baseline/UO <0.5mL/kg/hr for >12hrs
- Stage 3: >3x baseline/UO <0.3mL/kg/hr for >24hrs OR anuria >12hrs
Breakdown by pathology:
-
Pre-renal - HYPOPERFUSION
- Hypovolemia (e.g. dehydration/upper GI bleed -> less circulating volume)
- Sepsis/Anaphylaxis (widespread vasodilation -> reduced perfusion pressure)
- HF (heart pumping less effectively -> less blood reaches kidneys)
- RAS (mechanical obstruction of blood flow to kidneys)
-
Renal - KIDNEY-SPECIFIC –> renal referral
- Acute tubular necrosis (following pre-renal AKI, high CK)
- Glomerulus = Glomerulonephritis
- Interstitium = acute interstitial nephritis (low-grade fever, elevated urinary eosinophils, commonly from NSAIDs)
- Blood vessels = vasculitis
- Toxin accumulation = nephrotoxic drugs (ACEi, thiazide diuretic), rhabdomyolysis (myoglobin)
-
Post-renal - OBSTRUCTION –> urology referral
- Ureteric calculus
- BPH
- Cancer (prostrate, bladder)
Key things to do:
- Check trend (compared to baseline creatinine)
- Check drug chart (any nephrotoxic?) –> remove/replace
- CANDA: Contrast (keep very hydrated), Aminoglycosides (Gent), NSAIDs, Diuretics, ACEi
- NOTE: DO NOT GIVE Metformin if kidney issue/low GFR - increases risk of lactic acidosis but unlikely to cause AKI
- 3) Check fluids (pre-renal - dehydration) –> give fluids
Ix:
- Bedside - urinalysis (haematuria, inf, BM, PCR)
- Red cell casts - glomerulonephritis
- White cell casts = pyelonephritis
- Bloods - U&E, AI screen (ANCA), CK
- Imaging - renal USS (stones, vascular thrombosis)
Mx:
- Identify & Mx the cause
- Hypovolaemic - IV fluid bolus
- Hypervolaemic - if pul oedema –> loop diuretic (furosemide) + Na restriciton
Haemodialysis - access? How does it work? How often? Indications? Complications?
Access - 2 points (one for blood to come out of and one to go back into):
- AV fistula (surgical anastomoses between artery & vein) OR Tesio (tunnelled central line)
How does dialysis machine work:
- Box with dialysate fluid in it
- Blood in separate tube going through box
- Semi-permeable membrane between dialysis fluid & blood - diffusion between the two - K+, Na+, Ca2+, Mg2+, Cl-, Glucose, Bicarbonate
- End-stage renal failure will not be able to excrete potassium –> hyperkalemia - blood high in K+, dialysate low in K+ –> diffusion across concentration gradient
- End-stage renal failure will not be able to retain bicarbonate in kidneys = at risk of metabolic acidosis - blood low in bicarbonate, dialysate high in bicarbonate –> diffusion across concentration gradient
- End-stage renal failure = low UO –> fluid retention –> -ve pressure created in dialysate compartment –> H2O drawn into dialysate from blood = ULTRAFILTRATION
How often - 4 times per week
Dialysis indications: HUMP
- Hyperkalaemia (refractory)
- Uraemic complications
- Metabolic acidosis (context of poor renal funct)
- Pul oedema (refractory & hypoxic)
Complications: infection, CVD, fluid balance irregularities
CKD - Key kidney functions? How do these relate to kidney failure? Ix? Classification? Mx? Types of renal replacement therapy?
