Genitourinary Flashcards
Define Nephrolithiais/Urolithiasis
Refers to the presence of crystalline stones (calculi) forming within the renal parenchyma or collecting duct, eventually moving to the urinary system (kidneys/ureter)
Give 5 main functions of the kidney (in normal health)
Fluid management
Red blood cell production (EPO production)
Acid Base Balance (Excretes H+ and reabsorbes HCO3-)
Waste excretion
Vitamin D metabolism (25-Hydroxyvitamin D to 1,25 Dihydroxyvitamin D)
Name 3 areas where ureteric stones tend to manifest?
Pelviureteric junction
Pelvic brim
Vesicoureteric junction
What can ureteric stones be comprised of? (2)
Calcium oxalate (most common)
Calcium phosphate (uncommon)
Give 4 risk factors for ureteric stone formation?
Male
Diet (excessive oxalate, urate, sodium and animal protein)
Chronic dehydration
Obesity
Give 1 complication of ureteric stone formation
Obstruction of urinary flow and infection
Obstruction can decrease eGFR and perfusion to the kidneys, leading to irreversible kidney damage.
Give 5 clinical features of a renal colic
Rapid/Abrupt onset (awoken from sleep)
Pain from loin to groin (comes and goes in waves)
Often cannot lie still (differentiates from peritonitis)
Worse on fluid loading
Nausea/Vomiting/Haematuria
What is used to diagnose ureteric/renal colic? (non-pregnant)
Non-contrast CT KUB (kidney, ureter and bladder) within 24 hours of admission
What is used to diagnose ureteric/renal colic? (pregnant)
Ultrasound
What additional tests may be important to consider for a patient with ?ureteric/renal colic? (4)
Urine dipstick - To exclude UTI
Creatinine and electrolytes - To assess renal function
FBC/CRP - To look for associated infection
Serum Calcium - To exclude cystinuria, uric acid stones and primary hyperparathyroidism
How is pain from ureteric/renal stones managed? (3)
1st line - IM Diclofenac
2nd line - IV Paracetamol
3rd line - Opioids
What medication is used to treat distal ureteric stones <10mm?
Tamsulosin (alpha blocker)
How do alpha blockers (like tamsulosin) treat renal stones?
Promote smooth muscle relaxation and dilation of the ureter, potentially easing stone passage
Describe the management of renal stones based on their size (4)
Watchful wait if <5mm and asymptomatic
5-10mm - shockwave lithotripsy
10-20mm - shockwave lithotripsy or ureteroscopy
> 20mm percutaneous nephrolithotomy
Describe the management of uretic stones? (2)
<10mm = Shockwave lithotripsy +/- alpha blockers
10-20mm ureteroscopy
Give 3 complications of shockwave lithotripsy
Shockwaves can cause solid organ injury
Fragmentation of larger stones can cause ureteric obstruction
Procedure may be uncomfortable and require analgesia afterwards
Give one indication for using ureteroscopy as opposed to lithotripsy to manage uretic stones
Pregnant female
Give 5 methods of preventing renal stones
High fluid intake
Add lemon juice to drinking water
Avoid carbonated drinks
Limit salt intake
Avoid thiazide diuretics
Define AKI. How is it characterised clinically?
Acute Kidney Injury
Describes an acute decline in kidney function (over hours/days), resulting in failure to maintain fluid, electrolyte and acid-base homeostasis.
Characterised by a rise in serum creatinine and/or a fall in urine output.
