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Renal/Urology Flashcards

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USMLE® Step 1 flashcards
1
Q

Uraemia

  1. Symptoms
  2. Life threatening conditions
A
  1. Lethargy, confusion, convulsions, N+V, pruritis

2. Pericarditis, encephalopathy

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2
Q

Pre-renal vs renal causes - distinguish

A

Pre-renal reduced perfusion - urine concentrated

Renal - salt and water loss due to problems with kidney

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3
Q

Differentials for presentations

  1. Dysuria, urgency, frequency, nocturia
  2. Difficulty initiating voiding, poor stream, dribbling
  3. Oliguria
  4. Polyuria
  5. Ureteric colic (radiates anteriorly and to groin)
  6. Loin pain (including important non-renal differential)
  7. Visible haematuria
A
  1. UTI
  2. Prostatic aetiology
  3. AKI
  4. High fluid intake, DM, diabetes insipidus, hypercalcaemia, renal medullary disorders
  5. Renal stone, clot, sloughed papilla
  6. Pyelonephritis, renal cyst, renal infarct, AAA
  7. Malignancy, PKD, glomerular disease (IgA, anti-GBM), Alport disease
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4
Q

Systemic disorders with renal involvement

  1. Metabolic
  2. Auto-immune
  3. Infection
  4. Malignancy
  5. Pregnancy
  6. Drugs
A
  1. DM, sickle cell, tuberous sclerosis, Fabry disease, cystinosis
  2. ANCA vasculitis, SLE, HSP, systemic sclerosis, sarcoid, Sjogren’s
  3. Sepsis, TB, malaria, chronic hepatitis, HIV
  4. Obstruction, hypercalcaemia, direct toxicity i.e. myeloma
  5. Pre-eclampsia, obstruction
  6. NSAIDs, ACE-i, ARB, aminoglycosides e.g. gentamicin, chemotherapy
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5
Q

Proteinuria

  1. Normal albumin:creatinine ratio vs proteinuria A:CR
  2. Normal protein:creatinine ratio vs proteinuria P:CR
  3. Causes
  4. False positive causes
  5. Microalbuminuria - definition
  6. Microalbuminuria - cause
  7. Effect on specific gravity
A
  1. < 2.5 (men), < 3.5 (women) vs 30
  2. < 15 vs 50
  3. Glomerular disease - glomerulonephritis, DM, amyloidosis, myeloma
  4. Postural (repeat early morning sample), post-exercise, fever, heart failure
  5. Albumin excretion 30-300 mg/24 h
  6. Early glomerular disease e.g. DM, HTN
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6
Q

Haematuria

  1. Transient causes
  2. Main causes (KUB, prostate, systemic)
  3. False positive causes
  4. Painful causes
  5. Syndrome it differentiates from
  6. Questions to ask
  7. Bloods
  8. Urine tests
  9. Imaging
  10. Further tests
  11. 2ww urological/renal referral indications
  12. Non-urgent renal referral indication
A
  1. UTI, menstruation
  2. Malignancy (kidney, ureter, bladder*), calculi, trauma, glomerular disease (IgA, anti-GBM), Alport syndrome, PKD, schistosomiasis, Wilm’s nephroblastoma in young children, TB
  3. Myoglobinuria (check microscopy)
  4. Stones, UTI
  5. Nephritis, not nephrotic
  6. How much blood, which part of the stream, what colour, pain, B symptoms
  7. FBC, U+Es, CRP, clotting
  8. Urine dip, culture Early morning sample for TB
  9. X-ray KUB, CT urogram, US
  10. Cystoscopy, renal biopsy
  11. 45+ and VH without UTI, or 60+ and NVH with dysuria / raised WCC
  12. NVH with eGFR < 60, proteinuria, HTN, FH
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7
Q

Urine dipstick - significance of findings

  1. Glucose
  2. Ketones
  3. Leucocytes
  4. Nitrites
  5. Bilirubin
  6. Urobilinogen
  7. Specific gravity - normal range + use
  8. pH - normal range, cause for more acidic
A
  1. DM, pregnancy, sepsis, proximal renal tubular pathology
  2. Starvation, ketoacidosis
  3. UTI, vaginal discharge
  4. Gram negative UTI
  5. Haemolysis
  6. Liver disease, haemolysis
  7. 1.005-1.030, estimates urine osmolality, up in proteinuria
  8. 4.5-9, more acidic in renal tubular acidosis and meat diet
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8
Q

Urine microscopy - significance of findings

  1. Number of red cells /mm3 to be abnormal
  2. Isomorphic red cells
  3. Dysmorphic (abnormal size/shape) red cells
  4. Number of white cells /mm3 to be abnormal
  5. White cells
  6. Squamous epithelial cells
  7. Casts - what are they
  8. Hyaline cast
  9. Red cell cast
  10. White cell cast
  11. Granular cast - formed from what, and cause
  12. Eosinophilic cast
  13. Crystal - normal causes
  14. Uric acid crystal
  15. Calcium oxalate crystal
  16. Cystine crystal
A
  1. < 2
  2. Genitourinary/external bleeding
  3. Glomerular bleeding, tubular passage, pH / osmolality / protein changes
  4. > 10
  5. UTI, glomerulonephritis, tubulointerstitial nephritis, renal transplant rejection, malignancy
  6. Normal
  7. Cylindrical bodies formed in distal tubule lumen from Tamm-Horsfall protein and cells
  8. Normal
  9. Glomerular inflammation e.g. glomerulonephritis
  10. Pyelonephritis, interstitial nephritis, glomerulonephritis
  11. Formed from degenerated tubular cells, CKD
  12. Acute tubulointerstitial nephritis
  13. Old/cold urine
  14. Uric acid stone, tumour lysis syndrome
  15. Stones, high oxalate diet, ethylene glycol poisoning
  16. Cysteinuria
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9
Q

Urinary tract infection (UTI)

