Gastroenterology Flashcards
1
Q
what is the stepwise progression to becoming alcoholic liver disease?
A
alcohol related fatty liver - reversible
alcoholic hepatitis - reversible with permanent abstinence
cirrhosis - scar tissue, irreversible
2
Q
what is the recommended alcohol consumption?
A
no more than 14 units of alcohol per week for both men and women over 3 ore more days and no more than 5 a day
3
Q
how can harmful alcohol abuse be screened for?
A
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?
4
Q
how are people screened for harmful alcohol use?
A
Alcohol Use Disorders Identification Test (AUDIT) questionnaire
5
Q
what are the complications of alcohol?
A
Alcoholic Liver Disease
Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
Alcohol Dependence and Withdrawal
Wernicke-Korsakoff Syndrome (WKS)
Pancreatitis
Alcoholic Cardiomyopathy
6
Q
what are the signs of liver disease?
A
Jaundice
Hepatomegaly
Spider Naevi
Palmar Erythema
Gynaecomastia
Bruising – due to abnormal clotting
Ascites
Caput Medusae – engorged superficial epigastric veins
Asterixis – “flapping tremor” in decompensated liver disease
7
Q
which investigations are required for suspected liver disease?
A
FBC – raised MCV
LFTs – elevated ALT and AST (transaminases) and particularly raised gamma-GT. ALP will be elevated later in the disease. Low albumin due to reduced “synthetic function” of the liver. Elevated bilirubin in cirrhosis.
Clotting – elevated prothrombin time due to reduced “synthetic function” of the liver
U+Es may be deranged in hepatorenal syndrome.
8
Q
which scans could be used to establish liver disease and the results?
A
USS - fatty changes, fibrosis
endoscopy - assess and treat varices from portal hypertension
CT/MRI- fatty change, carcinoma, megaly, abnormal blood vessel changes and ascites
biopsy
9
Q
what is the general management of alcoholic liver disease?
A
Stop drinking alcohol
Consider a detoxication regime
Nutritional support with vitamins (particularly thiamine) and a high protein diet
Steroids improve short term outcomes (over 1 month) in severe alcoholic hepatitis but infection and GI bleeding need to be treated first and do not improve outcomes over the long term
Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)
Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral
10
Q
what are the complications of alcohol withdrawal and when do they occur?
A
6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”
11
Q
define delirium tremens
A
medical emergency
alcohol stimulates GABAr - relaxing
and inhibits glutamate r - also inhibitory
but chronic use - GABA downregulated and glutamate upregulated…excitability and adrenergic activity
12
Q
what does delirium tremens present with?
A
Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia (difficulties with coordinated movements)
Arrhythmias
13
Q
how can alcohol withdrawal be assessed?
A
CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised)
14
Q
what drugs is used to control alcohol withdrawal?
A
chlordiazepoxide - benzodiazepine
Iv high dose B vitamins and oral thiamine
15
Q
define wernicke-korsakoff syndrome
A
Alcohol excess leads to thiamine (vitamin B1) deficiency. . Wernicke’s encephalopathy comes before Korsakoffs syndrome
16
Q
what are the clinical fx of Wernicke’s encephalopathy?
A
Confusion
Oculomotor disturbances (disturbances of eye movements)
Ataxia (difficulties with coordinated movements)
17
Q
what are the clinical fx of korsakoffs syndrome?
A
Memory impairment (retrograde and anterograde)
Behavioural changes
18
Q
how is WKS treated/
A
stop alcohol
thiamine supplements
19
Q
wwhat are the most common causes of cirrhosis?
A
Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C
20
Q
what are the rarer causes of cirrhosis?
A
Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons Disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs (e.g. amiodarone, methotrexate, sodium valproate)
21
Q
what are the signs of cirrhosis?
A
Jaundice – caused by raised bilirubin
Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
Splenomegaly – due to portal hypertension
Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
Palmar Erythema – caused by hyperdynamic cirulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising – due to abnormal clotting
Ascites
Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease
22
Q
which investigations are required for cirrhosis?
A
Liver biochemistry is often normal, however in decompensated cirrhosis all of the markers (ALT, AST, ALP and bilirubin) become deranged.
The albumin level drops and the prothrombin time increases as the synthetic function becomes worse.
Hyponatraemia indicates fluid retention in severe liver disease.
Urea and creatinine become deranged in hepatorenal syndrome.
Further bloods can help establish the cause of the cirrhosis if unknown (such as viral markers and autoantibodies).
Alpha-fetoprotein is a tumour marker for hepatocellular carcinoma and can be checked every 6 months as a screening test in patients with cirrhosis along with ultrasound.
enhanced liver fibrosis - >7.7, not always possible
23
Q
what may imaging show of cirrhosis?
A
USS- nodularity, corkscrew appearance of arteries, enlarged portal vein, ascites, splenomegaly
fibro scan - every 2 yrs if at risk, elasticity, degree of cirrhosis
endoscopy -varices
CT/MRI
biopsy
24
Q
how is heptatocellular carcinoma screened for?