Give 3 divisions for causes of AKI
Pre-renal (most common)
Renal (intrinsic)
Post-renal (obstruction of urine outflow)
Give 5 risk factors for AKI
Sepsis
Major surgery
Cardiogenic shock (heart failure)
Hypovolemia
Drugs (ACEi, ARBs, NSAIDs, Iodinated contrast)
Give 4 drugs associated with causing AKI
ACEi (Ramipril)
ARBs (Candesartan)
NSAIDs (Ibuprofen)
Iodinated contrast
What electrolyte imbalances may be seen in AKI? (4)
Hyperkalaemia
Hyperphosphatemia
Hypermagnesemia
Hyponatraemia
Give 4 complications of AKI
Metabolic acidosis (altered consciousness, circulatory collapse, hyperventilation)
Volume overload (tachypnoea, tachycardia, cyanosis, lung crepitations)
Uraemia (high levels of urea in the blood)
CKD and end-stage renal disease
Give 5 clinical features of AKI
Nausea/Vomiting/Diarrhoea/Evidence of dehydration
Confusion, fatigue, drowsiness
Reduced urine output/changes in colour
Pulmonary/peripheral oedema + basal crepitations
Arrythmias (due to hyperkalaemia)
What diagnostic test is most important in detecting AKI?
U&E
Sodium, Potassium (most valuable), Urea and Creatinine (elevated)
What criteria are used to detect AKI?
p(RIFLE)
AKIN
KDIGO
Describe the KDIGO criteria for detecting AKI
Rise in serum creatinine of >26mmol/L within 48 hours.
A >50% rise in serum creatinine known or presumed to have occurred within the last 7 days
A fall in urine output to <0.5ml/Kg/hour for >6 hours in adults or >8 hours in children
A >25% fall in eGFR in children or young people within the last 7 days
Give 3 investigations which are important to conduct in a patient with ?AKI
Urinalysis (urine dipstick) - If shows haematuria and proteinuria without UTI/trauma, consider acute nephritis
Ultrasound - Gives assessment of kidney size
ECG - May show signs of hyperkalaemia
Give 4 signs of hyperkalaemia seen on an ECG
Flat/broad P waves
Tall tented T waves
Prolonged QRS
Prolonged PR
Describe how AKIs are staged according to KDIGO
Stage 1 = Creatinine = >26.5mmol/L and Urine Output = <0.5ml/Kg/h for 6-12h
Stage 2 = Creatinine = 2.0-2.9x baseline and Urine Output = <0.5ml/Kg/h for >12h
Stage 3 = Creatinine = >3x increase or increase of >353.6mmol/L and Urine Output = <0.3ml/Kg/h for 24h or anuria for 12h
Define pre-renal AKI
Characterised by reduced kidney perfusion (blood flow) resulting in ischaemia.
Typically leads to a decrease in GFR.
Give 3 pre-renal causes of AKI
Hypovolemia (decreased vascular volume) (haemorrhage, burns, pancreatitis)
Reduced cardiac output (heart failure, cardiogenic shock, liver failure, MI, sepsis)
Renal vasoconstriction (ACEi, ARBs, NSAIDs, Loop diuretics)
Define renal AKI
Characterised by structural damage to the kidneys
Give 4 causes of renal AKI
Toxins and Drugs (antibiotics, contrast, chemotherapy)
Vascular pathology (vasculitis, thrombosis, haemolytic uraemic syndrome, TTP, dissection, DIC)
Glomerular pathology (glomerulonephritis)
Tubular pathology (acute tubular necrosis)
Define post-renal AKI
Characterised by an acute obstruction of the outflow of urine, resulting in increased intratubular pressure and decreased GFR
Give 1 cause of post-renal AKI
Obstruction (renal stones, renal tract malignancy, enlarged prostate, blocked catheter)
How is pre-renal AKI primarily managed?
Correct volume depletion and/or increase renal perfusion
What medications should not be used to increase urine output/kidney perfusion respectively in pre-renal AKI?
Loop diuretics
Low dose dopamine
When (and only when) should loop diuretics be considered in a patient with pre-renal AKI?
When patient is awaiting renal replacement therapy.
or
When renal function is recovering in a patient not awaiting renal replacement therapy
How should renal cause of AKI be managed?
Refer for biopsy and specialist treatment for intrinsic renal disease
How should post-renal AKI be managed?