Kidney key functions –> failure:
- Fluid balance –catheter–> fluid overload
- Electrolyte homeostasis –> hyperkalemia, acidosis
- Waste excretion –> uraemia
- Hormone production (EPO, Vit D activation with 1alpha-hydroxylase, renin –> angiontensin –> aldosterone axis) –> anaemia, hypocalcemia, hyperkalaemia/hyponatremia/low BP
CKD Ix:
- FBC, U&E (GFR, potassium), blood glucose (diabetic nephropathy), abs (e.g. anti-DNA for SLE)
- US, renal biopsy
Classification by eGFR:
- 1 ≥90, 2 ≥60, 3a ≥45, 3b ≥30, 4 ≥15, 5 <15
- NOTE: 5 needs renal replacement therapy
CKD Mx:
- Modify RFs - anti-HTN, good glycaemic control (DM)
- Fluid balance - fluid & salt restriction
- Anemia - EPO-stimulating agents
- Hypocalcemia (& hyperphosphatemic) - vit D supplements, phosphate binders
- Renal replacement therapy - for stage 5 disease (end-stage renal failure) - GFR <15
- Haemodialysis
- Blood passed through dialyzer - removes waste & balances electrolytes
- Vascular access via tunneled central line or AV fistula
- 4 times/wk
- Complications: inf, CVD, fluid balance irregularities
- Peritoneal dialysis
- Peritoneum is used as membrane and dialysate instilled into peritoneum
- Can be done @home BUT increased risk of infection
- Renal transplant - lasts 10-20yrs
- Complications: rejection, recurrence of disease, immunosupression
- Haemodialysis
Nephrotic vs nephritic syndrome
- Glomerular structure and podocyte function?
- Nephritic - def? key signs? causes?
- Nephrotic - def? key signs? causes?
Kidney glomerular structure:
- Capillary > Endothelial cells > Glomerular basement membrane (GBM) > Foot processes of podocyte
- Podocyte function: prevent protein leaking into the filtrate
Nephritic = proliferative - inflammation of glomerulus & nephrons –> capillary becomes leaky –> blood & protein leak
- Key: blood, protein, increased creatinine, possible trigger (e.g. inf), acute/subacute disease progression
- Causes: often immune-mediated
-
Post-streptococcal glomerulonephritis - molecular mimicry - antigen in kidneys accidentally recognised as strep antigen after inf
- Nephritic - more HTN
- Weeks after GAS inf (pharyngitis, skin)
- Ix: ASO titre (high/low C3)
- Mx: conservative - BP control
- No long-term problems
-
IgA nephropathy (Berger’s disease) - generate abn IgA –> abs attach & form immune complexes = sticks & get stuck in glomerular capillaries –> activate compliment –> inflammation
- Nephritic - more proteinuria
- Sx: abdo pain, rash, arthritis
- Days post-resp/GI inf
- Mx: BP control, steroid
- 40% get renal failure
- Assoc w/ IgA conditions (HSP, Coeliac disease)
-
Henoch-Schonlein Purpura (HSP) - related to IgA nephropathy but is WIDESPREAD (IgA limited to kidneys)
- Purpuric rash (buttocks/extensors), arthritis, abdo pain, Hx URTI
- Mx: spontaneous resolution ± steroids
- Haemolytic Uraemic Syndrome (HUS) - MAHA, thrombocytopenia, E.Coli (O157)
- Goodpasture’s syndrome (anti-GBM disease) - pul haemorrhage, rapidly progressing glomerulonephritis + anti-GBM abs
- Granulomatosis with polyangiitis (Wegner’s) - chronic sinusitis + lung haemorrhage, PR3 (cANCA)
- SLE
-
Post-streptococcal glomerulonephritis - molecular mimicry - antigen in kidneys accidentally recognised as strep antigen after inf
Nephrotic = non-proliferative - (urinary protein loss >3.5g/day) from Podocyte effacement
- NOTE: 24-hr urine collection not commonly done so better marker is spot urine protein: creatinine ratio >300mg/mmol
- Key: high protein, hypoalbuminaemia, oedema (face), thrombosis (main coag factor loss in urine is anti-thrombin 3 = one of the bodies main anticoagulant mechanisms –> hypercoagulable state) –> VTE
-
Renal biopsy to determine type –> causes:
- Minimal change disease - children –> Tx: steroids
- Focal segmental glomerulosclerosis - most common in adults, assoc w/ obesity, DM & HIV
- Membranous glomerulonephritis - 2nd most common in adults, idiopathic
- Amyloidosis –> Ix: CONGO RED STAIN
Benign prostatic hyperplasia (BPH) - def? Sx? Ix? Mx?
