Neuro, GI, Uro Flashcards
What is hydronephrosis?
Swelling of the renal pelvis and calyces in the kidney. This occurs due to obstruction of the urinary tract, leading to back-pressure into the kidneys.
What is vesicoureteral reflux?
Vesicoureteral reflux (VUR) refers to urine refluxing from the bladder back into the ureters.
Give a cause of pre-renal AKI
Hypoperfusion of the kidneys (e.g., due to dehydration, sepsis or acute blood loss)
Give a cause of renal AKI
Damage within the kidney itself (e.g., due to glomerulonephritis or nephrotoxic medications).
How does upper urinary tract obstruction present?
Loin to groin or flank pain on the affected side (due to stretching and irritation of ureter and kidney)
Reduced or no urine output
Non-specific systemic symptoms, such as vomiting
Impaired renal function on blood tests (i.e. raised creatinine)
How does lower urinary tract obstruction present?
Difficulty or inability to pass urine (e.g., poor flow, difficulty initiating urination or terminal dribbling)
Urinary retention, with an increasingly full bladder
Impaired renal function on blood tests (i.e. raised creatinine)
Give three common causes of upper urinary tract obstruction
Kidney stones
Tumours pressing on the ureters
Ureter strictures (due to scar tissue narrowing the tube)
Retroperitoneal fibrosis (the development of scar tissue in the retroperitoneal space)
Bladder cancer (blocking the ureteral openings to the bladder)
Ureterocele (ballooning of the most distal portion of the ureter – this is usually congenital)
Give three common causes of lower urinary tract obstruction
Benign prostatic hyperplasia (benign enlarged prostate)
Prostate cancer
Bladder cancer (blocking the neck of the bladder)
Urethral strictures (due to scar tissue)
Neurogenic bladder
Give three causes of neurogenic bladder
MS
Diabetes
Stroke
PD
Brain or spinal cord injury
Spina Bifida
What is a nephrostomy?
Used to bypass an obstruction in the upper urinary tract (e.g., a ureteral stone). A nephrostomy involves surgically inserting a thin tube through the skin at the back, through the kidney and into the ureter. This tube allows urine to drain out of the body, into a bag.
What is a urethral or suprapubic catheter used for?
Used to bypass an obstruction in the lower urinary tract (e.g., a urethral stricture or prostatic hyperplasia). A urethral catheter is a tube, inserted through the urethra, into the bladder. A suprapubic catheter is a tube, inserted through the skin just above the pubic bone, directly into the bladder.
What is a pyeloplasty used for?
An operation to treat idiopathic hydronephrosis, which corrects the narrowing and restructures the renal pelvis
How do we classify prostatitis?
Acute bacterial prostatitis – acute infection in the prostate, presenting with a more rapid onset of symptoms
Chronic prostatitis – symptoms lasting for at least 3 months
How do we sub-divide chronic prostatitis?
Chronic prostatitis or chronic pelvic pain syndrome (no infection)
Chronic bacterial prostatitis (infection)
How does chronic prostatitis present?
Pelvic pain, which may affect the perineum, testicles, scrotum, penis, rectum, groin, lower back or suprapubic area
Lower urinary tract symptoms, such as dysuria, hesitancy, frequency and retention
Sexual dysfunction, such as erectile dysfunction, pain on ejaculation and haematospermia (blood in the semen)
Pain with bowel movements
Tender and enlarged prostate on examination (although examination may be normal)
How do we manage acute bacterial prostatitis?
Hospital admission for systemically unwell or septic patients (for bloods, blood cultures and IV antibiotics)
Oral antibiotics, typically for 2-4 weeks (e.g., ciprofloxacin, ofloxacin or trimethoprim)
Analgesia (paracetamol or NSAIDs)
How do we manage chronic prostatitis?
Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms
Analgesia (paracetamol or NSAIDs)
Psychological treatment, where indicated (e.g., cognitive behavioural therapy and / or antidepressants)
Antibiotics if less than 6 months of symptoms or a history of infection (e.g., trimethoprim or doxycycline for 4-6 weeks)
What is a hydrocele?
A hydrocele is a collection of fluid within the tunica vaginalis that surrounds the testes. They are usually painless and present with a soft scrotal swelling.
What would you see on examination with a hydrocele?
The testicle is palpable within the hydrocele
Soft, fluctuant and may be large
Irreducible and has no bowel sounds (distinguishing it from a hernia)
Transilluminated by shining torch through the skin, into the fluid (the testicle floats within the fluid)
What can cause hydrocele?