Refer for catheter, nephrostomy or urological intervention (stenting)
Give 3 other general managements of AKI
STOP nephrotoxic drugs (ACEi, ARB, NSAIDs, Genamicin, Amphotericin)
Treat hyperkalaemia (IV insulin + Dextrose + Calcium gluconate + nebulised salbutamol)
Treat metabolic acidosis (Sodium bicarbonate)
When should AKI patients be referred for Renal Replacement Therapy? (dialysis or transplantation)(4)
Hyperkalaemia
Metabolic acidosis
Symptoms or complications of uraemia (pericarditis/encephalopathy)
Fluid overload (peripheral/pulmonary oedema/crackles or basal crepitations)
Define CKD
Describes a reduction in kidney function and/or structural damage present for >3 months, with associated health implications.
What does GFR indicate?
Glomerular Filtration Rate
Describes how quickly blood is travelling through the kidney and so provides an indication to kidney function
What is the GFR of a normal functioning kidney?
> 60ml/min/1.73m2
Describe the 6 stages of CDK
Stage 1 (G1) = GFR = >90
(Only CKD if there is evidence of kidney damage, such as; Proteinuria and/or haematuria)
Stage 2 (G2) = GFR = 60-89 (Pathology on biopsy, tubular disorder, transplant)
Stage 3a (G3a) = GFR = 45-59 (Mild-moderate reduction in GFR)
Stage 3b (G3b) = GFR = 30-44 (Moderate-severe reduction in GFR)
Stage 4 = GFR = 15-29 (Severe reduction in GFR)
Stage 5 = GFR = <15 (Kidney Failure)
What are the 3 most common causes of CKD in the UK?
Diabetes (24%)
Glomerulonephritis (post-streptococcal -13%)
Hypertension (11%)
Give 8 complications of CKD (CRF HEALS)
C - Cardiovascular Disease
R - Renal osteodystrophy (decreased Ca, increased P04, increased pTH)
F - Fluid (oedema)
H - Hypertension
E - Electrolyte disturbances (K,H)
A - Anaemia (normocytic, normochromic due to reduced EPO production)
L - Leg restlessness
S - Sensory neuropathy
Give 6 clinical features of CKD
Fatigue
Oedema
Nausea +/- vomiting
Pruritis (due to urea accumulation from impaired renal excretion)
Restless legs (symptoms of uraemia)
Anorexia
Give 5 diagnostic tests used to investigate CKD
Renal ultrasound
Urine dipstick (test of haematuria)
Creatinine based eGFR
Albumin:Creatinine Ratio (test for proteinuria)
Biochemistry (may show raised PTH, Low Ca, High PO4 - vitamin D deficiency)
Describe the pharmaceutical management of CKD (2)
Blood pressure control - ACEi or ARB
Prevent/treat cardiovascular cause - Aspirin, Apixiban, Atorvastatin
Describe prostate cancer
Describes an adenocarcinoma arising from the peripheral zone of the prostate gland
Majority are multifocal
Prostate cancer is the most common cancer that metastasizes to what?
Bone
What is PSA?
Prostate Specific Antigen
Describes a protein produced by normal and cancerous prostate cells (isn’t prostate cancer specific).
Is secreted by the prostate epithelial cells into the prostatic fluid where it functions to liquify semen and allow spermatozoa to move more freely
Give 1 pro of using PSA
Early detection and early treatment
Give 4 cons of using PSA
False negative PSA tests - 15% of men with negative PSA may have prostate cancer
False positive PSA tests - 75% of men with a positive PSA test have a negative prostate biopsy
Unnecessary investigation - False positives may lead to invasive investigations (biopsy) which may have adverse effects (bleeding, infection ect)
Unnecessary treatment - Adverse effects from treatment, such as urinary incontinence and sexual dysfunction are common)
Give 6 risk factors for prostate cancer
Male
Increasing age
Black ethnicity
Family history - BRCA1, BRCA2, HOXB13
Overweight/obesity
Elevated testosterone
What is the main driver of prostate cancer formation?
