Liver + Kidneys + Urinary Tract Flashcards
What do abnormalities in the different LFTs signify
ALT (3-40) / AST (3-30), liver enzymes, raised in pathologies that cause liver cell inflammation or damage; hepatitis, liver cirrhosis, drug / toxin induced liver injury, malignancy. Alcoholic liver disease AST:ALT >2:1 (L = less)
ALP (30-100), biliary epithelial cells and in bones, cholestasis or bone disease
GGT (8-60), hepatocytes and biliary epithelial cells, non specific but highly sensitive marker of liver damage and cholestasis. Isolated GGT in alcoholics
Bilirubin (3-17), haemoglobin breakdown, jaundice >50, unconjugated = prehepatic, conjugated = hepatic / post. Post has dark urine and pale stools (not metabolised in gut)
Albumin (35-50), nonspecific marker of function, also malnutrition / nephrotic syndrome
Hepatocellular injury = >ALT 10 + <ALP3, cholestasis >ALT10 + <ALP3, bone isolated ALP without GGT, albumin and coagulation studies for synthetic function and severity
Describe the pathogenesis of liver failure
Range of causes: hepatitis viruses, EBV, herpes simplex, paracetamol, alcohol, hepatocellular carcinoma, alpha-1 antitrypsin deficiency
Fulminant hepatic failure: syndrome resulting in rapid massive necrosis of liver cells leading to severe impairment of liver function and hepatic encephalopathy
Hepatic encephalopathy: as liver fails ammonia builds up in circulation and passes to brain, neurotoxic (halts krebs cycle), resulting in irreparable cell damage and neuronal death
What is the presentation, investigations and treatment for liver failure
Jaundice, small liver, bruising, clubbing, fever, vomiting. Ascites is rare
Bloods (LFTs, clotting screen, albumin, FBC, U+Es, ammonia), ultrasound +/- elastography, EEG useful for encephalopathy, microbiology to rule out infection
Non invasive liver screen: US, hep B+C serology, autoantibodies + immunoglobulins, ceruloplasmin (wilson’s), alpha-1 AT levels, ferritin + transferrin (haemochromatosis)
Treat cause (paracetamol poisoning - N-acetly-cysteine), IV glucose if necessary, mannitol for raised ICP, IV vitamin K + blood / platelets, lansoprazole to reduce GI bleeds
Liver transplant
What is the difference between cholecystitis, acute / biliary / sclerosing cholangitis
Acute cholecystitis (obstruction of gallbladder emptying): increased secretions - progressive distension (may compromise vascular supply), inflammatory response due to retained bile, increases risk of infection. Complication of cholelithiasis
Acute / ascending cholangitis (bile duct inflammation): infection of biliary tree most commonly secondary to a gallstone obstructing the common bile duct, infection often from bacteria rising from duodenum, causes entire biliary stasis and dilated ducts. Risk of sepsis
Biliary: progressive intrahepatic bile duct damage and loss, autoimmune with PBC-specific antibodies
Sclerosing: associated with IBD, inflammation and fibrosis of intra / extra hepatic bile ducts, diffuse stricture formation
Describe cholelithiasis
Cholesterol gallstones (80%): cholesterol crystallisation in bile due to high concentrations, deficiency in bile salts / phospholipids (cirrhosis, Crohn’s, ileal disease), excess cholesterol (diabetes, diet, obesity), also stasis (pregnancy, age)
Bile pigment stones (mostly calcium): mostly due to haemolysis (anaemia, sickle cell, thalassaemia), stasis
Majority of gallstones are asymptomatic, once symptomatic recurrence common. Biliary colic, related to eating fatty food
Biliary colic / gallstones - abdominal ultrasound (thin walls, non dilated ducts), normal lab results
All symptomatic gallbladder stones - laparoscopic cholecystectomy, paracetamol +/- hyoscine (antispasmodic). Asymptomatic: avoid fatty foods, statins. No evidence for ursodeoxycholic
5 Fs: fair, female, fat, fourty, fertile
pathogenesis and presentation of cholecystitis
Acute cholecystitis (obstruction of gallbladder emptying): increased secretions - progressive distension (may compromise vascular supply), inflammatory response due to retained bile, increases risk of infection. Complication of cholelithiasis
Initially continuous epigastric pain that develops into localised RUQ pain, associated with tenderness / guarding / rigidity, signs of inflammation, palpable mass
Investigations and treatment of cholecystitis
Imaging - abdo US or CT / MRCP if sepsis is suspected, bloods (FBC - raised WCC, raised CRP, elevated bilirubin, ALP, ALT, GGT), culture to rule out sepsis
US: pericholecystic fluid, distended, thickened wall (>3mm), sonographic murphy’s sign
(Organ dysfunction - ICU admission)
IV fluids, paracetamol / diclofenac, IV abx if sepsis suspected, if required cholecystectomy / cholecystostomy (drain fluid) / lithotripsy / ursodeoxycholic acid
Describe the pathogenesis and presentation of acute cholangitis
Acute / ascending cholangitis (bile duct inflammation): infection of biliary tree most commonly secondary to a gallstone obstructing the common bile duct, infection often from bacteria rising from duodenum, causes entire biliary stasis and dilated ducts. Risk of sepsis
Rare causes: strictures following surgery, pancreatic cancer, parasites
Cholangitis: biliary colic, fever, rigours, jaundice, right upper quadrant pain
Jaundice is cholestatic - dark urine, pale stools, itchy skin
Investigations and treatment for acute cholangitis
Ascending cholangitis: bloods, transabdominal ultrasound / MRCP (dilatation of CBD)
Raised WCC, blood culture / lactate / urine (sepsis), LFTs (bilirubin, AST, ALT, ALP), CRP