Def: slowly progressive hyperplasia of periurethral (transition) zone of prostate gland –> urinary outflow obstruction
- Common - occuring primarily in elderly men
Sx: lower urinary tract symptoms (FUND HIPS)
Ix: urinalysis (UTI), PSA (cancer) ± US/CT (abdo/pelvis)/cystoscopy
Mx:
- Acute retention = CATHETERISE
- Conservative - watchful waiting
- Medical:
- Alpha-blocker (relax sm muscle around prostatic urethra) e.g. tamsulosin
- 5-alpha-reductase inhibitor (reduce conversion of testosterone –> dihydrotestosterone - reducing androgenic stimulation of prostate) e.g. finasteride
- Surgical: TURP (transurethral resection of the prostate - shave extra prostate), open prostatectomy
- NOTE: TURP not curative - will continue to grow
Mneumonic for urinary Sx?
LUTS - FUND HHIPS
- Storage Sx (difficulty keeping urine in bladder):
- Frequency
- Urgency
- Nocturia
- Dysuria
- Voiding Sx (difficulty emptying urine from bladder):
- Hesitancy (long time to start) & Haematuria
- Incomplete emptying
- Poor stream
- Straining (effort to start)
Urinary tract calculi - def? presentation? Stone types? Ix? Mx? When to ADMIT/what to do if managed @home?
Def: crystal deposition within the urinary tract
Presentation: severe loin to groin pain (ureteric colic - starts around back and moves towards groin)
Stone types:
- Ca oxalate (80%)
- Mg Ammonium Phosphate (struvite) - likely staghorn calculi
- Associated with proteus mirabilis inf
- Urate
- Cysteine
Ix:
- Bedside - urine dip (microscopic haematuria)
- Bloods - U&E (post-renal AKI)
- Imaging - gold standard non-contrast CT KUB (kidneys, ureters, bladder)
- Contrast is excreted by kidneys - looking for bright white light of Ca –> if you give contrast it will mask the finding
Mx:
- Infected & obstructed = pyonephrosis –> URGENT decompression via NEPHROSTOMY (or retrograde w/ JJ stent)
- Opening between kidney & skin w/ nephrostomy bag for external collection
- Nephro (kidney) stomy (opening)
- <5mm (on CT) - allow spontaneous passing, retain stone for analysis
- >5mm (on CT):
-
Ureteroscopic lithotripsy - endoscope into ureter & using mechanical force/laser to destroy stone
- Uretero (through ureter) scopic (camera) Litho (stone) tripsy (crush)
-
Extracorporeal shockwave lithotripsy - external USS to destroy stone
- Extra (outside) corporeal (body) shockwave (USS) Lithtripsy (crushing stone)
-
Percutaneous nephrolithotomy - ONLY if stone in kidney (e.g. staghorn calculi), extract stone through skin in back
- Percutaneous (through skin) Nephro (kidney) lith (stone) otomy (cutting)
-
Ureteroscopic lithotripsy - endoscope into ureter & using mechanical force/laser to destroy stone
When to ADMIT:
- Pain not controlled
- Significantly impaired renal function
- Single kidney
- Pyrexia/sepsis
- Stone >5mm
If managed at home:
- High fluid intake + return if pain worsening/develop temperature
- OPA in 4 weeks with CT-KUB on arrival –> if stone still present need lithotripsy/nephrolithotomy
Scrotal masses - ddx?
DDx:
-
Testicular torsion - EMERGENCY & TIME-URGENT
- Elevated testis, loss of cremasteric reflex, very tender
- Tx: bilateral orchidopexy (orchidectomy - if necrotic)
-
Can you feel above swelling?