Androgenic stimulation
What score is used to assess the likelihood that a patient has prostate cancer?
Likert score;
1 - Very unlikely
2 - Unlikely
3 - Difficult to tell
4 - Likely
5 - Very likely
What is the 1st line investigation for suspected prostate cancer? When is it’s use considered?
Multiparametric MRI
Offered if Likert scale is >=3
If Likert scale is 1-2 then discuss pros/cons of having a biopsy
What do NICE recommend with regards to PSA screening?
Men aged 50-69 should be referred if PSA is >=3.0ng/ml OR there is an abnormal DRE
Describe other investigations used in prostate cancer (3)
DRE - Examine size and structure of prostate
PSA - Determines risk (low, intermediate, high)
Prostate biopsy
Give 5 causes of raised PSA
Benign prostatic hyperplasia (BPH)
Prostatitis and UTI (NICE recommend postponing the PSA for 1 month after treatment)
Ejaculation
Vigorous exercise
Urinary retention
Give 5 clinical features of prostate cancer
Localised prostate cancer is often asymptomatic.
Bladder outlet obstruction (hesitancy, urinary retention)
Haematuria, haematospermia
Pain; back, perineal or testicular
DRE - Asymmetrical, hard, nodular enlargement with loss of medial sulcus
What may a digital rectal examination show in a patient with prostate cancer?
Asymmetrical, hard, nodular, enlargement with loss of medial sulcus
How is prostate cancer graded? Describe this
Graded using the Gleason Score.
Refers to how the cancer looks histologically on biopsy. The mor aggressive the cancer, the more malignant the cancer is.
Low risk = <6
Intermediate risk = 7
High risk = 8-10
How is prostate cancer staged? Describe this
Staged using TNM staging.
Refers to where the cancer is present in the body.
T1 – Clinically unapparent tumour (not detected by DRI nor visible through imaging)
T2 – Confined within the prostate
o T2a – Involves half a lobe or Less
o T2b – Involves > half of one lobe but not both
o T2c – Involves both lobes
T3 – Tumour extends through the prostate capsule but has not spread to other organs
T4 – Tumour is fixed or invades adjacent structures other than the seminal vesicles
How is localised prostate cancer managed?
Low/Intermediate risk;
- Active surveillance
- Radical prostatectomy
- Radical radiotherapy
High risk
- Offer either prostatectomy or radical radiotherapy
-Discuss option of Docetaxel Chemotherapy
Describe the active surveillance of low/intermediate risk prostate cancer (3)
Aim to keep patient with localised disease within a window of curability.
1st year - Involves testing PSA every 3-4 months and having a DRE after 12 months
2nd year - Involves testing PSA every 6 months and having DRE after 12 months
How is metastatic prostate cancer managed? (2)
External beam radiotherapy
Androgen deprivation therapy - Groserelin and Leuprorelin (LHRH antagonists)
Name 3 adverse effects of hormone therapy (treating prostate cancer) and describe how they are managed.
Hot flushes - Medroxyprogesterone
Sexual Dysfunction - Phosphodiesterase 5 inhibitors (sildenafil)
Osteoporosis - Bisphosphonates
Define BPH
Benign Prostatic Hyperplasia
Describes enlargement of the inner (transitional) zones of the prostate.
Typically leads to lower urinary tract symptoms
How may BPH present? (3)
Lower urinary tract symptoms;
Storage symptoms; Nocturia/Frequency/Urgency
Voiding symptoms; Poor stream/Hesitancy/Straining/Incomplete emptying/post void dribbling
Haematuria (may suggest cancer)
Give 4 investigations used to assess BPH
Urinalysis - Investigate complicated UTI
DRE - prostate nodules/asymmetry more consistent with prostate cancer
PSA - Likely elevated
International Prostate Symptom Score - Used to classify the severity of LUTI symptoms to assess impact.