Hydroceles can be idiopathic, with no apparent cause, or secondary to:
Testicular cancer
Testicular torsion
Epididymo-orchitis
Trauma
What is varicocele?
A varicocele occurs where the veins in the pampiniform plexus become swollen. They are common, affecting around 15% of men.
What is a common complication of varicocele?
They can cause impaired fertility, probably due to disrupting the temperature in the affected testicle. They may result in testicular atrophy, reducing the size and function of the testicle.
What is the aetiology of varicoceles?
Varicoceles are the result of increased resistance in the testicular vein. Incompetent valves in the testicular vein allow blood to flow back from the testicular vein into the pampiniform plexus.
The right testicular vein drains directly into the inferior vena cava. The left testicular vein drains into the left renal vein. Most varicoceles (90%) occur on the left due to increased resistance in the left testicular vein. A left-sided varicocele can indicate an obstruction of the left testicular vein caused by a renal cell carcinoma.
How do varicoceles present symptomatically?
Throbbing/dull pain or discomfort, worse on standing
A dragging sensation
Sub-fertility or infertility
How do varicoceles present on examination?
A scrotal mass that feels like a “bag of worms”
More prominent on standing
Disappears when lying down
Asymmetry in testicular size if the varicocele has affected the growth of the testicle
What might varicoceles that do not disappear when lying down indicate?
Retroperitoneal tumours obstructing the drainage of the renal vein = urgent referral to urology
How do epididymal cysts present OE?
Soft, round lump
Typically at the top of the testicle
Associated with the epididymis
Separate from the testicle
May be able to transilluminate large cysts (appearing separate from the testicle)
From which cells does testicular cancer arise from?
Testicular cancer typically arises from the germ cells in the testes. Germ cells are cells that produce gametes (sperm in males).
When is the highest incidence of testicular cancer?
15-35 years
What are the two types of testicular cancer?
Seminomas and non-seminomas
Give three RFs for testicular cancer
Undescended testes
Male infertility
Family history
Increased height
How does testicular cancer present symptomatically?
The typical presentation is a painless lump on the testicle. Occasionally it can present with testicular pain.
How does testicular cancer present on examination
The lump will be:
Non-tender (or even reduced sensation)
Arising from testicle
Hard
Irregular
Not fluctuant
No transillumination
Describe the Royal Marsden staging system.
Stage 1 – isolated to the testicle
Stage 2 – spread to the retroperitoneal lymph nodes
Stage 3 – spread to the lymph nodes above the diaphragm
Stage 4 – metastasised to other organs
What is a radical orchidectomy?
Surgery to remove the affected testicle (radical orchidectomy) – a prosthesis can be inserted
What is a lower UTI?
Lower urinary tract infections (UTIs) involve infection in the bladder, causing cystitis (inflammation of the bladder).
How does pyelonephritis differ from lower UTI?
Fever
Loin/back pain
Nausea/vomiting (triad)
Renal angle tenderness on examination
How would you use a urine dipstick to determine whether you would treat a lower UTI?
Nitrites are a better indication of infection than leukocytes. The NICE clinical knowledge summaries (2020) suggest that the presence of nitrites or leukocytes plus red blood cells indicate that the patient is likely to have a UTI.
If both are present, the patient requires treatment for a UTI. If only nitrites are present, it is worth treating as a UTI. If only leukocytes are present, the patient should not be treated as a UTI unless there is clinical evidence they have one.
When might you consider sending a midstream urine sample for microscopy in lower UTI?
Pregnant patients
Patients with recurrent UTIs
Atypical symptoms
When symptoms do not improve with antibiotics
Which bacteria break down nitrites into nitrates?
Nitrites – gram-negative bacteria (such as E. coli) break down nitrates, a normal waste product in urine, into nitrites. The presence of nitrites suggests bacteria in the urine.
When should nitrofurantoin be avoided in pregnancy?
Nitrofurantoin needs to be avoided in the third trimester as there is a risk of neonatal haemolysis (destruction of the neonatal red blood cells).
How do we manage pyelonephritis?
NICE guidelines (2018) recommend the following first-line antibiotics for 7-10 days when treating pyelonephritis in the community:
Cefalexin
Co-amoxiclav (if culture results are available)
Trimethoprim (if culture results are available)
Ciprofloxacin (keep tendon damage and lower seizure threshold in mind)
What are the sepsis six?