- YES - swelling separate from testis?
- YES - Epididymal cyst OR Varicocele
- NO - Tender?
- YES - Epididymo-orchitis
- NO - Hydrocele OR Tumour
- NO - Inguinal hernia
- YES - swelling separate from testis?
Hydrocele - def? Ix?
Def: collection of fluid in tunica vaginalis
Ix: US, testicular tumour markers (AFP & bHCG - secreted by tumour, LDH - necrosis), urine culture (inf)
Causes: idiopathic, inf, trauma, tumour
Varicocele - def? What side is more common? What is it associated with x2? How can I reduce swelling?
Def: distended veins of pampiniform plexus
Key points:
- More common on left (the way left testicular vein drains into left renal vein)
- Assoc w/ infertility, renal cancer
- Swelling may reduce when lying down
Testicular cancer - Epidemiology & mets? Ix? Mx?
Epidemiology & mets:
- Mets to para-aortic LNs
- Most common malignancy in males 20-40yrs
Ix:
- Blood testicular tumour markers: alpha-fetoprotein, beta-hCG, LDH (necrosis, others secreted by tumour itself)
- Testicular US –> CT-CAP for staging (would likely do orchidectomy before CT)
- Urine dip (look for infection) –> culture
Mx:
- Orchidectomy – take inguinal approach (scrotal approach risks mets and inguinal is coming out the same way the testicle drops) - only time would not do this first is when respiratory compromise then would do chemo first
- BEP chemotherapy follow-up = very good response typically
- Very good prognosis - good/intermediate prognosis groups have >90% 5-yr survival
Hyperkalemia on ECG? Mx?
Worried about arrhythmia
ECG: tented T-waves, widened QRS complex
- NOTE: hypokalemia - flattened (or inverted) T-waves & U waves
Mx:
- Call for senior help = emergency
- Ca Gluconate –> cardiac protection
- 10 U Actrapid + 100ml 20% glucose –> insulin drives K into cells + prevent hypoglycaemia
- Salbutamol –> drives K into cells
- Bicarbonate –> reduce metabolic acidosis
- Haemodialysis if refractory
Casts in urine on microscopy
- RBC casts = glomerular disease –> PS glomerulonephritis, Buerger’s disease
- WBC casts (neutrophils & eosinophils) –> acute interstitial nephritis, acute pyelonephritis
- Fatty casts (lipids) - in polarised light have ‘Maltese Cross sign’ = nephrotic syndrome
- Granular brown casts (degen epithelial cells from ischaemia) = pre-renal injury/nephrotoxic injury (e.g. meds) –> acute tubular necrosis
- Waxy casts = chronic renal failure (often end-stage renal disease = <15 eGFR)
- Hyaline casts (clear) = non-specific
Bladder cancer - presentation? Ix? Mx?
Most common = transitional cell carcinoma (urothelial)
Presentation:
- Painless visible haematuria (or asymptomatic non-visible haematuria)
- Irrigative LUTS (urgency, suprapubic pain)
- Recurrent UTIs
- Pain, weight loss, lymphoedema
Ix:
- Initial:
- Urine dip (blood, leucocytes)
- MC&S (use MSU - RBCs & WBCs, no bacterial growth)
- Bloods - FBC
- Flexible cystoscopy (lower urinary tract) + CT-urogram (upper urinary track if visible haematuria –> if non-visible low-risk use US)
- Dx & staging = Transurethral Bladder Tumour Resection (TURBT) - resects full tumour + histology
- Intravesical therapy:
- Bacillus Calmette-Guerin (BCG) instilled into bladder –> reduces superficial bladder cancer recurrence (causes immune response to remaining tumour cells, same substance as in BCG vaccine)
- Mitomycin - cytotoxic chemo agent
- Intravesical therapy:
Mx: 2wk wait urology
- Muscle invasive = cystectomy (young people) or radiotherapy/chemotherapy (older)
- Superficial = surveillance cystoscopies, intravesical chemo
- Mets = systemic therapy
AD Polycystic Kidney Disease (PCK)
Presentation? Associations? Screening?