How is BPH managed? (3)
Alpha blockers - Tamsulosin
5a reductase inhibitors - Dutasteride/Finisteride
Surgery - Transuretheral resection of prostate (TURP)
Give 1 common side effect of Tamsulosin (alpha blocker)
Postural hypotension (alpha blockers induce dilation of venous capacitance vessels)
In what patients is Dutasteride/Finasteride contraindicated?
5a reductase inhibitor
Contraindicated in patients with severe liver disease
Give 1 possible complication of Transurethral resection of the prostate (TURP)
Impotency
Give 4 possible side effects of 5 alpha reductase inhibitors (such as finasteride)?
Erectile dysfunction
Reduced libido
Ejaculation problems
Gynaecomastia
What is the MOA of 5 alpha reductase inhibitors (such as finasteride)
Blocks conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH
How is a nephrotic syndrome characterised?
Characterised by proteinuria due to podocyte pathology
What triad is seen in nephrotic syndrome?
Proteinuria (>3g/24h)
Hypoalbuminaemia (<30g/L)
Oedema
How is nephritic syndrome characterised?
Characterised by haematuria due to inflammatory damage
What symptoms are seen in nephritic syndromes? (4)
Haematuria + Red cast cells
Proteinuria > oedema
Hypertension
Oliguria and progressive renal impairment
Name 3 nephrotic syndromes
Minimal change disease (most common - children)
Focal segmental glomerulosclerosis
Membranous nephropathy
How does minimal change disease present in children? (4)
Triad; Proteinuria, Hypoalbuminaemia and Oedema
Facial/Leg oedema
Normotensive
No presence of haematuria
How is minimal change disease diagnosed? What will it show?
Renal biopsy + Electron microscopy
Shows effacement (shortening) of podocyte foot processes
How is minimal change disease treated? (2)
Relapse and remission
1st - Prednisolone
2nd - Cyclophosphamide
Describe the prognosis of minimal change disease
1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood
Describe the proteinuria seen in minimal change disease
Only intermediate sized proteins (Albumin and transferrin) leak through the glomerulus
Give 3 causes of minimal change disease
Drugs; NSAIDs/Rigampicin
Hodgkin’s lymphoma, thymoma
Infectious mononucleosis
Describe focal segmental glomerulosclerosis
Describes a histological lesion characterised by segmental areas of glomerular sclerosis.
Give 4 secondary causes of focal segmental glomerulosclerosis
HIV, Heroin, Lithium, Lymphoma
Give 4 symptoms of focal segmental glomerulosclerosis
Triad of; Proteinuria, Hypoalbuminaemia and Oedema
Foamy Urine
Hypertension (Due to salt retention)
Xamthelasma/Xanthomata/Muehrcke’s lines (on nails)
How is focal segmental glomerulosclerosis treated? (3)
1st - Prednisolone
2nd - Mycophenolate motefil + High dose dexamethasone
Adjunct- ACEi/ARB - to control blood pressure
Describe membranous nephropathy
Most common nephrotic syndrome in adults.
Describes an immune mediated disease of the glomerular basement membrane.
Give 4 causes of membranous nephropathy
Idiopathic - Due to anti-phospholipase A2 antibodies
Infection - Hep B, Malaria, Syphilis
Malignancy - Prostate, lung, lymphoma, leukaemia
Autoimmune disease - SLE, thyroiditis, rheumatoid
What antibody may be present in idiopathic membranous nephropathy?
Anti-phospholipase A2 antibody (PLA2)
What will a renal biopsy show in a patient with membranous nephropathy?
Thickened basement membrane with subepithelial electron dense deposits.