  1. Uncomplicated - definition
  2. Complicated - definition and causes
  3. Risk factors (4 groups)
  4. Cystitis (lower UTI - bladder irritation) symptoms
  5. Pyelonephritis (upper UTI) symptoms
  6. Prostatitis symptoms
  7. Bedside tests
  8. Blood tests (if systemically unwell)
  9. Imaging / referral - type and indication
  10. Commonest organism
  11. Bacteria associated with stone formation
  12. Cystitis - management in non-pregnant
  13. Pyelonephritis - management
  14. Pregnancy - antibiotics to avoid
  15. Prostatitis - management
  16. Sterile pyuria - differentials and investigation
A
  1. Normal renal tract structure/function
  2. Abnormal structure/function, e.g. from obstruction, catheter, stones, neurogenic bladder, renal transplant
  3. Bacterial inoculation (sexual activity, incontinence, constipation), bacteria binding (spermicides, low oestrogen), low urine flow (dehydration, obstructed tract), bacterial growth (DM, immunosuppression, obstruction, stones, catheter, pregnancy)
  4. Frequency, dysuria, nocturia, urgency, suprapubic pain, polyuria, haematuria
  5. Fever, rigors, N+V, loin pain, sepsis, urinary symptoms
  6. Pain in perineum / rectum / scrotum / penis / bladder / lower back, fever, malaise, nausea, urinary symptoms
  7. Dipstick (if not pregnant), MSU culture
  8. FBC, U+E, CRP, blood culture
  9. USS in upper UTI / failure to respond / 2+ per year / unusual organism / persistent haematuria
  10. Anaerobes, gram negative bacteria from bowel e.g. E. coli, staphylococcus saprophyticus
  11. Proteus
  12. If 3+ symptoms, empirical with 3 day trimethoprim / nitrofurantoin (7 day if men). No culture initially.
  13. Admit, culture, cefalexin PO/cefuroxime IV, or co-amoxiclav if culture available and susceptible
  14. 1st trimester (trimethoprim as anti-folate, ciprofloxacin), 3rd trimester (nitrofurantoin as HDON)
  15. Ciprofloxacin (fluoroquinolone) 4 weeks
  16. Analgesia nephropathy, recently/partially treated UTI, chlamydia, appendicitis, catheter/other instrumentation, urinary tract TB (do acid-fast microscopy and microbacterial early-morning MSU)
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10
Q

Acute kidney injury (AKI)

  1. Stage 1 criteria
  2. Stage 2 criteria
  3. Stage 3 criteria
  4. Bedside tests - frequency required
  5. Monitoring requirements
  6. Bloods - frequency required
  7. Investigations
  8. Renal referral - indications
  9. What to suspect if urea rise is proportionally greater than the creatinine rise
A
  1. Creatinine rise > 26.5 umol/L in 24 hours, or > 1.5x baseline in 7 days, or urine output < 0.5 mL/kg/h for 6-12 hours
  2. Creatinine 2-2.9 x baseline, or UO < 0.5 for 12+ hours
  3. Creatinine >3x baseline, or 0.3 for 24 hours / anuric for 12 hours
  4. Heart rate, BP, JVP, capillary refill, palpate bladder - look for pulmonary oedema or hypovolaemia - observations 4 hourly
  5. Fluid balance (catheter/hourly UO)
  6. FBC (Hb), potassium, creatinine (daily), bicarb/lactate (if sepsis), LFTs (hepatorenal), platelets (low then blood film for HUS/TTP), intrinsic disease tests if indicated (immunoglobulin, paraprotein, complement, autoantibodies e.g. ANA, ANCA, anti-GBM)
  7. Dipstick (proteinuria quantification), USS within 24 hours if cause unknown/not improving
  8. Not responding, complications (potassium, fluid overload, acidosis), stage 3, HTN, possible intrinsic disease
  9. Dehydration
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11
Q

AKI - causes

  1. Pre-renal (low volume) (4 groups)
  2. Renal (3 groups)
  3. Post-renal (obstruction) (2 groups)
A
  1. Low vascular volume (D+N+V, burns, haemorrhage, pancreatitis), low cardiac output (cardiogenic shock, MI), systemic vasodilation (sepsis), renal vasoconstriction (NSAIDs, ACE-i, ARB), hepatorenal syndrome
  2. Glomerular (glomerulonephritis, acute tubular necrosis), interstitial (drug reaction, infection, infiltration e.g. sarcoid), vessels (vasculitis, HUS, TTP, DIC)
  3. Within renal tract (stone, malignancy, stricture, clot- thrombosis), extrinsic compression (pelvic/prostatic malignancy, retroperitoneal fibroids)
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12
Q

AKI - management

  1. Pre-renal
  2. Renal
  3. Post-renal
  4. Hypovolaemia - how much, which, cautions
  5. Hypervolaemia - causes and management
  6. Acidosis - staging and management
  7. Hyperkalaemia - ECG changes
  8. Hyperkalaemia - indications for management
  9. Hyperkalaemia - management
A
  1. Treat cause - correct volume depletion / increase renal perfusion, treat underlying sepsis
  2. Refer to renal for likely biopsy and specialist treatment
  3. Nephrostomy, catheter, urological intervention
  4. 500mL crystalloid over 15 minutes, then further 250-500mL boluses up to maximum 2L, reassess each time. 0.9% normal saline (hyperchloraemic metabolic acidosis), buffered e.g. Hartmann’s / Ringer’s / Plasmalyte (hyperkalaemia)
  5. IV fluids and oliguric/septic. Give O2 as required, fluid restriction, diuretics if symptomatic, RRT.
  6. Mild 7.3-7.35, moderate 7.2-7.29, severe < 7.2. Treat underlying disorder
  7. Absent P, long PR, wide bizarre QRS, tall peaked T - asystole, ventricular fibrillation, bizarre wide complex PEA.
  8. ECG if >6, treat if ECG changes or K+ >6.5
  9. Calcium gluconate 10% 10ml IV over 5-10 minutes. 10 units IV soluble insulin in 25g glucose. Salbutamol 10-20mg nebulised. Confirm underlying pathology/RRT for K+ removal.
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13
Q