Presentation: HTN, abdo discomfort, blood in urine, FHx of IC haemorrhage
- Cysts in kidneys prod renin –> HTN
- Space occupying masses in abdo (renal/liver cysts)
- Can bleed into cysts –> blood in urine
Associations:
- Hepatic cysts
- Berry aneurysms –> risk of ICH
- Mitral valve prolapse
Family screening - renal USS
Urinary retention breakdown? Ix? Mx acute retention?
- Acute - pain
- Chronic – no pain
- Low pressure
- High pressure – renal impairment + hydronephrosis
- LUTS with nocturnal enuresis
Acute Ix:
- DRE - men & women (also PV exam)
- Urine dip + MC&S
- Bloods - FBC, U&E, PSA
- Imaging - bladder scan (for acute), US KUB (for chronic)
- Meds review:
- stop anticholinergics
- analgesia if needed
- laxatives for constipation
Acute urinary retention causes?
Men - usually enlarged prostate
Women - rare, detrusor instability
What are anticholinergic effects?
Acute retention
ACute glaucoma
Tachycardia
Dry eyes/mouth
What is post obstructive diuresis? Tx?
Prolonged urine production after catheter
Tx: IV fluids of half what urine production is
What test would you do if there is left-sided varicocele?
kidney USS (can block of renal vein)
Testicular torsion - presentation? Tx?
Presentation: sudden-onset pain, high fixed position, absent cremasteric reflex
Tx: bilateral orchidopexy (both sides as increased risk of torsion in the other side)
Painless testicular lump, male >60yrs
Benign seminoma (spermatocytic)
Young male, testicular lump, Beta-hCG
Non-seminoma
Prolonged pain + swollen testicle, Hx >1 day - Dx? Tx?
Epididymo-orchitis (young = STI, old = E. coli)
- Tx = ceftriaxone + doxy if secondary to STI
- Gradual onset + pain relieved by testicular elevation
Lower urinary tract Sx (LUTS) - def? Sx?
Def: a group of Sx involving the bladder, urinary sphincter, urethra and prostate gland
- Storage - issues keeping urine in the bladder
- Frequency
- Urgency
- Nocturia
- Dysuria
- Voiding - issues passing urine
- Hesitancy
- Incomplete emptying
- Poor stream
- Straining
What is paraphimosis? Causes? Pathophysiology? Mx?
Paraphimosis def: unable to pull back the foreskin
Causes: tight foreskin (phimosis), a complication of urinary catheter (always remember to replace foreskin after withdrawing for catheter insertion)
Pathophysiology: constrictive effect of foreskin –> oedema of distal penis –> ischaemia/necrosis (if severe)
Mx: UROLOGICAL EMERGENCY - must be reduced ASAP
- Reduce with - Lubricating jelly OR dextrose-soaked gauze
- If difficult - needle used to make small holes in penis –> drainage of oedema
Prostate cancer - Ix? Mx?
Ix:
- PR exam, PSA
- FBC, U&E, LFTs
- Transrectal ultrasound (TRUS)-guided needle biopsy
- Gleason score = PC grading
- TNM staging
- Multiparametric MRI
Mx: surgery/radiotherapy
- Radial prostatectomy ± LN dissection
- External beam radiotherapy/brachytherapy
- Androgen-deprivation therapy (ADT)
Crohn’s flair, AKI with very high urine protein: creatinine ratio, Dx? Key types?
Nephrotic syndrome caused by amyloidosis
Types:
- AA – acute phase protein that increases in inflammatory conditions (e.g. IBD, RA)
- AL – light chain, multiple myeloma –> clump in kidneys
What do you need to do after inserting catheter for acute-on-chronic urinary retention?