A
USS, every 6 mths
25
how is the severity of cirrhosis scored?
child-pugh score
- billirubin
- albumin
- INR
- ascites
- encephalopathy
if compensated - MELD score
26
what does the general management of cirrhosis involve?
Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
Endoscopy every 3 years in patients without known varices
High protein, low sodium diet
MELD score every 6 months
Consideration of a liver transplant
Managing complications as below
27
what are the complications of cirrhosis?
Malnutrition
Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma
28
how does cirrhosis lead to malnutrition and how is this managed?
increased use of muscle tissue as fuel and reduces protein available in body for muscle growth
also disrupts livers ability to store glucose as glycogen when required...muscle wasting and weight loss
- regular meals
- low sodium
- high protein and calorie
- avoid alcohol
29
how does liver cirrhosis lead to portal hypertension?
increases resistance of blood flow...back flow in portal system..vessels at the sites where portal system to anastome with systemic venous system to become sweollen and tortuouse...varices
at gastro-oesophageal, ileocaecal, rectal, ant abdo walla via umbilical vein (Caput medusae)
once start bleeding wont stop, but asx
30
how are stable varices managed?
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) is a technique where an interventional radiologist inserts a wire under xray guidance into the jugular vein, down the vena cava and into the liver via the hepatic vein. They then make a connection through the liver tissue between the hepatic vein and the portal vein and put a stent in place. This allows blood to flow directly from the portal vein to the hepatic vein and relieves the pressure in the portal system and varices.
31
how are bleeding oesophageal varices managed?
resus - vasopressin analogues - vasoconstriction, correct coagulopathy with vit K and FFP, prophylactic abx, intubation and ICU
urgent endoscopy - inject sclerosant, elastic band ligation
sengstaken-blakemore tube into oesophagus if endoscopy fails
32
how do ascites form from cirrhosis?
increased pressure in portal system causes fluid to leak out of capillaries in the liver and bowel into peritoneal cavity...hypovolaemic so reduced blood flow to kindyes....so releases renin -> RAAS causing fluid and sodium reabsorption
it is a transudate - low protein content
33
how are ascites managed?
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
Consider TIPS procedure in refractory ascites
Consider transplantation in refractory ascites
34
how does spontaneous bacterial peritonitis present?
Can be asymptomatic so have a low threshold for ascitic fluid culture
Fever
Abdominal pain
Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
Ileus
Hypotension
35
what are the most common organisms causing spontaneous bacterial peritonitis?
Escherichia coli
Klebsiella pnuemoniae
Gram positive cocci (such as staphylococcus and enterococcus)
36
how is spontaneous bacterial peritonitis managed?
ascitic culture
IV cephalosporin
37
define hepatorenal syndrome
Hypertension in the portal system leads to dilation of the portal blood vessels, stretched by large amounts of blood pooling there. This leads to a loss of blood volume in other areas of the circulation, including the kidneys. This leads hypotension in the kidney and activation of the renin-angiotensin system. This causes renal vasoconstriction, which combined with low circulation volume leads to starvation of blood to the kidney. This leads to rapid deteriorating kidney function. Hepatorenal syndrome is fatal within a week or so unless liver transplant is performed.
38
define hepatic encephalopatjy
causes by build up of toxins in brain..ammonia - functional impairment of liver in cirrhosis to metabolise, and collateral vessels develop to bypass liver cause ammonia to enter blood system directly
39
what are the precipitating factors of hepatic encephalopathy?
Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications (particularly sedative medications)
40
how is hepatic encephalopathy managed?
laxatives - promote excretion of ammonia
abx - rifaximin - less bacteria producing ammonia
nutrition - NG feeding
41
define non alcoholic fatty liver disease
forms part of the “metabolic syndrome” group of chronic health conditions relating to processing and storing energy that increase risk of heart disease, stroke and diabetes - fatty deposits in liver cells intefering with function, can progress to hepatitis and cirrhosis
42
what are the risk factors for NAFLD?
Obesity
Poor diet and low activity levels
Type 2 diabetes
High cholesterol
Middle age onwards
Smoking
High blood pressure
43
what is a non invasive liver screen?
abnormal LFT'S-? next action
Ultrasound Liver
Hepatitis B and C serology
Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis)
Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis)
Caeruloplasmin (Wilsons disease)
Alpha 1 Anti-trypsin levels (alpha 1 anti-trypsin deficiency)
Ferritin and Transferrin Saturation (hereditary haemochromatosis)
44
which autoantibodies attack the liver?
Antinuclear antibodies (ANA)
Smooth muscle antibodies (SMA)
Antimitochondrial antibodies (AMA)
Antibodies to liver kidney microsome type-1 (LKM-1)
45
how is non alcoholic fatty liver disease diagnosed?
liver USS - hepatic steatosis
ELF blood test - fibrosis (first line)
NAFLD fibrosis score
fibroscan
46
how is alcoholic fatty liver disease managed?