Chronic kidney disease (CKD)

  1. Definition
  2. History questions
  3. Cardiac symptoms
  4. GI symptoms
  5. CNS symptoms
  6. Causes (‘HIDDEN’)
A
  1. Abnormal kidney structure/function present for >3 months
  2. Previous UTI, lower tract symptoms, PMH of HTN/DM/IHD, renal colic, drug history, FH of renal disease/SAH, malignancy, eyes/skin/joints
  3. Pericarditis, oedema, SOB, arrhythmias
  4. N+V, anorexia, pruritis, bone pain
  5. Fatigue, weakness, confusion, seizures, coma
  6. HTN, (recurrent) Infections, Diabetes, Drugs, Exotica (SLE / vasculitis), Nephritis
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14
Q

CKD - classification

  1. G1
  2. G2
  3. G3a
  4. G3b
  5. G4
  6. G5
  7. GFR when potentially symptomatic
  8. A1
  9. A2
  10. A3
  11. Renal failure
A
  1. GFR >90, only CKD if other evidence of kidney damage
  2. GFR 60-89, only CKD if other evidence of kidney damage
  3. GFR 45-59, mild-moderate
  4. GFR 30-44, moderate-severe
  5. GFR 15-29, severe
  6. GFR <15, renal failure
  7. GFR <30 (stage 4/5)
  8. <30 mg/24h albumin excretion, A:CR <3mg/mmol
  9. 30-300 mg/24h albumin excretion, A:CR 3-30mg/mmol
  10. <300mg/24h albumin excretion, A:CR >30mg/mmol
  11. Creatinine >50% above baseline
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15
Q

CKD - management

  1. Renal referral - indications
  2. ACE-i - indications
  3. HbA1C - target
  4. Lifestyle
  5. Anaemia
  6. Acidosis
  7. Oedema
  8. Bone-mineral disorder
  9. Cardiovascular disease
A
  1. Stage G4/5 CKD, quick GFR fall, HTN despite 4+ drugs
  2. DM and A:CR >3, HTN and A:CR >30, any CKD and A:CR >70
  3. 53 mmol/mol
  4. Exercise, healthy weight, no smoking, low salt diet
  5. EPO injections, IV iron
  6. Sodium bicarb supplements if GFR <30 and low (<20) serum bicarb
  7. Fluid restriction, furosemide, + thiazide potentially
  8. Dietary restriction (e.g. dairy) and binders if phosphate >1.5 mmol/L, vitamin D supplements (e.g. colecalciferol) or activated analogue (e.g. calcitriol) if PTH still high
  9. Low-dose aspirin, 20mg atorvastatin
    5.
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16
Q

CKD - Investigations

  1. Baseline bloods - U+E, FBC, Ca2+, phosphate, ABG, haematinics, glucose
  2. Potential other bloods
  3. Imaging - CKD, AKI, renovascular how to distinguish chronic from acute (and exceptions)
  4. Biopsy indications
  5. CXR changes
  6. Cause of low calcium, + what this leads to
A
  1. U+E (compare to previous) - uraemia, high Na+ and K+, Hb (normocytic, normochromic anaemia), low Ca2+, high phosphate, metabolic acidosis (with/without respiratory compensation - can’t secrete H+ or reabsorb HCO3-), low ferritin, BM high (if DM)
  2. ANA, ANCA, antiphospholipid antibodies
  3. Chronic usually bilaterally small (<9cm) kidneys (except amyloid, myeloma, APKD, DM), AKI normal size, vascular asymmetrical
  4. Progressive, nephrotic, systemic disease, AKI without recovery
  5. Overload (pulmonary oedema)
  6. Unable to produce calcitriol (activated vit D) so Ca2+ not reabsorbed; leads to secondary hyperparathyroidism
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17
Q

CKD - examination findings

  1. Periphery
  2. Face
  3. Neck
  4. Cardiovascular
  5. Respiratory
  6. Abdomen
A
  1. Peripheral oedema, signs of peripheral vascular disease/neuropathy (DM), AV fistula, uraemic flap/encephalopathy if GFR <15, immunosuppression signs (bruising etc.)
  2. Anaemia, xanthelasma, yellow tinge (uraemia), jaundice (hepatorenal syndrome)
  3. JVP (fluid state), tunnelled line (small scar over EJV and large scar over ‘breast pocket’ area), parathyroidectomy scar
  4. BP, cardiomegaly
  5. Pulmonary oedema or effusion
  6. PD catheter/previous scars (diagonal from umbilicus), previous transplant signs (scar, palpable graft), palpable liver, ballotable polycystic kidneys
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18
Q

Renal replacement therapy (RRT) - dialysis and filtration

  1. Indication in CKD and AKI
  2. Types used in AKI
  3. AV fistula - Artery and vein normally used
  4. AV fistula - Cause of thrill and bruit
  5. AV fistula - Complications (4)
  6. Haemodialysis - location and method
  7. Haemodialysis - non-fistula complications
  8. Peritoneal dialysis - location and method
  9. Peritoneal dialysis - complications
  10. Haemofiltration - method and indication
  11. RRT - general complications
A
  1. Low creatinine clearance <20/15, symptomatic uraemia e.g. pruritis despite treatment, unresponsive fluid overload, bone disease, severe hyperkalaemia, severe acidosis
  2. Haemodialysis, haemofiltration
  3. Radial artery, cephalic vein
  4. Arterial blood from the radial artery
  5. Thrombosis, infection, stenosis, bleeding
  6. Blood passed over semi-permeable membrane, dialysis fluid flowing other way, solutes diffuse down concentration gradient. Done 3+ times/week, in hospital or at home
  7. Dialysis disequilibrium (between cerebral and blood solutes) leading to cerebral oedema so start slowly, hypotension, time-consuming
  8. Home; catheter into peritoneal cavity, fluid with osmotic agents e.g. glucose pumped in, drains intermittently (continuous process)
  9. Catheter site infection, PD peritonitis, hernia, gradual loss of membrane function
  10. Filtered using positive pressure; used short term in critical care when haemodialysis not possible due to hypotension
  11. CVD (HTN, calcium/phosphate dysregulation, vascular stiffness, abnormal endothelial function), protein-calorie malnutrition, renal bone disease (high turnover, osteodystrophy, osteitis fibrosa),
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19
Q