Monitor catheter for urine output (may be a lag where kidneys struggle to reabsorb enough water)
What is someone with CKD due to receive IV contrast at risk of? What should be given before hand?
Contrast nephropathy
IV 0.9% NaCl (1mL/kg) for volume expansion
Elderly lady admitted after being found collapsed at home, how do I determine the most likely cause of her AKI?
1) Hypovolaemia if dehydration picture
2) Rhabdomyolysis if CK >10,000
Nephrotic syndrome - test to determine type?
Renal biopsy
Transmural inflame, “beads on a string” on renal angiography - Dx? Def? Presentation? Ix? Mx?
Polyarteritis nodosa - systemic vasculitis, only medium-sized vessels
- NO anti-neutrophil cytoplasmic antibodies (ANCA) and does not involve small vessels unlike ANCA-associated vasculitis (GPA, EGPA, microscopic polyangiitis)
Presentation:
- RFs: 40-60yrs, hep B inf (prevalence of hep B-PAN has reduced with hep B vaccination), hairy cell leukaemia
- NOTE: hep C associated with purely cutaneous form of PAN –> high cryoglobulins
- Skin - livedo reticularis, skin ulcers, bullous or vesicular eruptions, purpura, or skin infarction
- Mononeuritis multiplex, paraesthesia (motor/sensory loss in peripheral nerve distribution)
- Myalgia/arthralgia/muscle tenderness, abdo pain (ischaemia/infarct of bowel)
- High diastolic BP (>90mmHg)
- Systemic - fever, weight loss
Ix:
- Bedside - MSU (rule out inf, RCC/severe proteinuria –> alternative Dx)
- Bloods:
- FBC (normocytic anaemia, raised Pl), U&E, LFTs (hep B/ischaemic hep)
- CRP, ESR, CK, complement (esp in Hep-B-PAN), BC (endovascular inf can mimic)
- HBV/HCV serology, cryoglobulins
- Ab screen - ANCA, ANA (CTD)/DS-DNA, RF/CCP, lupus-anticoag/IgG antiphospholipid/B2 glycoprotein (anti-phospholipid syndrome)
- Imaging: angiography, echo (exclude endocarditis, atrial myxoma, or a left ventricular thrombus)
- ± Biopsy of affected tissue = focal and segmental transmural necrotising inflammation in a medium-sized vessel
Mx:
- Remission: cyclophosphamide + CSs
- Maintenance: low-dose CSs + methotrexate
Acute tubular necrosis - causes? def?
Def: renal tubular dysfunction/detachment from the basement membrane
- Most common intrinsic renal cause of AKI
- Causes:
- Chronic ischaemia of renal tubules (shock/LVF) - initially pre-renal AKI
- Nephrotoxic (lots of myo/haemoglobin, contrast, aminoglycosides e.g. gent, Ig light chains)
- Can’t concentrate urine or regulate electrolytes –> high UO, high urine sodium
Orthostatic hypotension, high protein on urine dip, constipation, bilateral carpal tunnel - what is the kidney biopsy likely to show?
Autonomic neuropathy (orthostatic hypotension, constipation)
Bilateral carpal tunnel DDx: protein infiltration (amyloidosis), pregnancy, hemochromatosis, acromegaly etc…
Dx: Amyloidosis - neuropathy, autonomic dysfunction, end-organ involvement
- Apple green birefringence in polarised light with Congo Red stain
low-grade fever, raised eosinophils in urine, red eyes, prev NSAID use, Dx?
TINU syndrome = red eyes (uveitis) AND acute interstitial nephritis
Renal causes of raised eosinophils?