Weight loss
Exercise
Stop smoking
Control of diabetes, blood pressure and cholesterol
Avoid alcohol
47
when would you refer a pt to a liver specialist?
when have significant fibrosis - so need to be treated with vit E or pioglitazone
48
what are the causes of hepatitis?
Alcoholic hepatitis
Non alcoholic fatty liver disease
Viral hepatitis
Autoimmune hepatitis
Drug induced hepatitis (e.g. paracetamol overdose)
49
how does hepatitis present?
Abdominal pain
Fatigue
Pruritis (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice
Fever (viral hepatitis)
50
what are the biochemical results for hepatitis?
high AST/ALT, proportionally more than ALP
billirubin rise
51
how common is hep A?
not in UK, most common worldwide
52
how is hep A transmitted and what sx does it cause?
faecal-oral route, usually by contaminated water or food
- N+V, anorexia, jaundice, cholestasis causing dark urine and pale stools, hepatomegaly
53
how is hep A managed?
analgesia- resolves in 1-3 months
vaccinated
notifiable disease to public health
54
how does hep B spread?
direct contact with blood or bodily fluids - sex, sharing needles, contaminated products such as toothrushes or minor cuts
mother to child
55
what is the prognosis of hep B?
most people recover within 2 months
10% develop chronic hep B carriers
56
what do the viral markers tell you about the presence of disease?
Surface antigen (HBsAg) – active infection
E antigen (HBeAg) – marker of viral replication and implies high infectivity
Core antibodies (HBcAb) – implies past or current infection
Surface antibody (HBsAb) – implies vaccination or past or current infection
Hepatitis B virus DNA (HBV DNA) – this is a direct count of the viral load
57
what does core antibodies tell you about the hepatitis sttatus?
IgM and IgG versions of the HBcAb. IgM implies an active infection and will give a high titre with an acute infection and a low titre with a chronic infection. IgG indicates a past infection where the HBsAg is negative.
58
what does hep B e antigen tell about the hepatitis status?
Hepatitis B e antigen (HBeAg) is important. Where the HBeAg is present it implies the patient is in an acute phase of the infection where the virus is actively replicating. The level of HBeAg correlates with their infectivity. If the HBeAg is higher, they are highly infectious to others. When they HBeAg is negative but the hepatitis B e antibody is positive this implies they have been through a phase where the virus was replicating and but the virus has now stopped replicating and they are less infectious
59
how are people vaccinated against hep B?
with hep B surface antigen
60
how do you manage hepatitis B?
Have a low threshold for screening patients that are at risk of hepatitis B.
Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases
Refer to gastroenterology, hepatology or infectious diseases for specialist management
Notify Public Health (it is a notifiable disease)
Stop smoking and alcohol
Education about reducing transmission and informing potential at risk contacts
Testing for complications: FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma
Antiviral medication can be used to slow the progression of the disease and reduce infectivity
Liver transplantation for end-stage liver diseas
61
how does hep C spread?
blood and bodily fluids
62
how is hep C managed?
NO VACCINE
curable with direct acting antiviral meds - need genotype
screen
notify public health
refer for specialist management
stop smoking and drinking
educate
test for complications - fibroscan for cirrhosis and USS for hepatocellular carcinoma
liver transplant for end stage liver disease
63
what is the prognosis of hep C?
1 in 4 rceovery
3 in 4 becomes chronic
64
what are the complications of hep C?
liver cirrhosis
heptacocellular carcinoma
65
how is hep C tested for?
hep C antibody
calculate viral load and assess for individual genotype
66
how does a hep D spread?
only survives in patients who already have a hep V infection..attaching to HBsAg
67
how serious is hep D and how is it treated?
Hep D increases complications and disease severity of hep B
notifiable disease
68
how is hep E transmitted?
faecal-oral route
69
how is hep E treated?
cleared within a month and no tx is usually required
rarely can progress to chronic hep and liver failure
NO VACCINATION
notified
70
what is the cause of autoimmune hepatitis?
unknown
genetic and environmental causing T cell mediated response against liver cells
71
what are the two types of autoimmune hepatitis?
type 1 - middle aged wmen, around or after menopause with fatigue and fx of liver disease
type 2 - teenage/early twenties present with acute hepatitis, high transaminases and jaundice
72
what biochemical results are there for autoimmune hepatitis?
raised ALT, AST
raised IgG
autoantibodies, type 1 - ANA, anti-actin, anti SLA/LP
type 2 - anti-LKM1, anti-LC1
confirmed with biopsy
73
how is autoimmune hepatitis treated?
high dose prednisolone
azathioprine
liver transplant
74
define haemochromatosis
iron storage disorder that results in excessive total body iron and deposition of iron in tissues
75
what is the genetic mutation involved in haemachromatosis?