Cholangitis: IV antibiotics for all suspected (cefotaxime / metronidazole, piperacillin / tazobactam), removal of stones with ERCP or lithotripsy if large (non invasive preferred), analgesia (morphine, oxycodone, paracetamol)
Describe the pathogenesis and presentation of biliary and sclerosing cholangitis
Biliary: progressive intrahepatic bile duct damage and loss, autoimmune with PBC-specific antibodies
Sclerosing: associated with IBD, inflammation and fibrosis of intra / extra hepatic bile ducts, diffuse stricture formation
Fatigue, xanthelasma, dry eyes + mouth, abdo discomfort, pruritus
Pathogenesis of pancreatitis
Acute - syndrome of inflammation initiated by any acute injury, in most severe form there is extensive pancreatic / peripancreatic necrosis and haemorrhage
Gallstones (60%), alcohol (30%), trauma, idiopathic, autoimmune, drugs
Destructive effect of premature activation of pancreatic enzymes - enzyme autodigestion
Gallstones - obstruction of pancreatic duct so enzyme fluid builds up. Alcohol - interferes with calcium homeostasis - increased enzyme secretion due to contraction of ampulla of vater
Chronic: reduction in bicarbonate secretion, alkaline pH, activation of trypsinogen - necrosis and fibrosis. Protein plugs form and become calcified (obstruction and further damage)
Long term alcohol (75%), idiopathic, chronic kidney disease, genetic (CF), recurrent acute, autoimmune
What is the presentation of pancreatitis
Upper abdominal pain (severe that radiates to back), anorexia, N+V, fever, jaundice, shock + hypotension
Exocrine dysfunction in chronic: malabsorption, steatorrhoea, jaundice. Endocrine - diabetes
Investigations and scoring for pancreatitis
History + elevated lipase / amylase diagnostic
Bloods: clearly raised amylase + lipase (more specific), CRP (severity), FBC, LFTs, calcium (hypercalcaemia rare cause); urine amylase can be diagnostic if levels remain elevated
Abdo US (gallstones, pancreatic inflammation), CXR (pleural effusion, basal atelectasis, exclude others)
Pancreatic Glasgow scoring system (PANCREAS): PaO2 <8 kPa, Age >55, Neutrophils (WCC) >15*109, Calcium <2, Renal (urea) >16, Enzymes LDH >600 AST >200, Albumin <32, Sugar >10
3+ severe
What is the management for acute and chronic pancreatitis
Acute: IV fluids, analgesia, IV abx if infection; if required: oxygen, ondansetron
severity assessment + appropriate dietary supplements (nasogastric tube, nil by mouth), urinary catheter
Abx: carbapenem (imipenem / cilastatin) FL, fluoroquinolone (ciprofloxacin), metronidazole
Chronic: cessation of alcohol / smoking, dietary intervention, analgesia (paracetamol / ibuprofen / opiates), surgical duct drainage if required
Dietary: address malabsorption of fat, fat soluble vitamins (A, D, E, K), protein. Enzyme replacement
Gallstones - shockwave lithotripsy, steatorrhoea - enzyme supplements + PPI, diabetes - insulin
What is the pathogenesis of alcoholic liver disease
When alcohol is metabolised Acetyl-CoA is the final product (fatty acid), NADH is produced, increasing NADH/NAD+ ratio (decreased FA oxidation), converted to triglycerides in hepatocytes
Steatosis (worst in zone 3 with least O2) - hepatocellular ballooning blocking ducts
Changes in oxidation / reduction also impair carbohydrate and protein metabolism → necrosis of hepatic acinus
Acetaldehyde is toxic in high quantities, alcohol increases effects of toxic metabolites of drugs
Infiltration of leucocytes, necrosis (also TNF-alpha from kupffer), leads to cirrhosis
Investigations and treatment for alcoholic liver disease
Alcoholic liver disease: raised AST and ALT, AST:ALT >2:1, raised ALP + GGT. Function impaired disease: elevated bilirubin, decreased albumin, hyponatraemia, elevated prothrombin time. US
Cessation of alcohol + weight loss, fatty liver will heal, hepatitis requires nutrition supplementation and prednisolone (if bilirubin falls continue, if no change after 7 days stop)
Influenza and pneumococcal vaccines, hep A and hep B
Cirrhosis may require transplant
Symptomatic: diazepam for withdrawal (delirium tremens), thiamine to prevent encephalopathy, fluid and sodium restriction for ascites
What is the pathogenesis of cirrhosis, portal hypertension and varices
Cirrhosis (irreversible damage): inflammation, matrix deposition, necrosis, angiogenesis → fibrosis
Injury: necrosis, apoptosis, reactive oxygen species. Stellate: neutrophils, macrophages - inflammation. Kupffer cells: phagocytose and inflammatory mediators. Myofibroblasts deposit collagen
Alcohol abuse, NA fatty liver, hepatitis viruses. Also primary biliary cirrhosis, autoimmune
Portal hypertension (hepatic venous pressure > 5mmHg): 80% cirrhosis - contraction of myofibroblasts, portal vein thrombosis, schistosomiasis (most common global), sarcoidosis, right heart failure, IVC obstruction
Reduced venous flow to liver, splanchnic vasodilation, salt and water retention, formation of collaterals / varices, fluid leaks - ascites. drop in BP, compensating increase in cardiac output
Varices: compensating venous dilation (oesophageal, gastric, rectum, left renal, umbilical), potential to rupture (especially oesophageal)
Describe the presentation of cirrhosis
Ascites (distention), hepatic jaundice + pruritus, haematemesis / melaena (blood in stool); general: fatigue, weakness, weight loss, peripheral oedema
Physical signs:
Hands: leukonychia (white nails), palmar erythema, spider naevi, clubbing, cholesterol deposits, dupuytren’s in alcoholics
Facial: telangiectasia (red lesions) / spider naevi, jaundiced sclera, xanthelasma (lipid plaques on eyelids)
Abdo: caput medusae (swollen veins around umbilicus), hepatosplenomegaly, shifting dullness, hepatic bruit