Blood lactate level
Blood cultures
Urine output
Oxygen to maintain oxygen saturations of 94-98% (or 88-92% in COPD)
Empirical broad-spectrum IV antibiotics (according to local guidelines)
IV fluids
When do we use DMSA scans?
Dimercaptosuccinic acid (DMSA) scans involve injecting radiolabeled DMSA, which builds up in healthy kidney tissue. When imaged using gamma cameras, it indicates scarring or damage in areas that do not take up the DMSA. They are used in recurrent pyelonephritis to assess for renal damage.
What is interstitial cystitis?
Interstitial cystitis is a chronic condition causing inflammation in the bladder, resulting in lower urinary tract symptoms and suprapubic pain. It is also called bladder pain syndrome and hypersensitive bladder syndrome.
There is no simple explanation for the symptoms, and the pathophysiology is likely a complex combination of various factors, including dysfunction of the blood vessels, nerves, immune system and epithelium.
How does interstitial cystitis present?
The typical presentation is more than 6 weeks of:
Suprapubic pain, worse with a full bladder and often relieved by emptying the bladder
Frequency of urination
Urgency of urination
Symptoms may be worse during menstruation
How do we investigate interstitial cystitis?
Urinalysis for urinary tract infections
Swabs for sexually transmitted infections
Cystoscopy for bladder cancer
Prostate examination for prostatitis, hypertrophy or cancer
Where do you find bladder cancer?
In the urothelium
Give four RFs of bladder cancer.
Smoking and increased age are the main risk factors for bladder cancer.
Aromatic amines are worth noting as a carcinogen that causes bladder cancer. Aromatic amines were used in dye and rubber industries but have been heavily regulated or banned for many years. They are also found in cigarette smoke and seem to be the reason smoking causes bladder cancer.
Schistosomiasis causes squamous cell carcinoma of the bladder in countries with a high prevalence of the infection.
What is the most common type of bladder cancer?
Transitional cell carcinoma (90%)
Squamous cell carcinoma (5% – higher in areas of schistosomiasis)
Rarer causes are adenocarcinoma (2%), sarcoma and small-cell carcinoma
How does bladder cancer present?
Painless haematuria is the symptom to remember for your exams.
When do we offer a 2wwr for a patient with haematuria?
Aged over 45 with unexplained visible haematuria, either without a UTI or persisting after treatment for a UTI
Aged over 60 with microscopic haematuria (not visible but positive on a urine dipstick) PLUS:
Dysuria or;
Raised white blood cells on a full blood count
The NICE guidelines also recommend considering a non-urgent referral in people over 60 with recurrent unexplained UTIs.
How do we diagnose bladder cancer?
Cystoscopy (a camera through the urethra into the bladder) can be used to visualise bladder cancers. The cystoscope can be rigid or flexible. Cystoscopy can be performed under local or general anaesthetic.
What is TURBT?
Transurethral resection of bladder tumour (TURBT) may be used for non-muscle-invasive bladder cancer. The involves removing the bladder tumour during a cystoscopy procedure.
How do we reduce the risk of recurrence after TURBT?
Intravesical chemotherapy (chemotherapy given into the bladder through a catheter) is often used after a TURBT procedure to reduce the risk of recurrence.
What is Intravesical Bacillus Calmette-Guérin (BCG) used for?
may be used as a form of immunotherapy. Giving the BCG vaccine (the same one as for tuberculosis) into the bladder is thought to stimulate the immune system, which in turn attacks the bladder tumours.
What is a radical cystectomy?
Radical cystectomy involves the removal of the entire bladder.
What are the CAGE questions?
C – CUT DOWN? Ever thought you should?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Ever feel guilty about drinking?
E – EYE OPENER? Ever drink in the morning to help your hangover/nerves?
Name a questionnaire used to screen for people with harmful alcohol use.
Alcohol Use Disorders Identification Test (AUDIT)
What is a fibroscan used for?
Can be used to check the elasticity of the liver by sending high frequency sound waves into the liver. It helps assess the degree of cirrhosis.
Describe the early stages of alcohol withdrawal
6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”
What is delirium tremens?
Delirium tremens is a medical emergency associated with alcohol withdrawal with a mortality of 35% if left untreated.
Describe the pathophysiology behind delirium tremens
Alcohol stimulates GABA receptors in the brain. GABA receptors have a “relaxing” effect on the rest of the brain. Alcohol also inhibits glutamate receptors (also known as NMDA receptors) having a further inhibitory effect on the electrical activity of the brain.