HFE gene located on chromosome 6
autosomal recessive
76
what are the sx of haemochromatosis?
Chronic tiredness
Joint pain
Pigmentation (bronze / slate-grey discolouration)
Hair loss
Erectile dysfunction
Amenorrhoea
Cognitive symptoms (memory and mood disturbance)
presenting at age of 40 or later in females as menstruation eliminates iron from body
77
how is haemochromatosis diagnosed?
serum ferritin level (can rise in inflammation) so 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 both high, perform genetic test to confirm
liver biopsy with Perl's stain - iron conc in parenchymal cells
CT abdo - attenuation
MRI - liver depositis of iron
78
what are the 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)
Hepatocellular Carcinoma
Hypothyroidism (iron deposits in the thyroid)
Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
79
how is haemtochromatosis managed?
Venesection (a weekly protocol of removing blood to decrease total iron)
Monitoring serum ferritin
Avoid alcohol
Genetic counselling
Monitoring and treatment of complications
80
define wilson disease
excessive accumulation of copper in the body and tissue
81
what is the genetic mutation causing wilson's disease?
mutation in the “Wilson disease protein” on chromosome 13. The Wilson disease protein also has the catchy name “ATP7B copper-binding protein”
autosomal recessive
82
what are the features of wilson's disease?
Hepatic problems (40%)-
chronic hepatitis and cirrhosis,
Neurological problems (50%)
concentration and coordination difficulties, dysarthria, dystonia, parkinsonism, motor sx are assymetrical
Psychiatric problems (10%) -
mild depression, full psychosis
kayser-fleischer rings in cornea - brownish cirlces in iris
haemolytic anaemia
renal tubular acidosis
osteopenia
83
how is wilson's disease diagnosed?
serum caeruloplasmin - low (can be falsely normal or elevated in cancer/inflammation)
liver biopsy - liver copper content (gold standard)
24 hour urine copper assay elevated
low serum copper
kayser-fleischer rings
MRI brain - non specific changes
84
how is wilson's disease treated?
copper chelation -
Penicillamine
Trientene
85
what is the cause of alpha 1 antitrypsin defiency?
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
86
what are the two main organs affected by alpha 1 antitrypsin defiency?
liver - cirrhosis
lungs - bronchiecatsis and emphysema
87
how is cirrhosis caused by alpha 1 antitrypsin defiency?
normally alpha 1 antitrypsin created in liver - instead mutant version is produced, which gets trapped in liver, building up and causes damage...cirrhosis and then carcinoma
88
how are the lungs damaged by alpha 1 antitrypsin defieincy?
lack of normal alpha 1 leads to excess of protease which attacks C.T of lungs
89
how is alpha 1 antitrypsin defiency diagnosed?
Low serum-alpha 1-antitrypsin (screening test of choice)
Liver biopsy - cirrhosis and acid-Schiff-positive staining globules (this stain highlights the mutant alpha-1-antitrypsin proteins) in hepatocytes
Genetic testing - A1AT gene
High resolution CT thorax - bronchiectasis and emphysema
90
how is alpha 1 antitrypsin defiency treated?
stop smoking
symptomatic tx
NICE recommend against the use of replacement alpha-1-antitrypsin, however the research and debate is ongoing regarding the possible benefits
Organ transplant - end-stage liver or lung disease
Monitoring for complications (e.g. hepatocellular carcinoma)
91
define primary billiary cirrhosis?
a condition where the immune system attacks the small bile ducts within the liver- the intralobar ducts, also known as the Canals of Hering are first affected. 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. lack of bile acids in stool - malabsorption of fats. bile acids, bilirubin and cholesterol build up in blood
92
how does primary biliary cirrhosis present?
Fatigue
Pruritus
GI disturbance and abdominal pain
Jaundice
Pale stools
Xanthoma and xanthelasma
Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)
93
what are the associations of primary biliary cirrhosis?
middle aged women
autoimmune conditions - thyroid
rheumatoid conditions - RA, sjogrens
94
how is primary biliary cirrhosis diagnosed?
LFT's - ALP raised
autoantibodies - anti-mitochondrial antibodies, ANA
ESR raised
IgM raised
liver biopsy
95
how is primary biliary cirrhosis treated?
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
96
what are the complications of primary biliary cirrhosis?
cirrhosis
portal hypertension
Symptomatic pruritus
Fatigue
Steatorrhoea (greasy stools due to lack of bile salts to digest fats)
Distal renal tubular acidosis
Hypothyroidism
Osteoporosis
Hepatocellular carcinoma
97
define primary sclerosing cholangitis?
intrahepatic and extrahepatic ducts become strictured and fibrotic...obstructing flow of bile out of liver and into intestine...liver inflammation, fibrosis and cirrhosis
98
what is primary sclerosing cholangitis caused by?
genetic
autoimmune
microbiome
evironment
association with UC
99
what are the risk factors for primary sclerosing cholangitis?