Investigations and score for cirrhosis
Liver biopsy gold standard but often not required, LFTs, US + US elastography, CT / MRI if indicated, most sensitive and specific indicator is thrombocytopenia (platelets < 150,000 / micL)
Elastography assesses the stiffness of organs
LFTs: raised AST, ALT, ALP + GGT. Decreased albumin, bilirubin can be compensated, prolonged prothrombin time
Other blood tests: FBC, albumin, clotting screen, hepatitis serology
Child-Pugh classification: ascites, encephalopathy, high bilirubin, low albumin, long prothrombin
1y survival rates of cirrhosis patients
Fibrosis-4 score: age, AST, platelets, ALT
Management for cirrhosis
Treatment of underlying liver disease, monitor complications, support and palliative care
Good nutrition vital, alcohol abstinence, screening for cancer, hep A+B vaccinations, no NSAIDs
Transjugular intrahepatic portosystemic shunts (TIPSS) - for ascites. Transplant only cure
Ruptured varices: resuscitation, blood transfusion if anaemic, vitamin K + platelet transfusion, terlipressin to vasoconstrict, prophylactic antibiotics
Variceal banding, balloon tamponade, transjugular intrahepatic portocaval shunt
Describe the pathogenesis of the different types f hepatitis
Viral: infection of liver cells activates immune system, inflammation and cell death, chronic - fibrosis
Hep A: faecal-oro (a=anus), always acute and usually symptomatic
Hep B: blood-borne (sex, mother to child, IV drugs), ~70% asymptomatic in acute, risk of becoming chronic largely dependent on age (90% infants, 2-6% adults), chronic risk of cirrhosis and HCC
Hep C: blood borne (often iatrogenic), 30% spontaneous resolution, 70% chronic (30% will develop cirrhosis)
Hep D: is only simultaneous with or following B, also blood borne, secondary acute and increased rate of progression, increased risk of fulminant and carcinoma
Hep E: acute only, faecal-oro (usually water or food), self limiting but can cause fulminant
(A+E, the two ends are transmitted faecal - orally, end to end)
What is the presentation of hepatitis
Acute: fever, malaise, N+V, jaundice later (light stools), RUQ pain. Hepatomegaly.
Chronic (B+C) often asymptomatic until they develop: cirrhosis, liver failure, cancer. Jaundice, RUQ pain, hepatomegaly, ascites, fever, fatigue
95% of E are asymptomatic
Investigations and treatment for hepatitis
Serology tests for diagnosis and progression - surface antigens, antibodies for surface antigens, viral DNA / RNA (C)
Other bloods: LFTs, FBCs, clotting screen, U+Es (hyponatraemia), alpha-fetoprotein (HCC)
All acute, supportive treatment, monitor liver function. E can only be affected once. 95% of immunocompetent will clear B
Supportive: analgesia, metoclopramide, ursodeoxycholic acid / steroids if required
B (+D): acute - at 6 months measure for full clearance; chronic - pegylated interferon alpha 2a (weekly sc injection for 48 weeks), nucleotide analogues (daily tablet, may be life long)
Risk of autoimmune and lifelong immunosuppression
C: observe for viral clearance, pegylated interferon alpha 2a + oral ribavirin. Alternatively triple therapy direct acting antivirals
We have vaccines for A and B. antivirals (entecavir, tenofovir) and transplant if required
Describe haemochromatosis
Haemochromatosis: disorder of iron metabolism, deposited in liver, joints, heart, pancreas, pituitary, adrenals, skin. Iron precipitates fibrosis, late feature - cirrhosis
Increased iron absorption, stored in hepatocytes, oxidative stress and tissue damage
Classic triad of bronze skin, hepatomegaly, diabetes. Early - tiredness, weakness and arthralgia; hypogonadism (impotence / amenorrhoea); later - chronic liver, osteoporosis, cardiomyopathy
Serum iron + ferritin, genetic testing, MRI (iron overload), liver biopsy
Lifelong venesection (removal of blood), treat diabetes, testosterone replacement, low iron diet
Describe Wilson’s
Wilson’s: failure of biliary copper excretion, too much copper in liver and CNS, cirrhosis and damage to basal ganglia. Also kidney tubular degeneration and bone erosion
Hepatitis / liver failure, kayser-fleischer rings, behaviour changes, tremor, dysarthria, dystonia
LFTs, 24h urinary copper, slit-lamp exam, serum ceruloplasmin
24h copper excretion high, liver biopsy, haemolysis and anaemia, MRI shows degeneration
Slit lamp: see kayser-fleischer rings (gold-brown copper rings in cornea)
Lifelong chelating agent (penicillamine), avoid high copper foods, liver transplant if severe
Describe Alpha1 antitrypsin
Alpha1 antitrypsin deficiency: lack of inhibition of neutrophil elastase (protease enzyme to kill pathogens) in liver and lung; results in emphysema, liver cirrhosis, hepatocellular carcinoma
In lungs lack of elastin (they lose stretch): bronchiectasis, emphysema and potential of COPD
In liver toxic proteins are made: cirrhosis, fibrosis, hepatocellular carcinoma in adults, cholestasis in children
Emphysema and obstructive lung disease are the most common, bronchiectasis; liver: hepatitis, jaundice, ascites. Obstructive: dyspnoea, wheeze, cough, chest tightness
Plasma AAT, spirometry, CXR / CT, LFTs. Spiro: reduced FEV1, FVC, FEV1/FVC, increased TLC
no smoking, supportive (bronchodilators, physio), IV A1AT protein concentrates, lung reduction surgery + transplant
Describe the pathogenesis of liver cancer
Primary tumours - hepatocellular carcinoma, cholangiocarcinoma. Most common is actually secondary, often from GI / breast / lung. Hemangioma and hepatic adenoma are both benign tumours, HA only surgery if symptomatic and > 5cm.