Chronic alcohol use results in the GABA system becoming down-regulated and the glutamate system becoming up-regulated to balance the effects of alcohol. When alcohol is removed from the system, GABA under-functions and glutamate over-functions causing an extreme excitability of the brain with excess adrenergic activity.
How does delirium tremens present?
Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia (difficulties with coordinated movements)
Arrhythmias
How do we manage alcohol withdrawal?
Chlordiazepoxide for 5-7 days
Intravenous high-dose B vitamins (pabrinex). This should be followed by regular lower dose oral thiamine.
What is Wernicke-Korsakoff Syndrome?
Alcohol excess leads to thiamine (vitamin B1) deficiency. Thiamine is poorly absorbed in the presence of alcohol and alcoholics tend to have poor diets and rely on the alcohol for their calories. Wernicke’s encephalopathy comes before Korsakoffs syndrome. These result from thiamine deficiency.
How does Wernicke’s encephalopathy present?
Confusion
Oculomotor disturbances (disturbances of eye movements)
Ataxia (difficulties with coordinated movements)
How does Korsakoff’s syndrome present?
Memory impairment (retrograde and anterograde)
Behavioural changes
How severe is Wernicke-Korsakoff syndrome?
Wernicke’s encephalopathy is a medical emergency and has a high mortality rate if untreated. Korsakoffs syndrome is often irreversible and results in patients requiring full time institutional care. Prevention and treatment involve thiamine supplementation and abstaining from alcohol.
What are the four most common causes of liver cirrhosis?
Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C
Lots of inflammation leads to fibrotic changes
What is the Child-Pugh score used for?
The score indicates the severity of the cirrhosis and the prognosis.
What is the MELD score used for?
The MELD score is recommended by NICE to be used every 6 months in patients with compensated cirrhosis. It is a formula that takes into account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis. It gives a percentage estimated 3 month mortality and helps guide referral for liver transplant.
How do we manage malnutrition?
Regular meals (every 2-3 hours)
Low sodium (to minimise fluid retention)
High protein and high calorie (particularly if underweight)
Avoid alcohol
How does portal hypertension occur? What are varices?
Liver cirrhosis increases the resistance of blood flow in the liver. As a result, there is increased back-pressure into the portal system. This back-pressure causes the vessels at the sites where the portal system anastomoses with the systemic venous system to become swollen and tortuous. These swollen, tortuous vessels are called varices.
How do we treat stable varices?
Propranolol reduces portal hypertension by acting as a non-selective beta blocker
Elastic band ligation of varices
Injection of sclerosant (less effective than band ligation)
Transjugular Intra-hepatic Portosystemic Shunt (TIPS) last line
How do we treat bleeding oesophageal varices?
Resuscitation
Vasopressin analogues (i.e. terlipressin) cause vasoconstriction and slow bleeding in varices
Correct any coagulopathy with vitamin K and fresh frozen plasma (which is full of clotting factors)
Giving prophylactic broad spectrum antibiotics has been shown to reduce mortality
Consider intubation and intensive care as they can bleed very quickly and become life threateningly unwell
Urgent endoscopy
Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel
Elastic band ligation of varices
Describe the pathophysiology behind ascites
Ascites is basically fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel and in to the peritoneal cavity. The drop in circulating volume caused by fluid loss into the peritoneal space causes a reduction in blood pressure entering the kidneys. The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion (via the renin-angiotensin-aldosterone system) and reabsorption of fluid and sodium in the kidneys.
How do we manage ascites?
Low sodium diet
Anti-aldosterone diuretics (spironolactone)
Paracentesis (ascitic tap or ascitic drain)
Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid
What is spontaneous bacterial peritonitis?
This occurs in around 10% of patients with ascites secondary to cirrhosis and can have a mortality of 10-20%. It involves an infection developing in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary to an ascitic drain or bowel perforation).
Give a toxin that can lead to hepatic encephalopathy
Firstly, the functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products. Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly.
How do we treat hepatic encephalopathy caused by ammonia
By giving laxatives, e.g. lactulose, we help clear the ammonia from the gut before it is absorbed and by giving antibiotics we reduce the number of bacteria in the gut producing ammonia.
What is the first line recommended investigation for assessing liver fibrosis?
Enhanced Liver Fibrosis (ELF) blood test. This is the first line recommended investigation for assessing fibrosis but it is not currently available in many areas. It measures three markers (HA, PIIINP and TIMP-1) and uses an algorithm to provide a result that indicates the fibrosis of the liver:
< 7.7 indicates none to mild fibrosis
≥ 7.7 to 9.8 indicates moderate fibrosis
≥ 9.8 indicates severe fibrosis
When is the NAFLD fibrosis score used?