Male
Aged 30-40
Ulcerative Colitis
Family History
100
how does PSC present?
Jaundice
Chronic right upper quadrant pain
Pruritus
Fatigue
Hepatomegaly
101
what are the biochemical results of PSC?
LFTs - raised ALP, billirubin and as progresses ALT and AST
autoantibodies - p-ANCA, ANA, aCL
102
what is the gold standard investigations for PSC?
MRCP
103
what are the associations and complications of PSC?
Acute bacterial cholangitis
Cholangiocarcinoma develops in 10-20% of cases
Colorectal cancer
Cirrhosis and liver failure
Biliary strictures
Fat soluble vitamin deficiencies
104
how is PSC managed?
liver transplant
ERCP
105
what are the risk factors for hepatocellular carcinoma?
Viral hepatitis (B and C)
Alcohol
Non alcoholic fatty liver disease
Other chronic liver disease- screened for HCC
106
what condition is associated with cholangiocarcinoma?
PSC
107
how does HCC present?
Weight loss
Abdominal pain
Anorexia
Nausea and vomiting
Jaundice
Pruritus
108
how does cholangiocarcinoma present?
painless jaundice
109
what are the tumour markers of HCC and cholangiocarcinoma?
HCC - alpha-fetoprotein
cholangiocarcinoma - CA19-9
110
how are liver cancers diagnosed?
liver USS
CT/MRI
ERCP
111
how is HCC treated?
resection
liver transplant
kinase inhibitors - inhibiting prolieration of cancer cells - sorafenib, regorafenib and lenvatinib
112
how is cholangiocarcinoma treated?
resection
ERCP
113
define haemangioma
benign tumours of liver
114
define focal nodular hyperplasia
benign liver tumour made of fibrotic tissue
usually asx and has no malignant potention
related to oestrogen - COCP
115
define orthotopic transplant
entire liver is transplanted from a deceased patient to a recipient
116
defin liver donor transplant
portion of the organ from a living donor, transplant it into a patient and have both regenerate to become two fully functioning organs
117
define split donation
split the organ of a deceased person into two and transplant it into two patients and have them regenerate to their normal size in each recipient
118
what are the indications for liver transplant?
acute liver failure - immediate, top of list - acute viral hepatitis, paracetamol overdose
chronic liver failure - around 5 months
119
what are the factors suggesting unsuitability for liver transplantation?
Significant co-morbidities (e.g. severe kidney or heart disease)
Excessive weight loss and malnutrition
Active hepatitis B, hepatitis C or other infection
End-stage HIV
Active alcohol use (generally 6 months of abstinence is required)
120
what incision is required for liver transplant surgery?
rooftop
121
what is involved in post transplantation care?
lifelong immunosuppression - steroids, azathioprine, tacrolismus
avoid alcohol and smoke
treat any infection
monitor for recurrence
monitor for cancer
122
how do you monitor for transplant rejection?
Abnormal LFTs
Fatigue
Fever
Jaundice
123
what are the sx of GORD?
dyspepsia
heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice
124
when does GORD require an endoscopy referral?
concerning features
GI bleed - malaena
125
what are the NICE guidlines for a 2 week referral for endoscopy?
Dysphagia (difficulty swallowing) at any age gets a two week wait referral
Aged over 55 (this is generally the cut off for urgent versus routine referrals)
Weight loss
Upper abdominal pain / reflux
Treatment resistant dyspepsia
Nausea and vomiting
Low haemoglobin
Raised platelet count
126
how is GORD managed?
lifestyle - reduced caffeine, alcohol, weight loss, small meals, avoid heavy meals before bed, stay upright after meals, gaviscon/rennie, PPI, ranitidine (H2 receptor antagonist)
surgery - laprascopic fundoplication
127
what is H.pylori?
causes damage to epithelial lining of stomach...forces its way into gastric mucosa breaking it so epithelial cells are exposed to the acid
also produces ammonia to neutralise the stomach acid and damages the epithelial cells directly
128
when is an H.pylori test used?
anyone with dyspepsia - Urea breath test using radiolabelled carbon 13, Stool antigen test, Rapid urease test can be performed during endoscopy.
129
how does a rapid urease work?
performed during endoscopy and involves taking a small biopsy of the stomach mucosa. Urea is added to this sample. If H. pylori are present, they produce urease enzymes that converts the urea to ammonia. The ammonia makes the solution more alkali giving a positive result on when the pH is tested.
130
how is H pylori eradicated?
PPI, amoxicillin and clarithromycin for 7 days
131
define barretts oesophagus
metaplasia from squamous to columnar epithelium
premalignant changes - risk factor for adenocarcinoma
require regular endoscopy
treated with PPI and possibly ablation tx during endoscopy
132
what are peptic ulcers caused by?
medications - steroids, NSAIDS
H.pylori
increased acid - stress, caffeine, alcohol, smoking, spicy foods
133
how does peptic ulcer present?
Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia
Bleeding causing haematemesis, “coffee ground” vomiting and melaena
Iron deficiency anaemia (due to constant bleeding)
134
how can you differentiate between the presenting fx of gastric and duodenal ulcers?
eating worsens pain of gastric ulcers and improves duodenal ulcers
135
how are peptic ulcers managed?
diagnosed by endoscopy and raised urease test to check h pylori + biopsy to exclude malignancy
treated with PPI
136
what are the complications of peptic ulcer?
bleeding from ulcer
perforation -> peritonitis
scarring and strictures of muscle and mucosa...narrowing of pylorus so hard to empty contents...pyloric stenosis
137
what are the 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
138
how does upper GI bleed present?
haematemesis
coffee ground vomit
malaena
haemodynamic unstability - low BP, tachycardic, other signs of shock
epigastric pain and dyspepsia - peptic ulcer
jaundice - ascites in liver disease with varices
139
what is the scoring system in suspected upper GI bleed?
glasgow-blatchford score
>0 = high risk
Drop in Hb
Rise in urea (blood broken down by acid and enzymes)
Blood pressure
Heart rate
Melaena
Syncopy
140
how is the risk of rebleeding and mortality scored in an upper GI bleed?
rockall score
Age
Features of shock (e.g. tachycardia or hypotension)
Co-morbidities
Cause of bleeding (e.g. Mallory-Weiss tear or malignancy)
Endoscopic stigmata of recent haemorrhage such as clots or visible bleeding vessels
141
how is an upper GI bleed managed?
A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 large bore cannula)
T – Transfuse
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)
send bloods - FBC, UE, coag, LFT, crossmatch
142
in which circumstances is a tranfusion required?
transfuse fresh frozen plasma to patients with massive haemorrhage
not too much blood
platelets in active bleeding and thrombocytopenia
prothrombin complex concentrate for patients with warfarin that are actively bleeding
143
what is required in addition if varices are caused by chronic liver disease?
terlipressin
prophylactix abx
band varices with OGD or cauterisation
144
what are the clinical fx of crohns?
N – No blood or mucus (less common)
E – Entire GI tract
S – “Skip lesions” on endoscopy
T – Terminal ileum most affected and Transmural (full thickness) inflammation
S – Smoking is a risk factor (don’t set the nest on fire)
- weight loss. strictures and fistulas
145
what are the clinical fx of UC?
C – Continuous inflammation
L – Limited to colon and rectum
O – Only superficial mucosa affected
S – Smoking is protective
E – Excrete blood and mucus
U – Use aminosalicylates
P – Primary Sclerosing Cholangitis
146
what are the sx of IBD?
diarrhoea
abdo pain
passing blood
weight loss
147
which investigations are required for IBD?
Bloods - anaemia, infection, thyroid, kidney, LFT
CRP
faecal calprotectin (> 90% sensitive and specific to IBD in adults)
OGD and colonoscopy with biopsy
USS, CT, MRI
148
how is crohns managed?
steroids to induce remission - oral prednisolone
immunosuppressants such as azathioprine
maintain remission with azathioprine
surgery - resect terminal ileum or treat fistulas and strictures
149
how is UC managed?
induce remission with aminosalicylate - mesalazine or corticosteroids, if severe - IV corticosteroids
to maintain remission - mesalazine, azathioprine
surgery - panprotocolectomy and left with permanent ileostomyx or ileo-anal anastomosis - J pouch
150
what are the sx of IBS?
Diarrhoea
Constipation
Fluctuating bowel habit
Abdominal pain
Bloating
Worse after eating
Improved by opening bowels
151
what is the criteria for diagnosing IBS?
FBC, ESR, CRP
faecal calprotectin neg to exclude IBD
negative coeliac diseae serology (anti-TTG antibodies)
cancer is not suspected
and sxz should suggest IBS -
Abdominal pain / discomfort:
Relieved on opening bowels, or
Associated with a change in bowel habit
AND 2 of:
Abnormal stool passage
Bloating
Worse symptoms after eating
PR mucus
152
how is IBS managed?
Adequate fluid intake
Regular small meals
Reduced processed foods
Limit caffeine and alcohol
Low “FODMAP” diet (ideally with dietician guidance)
Trial of probiotic supplements for 4 weeks
1st line medications - loperamide for diarrhoea, laxative for constipation - linaclotide, antispasmodic for cramps - hyoscine butylbromide (buscopan), then try TCA, then SSRI
CBT for psychological
153
define coeliac disease
autoantibodies are created in response to exposure to gluten that target epithelial cells of the intestine...inflammation
- anti-TTG
- anti-EMA
affects jerjenum and causes atrophy of villi so malabsoprtion of nutrients
154
how does coeliac disease present?
asx
Failure to thrive in young children
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)
neurological sx - peripheral neuropathy, cerebellar ataxia, epilepsy
155
what condition is coeliac disease linked to?
type 1 DM (mainly)
Thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
156
what are the genetic associations of coeliac disease?