RRT - Transplant

  1. Contraindications (absolute, temporary, relative)
  2. Expanded criteria donor - examples and prognosis
  3. Perioperative immunosuppression
  4. Long-term immunosuppression
  5. Acute rejection - cause, diagnosis, treatment
  6. Chronic rejection - cause
  7. Malignancy - more at risk of
  8. Commonest infection post-transplant, and signs
A
  1. Absolute (metastatic cancer), temporary (active infection, HIV with viral replication, unstable CVD), relative (congestive heart failure, CVD)
  2. Older kidney, donor had CVA/HTN/CKD; lasts for shorter period but better than dialysis
  3. Monoclonal antibodies
  4. Calcineurin inhibitors e.g. tacrolimus/cyclosporin, antimetabolites e.g. MMF
  5. Cellular (commonest) or antibody mediated, diagnosed with biopsy, treat with high dose steroids and increased tacrolimus/MMF
  6. Immune response from donor-specific antibodies damaging renal microcirculation
  7. Skin (melanoma), lymphoproliferative, gynaecological
  8. CMV - jaundice, hepatomegaly, widespread lymphadenopathy
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20
Q

Glomerulonephritis - general

  1. Presentation
  2. Blood tests
  3. Non-blood investigations
  4. Management
  5. Commonest cause
A
  1. Nephrotic (podocyte damage/proteinuria from scarring) to nephritic (inflammation)
  2. FBC, U+E, LFT, CRP, blood film, ABG
  3. Urine (dip, protein and creatinine levels), CXR (pulmonary haemorrhage in anti-GBM), renal USS (size/anatomy for biopsy), renal biopsy (necessary for diagnosis)
  4. Treat cause (immunosuppression), BP monitoring, fluid control, consider transplant
  5. IgA nephropathy
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21
Q

Other nephritic glomerulonephritis - presentation, diagnosis, treatment

  1. HSP
  2. Post-streptococcal
  3. Anti-GBM (Goodpastures)
  4. Rapidly progressive
A
  1. Small vessel vasculitis (IgA deposits in skin/joints/gut as well as kidney), purpuric rash on extensor surfaces (typically legs), polyarthritis and abdominal pain, treat with ACE-i/ARB and steroids for gut
  2. Post infection (2 weeks throat, 3-6 weeks skin), streptococcal antigen in glomerulus, presents with haematuria maybe with oedema/HTN/oliguria, give ABX and supportive
  3. Auto-antibodies to type IV collagen, presents as both renal and lung disease (haemoptysis), anti-GBM antibodies to diagnose, treat with plasma exchange, corticosteroids, cyclophosphamide
  4. Any aggressive GN (from lupus, ANCA/small vessel vasculitis, anti-GBM), crescents seen on biopsy, treat with corticosteroids and cyclophosphamide
22
Q

Nephrotic syndrome

  1. Triad
  2. Causes
  3. Blood tests
  4. Urine tests
  5. Non-bedside tests
  6. Complications
  7. Why does this lead to hypercoagulable state
  8. Management
A
  1. Oedema, hypoalbuminaemia, proteinuria >3g/24h or P:CR >300
  2. SLE, myeloma, DM, glomerulonephritis
  3. Renal profile, albumin, clotting, cholesterol, glucose, TFT (low total, but not free, T4)
  4. Protein and creatinine, Bence-Jones
  5. Renal US, biopsy
  6. Hypercoagulability, hypercholesterolaemia, infection
  7. Due to loss of antithrombin III via the kidneys and platelet abnormalities
  8. Reduce oedema (fluid <1L/day, salt restriction, furosemide, daily weights), treat underlying cause (biopsy in adults, reduce proteinuria (ACE-i/ARB)
23
Q

Nephrotic glomerulonephritis - presentation, diagnosis, treatment

  1. Minimal change disease
  2. Focal segmental glomerulosclerosis
  3. Membranous nephropathy
  4. Membranoproliferative
A
  1. Commonest in children, 25% adults, can be idiopathic (most), drugs (NSAIDs, lithium) or paraneoplastic (Hodgkin’s lymphoma). Light microscopy normal (hence name), electron microscopy shows effacement of podocyte foot processes. Treat with prednisolone 1mg/kg for 6 weeks, and relapses with immunosuppression
  2. Commonest seen on biopsy, glomeruli scarring of certain segments, treat with ACE-i/ARB in all and corticosteroids if primary (idiopathic) disease
  3. Idiopathic (primary) or secondary to malignancy, infection, autoimmune. Diagnose from antiphospholipase A2 receptor antibody, diffusely thickened GBM from subepithelial deposits, ‘spikes’ on silver stain. Treat with ACE-i/ARB, ‘Ponticelli’ immunosuppression regimen if high risk of progression
  4. Proliferative GN with electron dense deposits
24
Q

Diabetic Nephropathy

  1. Signs
  2. Diagnosis
  3. Management
A
  1. Microalbuminuria 1st, then glomerulosclerosis, nodule formation (Kimmelstiel-Wilson lesions), fibrosis
  2. DM with microalbuminuria (A:CR 3-30 mg/mmol)
  3. Intensive DM control, BP <130/80 via ACE-i/ARB, sodium restriction, statins
25
Q