NAFLD fibrosis score is the second line recommended assessment for liver fibrosis where the ELF test is not available. It is based on an algorithm of age, BMI, liver enzymes, platelets, albumin and diabetes and is helpful in ruling out fibrosis but not assessing the severity when present.
How does hepatitis present symptomatically?
Abdominal pain
Fatigue
Pruritis (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice
Fever (viral hepatitis)
What is a hepatitic picture on LFT?
Typical biochemical findings are that liver function tests become deranged with high transaminases (AST / ALT) with proportionally less of a rise in ALP. Transaminases are liver enzymes that are released into the blood as a result of inflammation of the liver cells. Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.
What is haemochromatosis?
an iron storage disorder that results in excessive total body iron and deposition of iron in tissues. The human haemochromatosis protein (HFE) gene is located on chromosome 6. The majority of cases of haemochromatosis relate to mutations in this gene, however there are other genes that can cause the condition. The haemochromatosis genetic mutation is autosomal recessive.
How does haemochromatosis present?
Chronic tiredness
Joint pain
Pigmentation (bronze / slate-grey discolouration)
Hair loss
Erectile dysfunction
Amenorrhoea
Cognitive symptoms (memory and mood disturbance)
How do we diagnose haemochromatosis?
The main diagnostic method is to perform a serum ferritin level. Ferritin is an acute phase reactant, meaning that it goes up with inflammatory conditions such as infection. Performing a transferrin saturation is helpful in distinguishing between a high ferritin caused by iron overload (in which case transferrin saturation is high) from a high ferritin due to other causes such as inflammation or non alcoholic fatty liver disease. If serum ferritin and transferrin saturation is high and there is no other reason then genetic testing can be performed to confirm haemochromatosis.
Give three complications of haemochromatosis
Type 1 Diabetes (iron affects the functioning of the pancreas)
Liver Cirrhosis
Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)
Cardiomyopathy (iron deposits in the heart)
How do we manage haemochromatosis?
Venesection (a weekly protocol of removing blood to decrease total iron)
Monitoring serum ferritin
Avoid alcohol
Genetic counselling
Monitoring and treatment of complications
How do we investigate Wilson’s disease?
The initial investigation of choice is serum caeruloplasmin. A low serum caeruloplasmin is suggestive of Wilson disease. This is the protein that carries copper in the blood. It can be falsely normal or elevated in cancer or inflammatory conditions. It is also not specific to Wilson disease.
Liver biopsy for liver copper content is the definitive gold standard test for diagnosis
How do we manage Wilson’s disease?
Treatment is with copper chelation using:
Penicillamine
Trientene
What is alpha-1-antitrypsin deficiency?
Alpha-1-antitrypsin deficiency is a condition caused by an abnormality in the gene for a protease inhibitor called alpha-1-antitrypsin.
What is the pathophysiology of alpha-1-antitrypsin deficiency?
Elastase is an enzyme secreted by neutrophils. This enzyme digests connective tissues. Alpha-1-antitrypsin (A1AT) is mainly produced in the liver, travels around the body and offers protection by inhibiting the neutrophil elastase enzyme. A1AT is coded for on chromosome 14. In A1AT deficiency, there is an autosomal recessive defect in the gene for A1AT.
It leads to:
Liver cirrhosis after 50 years old
Bronchiectasis and emphysema in the lungs after 30 years old
How do we diagnose alpha-1-antitrpysin deficiency?
Low serum-alpha 1-antitrypsin (screening test of choice)
Liver biopsy shows cirrhosis and acid-Schiff-positive staining globules (this stain highlights the mutant alpha-1-antitrypsin proteins) in hepatocytes
Genetic testing for the A1AT gene
High resolution CT thorax diagnoses bronchiectasis and emphysema
How do we manage alpha-1-antitrypsin deficiency?
Stop smoking (smoking dramatically accelerates emphysema)
Symptomatic management
NICE recommend against the use of replacement alpha-1-antitrypsin, however the research and debate is ongoing regarding the possible benefits
Organ transplant for end-stage liver or lung disease
Monitoring for complications (e.g. hepatocellular carcinoma)
What is primary biliary cirrhosis?
Primary biliary cirrhosis is a condition where the immune system attacks the small bile ducts within the liver. This causes obstruction of the outflow of bile, which is called cholestasis. The back-pressure of the bile obstruction and the overall disease process ultimately leads to fibrosis, cirrhosis and liver failure.