HCC: cells resemble hepatocytes, can be multiple nodules in liver, can metastasise via hepatic or portal veins to lymph nodes / bone / lungs
Cholangiocarcinoma - cancer of biliary tree (biliary endothelium), usually slow growing
Presentation and investigations for liver cancer
Weight loss, fever, fatigue, jaundice, ache in right hypochondrium, ascites, varices (+ haemorrhage)
Rapid development of features in cirrhotic patients
Examination - large, irregular, tender liver
Raised alpha-fetoprotein, ultrasound (filling defects), enhanced CT (lesion > 1cm), liver biopsy (used less due to risk of spread)
FBC, metabolic panel, LFTs, clotting screen
Cholangocarcinoma: often asymptomatic
Raised but unspecific: CA 19-9, CA 125, carcinoembryonic antigen (CEA)
How is liver cancer managed
Isolated lesion - surgical resection / thermal ablation / radiofrequency ablation / transarterial chemoembolization, liver transplant only cure
Biologics: atezolizumab / bevacizumab
Describe the pathogenesis and presentation of pancreatic cancer
Adenocarcinoma, 99% occurs in exocrine component, ductal epithelium, progresses to fully invasive, most metastasise early so present late
5 year survival rate is 3%
PRESENTATION
Weight loss, diabetes, acute pancreatitis (obstructive jaundice, upper abdo discomfort). Many present minor - back / abdo pain, bowel habit change
Head of pancreas: painless obstructive jaundice (pale stools and dark urine)
Body and tail: epigastric pain, radiated to back and relieved by sitting forwards
What are the investigations and treatment for pancreatic cancer
Transabdominal ultrasound + CT - mass and dilated biliary tree, biopsy to stage
LFTs (obstructive jaundice): raised bilirubin, ALP, GGT. raised CA 19-9, staging laparoscopy, biopsy
Resectable disease: Whipple procedure (pancreaticoduodenectomy) for head of pancreas, extended resections if required
Resectable = no involvement of superior mesenteric artery, coeliac axis, common hepatic artery
Palliative: biliary stenting for jaundice, opiates, nutrition - pancreatic enzymes
Chemo: gemcitabine, FOLFIRINOX regimen
What are the causes of ascites
Local inflammation - peritonitis, intra abdominal surgery, infection (TB)
Low protein - hypoalbuminaemia, nephrotic syndrome, malnutrition
Low flow of fluid (fluid leaks out of vessels) - clot, cirrhosis (portal hypertension), cardiac failure, constrictive pericarditis
Describe primary and secondary peritionitis and the presentation
Primary: spontaneous bacterial peritonitis, ascites
Secondary: medical procedures (peritoneal dialysis), ruptured appendix, stomach ulcer, perforated colon, pancreatitis, diverticulitis, trauma, liver disease - cirrhosis, ruptured ectopic pregnancy
Abdominal pain, bloating / ascites, fever, N+V, loss of appetite, diarrhoea, low urine output
Perforation = sudden onset, secondary to inflammatory disease = gradual
Poorly localised at first (visceral peritoneum), then localised (parietal)
Investigations and treatment for peritonitis
Blood tests, erect CXR (air under diaphragm = perforated colon), abdominal X ray (bowel obstruction, foreign body), CT (exclude ischaemia)
Bloods: FBC (leukocytosis), blood cultures, LFTs (rule out)
Ascitic fluid appearance, absolute neutrophil count (ANC), culture
Empirical Iv Abx: cefotaxime / ceftriaxone. IV albumin infusion, large volume paracentesis
ABC, underlying cause, nasogastric tube, IV fluids
Surgery - peritoneal lavage (cleaning)
Describe the different segments of the nephron
Glomerulus surrounded by Bowman’s capsule, collection of capillaries that allow water and small particles out of the blood, Bowman’s capsule continues to proximal tubule. Blood enters through afferent arteriole, filtrate into tubule (no proteins), blood out efferent arteriole
Glomerular filtration rate - volume of fluid into Bowman’s space per minute. Normal is 120ml/min or > 90ml/min/1.73m2
Estimated GFR based on serum creatinine level, age, gender. Used to predict kidney function
Proximal convoluted tubule reabsorbs: all sugar, amino acids and bicarbonates, 70% of water, Na, Cl-, K+, HCO3-. Most vulnerable to damage and ischaemic injury, where most drugs are secreted
Loop of Henle reabsorbs 25% of water (descending only), loop diuretics inhibit NKCC2 inhibiting Na and therefore water reabsorption, osmosis, reabsorption of Na, K, Cl-
Distal 5% Na, controlled by aldosterone, thiazide diuretics. Where Ca is reabsorbed (PTH)
Collecting duct secretes K+ and H+, water absorbed through aquaporin 2 channels, controlled by aldosterone, acid base balance through secretion of H+ / HCO3-
Describe how blood pressure is affected by the nephrons
Blood pressure control: macula densa measures the rate of Na (GFR) from afferent arteriole
Decreased blood pressure / decrease in afferent arteriole diameter - decreased Na - prostaglandins make afferent dilate + renin is released by juxtaglomerular cells (will increase blood pressure)
High blood pressure / high Na detected, contraction of the afferent arterioles and less Na reabsorption
Presentation of lower UTI