Renal manifestations of systemic disease - presentation, diagnosis, treatment

  1. Lupus nephritis
  2. Small vessel vasculitis
  3. Myeloma
  4. Amyloid
  5. TTP
  6. Scleroderma renal crisis
  7. Sickle cell nephropathy
A
  1. Rash, photosensitivity, ulcers, arthritis, serositis. Clinical diagnosis; positive ANA and anti-dsDNA. ACE-i-ARB and hydroxychloroquine if stage 1-2, add immunosuppressants if classes 3-5.
  2. Lethargy, fever, myalgia, anorexia. Diagnosis: clinical + ANCA + biopsy (rapidly progressive GN without immune deposits). Treat with high dose glucocorticoid, cyclophosphamide/rituximab, plasma exchange if pulmonary haemorrhage or renal failure
  3. Proteinuria, hypercalcaemia, renal tract infection. Diagnose from light chain casts / Bence Jones protein / serum electrophoresis etc. Treatment: hydration, bisphosphonates for high Ca2+, ant-myeloma treatment e.g. glucocorticoids.
  4. AL amyloid has light chains in myeloma, AA amyloid has serum amyloid A (chronic inflammation). Diagnosis: congo red staining on biopsy, SAP scan.
  5. Microangiopathic haemolytic anaemia, low platelets, AKI, fever, neurological symptoms (headache, palsies, seizure, confusion, coma). Diagnosis: clinical with ADAMTS13 activity. Treatment: plasma infusion/exchange, corticosteroids
  6. Accelerated HTN (new >150/85) and AKI. Biopsy shows collapsed glomeruli, onion-skin arteriole thickening. Treatment: ACE-i/ARB, IV vasodilators
  7. Hyperfiltration (lower than expected creatinine) and albuminuria. Clinical diagnosis. Treat with ACE-i/ARB.
26
Q

HUS

  1. Triad
  2. Common cause
  3. Blood tests
  4. Other tests
  5. Management
A
  1. Haemolysis (microangiopathic haemolytic anaemia), thrombocytopaenia, acute renal failure
  2. Post infection - renal failure (Shiga toxin producing E.coli in children - ‘STEC’, also pneumococcal and HIV), can also be complement dysregulation
  3. FBC (anaemia, thrombocytopaenia, fragmented blood film), U+E (AKI), raised LDH
  4. Stool sample
  5. Supportive if STEC, plasma infusion/exchange if complement problem
27
Q

The renal tubule - solute movement, tubular pathology, diuretic

  1. Proximal tubule
    Pathology
    Diuretics
  2. Thick ascending loop
  3. Distal tubule
  4. Collecting duct
  5. RTA Type 1 - definition, cause, bloods
  6. Type 2
  7. Type 4
A
  1. Reabsorbs Na+, bicarb, phosphate, sugars + AAs
    Pathology: Fanconi syndrome (replace phosphate) + proximal (T2) RTA
    Diuretics: mannitol and carbonic anhydrase inhibitor e.g. acetazolamide.
  2. Reabsorbs Na+, K+, Cl-.
    Bartter syndrome (low K+/Cl- metabolic alkalosis from childhood - replace salt and use NSAID).
    Diuretics: loop e.g. furosemide
  3. Reabsorbs Na+/Cl-.
    Gitelman syndrome (loss of NaCl co-transporter, milder form of Bartter, mimics thiazide diuretics).
    Diuretic: thiazide
4. Excretes K+/H+ and retains Na+ (via aldosterone). 
Type 1 (distal) RTA, Type 4 RTA
Diuretics: K+ sparing e.g. aldosterone antagonists (spir)
  1. Distal, not enough H+ secretion into filtrate in distal tubule (genetic, lithium, amphoteracin).
    Low blood K+ as not reabsorbed. Give bicarb
  2. Proximal, not enough bicarb reabsorbed into blood (replace bicarb)
  3. Low/absent aldosterone (so low Na+/high K+) from adrenal insufficiency/DM/ACE-i/ARB - medication review
28
Q

Tubulointerstitial nephropathy

  1. Acute tubulointerstitial nephritis - presentation +diagnosis
  2. Acute tubulointerstitial nephritis - cause
  3. Acute tubulointerstitial nephritis - treatment
  4. Chronic tubulointerstitial nephritis - presentation + diagnosis
  5. Chronic tubulointerstitial nephritis - cause
  6. Chronic tubulointerstitial nephritis - treatment
A
  1. AKI, eosinophilia (+ eosinophilic casts), ‘allergic triad’ of fever/rash/arthralgia. Inflammatory cell infiltrate in interstitium and tubule.
  2. Drugs (NSAIDs, ABX, PPIs), infection, autoimmune
  3. Stop causative agent, treat underlying cause, steroid
  4. Insidious, slowly progressive, interstitial fibrosis, tubular atrophy.
  5. Drugs (commonest), infection, immune
  6. Stop causative agent, treat underlying cause, management as if CKD to stop progression
29
Q

Nephrotoxins - presentation and management

  1. Analgesics
  2. Aminoglycosides e.g. gentamicin, streptomycin
  3. Radiocontrast
  4. Rhabdomyolysis
  5. Urate
A
  1. Small, irregular kidneys, sterile pyuria, proteinuria. IVU ‘cup and spill’ appearance. Biopsy: CTIN from papillary necrosis. Stop drug, manage CKD
  2. Tubular necrosis with mild, non-oliguric AKI after 1-2 weeks of therapy. Treatment: prevention.
  3. AKI 2-3 days post-contrast. Prevent by pre-hydration with IV crystalloid. Stop other nephrotoxins 24h pre- and post-procedure.
  4. Red-brown urine. Diagnose from serum myoglobin. Supportive treatment e.g. rehydration and hyperkalaemia.
  5. Seen in tumour lysis syndrome. Treat with aggressive hydration and allopurinol/rasburicase.
30
Q

Acute tubular necrosis

  1. Commonest cause of what
  2. Causes (2 broad)
  3. Clinical features
  4. Histopathology
A
  1. AKI
  2. Renal ischaemia (e.g. shock, sepsis) or toxins (aminoglycosides, myoglobin from rhabdomyolysis)
  3. Usual AKI features plus muddy red-brown casts in urine
  4. Tubular epithelium necrosis (no nuclei, eosinophilic homogeneous cytoplasm), tubular dilatation, necrotic cells obstructing tubule lumen
31
Q