Acute interstitial nephritis - AKI, NSAIDs, raised urinary eosinophils
- NOTE: TINU syndrome = red eyes + AIN
Churg-strauss syndrome aka eosinophilic granulomatosis with polyangiitis (EGPA)
- Vasculitis (microscopic polyangitis), pANCA +ve (aka MPO)
- Asthma + eosinophils + mononeuritis multiplex
Cholesterol embolism (rare) - livedo reticularis rash (same rash in anti-phospholipid syndrome)
What can result in false urine +ve for blood?
Rhabdomyolysis - myoglobin
Ascorbic acid
Haemoglobinuria (haemolytic anaemia)
Signs on blood that have CKD > AKI
Phosphate high (low Ca –> secondary hyperparathyroidism)
Hb low (low erythropoietin prod by the kidney)
80yrs fallen at home + clinically dehydrated, very high CK, high serum creatinine, urine dip +ve for blood
What is going on? Tx? What finding is likely on biochem? Why is urine dip +ve for blood?
Rhabdomyolysis leaking myoglobin from muscle (due to injury/seizure/statins) –> acute tubular necrosis
Tx: fluids ± haemodialysis
Myoglobin has lots of phosphate and potassium (cells burst):
- PO4 binds Ca = Hypocalcaemia
- Hyperkalaemia
High myoglobin (cause false +ve reading)
ATN vs pre-renal AKI?
If your tubules still work then they can control your electrolytes
In pre-renal: dehydration –> retention of Na to maintain oncotic pressure via aldosterone –> low urinary Na (<20)
In ATN: necrosis so above does not happen –> high urinary Na (>20)
- ATN follows pre-renal AKI
ANCA-assoc vasculitis breakdown? Presentation? Ix? Types based on Ix? Tx?
Presentation: ALL can cause renal impairment + rash (e.g. shins) ± low-grade pyrexia/fatigue
Ix - Rheumatological Ab screening:
- ANA
- ANCA
- biopsies of BVs/affected organs e.g. kidneys
cANCA = PR3 (note: c=3):
-
Granulomatosis with polyangiitis (GPA) aka Wegener’s
- Nasal bridge collapse/epistaxis, chronic sinusitis
- DDx for nasal bridge collapse can be cocaine abuse
- Can develop pulmonary nodules/haemorrhage
- Granulomas
- Case: 52yrs, cough with blood, malaise, rashes, SoB, sinusitis for yrs
- ABG - reduced PaO2, raised creatinine, cANCA +ve
- Nasal bridge collapse/epistaxis, chronic sinusitis
pANCA = MPO (myeloperoxidase):
-
Eosinophilic granulomatosis with polyangiitis (EGPA) aka Churg-Strauss
- Asthma + eosinophilia + mononeuritis multiplex (e.g. weakness in hand)
- Granulomas
- Microscopic polyangiitis - no granulomas
Tx:
- Remission: cyclophosphamide + CSs
- Maintenance: low-dose CSs + methotrexate
Vasculitis breakdown
Large vessel - Aorta & major branches
- GCA (temporal arteritis), Takayasu’s arteritis (occlusive vasculitis –> upper limb claudication, diminished/absent pulse)
Medium vessel - smaller arteries that supply blood to end organs
- Polyarteritis nodosa (PAN), Kawasaki’s arteritis
Small vessel - arterioles & capillaries
- ANCA-assoc: GPA, EGPA, microscopic polyangiitis
- Immune-complex: anti-GBM, IgA vasculitis (HSP), cryoglobulinemic vasculitis, hypocomplementemic urticarial vasculitis
Thromboangitis obliterans (Buerger’s disease) - affects small & medium vessels in lower limb
- Segmental occlusion, young male smokers, tortuous corkscrew collateral vessels on angiography
Urinary incontinence - types & drug Tx?
Stress-incontinence (leak on laugh/cough): pseudoephedrine (2nd - Duloxetine)
Urge-incontinence (preceded by the urge to pass urine): anticholinergic e.g. Oxybutynin (not if >80yrs), Tolterodine
Overactive bladder syndrome (urge but not incontinence - increased freq + nocturia): same as urge incontinence