Dysuria, new nocturia, cloudy / smelly urine; frequency, urgency, suprapubic tenderness, haematuria. In older patients often only presents with confusion
(Prostatitis: fever, malaise, nausea, urinary symptoms, pain: perineum, rectum, scrotum, penis, lower back, on PR)
Investigations and treatment for lower UTI
Dipstick (nitrites, leucocytes) (not in catheter or >65), MSU culture, consider US and referral if pyelonephritis / treatment resistant / recurrent unexplained / persistent haematuria, blood culture if systemic
Follow Abx guidelines, trimethoprim / nitrofurantoin, 3d for simple women, 5-10d for immunosuppressed / abnormal anatomy / impaired kidney function, 7d for men / pregnant / catheter
Nitrofurantoin not suitable if eGFR <45 or third trimester, trimethoprim is teratogenic
Treat asymptomatic bacteriuria in pregnant women, risk of pyelonephritis and preterm
Alternatives: amoxicillin (good for severe), cefalexin, pivmecillinam
Prostatitis: 14d ciprofloxacin / olfloxacin
presentation and treatment for pyelonephritis
fever, n+v, loin pain; rigours, costovertebral pain, cystitis, myalgia, haematuria
Cefalexin 10d; alternatively co-amoxiclav, trimethoprim, ciprofloxacin
Pregnancy: cefuroxime or cefalexin
Pathophysiology of nephroliathiasis
Stones form in supersaturated urine from urine constituents in the renal pelvis, 80% are calcium based (oxalate most common, phosphate), also uric acid, struvite, cystine
Uric acid not visible on x ray, struvite made by bacteria, cystine - cystinuria (genetic)
Reasons for increased concentration: excess calcium/ oxalate in diet, decreased absorption (gut or kidneys), hyperparathyroidism, dehydration, ileostomies
Pass out of the kidney and usually block: pelviureteric junction, pelvic brim, vesicoureteric junction
Can pass to bladder and develop into a bladder stone
Presentation of nephrolithiasis
Majority asymptomatic
Renal colic: rapid onset, excruciating ureteric spasms, waves of pain
Nausea and vomiting, worse with fluid loading, can radiate to groin + testis/labia, dysuria / oliguria, recurrent UTIs, haematuria; sepsis features if infectious
Investigations for nephrolithiasis
Urine dipstick (most haematuria, infection), FBC, U+Es, pregnancy test
Non contrast CT KUB initially (within 24h), US KUB (pregnant, children), abdo x ray (only calcium)
Analysis of stones following surgery
Management of nephrolithiasis
IM diclofenac GS, other NSAIDs, IV paracetamol. Hydration, antiemetics (metoclopramide, cyclizine)
Infection - IV cefuroxime / gentamicin
Obstruction - drainage with ureteric stent / percutaneous nephrostomy
<5mm, watch and wait, 50-80% pass without intervention, fails - shockwave lithotripsy, medical expulsive therapy with tamsulosin
>10mm: ureteroscopy or percutaneous nephrolithotomy, open surgery last resort
Prevent recurrence: potassium citrate, alkalizes the urine (less likely to form)
Lifestyle: overhydration (add lemon juice), low sodium diet, increase fibre, avoid fizzy drinks, reduce BMI, active lifestyle
Reducing calcium intake actually increases risk
Describe bladder stones
Form when bladder can’t empty: infection, benign prostate hyperplasia, neuropathic, catheters. Symptoms: lower abdominal pain, dysuria, frequency, interrupted flow, haematuria, UTI. Diagnosis and treatment the same
What are the causes and phases of AKI
Pre renal - decreased renal perfusion: heart failure, shock (hypovolemia, sepsis, trauma resulting in massive haemorrhage), dehydration
Intrinsic/ renal - renal parenchyma damage: acute tubular necrosis, thrombosis, glomerulonephritis, acute interstitial nephritis, haemolytic uraemic syndrome, rhabdomyolysis, drugs
Post renal - obstruction: urinary tract stones, clots, malignancy, BPH, strictures, neurogenic bladder
4 phases: initiation, oligo-anuria (symptoms start, urine output 30%), polyuria (significant loss of water), restitution
Presentation of AKI
Oliguria, arrhythmias (hyperkalaemia), oedema, fatigue, shortness of breath, nausea, chest pain
Examination: palpable bladder, palpable kidneys, masses
Investigations and criteria of AKI
U+Es, LFTs, FBC. Determine pre/ renal/ post: urine dipstick, blood count (anaemia), cultures, ultrasound (size, obstruction), DRE, biopsy
Dipstick: leucocytes + nitrites (infection), protein + blood (acute nephritis), glucose (DM)
Renal cause - biopsy
Criteria: rise of creatinine of >26 in last 48 hours (or just high) and rise of >50% in 7d, fall in urine to less than 0.5mL/kg/hour for more than 6 hours
Severity: stage 1 creatinine 1.5-1.9x baseline and <0.5ml/kg/h for 6-12h; stage 2 2-2.9x baseline and <0.5 for >12h; stage 3: >3x creatinine and <0.3 for >12h
Management of AKI
Treat underlying cause, stop nephrotoxic drugs, increase fluids (oral or IV)
Prerenal - give fluids, antibiotics if necessary. Post renal: catheterise, cystoscopy, stents or nephrostomy
Hyperkalaemia - insulin (drives potassium uptake) + dextrose, acidosis - sodium bicarbonate, pulmonary oedema - furosemide
Renal replacement in severe cases, haemodialysis and haemofiltration preferred but peritoneal in rare cases
What are the causes of CKD