Inherited kidney disease

  1. ADPKD - cause
  2. ADPKD - presentation (+ extra-renal)
  3. ADPKD - diagnosis
  4. ADPKD - management
  5. ARPKD - cause + presentation
  6. Tuberous sclerosis complex - cause and presentation
  7. Von Hippel-Lindau - cause and presentation
  8. Alport syndrome - cause and presentation
  9. Fabry disease - cause and presentation
A
  1. PKD1 (chromosome 16 - more aggressive), or PKD2 (chromosome 4) mutations
  2. May be clinically silent but also loin pain, visible haematuria, renal calculi, HTN. Extra-renal: liver cysts, intracranial aneurysm leading to SAH.
  3. USS (3 cysts <40, 2 in each kidney >40)
  4. Drink lots of water, BP <130/80 via ACE-i/ARB, then thiazide-like e.g. indapamide.
  5. Chromosome 6. Presents ante/perinatally with ‘salt and pepper’ renal cysts on USS, plus congenital hepatic fibrosis leading to portal hypertension.
  6. Autosomal dominant, TSC1/TSC2 (chromosomes 9 and 16); presents with systemic hamartomas.
  7. Autosomal dominant, chromosome 3 mutation, familial renal cysts and clear cell renal carcinoma by 40s.
  8. X-linked, COL4A5 gene mutation (codes for type 4 collagen). Haematuria, proteinuria, progressive CKD, high tone sensorineural hearing loss, anterior lenticonus.
  9. X-linked, lysosomal storage disorder, deficient of a-galactosidase-A enzyme. Proteinuria and progressive renal failure. Lipid deposits in urine and biopsy ‘zebra body’.
32
Q

Nephrogenic diabetes insipidus

  1. What is it
  2. Cause
  3. Symptoms
  4. Investigation result (3)
  5. Management (2)
A
  1. Kidneys insensitive to ADH/vasopressin
  2. Genetic (ADH receptor/mutation of gene encoding aquaporin 2 channel), electrolytes (high Ca2+, low K+), drugs (demeclocycline, lithium), tubulo-interstitial disease (obstruction, sickle-cell, pyelonephritis)
  3. Polyuria, polydipsia
  4. High plasma osmolality, low urine osmolality (urine osmolality of >700 mOsm/kg excludes DI), still low after water deprivation test, still low after exogenous ADH
  5. Thiazides (e.g. chlorothiazide), low salt/protein diet
33
Q

Renovascular disease

  1. Main causes (2)
  2. Common patient cohort in rarer cause
  3. Features of rarer cause
  4. What happens in rarer cause
  5. What is seen in MR angiography
A
  1. Renal artery stenosis secondary to atherosclerosis (90%), fibromuscular dysplasia (10%)
  2. Female
  3. HTN, CKD/AKI secondary to ACE-inhibitor initiation,
    ‘flash’ pulmonary oedema
  4. Proliferation of cells in the walls of the arteries causing the vessels to bulge or narrow
  5. ‘String of beads’ appearance of renal arteries
34
Q

IgA Nephropathy (Berger’s disease)

  1. Classic patient cohort
  2. Presentation
  3. Histological findings
  4. Associated conditions (4)
  5. Management

Differences from post-streptococcal

  1. Time post-URTI
  2. Haematuria
  3. Proteinuria
  4. Complement levels
  5. PSGN - causative organism, therefore suspect when
  6. Diagnostic criteria (2)
A
  1. Young men/teens
  2. Recurrent frank haematuria (asymptomatic non-visible or post-infectious visible), associated with URTIs
  3. Mesangial hypercellularity (proliferation), positive immunofluorescence for mesangial IgA + C3 deposits
  4. HSP, alcohol cirrhosis, coeliac, dermatitis herpetiformis
  5. ACE-i/ARB (reduce proteinuria, protect renal function), corticosteroids + fish oil if proteinuria after 3-6 months
  6. 1-2 days (vs 1-2 weeks)
  7. Frank (as opposed to microscopic)
  8. Lower (higher in PSGN)
  9. Normal/higher (lower in PSGN)
  10. β-haemolytic streptococcus (e.g. pyogenes) - suspect if AKI symptoms 1-3 weeks post strep-tonsillitis
  11. Positive throat swab, ASO antibody in blood
35
Q

Bladder Cancer

  1. Risk factors
  2. Commonest type
  3. Commonest presenting symptom
  4. Gold standard investigation
  5. Superficial disease - management
  6. Invasive disease - management
A
  1. Smoking, aromatic amine exposure
  2. Transitional cell carcinoma
  3. Haematuria
  4. Cystoscopy
  5. Endoscopic resection, intravesical chemotherapy
  6. Radical cystectomy / radical radiotherapy
36
Q

Kidney cancer

  1. Commonest type
  2. Familial renal cell carcinoma - aka
  3. Clinical features
  4. Usually spreads to (3)
  5. Gold standard imaging
  6. Type usually causing canon-ball lung metastases
  7. 1st line management
A
  1. Adenocarcinoma
  2. Von-Hippel Lindau syndrome
  3. Haematuria, loin pain, weight loss, abdominal mass, HTN, hypercalcaemia
  4. Lungs / bone / lymph
  5. USS CT (for staging)
  6. Renal cell carcinoma
  7. Nephrectomy
37
Q

Benign Prostatic Hyperplasia

  1. Urinary obstruction symptoms
  2. Usual location for BPH to develop
  3. Blood tests
  4. Conservative management
  5. Medical management - smooth muscle relaxer
  6. SMR side effects
  7. Medical management - prostate size reducer
  8. PSR side effects
  9. Surgical management
  10. TURP complications
  11. TURP syndrome - cause
  12. TURP syndrome - components (3)
A
  1. Hesitancy, poor stream, dribbling, incomplete voiding, retention, + ED (BPH specifically)
  2. Urethral prostate (centre)
  3. FBC, U+E, PSA (look for trend/big jump/ >10)
  4. Watch and wait, catheterise for retention
  5. Tamsulosin (alpha blocker)
  6. Hypotension, incontinence, retrograde ejaculation
  7. Finasteride (5 alpha 2 reductase inhibitors)
  8. Gynaecomastia, erectile dysfunction, retrograde ejaculation, can take 6 months to work
  9. TURP
  10. TURP syndrome, urethral stricture/UTI, retrograde ejaculation, prostate perforation
  11. Irrigation fluid entering systemic circulation
  12. Dilutional hyponatraemia, fluid overload, glycine toxicity
38
Q