HLA-DQ2 gene (90%)
HLA-DQ8 gene
157
what is important about testing the autoantibodies linked with coeliac disease?
Anti-TTG and anti-EMA antibodies are IgA. Some patients have an IgA deficiency. When you test for these antibodies, it is important to test for total Immunoglobulin A levels because if total IgA is low because they have an IgA deficiency then the coeliac test will be negative even when they have coeliacs. In this circumstance, you can test for the IgG version of anti-TTG or anti-EMA antibodies or simply do an endoscopy with biopsies.
158
how is coelic disease diagnosed?
investigations carried out while reamining on diet containing gluten -
total IgA levels to exclude IgA defiency
then check autoantibodies - anti TTG is first line
endosocpy and biopsy - crypt hypertrophy, villous atrophy
159
what are the complications of untreated coeliac disease?
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL) of the intestine
Non-Hodgkin lymphoma (NHL)
Small bowel adenocarcinoma (rare)
160
how is coeliac disease treated?
lifelong gluten free diet
161
when should non alcoholic fatty liver disease be suspected
T2DM with abnormal LFTs - ? non-alcoholic fatty liver diseas
162
what abx is related to c diff
Cephalosporins, not just clindamycin, are strongly linked to C.difficile
163
what is used for the secondary prophylaxis of hepatic encephalopathy
Lactulose and rifaximin are used for the secondary prophylaxis of hepatic encephalopathy
164
what is the abx of choice for c diff
Oral vancomycin is the first line antibiotic for use in patients with C. difficile infection. ADD iv metronidazole if severe infection
165
how is ibs and ibd diagnosed as differentials
faecal calprotectin - A positive result does not indicate definite IBD but patients should be referred on to secondary care for further investigation.
166
how is a pt with crohns and perianal fistal investigated
MRI is the investigation of choice for suspected perianal fistulae in patients with Crohn's
167
upper Gi bleed v lower GI bleed
The isolated urea rise is more suggestive of an acute upper gastrointestinal bleed rather than a lower gastrointestinal bleed. Therefore, a colonoscopy within 24 hours is not necessary at this stage.
168
vit b12 how investigated
Intrinsic factor antibodies are more useful than gastric parietal cell antibodies when investigating vitamin B12 deficiency
169
what is a cause of a choletasis?
Co-amoxiclav is a well recognised cause of cholestasis
170
alcoholic hepatitis investigations
he AST/ALT ratio in alcoholic hepatitis is 2:1
171
ischaemic colitis
Ischaemic colitis is the most likely diagnosis given this man's classic presentation (after a meal, intermittent and severe pain, pain out of proportion to clinical findings) and given his predisposing factors (prev. myocardial infarction, atrial fibrillation, hypertension).
172
ascities
causes of ascites can be grouped into those with a serum-ascites albumin gradient (SAAG) <11 g/L or a gradient >11g/
173
SAAG >11
Liver disorders are the most common cause
cirrhosis/alcoholic liver disease
acute liver failure
liver metastases
Cardiac
right heart failure
constrictive pericarditis
Other causes
Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema
174
SAAG <11
Hypoalbuminaemia
nephrotic syndrome
severe malnutrition (e.g. Kwashiorkor)
Malignancy
peritoneal carcinomatosis
Infections
tuberculous peritonitis
Other causes
pancreatitisis
bowel obstruction
biliary ascites
postoperative lymphatic leak
serositis in connective tissue diseases
175
what lab finding would indicate cirrhosis in someone with chronic liver disease?
Thrombocytopenia (platelet count <150,000 mm^3) is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease
176
what are the associated cancers of HNPCC?
Endometrial cancer is the second most common association of HNPCC after colorectal cancer
177
what are people with coeliac at risk of?
People with coeliac disease receive the pneumococcal vaccine due to hyposplenism
178
buddai charri syndrom
Budd–Chiari syndrome - ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation
179
gilbert's syndrome
An isolated hyperbilirubinaemia in a 22-year-old male is likely to be secondary to Gilbert's syndrome. The normal dipstix urinalysis excludes Dubin-Johnson and Rotor syndrome as these both produce a conjugated bilirubinaemia. Viral infections are common triggers for a rise in the bilirubin in patients with Gilbert's
180
how is severe alcoholic hepatitis managed?