Range of aetiologies: diabetes, hypertension, atherosclerotic renal D, polycystic, primary glomerulonephritides, SLE, small/ medium vasculitis, acute injury
Diabetes and hypertension account for ⅔ of all cases
Presentation of CKD, when do symptoms occur
Usually asymptomatic (screen patients with comorbidities and chronically using nephrotoxins)
Symptoms when serum urea > 40mmol/L: fatigue, fluid overload (SOB, oedema), weight loss, n+v, insomnia, nocturia, itching, diarrhoea
Investigations and staging of CKD
U+Es. Also urine dipstick, microscopy, renal US, U+Es, BP, HbA1c, lipid profile, consider biopsy / hepatitis serology / antibodies
ECG for hyperkalaemia, urinalysis (haematuria, proteinuria), ultrasound (size, obstruction), CT (sontes, fibrosis), biopsy
Kidney failure risk equation: age, sex, eGFR, albumin:creatinine. 5y risk of needing dialysis
Staging: eGFR (serum creatinine), urine albumin:creatinine ratio
G1 eGFR >90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 <15
A1 <3 mg/mmol, A2 3-30, A3 >30
Accelerated progression: sustained decline in 1y of eGFR 25% or 15
Management of CKD
Treat underlying cause and prevent complications
Slow disease progression: ACE (ARB), SGLT2 (dapagliflozin) (also cardiac)
Reduce complications: statin, exercise, diet, stop smoking, low dose aspirin if clot risk
Manage complications: sodium bicarbonate (metabolic acidosis), iron + erythropoietin, vit D / phosphate binders / low phosphate diet
Dialysis if symptomatic uraemia, uncontrolled hyperkalemia, pulmonary oedema (symptoms outweigh complications)
(Haemodialysis: pump in hospital, time consuming, feel washed out, no training needed, good clearance
Peritoneal: can do at home, less hypertension, can maintain the remaining kidney function, infections, need training, can be inadequate
Haemofiltration: used in critical care)
Transplant: every patient progressing to G5 unless comorbidities like metastatic cancer, HIV, unstable CVD, frailty etc
Living donor has best function especially with HLA matching, immunosuppression required
What are the compications of CKD
Complications: anaemia (normocytic - reduced EPO production), bone disease (phosphate retention and impaired 1,25-dihydroxy vitamin D production), cardiovascular (hypertension, hyperlipidaemia, calcification) (MI, failure, stroke), peripheral neuropathy, dialysis related complications
Pathophysiology and presentation of renal cell carcinoma
Most common kidney tumour, adenocarcinoma from renal tubules
Clear cell 80%, papillary 15%, chromophobe 5%. Wilm’s in children under 5
Often spreads to renal vein then inferior vena cava, cannonball metastases in lungs classic feature of metastatic RCC
Classic triad: haematuria, flank pain, palpable mass. Also general cancer signs and symptoms
Paraneoplastic symptoms: polycythaemia (unregulated erythropoietin), hypercalcaemia, hypertension, Stauffer’s (raised ALT, AST, ALP, bilirubin) without liver mets
Investigations and management of renal cell carcinoma
Bloods: FBC, LDH (>1.5x normal bad prognosis), corrected calcium. LFTs, coagulation profile, creatinine, eGFR. Urinalysis
Abdo/ pelvis US, CT abdo / pelvis, MRI if contrast contraindicated
Stage 1: <7cm in kidney, 2: >7 in kidney, 3: local spread in Gerota’s fascia, 4: metastasis
2w wait: 45+, unexplained visible haematuria, without UTI or after UTI treatment
Surgery FL: parietal / radical nephrectomy
Arterial embolisation, percutaneous cryotherapy, radiofrequency ablation. Also radio and chemo
Pathophysiology and presentation of bladder cancer
Arises from urothelium (endothelium), 90% transitional cell carcinoma, 5% squamous CC, also adenocarcinoma, sarcoma, small cell
RF: smoking, age, aromatic amine exposure (dye, rubber), schistosomiasis → squamous
Painless haematuria main
2ww if 45+ with unexplained visible haematuria (without UTI or after treatment), 60+ with microscopic and dysuria / raised WCC
Investigations and management of bladder cancer
Urinalysis, cystoscopy, cytology - if suspicious CT / MR urogram
Transurethral resection of bladder tumour (non invasive), intravesical chemo to stop recurrence. Intravesical BCG vaccine, radical cystectomy (+ urostomy, continent urinary diversion, neobladder reconstruction, ureterosigmoidostomy), chemo + radio
What is renal tubular acidosis and what are the types
Metabolic acidosis (hyperchloraemic) due to pathology in renal tubules, 4 types
Type 1: distal tubule cannot excrete H+, high urine pH, low serum K
Genetic, SLE, Sjorgren’s, primary biliary cholangitis, hyperthyroidism, sickle cell, Marfan’s
2: proximal tubule cannot reabsorb HCO3-, high urine pH, low serum K
Genetic, multiple myeloma, Fanconi’s
3 (very rare): carbonic anhydrase II deficiency, combination of types 1+2
4 (most common): low aldosterone / impaired function, low urine pH, high serum K
Adrenal insufficiency, diabetic nephropathy, medications (ACE, spironolactone)
Presentation and treatment of renal tubular acidosis
Presentation: growth retardation, muscular weakness, rickets / osteomalacia, nephrolithiasis, recurrent UTIs, arrhythmias
Treatment depends on type