Prostate cancer

  1. Location of development and significance
  2. Metastasis sites
  3. Diagnosis
  4. Grading system used
  5. How to interpret grading system
  6. Test to monitor response to management
  7. Further imaging
  8. Local disease - management
  9. More advanced disease - management
  10. Radical prostatectomy - side effects (2)
A
  1. Peripheral (can therefore present late)
  2. Bone, lymph nodes, liver, lungs
  3. Biopsy / MRI (if on warfarin) post-high PSA
  4. Gleason score (6-10)
  5. Regular PSA if 6-8, immediate treatment if 9/10
  6. PSA
  7. Transurethral US CT, MR abdomen for staging, bone scan
  8. Radical prostatectomy (if stage T1/T2)
  9. Chemotherapy, radiotherapy (brachytherapy seeds in protstate), hormone therapy (goserelin - cover with anti-androgen flutamide at start) alongside radiotherapy (blocks/reduced effects of testosterone)
  10. Impotence (50%), urinary incontinence (10%)
39
Q

Polyuria

  1. Definition
  2. Causes (4 broad groups)
  3. Diuresis - causes (4)
  4. Associated symptoms
  5. Bedside tests
  6. Bloods
  7. Urine tests
A
  1. > 3.5L/ 24 hours
  2. Too much fluid intake, diuresis, DM, renal failure
  3. High glucose/Ca2+/urate, diuretics
  4. Polydipsia, weight loss
  5. Fluid balance, weight
  6. BM, FBC, U+E, Ca2+, LFTs, serum osmolality
  7. Dip, microscopy, culture, osmolality, 24 hour collection
40
Q

Oliguria

  1. Definition
  2. Causes
  3. Bedside tests
  4. Bloods
  5. Urine tests
  6. Imaging
A
  1. <300ml / 24 hours
  2. Hypotension (sepsis, cardiogenic, renal artery obstruction), AKI (e.g. ATN), glomerulonephritis
  3. BP, hydration status
  4. FBC, U+E, BM, serum osmolality, Ca2+, bicarbonate, urate
  5. Dip, osmolality
  6. US DMSA scan
41
Q

Testicular cancer

  1. Commonest overarching type
  2. Subtypes if age 20-40 (2)
  3. Subtype if <10
  4. Risk factors
  5. Commonest presenting feature
  6. First line test
  7. Tumour marker
A
  1. Germ cell
  2. Seminoma, teratoma
  3. Yolk sac
  4. Infertility, FH, cryptorchidism, Klinefelter’s, mumps orchitis
  5. Painless lump
  6. Testicular USS
  7. Beta HCG, AFP
42
Q

Penile rash/lump

  1. Differentials
A
  1. Viral wart, STD, fungal infection, penile cancer in situ
43
Q

Anatomy

  1. Renal pelvis at what spinal level
  2. Ureter narrowing locations (3)
A
  1. L1

2. Pelvic brim, PUJ, VUJ

44
Q

Bladder clot retention

  1. Symptoms
  2. Management
  3. Complications
A
  1. Haematuria and palpable bladder
  2. ABCDE, 3-way catheter with wash out
  3. Further bleeding (needing surgery), perforation
45
Q

Urology history

  1. Red flags
  2. Voiding symptoms (prostate, other obstruction)
  3. Storage symptoms (overactive/irritated bladder)
  4. Fluid questions
  5. PMH
  6. Social history
  7. Family history
A
  1. Haematuria, blood in stool, change in bowel habits, dysuria, fever, weight loss, bone pain
  2. Hesitancy, intermittent, weak, dribbling, straining, feeling of retention, erectile dysfunction
  3. Urgency, frequency, nocturia, incontinence, pads
  4. Alcohol, caffeine, late night drinking, limiting fluids
  5. STI, UTI, stones, surgery, HTN, IHD, DM
  6. Alcohol, smoking, occupation
  7. Prostate cancer, BPH etc.
46
Q

Prostate exam

  1. Introduction
  2. Equipment
  3. External inspection
  4. Things to comment on
  5. Normal
  6. Prostatitis
  7. Benign prostatic hypertrophy
  8. Malignancy
  9. Complete examination
  10. Further investigations
A
  1. Yourself, patient details, explain, consent, chaperone
  2. Gloves, apron, lubricant, paper towels
  3. Skin excoriation (sphincter dysfunction/incontinence), skin tags, rashes (STI), haemorrhoids (potentially thrombosed), anal fissures (often posterior + central), external bleeding (e.g. brisk GI bleeding or anal pathology such as squamous cell anal cancer), fistulae +
    abscesses (e.g. perianal Crohn’s)
  4. Size, symmetry, texture
  5. Walnut sized, symmetrical, palpable midline sulcus, smooth
  6. ‘Boggy’
  7. Enlarged, loss of sulcus, smooth (sometimes nodule)
  8. Enlarged, loss of sulcus, irregular
  9. Rotate finger 360 degrees for further irregularity, comment on stool (soft/impacted), anal tone (squeeze finger), remove and look for stool/mucus/blood (fresh/melaena)
  10. Full abdominal examination, bloods (FBC/haematinics for anaemia), faecal occult blood, AXR (constipation), scope, CTAP
47
Q

Urinary incontinence

  1. Risk factors
  2. Initial investigations

Urge incontinence

  1. Symptoms
  2. Cause
  3. Non-medical management
  4. 1st line medication (+ side effects)
  5. When to avoid oxybutinin

