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
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