How do we diagnose primary biliary cirrhosis?
Liver Function Tests
Alkaline phososphatase is first liver enzyme to be raised (as with most obstructive pathology)
Other liver enzymes and bilirubin are raised in later disease
Liver biopsy can be used to diagnose and stage the disease
How do we treat primary biliary cirrhosis?
Ursodeoxycholic acid reduces the intestinal absorption of cholesterol
Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
Liver transplant in end stage liver disease
Immunosuppression (e.g. with steroids) is considered in some patients
What is primary sclerosing cholangitis?
A condition where the intrahepatic or extrahepatic ducts become strictured and fibrotic. This causes an obstruction to the flow of bile out of the liver and into the intestines. Sclerosis refers to the stiffening and hardening of the bile ducts, and cholangitis is inflammation of the bile ducts. Chronic bile obstruction eventually leads to liver inflammation (hepatitis), fibrosis and cirrhosis.
Which condition is PSC associated with?
UC
How does PSC present on LFTs?
Liver function tests show a “cholestatic” picture. This means alkaline phosphatase is the most deranged LFT and may be the only abnormality at first.
There may be a rise in bilirubin as the strictures become more severe and prevents bilirubin from being excreted through the bile duct. Other LFTs (i.e. transaminases: ALT and AST) can also be deranged, particularly as the disease progresses to hepatitis.
How do we diagnose PSC?
The gold standard investigation for diagnosis is an MRCP, which is short for magnetic resonance cholangiopancreatography. This involves an MRI scan of the liver, bile ducts and pancreas. In primary sclerosis cholangitis it may show bile duct lesions or strictures.
How do we manage PSC?
Liver transplant can be curative but is associated with its own problems (around 80% survival at 5 years).
ERCP can be used to dilate and stent any strictures
Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
Monitoring for complications (such as cholangiocarcinoma, cirrhosis and oesophageal varices)
What are the two main types of primary liver cancer?
There are two main types: hepatocellular carcinoma (80%) and cholangiocarcinoma (20%).
Give three RFs for HCC.
Viral hepatitis (B and C)
Alcohol
Non alcoholic fatty liver disease
Other chronic liver disease
What is alpha-fetoprotein a tumour marker for?
Hepatocellular carcinoma.
What is CA19-9 a tumour marker for?
Cholangiocarcinoma & pancreatic cancer
What are haemangiomas?
Haemangiomas are common benign tumours of the liver. They are often found incidentally. They cause no symptoms and have no potential to become cancerous. No treatment or monitoring is required.
What is focal nodular hyperplasia?
Focal nodular hyperplasia is a benign liver tumour made of fibrotic tissue. This is often found incidentally. It is usually asymptomatic and has no malignant potential. It is often related to oestrogen and is therefore more common in women and those on the oral contraceptive pill. No treatment of monitoring is required.
What is the pathophysiology behind H. pylori infection?
H. pylori is a gram negative aerobic bacteria. It lives in the stomach. It causes damage the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer. It avoids the acidic environment by forcing its way into the gastric mucosa. The breaks it creates in the mucosa exposes the epithelial cells underneath to acid.
It also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells. Other chemicals produced by the bacteria also damage the epithelial lining.
How do we test for H. pylori?
We offer a test for H. pylori to anyone with dyspepsia. They need 2 weeks without using a PPI before testing for H. pylori for an accurate result.
Tests
Urea breath test using radiolabelled carbon 13
Stool antigen test
Rapid urease test can be performed during endoscopy.
How does eating impact the pain from duodenal ulcers?
Improves the pain
Give three complications of gastric ulcers
Bleeding from the ulcer is a common and potentially life threatening complication.
Perforation resulting in an “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic).
Scarring and strictures of the muscle and mucosa. This can lead to a narrowing of the pylorus (the exit of the stomach) causing difficulty in emptying the stomach contents. This is known as pyloric stenosis. This presents with upper abdominal pain, distention, nausea and vomiting, particularly after eating.
Give three causes of upper GI bleed
Oesophageal varices
Mallory-Weiss tear, which is a tear of the oesophageal mucous membrane
Ulcers of the stomach or duodenum
Cancers of the stomach or duodenum
How does upper GI bleed present?
Haematemesis (vomiting blood)
“Coffee ground” vomit. This is caused by vomiting digested blood that looks like coffee grounds.
Melaena, which is tar like, black, greasy and offensive stools caused by digested blood