Corticosteroids are used in the management of severe alcoholic hepatitis
181
primary billiary cholangitis
Primary biliary cholangitis - the M rule
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females
182
dysplasia on barretts oesophagus tx
Dysplasia on biopsy in Barrett's oesophagus requires an endoscopic intervention
183
UC falre up
In a mild-moderate flare of ulcerative colitis extending past the left-sided colon, oral aminosalicylates should be added to rectal aminosalicylates, as enemas only reach so far
184
gilberts
An isolated rise in bilirubin in response to physiological stress is typical of Gilbert's syndrome
185
pancreatitis
Mesalazine > sulfasalazine in terms of pancreatitis risk
186
ALT >1000
drug induced
autoimmune - igG and liver biopsy then azathioprine and steroids, monitor myelosuppression and LFT
viral - hepatitis, CMV, EBV
187
lot in portal vein
portal HTN occurs - collateral circ - splenomegaly - ischaemic changes to liver
tx with propranolol and varices banding
188
r sided HF hepatmegaly
Right heart failure is associated with a firm, smooth, tender and pulsatile liver edge
189
enteric fever
Rose spots appear in Salmonella typhi infections. They also appear in C.psittaci infections although it is more associated with typhoid than psittacosis.
190
barretts tx
Endoscopic intervention is the single most appropriate management option at this stage. High-grade dysplasia is treated with endoscopic therapy and is preferred over oesophagectomy or surveillance.
191
giardiasis
longest incubation period
192
recurrent c.diff tx
A recurrent episode of C. difficile within 12 weeks of symptom resolution should be treated with oral fidaxomicin
193
ischaemic colitis most likely to be affected
The splenic flexure is the most likely area to be affected by ischaemic colitis
194
high urea levels
High urea levels can indicate an upper GI bleed versus lower GI bleed
195
iron defieciency anaemia v anaemia of chronic disease
Iron defiency anaemia vs. anaemia of chronic disease: TIBC is high in IDA, and low/normal in anaemia of chronic disease
196
addisons electrolyte distubrance
Addison's disease/adrenal insufficiency can cause hyperkalaemic metabolic acidosis
197
scurvy deficient
This patient with a low body mass index and bleeding gums likely has scurvy due to ascorbic acid deficiency, which is the correct answer. It is also known as vitamin C.
198
zollinger elisson syndrom
Zollinger-Ellison syndrome: epigastric pain and diarrhoea
199
moderate UC flare up
If a mild-moderate flare of distal ulcerative colitis doesn't respond to topical (rectal) aminosalicylates then oral aminosalicylates should be added
200
scleroderma
a is a risk factor for this condition, which makes it the correct answer. This patient's clinical features and positive hydrogen breath test are consistent with small bowel bacterial overgrowth syndrome, a condition in which excessive bacteria accumulate in the small intestine, leading to symptoms such as abdominal bloating, diarrhoea, and malnutrition.
201
clinical fx of enteric fever - typhoid
initially systemic upset as above
relative bradycardia
abdominal pain, distension
constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid
rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid
202
recurrent c.diff treatment
A recurrent episode of C. difficile within 12 weeks of symptom resolution should be treated with oral fidaxomicin
203
pts must eat gluten for how many weeks before coeliac test
6 weeks
204
chronic mesenteric ischameia triad
classically characterised by a triad of severe, colicky post-prandial abdominal pain, weight loss, and an abdominal brui
205
most common inheritable form of colorectal cancer
HNPCC (Lynch syndrome) is the most common inheritable form of colorectal cancer
206
iron defiency anaemia v anaemia of chronic disease
Iron defiency anaemia vs. anaemia of chronic disease: TIBC is high in IDA, and low/normal in anaemia of chronic disease
207
type 1 v type 2 hepatorenal syndrome
Hepatorenal syndrome is split into type 1 and 2. Type 1 is a rapid onset hepatorenal syndrome (less than two weeks). This typically occurs following an acute event such as an upper GI bleed. Type 2 is a more gradual decline in renal function and is generally associated with refractory ascites.
208
coeliac disease
low total IgA and TTG
209
AMA negative
Negative antimitochondrial antibodies make the diagnosis of primary biliary cirrhosis less likely.
210
clindamyclin is reisk factor
c.diff
211
gastric carcinoma sign
Sister Mary Joseph nodule – sign of metastasis to periumbilical lymph nodes, classically from gastric cancer primary
212
carcinoid syndrome triad
This patient has abdominal pain, diarrhoea and flushing which are the classical features of carcinoid syndrome
213
definition of upper GI bleed
The definition of an Upper GI Bleed is a haemorrhage with an origin proximal to the ligament of Treitz
214
double duct sign
Double duct sign - not seen in all cases of pancreatic cancer but if it is present is either pancreatic or ampulla vater cancer. It is a dilated common bile duct and dilated pancreatic duct.
215
Wilson’s disease T’s
Pencillamine
216
IBS
This is a clinical diagnosis of irritable bowel syndrome, supported by relief on defaecation as well as a panel of normal blood tests. The first-line anti-motility agent for this presentation of diarrhoea would be loperamide, as recommended by NICE guidelines.
217
Clindamycin side effect
Clindamycin treatment is associated with a high risk of C. difficile
218
Long term PPI
Long term proton pump inhibitor therapy can cause hypomagnesaemia
219
Double duct sign
Pancreatic cancer
220
Severity of c.diff
WCC
221
Crohns associated
Gallstones