1 + 2: alkali replacement therapy - Shohl’s solution or oral sodium bicarbonate, K supplementation
3: fludrocortisone + dietary restriction of K; aldosterone resistance: furosemide, low potassium high salt diet
Describe haemolytic uraemic syndrome
Thrombosis in small blood vessels throughout the body, usually triggered by shiga toxins - E.coli / shigella
Most commonly affects children following gastroenteritis, antibiotics and anti-mobility meds (loperamide) increase the risk
Presentation, investigation and management of haemolytic uraemic syndrome
Presentation: microangiopathic haemolytic anaemia, AKI, thrombocytopenia; following diarrhoea that turns bloody in a child
Also: fever, abdo pain, lethargy, pallor, oliguria, haematuria, hypertension, bruising, jaundice, confusion
FBC + smear, renal function, U+Es
Medical emergency - hospital admission, stool culture to establish causative organism, supportive: IV fluids, antihypertensives (not ACE, CCB / BB), blood transfusion, dialysis
Describe rhabdomyolysis
Myocyte apoptosis, releasing: myoglobin, potassium, phosphate, creatinine kinase
Causing AKI, hyperkalaemia causes arrhythmias
Causes: prolonged immobility, extremely rigorous exercise, crush injuries, seizures, statins
Presentation, investigations and treatment of rhabdomyolysis
Presentation: muscle pain / weakness / swelling, oliguria, red-brown urine (myoglobinuria), fatigue, n+v, confusion (especially elderly)
Ix: creatinine kinase (main), urine dipstick (myoglobin), U+Es, ECg
IV fluids, calcium gluconate for K; debatable: IV sodium bicarbonate, IV mannitol
Presentation and management for interstitial cystitis
Presentation: suprapubic pain (worse with full bladder), frequency, urgency, may be worse during menstruation
Supportive Mx: avoid alcohol / caffeine / tomatoes / smoking, pelvic floor exercises, bladder retraining, CBT, transcutaneous electrical nerve stimulation
(Meds: analgesia, antihistamines, oxybutynin, mirebegron, ciclosporin
Also can use intravesical medications (directly into bladder) and surgery (botox injections, augmentation of bladder))
Pathophysiology and presentation of BPH
Epithelial and stromal proliferation and / or decreased apoptosis, may squeeze or partially block the urethra causing LUTS
Androgen do not cause BPH but are a requirement - castration of testicles protective
Lower urinary tract symptoms: hesitancy, weak flow, urgency, frequency, intermittency, straining, terminal dribbling, incomplete emptying, nocturia
Can develop bladder stones, haematuria, infections, chronic retention
Investigations and management of BPH
Examination: digital rectal, as well as abdominal, external genitalia
Urinalysis, PSA, international prostate symptom score, urine volume chart
Observation if only mild/ no symptoms (over 5 years 25% progress and 30% improve)
Alpha adrenergic antagonists (tamsulosin) and 5 alpha reductase inhibitors (finasteride). Both reduce flow, aa fast acting but not permanent, 5ar improve tone
Anticholinergics for overreactivity - tolterodine / oxybutynin
Indications for surgery: bladder stones, recurrent gross haematuria, recurrent infections, therapy failure, renal insufficiency, refractory retention
Pathophysiology and presentation of prostate cancer
Adenocarcinoma, usually in peripheral zone, 85% multifocal, spreads locally through prostate capsule, metastasises to lymph nodes and bones (sclerotic), occasionally to liver and lungs
Androgen driven
Can be asymptomatic
Lower urinary tract symptoms +- haematuria
New onset erectile dysfunction, discomfort when sitting
Investigations and treatment for prostate cancer
PSA, multiparametric MRI, transrectal ultrasound guided / transperineal biopsy, histopathology, isotope bone scan for metastasis
Watchful waiting/ active monitoring as won’t necessarily progress and complications of surgery
External beam radiotherapy (proctitis), brachytherapy, hormone, radical prostatectomy surgery
Pathophysiology and presentation of nephritis
Nephritis - inflammation of kidneys, glomerulonephritis - inflammation of glomerulus (pores in podocytes allow blood and urine to pass through)
IgA nephropathy, HSP, post-streptococcal, anti-glomerular basement membrane, membranous nephropathy, membranoproliferative GN, rapidly progressive GN, goodpasture, vasculitis, lupus nephritis
Nephritic: haematuria (micro or macroscopic), proteinuria, hypertension, oliguria, red cell casts
Proteinuria <3g / 24h
Investigations and management of nephritis
Biopsy required for most diagnoses, US (size + anatomy), urinalysis (ACR, RBC casts), bloods (FBC, U+Es, LFT, CRP), CXR for pulmonary haemorrhage
Cause: autoantibodies (ANA, ANCA, dsDNA, GBM), blood cultures and serology
Treat cause and supportive like CKD: BP control, ACE / ARB; May need immunosuppression (steroids), dialysis
Pathophysiology and presentation of nephrotic syndrome
Nephrotic = damage to basement membrane. Primary causes: minimal change disease (children), membranous nephropathy + focal segmental glomerulosclerosis. Secondary: diabetes, SLE, Sjorgen’s, HIV / Hep B / syphilis, amyloidosis, myeloma