Creates a spike and dome appearance
How is membranous nephropathy managed? (3)
ACEi/ARBs (reduces proteinuria)
Ponticelli regimen - Cyclophosphamide + Corticosteroid
Consider - Anticoagulation in high risk patients
Name 5 types of nephritic syndrome
IgA nephropathy (most common)
Goodpastures (Anti-GBM)
Post-streptococcal
SLE
Haemolytic uraemic syndrome
How is IgA nephropathy characterised on renal biopsy?
Characterised by mesangial deposition of IgA immune complexes
Give 3 causes of IgA nephropathy
Alcoholic cirrhosis
Coeliac disease/dermatitis herptiformis
Henoch Schonlein purpura
How does IgA nephropathy typically present?
Young male, presenting with recurrent episodes of macroscopic haematuria, typically following a respiratory tract infection.
How does IgA Nephropathy differ from Post-Streptococcal glomerulonephritis? (3)
IgA - Develops 1/2 days after URTI
PSG - Develops 1-2 weeks after URTI
IgA - No Proteinuria
PSG - Proteinuria
IgA - Macroscopic haematoria
PSG - Low compliment
How is IgA nephropathy managed?
No treatment if - Isolated haematorua, + no/minimal proteinuria (<500-1000mg/day) and normal eGFR
ACEi if - Persistent proteinuria (>500 - 1000mg/day) and reduced/normal eGFR
Corticosteroids if - Active disease (falling GFR or failure to respond to ACEi)
Give 1 marker for a good prognosis in IgA nephropathy
Frank haematuria
Give 4 markers for a poor prognosis in IgA nephropathy
Male gender
Proteinuria (>2g/day)
Hypertension
Hyperlipidaemia
What triad is seen in haemolytic uraemic syndrome?
Microangiopathic haemolytic anaemia
Thrombocytopenia
AKI
What majority of haemolytic uraemic syndrome cases in children are caused by what pathogen?
E.Coli (Shiga toxin producing)
Describe goodpastures syndrome (Anti-glomerular basement membrane disease)
describes a small vessel vasculitis associated with pulmonary haemorrhage and progressive glomerulonephritis.
Anti GBM antibodies are generated against what type of collagen? Where is this found?
Type IV collagen
Found in basement membranes of alveoli and glomeruli
Give 3 features of goodpastures syndrome
Pulmonary haemorrhage > Haemoptysis
Rapidly progressive glomerulonephritis (Reduced urine output - AKI)
Oedema
Describe the epidemiology of good pastures syndrome (2)
More common in males
Bimodal age distribution (peaks at 20-30 and then at 60-70)
How is goodpastures diagnosed? What test confirms diagnosis?
Renal biopsy - Shows linear IgG deposits along basement membrane
Anti- GBM antibody titre - Confirms diagnosis
How is goodpastures managed? (3)
Plasma exchange (plasmapheresis)
Oral Prednisolone
Cyclophosphamide
What test is used to distinguish between AKI and CKD?
Renal Ultrasound
CKD patients have bilateral small kidneys
CKD patients also have hypocalcaemia (due to lack of vitamin D)
What may be seen on histology in membranous glomerulonephritis? (3)
Basement membrane thickening on light microscopy
Subepithelial spikes on silver stain
Positive immunohistochemistry for PLA2
Describe Primary Biliary Cholangitis. What is the classic presentation?
Describes an autoimmune condition where the immune system attacks the small bile ducts (intrahepatic) in the liver, resulting in obstructive jaundice and liver disease
Classic presentation = A middle aged woman presenting with itching
Is primary biliary cholangitis intrahepatic or extrahepatic in nature?
Intrahepatic - Affects the small bile ducts within the liver
Describe the pathophysiology of primary biliary cholangitis
Inflammation + damage to epithelial cells of bile ducts > Obstruction of bile flow through these ducts (cholestasis) > Liver fibrosis, cirrhosis and failure.
Name 3 biochemical markers which may be raised in primary biliary cholangitis.