Stress incontinence

  1. Symptoms
  2. Cause
  3. Non-medical management
  4. Medical management
  5. Surgical management
  6. Overflow incontinence - symptoms and cause
  7. Other incontinence types (2)
  8. LUTS lifestyle advice
A
  1. Advanced age, previous pregnancy / childbirth, high BMI, hysterectomy, FH
  2. Bladder diary for 3 days, urine dip/culture, vaginal exam (exclude prolapse)
  3. Sudden intense need to urinate (urgency, frequency, nocturia, incontinence, pads) following position change , sound of running water, sex
  4. Overactive bladder
  5. Bladder retraining (6+ weeks, gradually increase voiding intervals), monitor with incontinence chart
  6. Anti-muscarinic - oxybutynin, tolterodine, darifenacin (can’t shit / spit / see (dizzy and dry eyes) / pee)
  7. Frail older women
  8. Pee when cough/laugh/sneeze/exercise
  9. Pelvic floor/detrusor muscle weakness (childbirth, age)
  10. Pelvic floor exercises - 8+ 3x a day for 3+ months
  11. Alpha agonist, HRT
  12. Retropubic mid-urethral tape
  13. Bladder outflow obstruction (e.g. BPH) causing chronic urinary retention, very large bladder, frequent small trickles, constant urgency
  14. Total, mixed
  15. Cut out alcohol / caffeine / limit late night fluids, physio
48
Q

Acute urinary retention

  1. Commonest patient cohort
  2. Commonest cause

Urethral obstruction

  1. Physical causes
  2. Drug causes
  3. Neurological causes
  4. Symptoms
  5. Examinations
  6. Investigations (urine, blood, imaging)
  7. Diagnostic criteria
  8. Management
  9. Interpretation of management
A
  1. Males >60
  2. Secondary to BPH (presses on urethra, making the bladder wall thicker and less able to empty)
  3. Stricture, calculi, cystocele, constipation, masses
  4. Anticholinergics, TAD, anti histamines, opioids, benzos
  5. Cauda equina syndrome
  6. Inability to pass urine, lower abdominal pain
  7. Abdominal, PR, neurological, pelvic (in women)
  8. Urine dipstick + culture, FBC/U+E/CRP, bladder USS
  9. Urine volume >300ml on USS
  10. Catheterisation, + measure drainage in 15 minutes
  11. <200 - not acute, >400 - catheter left in
49
Q

Testicular pain

  1. Differentials

Torsion

  1. Definition
  2. Symptoms
  3. Management

Epididymo-orchitis

  1. Usual cause if men < 35
  2. Causative drug
  3. Symptoms
  4. Investigations
  5. Management
  6. Testicular swelling - main imaging
A
  1. Epididymo-orchitis, torsion
  2. Twist of the spermatic cord resulting in testicular ischaemia and necrosis
  3. Extreme sudden whole testicular pain, abdominal pain, vomiting, loss of cremestaric reflex, sometimes skin colour change, hot, bell clapper deformity (horizontal lie and high riding)
  4. Three point fixation (if viable) and secure the other side, within 6 hours
  5. Infective (chlamydia, gonorrhoea)
  6. Amiodarone
  7. Only epididymal pain, swelling, dysuria, sweats/fever
  8. 1st catch urine, STI screen
  9. Doxycycline, add ceftriaxone if gonorrhoea suspected
  10. US
50
Q

Urinary tract calculi (uro/nephrolithiasis)

  1. Common sites (3)
  2. Commonest type (+ others)
  3. Painful presentation
  4. Other presentations
  5. Examination
  6. Blood tests
  7. Urine tests
  8. 1st line imaging
  9. Medical management (+ indication)
  10. 1st line surgical management (+ indication)
  11. Further surgical management options
  12. ABX to add if septic
A
  1. Pelviureteric junction, pelvic brim, vesicoureteric junction
  2. Calcium oxalate (+ magnesium ammonium phosphate, urate, hydroxyapatite)
  3. Renal colic (loin to groin), cannot lie still with N+V
  4. Infection/interrupted flow, haematuria, proteinuria, sterile pyuria, anuria
  5. No tenderness on palpation, except renal angle tenderness on percussion if retroperitoneal inflammation
  6. FBC, U+E, Ca2+, phosphate, glucose, bicarbonate, urate
  7. Dipstick (blood), MC+S, pH, 24 hour, stone biochemistry
  8. Non-contrast CT
  9. <10mm; Analgesia (ketolac or morphine), rehydration, anti-emetic, alpha blocker to promote stone passing (e.g. tamsulosin/alfuzosin)
  10. > 10mm; 1st line is extracorporeal shock wave lithotripsy (ESWL) + ureteroscopy (higher stone-free rate)
  11. Surgical decompression (ureteric stent / percutaneous nephrostomy)
  12. Gentamicin/ceftriaxone
51
Q

Groin/scrotal lumps

  1. Can’t get above it
  2. Separate from testes + cystic
  3. Separate from tests + solid
  4. Testicular + cystic
  5. Testicular + solid
  6. Epididymal cyst - age, fluid type, location
  7. Hydrocoele - what it is
  8. Causes
  9. Management
A
  1. Inguinoscrotal hernia, hydrocoele extending proximally
  2. Epididymal cyst
  3. Epididymitis, varicocoele
  4. Hydrocoele
  5. Tumour, haematocoele, granuloma, orchitis
  6. Adult, clear/white fluid, above/behind testes
  7. Fluid within tunica vaginalis (blood is haematocoele)
  8. Patent processus vaginalis (primary, larger, commonest, young men), trauma/tumour/infection (secondary)
  9. Aspirate, surgery
52
Q

Undescended testes

  1. Cryptorchidism - definition
  2. Restractile testes - commonly found where
  3. Ectopic testes - commonly found where
  4. Maldescended/ectopic - complications
  5. Management
A
  1. Complete absence of testis from scrotum (anorchism if both)
  2. External inguinal ring
  3. Superior inguinal pouch
  4. Infertility, 40x higher of testicular cancer, trauma, torsion, hernias (patient processus vaginalis)
  5. Surgery (orchidopexy) at 6-12 months old, hormonal (hCG) if in inguinal canal

Medical School (28 decks)

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