Pathology of podocytes / glomerular basement membrane / endothelial cells
Peripheral + facial oedema, hyperlipidaemia, fatigue, shortness of breath, recurrent infections, frothy urine, thrombosis
Investigations and management of nephrotic syndrome
Nephrotic: large proteinuria (> 3.g / 24h), hypoalbuminaemia (<30g / L), oedema
Protein-creatinine ratio, urinalysis (cellular casts, protein electrophoresis), autoimmune _ infection serology, renal biopsy
Treat cause, reduce oedema: fluid and salt restriction, loop (furosemide), aim for 0.5-2kg loss per day
Presentation, investigations and management of polycycstic kidney disease
Clinically silent for many years
Loin pain (the more the larger the kidneys), haematuria, water and salt loss, nocturia,
Enlarged kidneys, hypertension, renal stones
Ultrasound, diagnostic if 15-39 3+ cysts / 40-59 2+ cysts on each / > 60 4+ cysts on each
Blood pressure raised, genetic testing (hard)
Nothing to slow progression
Blood pressure - ACE-i, stones - analgesia, laparoscopic removal of cysts, renal replacement if end stage failure
Monitor progression with serum creatinine, family screening for children and siblings (ultrasound in 20s)
Pathophysiology of obstructive uropathy
Obstruction leads to back pressure, vesicoureteral reflux (into ureters), hydronephrosis (kidneys)
Common causes: upper: kidney stones, tumours, ureter strictures, retroperitoneal fibrosis, ureterocele; BPH, prostate / bladder cancer, urethral strictures, neurogenic bladder
Presentation, investigations and management of obstructive uropathy
Upper: Loin to groin / flank pain, reduced urine output, non specific (vomiting), impaired renal function
Lower: LUTS (hesitation, poor flow etc), urinary retention, impaired renal function
Urinalysis, renal US, U+Es, FBC, FBC, CT
nephrostomy, urethral / suprapubic catheter
Presentation, investigations and maangement of testicular cancer
Usually painless, lump, arising from testicle, hard + irregular, non fluctuant, no transillumination
Leydig cell tumours present with gynaecomastia
US FL, tumour markers, staging CT (royal marsden)
Markers: alpha fetoprotein (raised in teratomas), beta HCG (both), LDH very non specific
Stage 1 - testicle, 2 retroperitoneal lymph nodes, 3 distal lymph nodes, 4 other organs
Radical orchidectomy + prosthesis, chemo + radio, sperm banking. May become hypogandic
How are non-malignant scrotal diseases different on examination
Diagnosing: can you get above it, is it separate from the testis, cystic or solid
Cannot get above: inguinoscrotal hernia, proximally extending hydrocele
Separate: cystic - epididymal cyst; solid - epididymitis or varicocele
Testicular: cystic - hydrocele; solid - tumour, haematocele
Diagnose with ultrasound
Describe epididymal cysts
Epididymal cyst - smooth, extratesticular, spherical cyst in head of epididymis, if filled with sperm spermatocele (same management)
Often multiple, may be bilateral, small asymptomatic / large painful, well defined
Exam: soft + round, typically at top of testicle, associated with epididymis, separate from testicle, large cysts transilluminate
Surgical excision only if painful
Describe varicoceles
Varicocele - abnormal dilation of pampiniform plexus veins caused by venous reflux, 15% of men
Can cause: impaired fertility and testicular atrophy (impaired temperature control)
More common on left (L testicular vein to renal vein, increased resistance and angle; R into IVC)
Dull ache/ throbbing, worse when standing, subfertility. Mass feels like ‘bag of worms’, more prominent when standing / disappears when lying (if not indicates tumour)
US + doppler, concerns about function - semen analysis, hormones
Surgery or endovascular embolisation
Describe testicular torsion
Testicular torsion - twisting of spermatic cord resulting in occlusion of vessels (can rapidly lead ischaemia and infarct, loss of testis). Often an underlying congenital malformation (not fully fixed)
Any boy with abdominal pain should have testis checked, sudden onset pain in one testis (can’t walk), often occurs during physical activity, inflammation, may lie high and transverse
Exam: firm + swollen, elevated, absent cremasteric reflex, abnormal testicular lie (horizontal) (epididymis not posterior)
Scrotal US - if delayed skip, whirlpool sign
Surgery in < 6 hours salvage rate 90-100%, > 24 is 0-10%. Recognising early is key. Surgery: orchiopexy untwist and fix in place, orchidectomy (removal)
Describe epididymo orchitis
Epididymo Orchitis, infection caused by e coli, chlamydia trachomatis, neisseria gonorrhoea, mumps
Presentation: acute onset testicular pain, dragging / heavy, swelling, tender on palpation, urethral discharge (chlamydia / gonorrhoea), fever. Potential to cause sepsis
US immediate to rule out torsion; urine microscopy / culture / sensitivity, C+G NAAT / charcoal swab, saliva swab / serum Abs - mumps
E coli: ofloxacin 14d / levofloxacin 10d / co-amoxiclav 10d. STI: IM ceftriaxone, doxycycline, ofloxacin
Quinolones very broad for gram negative; important SE: tendon damage (especially achilles), low seizure threshold