Bile acids
Bilirubin
Cholesterol
(All are usually excreted through the bile ducts into the intestine)
Raised cholesterol increases the risk of what 2 diseases? And what 1 cosmetic symptom may it cause?
Increases risk of = Atherosclerosis and Cardiovascular Disease
Cosmetic symptom = Xanthelasma (cholesterol deposits in skin/tendons)
Name 2 conditions associated with primary biliary cholangitis
Sjogren’s syndrome (seen in 80% of patients)
Rheumatoid arthritis
Give 5 clinical features of primary biliary cholangitis
Pruritus (itching)
Jaundice
Pale, greasy stools
Dark urine
Xanthelasma/Xanthomata
What 2 test results are positive in Primary Biliary Cholangitis? (2)
Autoantibodies = AMA (Anti-Mitochondrial Antibodies) - Most specific
Liver function tests = Raised ALP
What is the most specific autoantibody marker for primary biliary cholangitis?
AMA (Anti-Mitochondrial Antibody)
What other autoantibodies may be positive in primary biliary cholangitis?
Anti-nuclear antibody (35% of patients)
IgM (immunoglobulin M) (non specific)
What imaging tools can be used to exclude extrahepatic biliary obstruction when investigating primary biliary cholangitis? (2)
Right Upper Quadrant Ultrasound
MRCP (magnetic resonance cholangiopancreatography)
What is the 1st line treatment to slow disease progression and improve symptoms of primary biliary cholangitis?
Ursodeoxycholic acid
What is the treatment for pruritus in primary biliary cholangitis?
Cholestyramine
Give 3 complications of primary biliary cholangitis
Cirrhosis > Portal Hypertension > Ascites + Variceal haemorrhage
Osteomalacia and osteoporosis
Hyperlipidaemia (raised cholesterol)
Define primary sclerosing cholangitis
Describes inflammation and damage to intrahepatic and extrahepatic bile ducts.
Results in sclerosis causing strictures that obstruct the flow of bile out of the liver into the intestines.
Which form of IBD is strongly associated with primary sclerosing cholangitis?
Ulcerative colitis
Give 4 clinical features of primary sclerosing cholangitis
Cholestasis = Jaundice, Pruritis, Raised bilirubin, Raised ALP
Right upper quadrant pain
Fatigue
Hepatomegaly/Splenomegaly
What is the standard diagnostic investigation for primary sclerosing cholangitis? What will it show?
ECRP or MRCP
Shows multiple biliary strictures (beaded appearance)
Which LFTs will be raised in primary sclerosing cholangitis?
Raised ALP
Which autoantibodies may be positive in primary sclerosing cholangitis?
p-ANCA
ANA
Anti-Smooth Muscle Antibodies
Name 2 complications/associations of primary sclerosing cholangitis
Ulcerative colitis
Cholangiocarcinoma
What are gallstones predominantly made up of?
Cholesterol
Name 3 possible complications of gallstones
Acute cholecystitis
Acute cholangitis
Pancreatitis (blocking the pancreatic duct)
Which 2 ducts join to become the ampulla of Vater?
Common bile duct + Pancreatic Duct
What is the name of the ring of muscle surrounding the ampulla of Vater that controls the flow of bile and pancreatic secretions into the duodenum?
Sphincter of Oddi
Define cholecystitis
Inflammation of the gallbladder
Define cholangitis
Inflammation of the bile ducts
Define Biliary colic
Intermittent right upper quadrant pain caused by gallstones irritating the bile ducts
Give 4 risk factors for gallstones (4Fs)
Fat
Fair
Female
Forty
Give 4 symptoms of biliary colic
Right upper quadrant pain
Triggered by meals (high fat meals)
Pain lasts 30mins to 8 hours
Nausea and vomiting
Why does ingestion of fat trigger biliary colic?
Fat causes cholecystokinin (CCK) secretion from duodenum > CCK triggers contraction of gallbladder > Biliary colic
What is the 1st line investigation for gallstones?
Ultrasound
What ultrasound findings may be present in a patient with gallstones? (3)
Gallstones in gallbladder/ducts
Bile duct dilatation (<6mm in diameter)
Acute cholecystitis (thickened gall bladder wall/fluid around gallbladder)
If ultrasound is inconclusive, what imaging tool may be used?
MRCP
What tool is used to clear stones from the bile ducts?
ERCP (Endoscopic retrograde cholangio-pancreatography)
Give 4 complications of ERCP
Excessive bleeding
Duodenal perforation
Cholangitis
Pancreatitis
What is the treatment for gallstones? (2)
Asymptomatic - Conservative management
Symptomatic - Laparoscopic cholecystectomy (removal of gallbladder)
What is the imaging and treatment for acute cholecystitis?
Ultrasound and cholecystectomy
Define ascending cholangitis
Bacterial infection (e.coli) of the biliary tree. Commonly caused by gallstones
What bacteria most commonly causes ascending cholangitis?
E.coli
What is Charcot’s triad? (Ascending cholangitis)
Right Upper Quadrant Pain
Fever
Jaundice
What is the 1st line investigation for ascending cholangitis?
Ultrasound (look for bile duct dilatation and stones)
How is ascending cholangitis managed? (3)
Fluid resuscitation
Broad spectrum IV antibiotics
ERCP after 24-48 hours
Name 2 causes of acute pancreatitis
Alcohol excess
Gallstones
Describe the pathophysiology of acute pancreatitis
Autodigestion of pancreatic tissue by pancreatic enzymes, leading to necrosis
Give 4 features of acute pancreatitis
Severe epigastric pain (may radiate through back)
Vomiting
Epigastric tenderness, ileus and log-grade fever
Periumbilical discolouration (cullen’s sign) and flank discolouration (grey-Turner’s sign)
Which 2 clinical signs may be present in acute pancreatitis
Cullen’s sign (Periumbilical discolouration)
Grey-Turner’s sign (Flank discolouration)
Give 3 investigation for acute pancreatitis
Raised Serum Lipase (most specific and sensitive)
Raised Serum Amylase
Ultrasound
When can a diagnosis of acute pancreatitis be made without an ultrasound scan?
If characteristic pain + Amylase/Lipase >3 times normal level
What is the most sensitive and specific marker for acute pancreatitis?
Raised Serum Lipase
What 3 scoring systems can be used to score acute pancreatitis?
Ranson score
Glasgow score
APACHE II
Give 4 causes of acute pancreatitis
Gallstones and alcohol (Most common)
ERCP
Scorpion Venom
Drugs (azathiopurine, mesalazine, bendroflumethiazide)
Give 3 complications of acute pancreatitis
Pseudocyts
Pancreatic necrosis
Pancreatic abscesses
How is acute pancreatitis initially managed? (3)
Fluid resuscitation with crystalloids
Analgesia (IV opioids)
Enteral nutrition (if severe acute pancreatitis)
How is acute pancreatitis managed surgically? (2)
Cholecystectomy (if due to gallstones)
ERCP (if due to obstructed biliary system)
What is the most common cause of chronic pancreatitis?
Alcohol excess
Other than alcohol, give 3 causes of chronic pancreatitis
Cystic fibrosis
Haemochromatosis
Ductal obstruction (tumour, stones)
Give 3 clinical features of chronic pancreatitis
Pain - Worse 15-30 minutes following a meal
Steatorrhea
Diabetes mellitus
What investigations are used to diagnose chronic pancreatitis?
CT (shows pancreatic calcification) (most specific and sensitive)
Abdominal x-ray
Faecal elastase
How is chronic pancreatitis managed? (4)
Abstinence from alcohol and smoking
Creon - Replacement of pancreatic enzymes
ERCP with stenting (if obstruction to biliary system/pancreatic duct)
Surgery (if pseudocysts, abscesses)
