Gastroenterology Flashcards
(354 cards)
1
Q
sx of coeliac disease?
A
Chronic or intermittent diarrhoea
Failure to thrive or faltering growth (in children)
Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
Prolonged fatigue (‘tired all the time’)
Recurrent abdominal pain, cramping or distension
Sudden or unexpected weight loss
Unexplained iron-deficiency anaemia, or other unspecified anaemia
folic acid deficiency
2
Q
pathophysiology of coeliac disease?
A
sensitivty to the protein gluten
autoimmune condition
repeated exposure results in villious atrophy - which then leads to malabsorption
3
Q
what genes are associated with coeliac disease?
A
HLA-DQ2 (95% of patients) and HLA-DQ8 (80%)
4
Q
what conditions are associated with coeliac?
A
Autoimmune thyroid disease
Dermatitis herpetiformis
Irritable bowel syndrome
Type 1 diabetes
First-degree relatives (parents, siblings or children) with coeliac disease
5
Q
what are the complications of untreated coeliac disease?
A
anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
hyposplenism
osteoporosis, osteomalacia
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility, unfavourable pregnancy outcomes
rare: oesophageal cancer, other malignancies
6
Q
how to diagnose coeliac disease?
A
Ttg- If patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at least 6 weeks prior to testing.
if positive - refer for a endoscopic intestinal biopsy - will show villous atrophy, crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes
7
Q
management of coeliac disease?
A
avoid gluten
yearly pneumococcal vaccination - as all pt have a degree of hyposplenism
8
Q
differential diagnosis of acute change in bowel habit?
A
viral gastroenteritis
food poisoning
medications
constipation with overflow
early presentation of acute cause
ectopic pregnancy
9
Q
differentials of chronic change in bowl habit?
A
IBS
IBD
coeliac disease
bowel Ca
ovarian Ca, lymphoma, small bowel cancer
bile acid malabsorption
hyper/hypo-thyroidism
chronic pancreatitis
pancreatic cancer
lactose intolerance - can follow an acute gastroenteritis
other food sensitivity
laxative misuse
10
Q
What investigations would you organise for change in bowel habit?
A
FIT test
stool culture
faecal calprotectin
bloods to consider - FBC, ferritin, U+E, LFT, TFT, bone profile, CRP/ESR, coeliac serology, ca125, b12/folate
11
Q
who should be offered a FIT test?
A
abdominal mass
change in bowel habit
IDA
>40yrs with unexplained weight loss and abdo pain
<50yrs with unexplained rectal bleeding/abdo pain/weight loss
>60 with anaemia even in absence of IDA
12
Q
differentials for acute abdominal pain?
A
appendicitis
acute obstruction + perforation
diverticulitis
Meckles diverticulum
ischamia
volvulus
intersussception
gastric and duodenal ulcer
pancreatitis
cholecystitis
biliary colic
empyema
renal colic
13
Q
what is the diagnostic criteria for IBS?
A
A diagnosis of IBS can be made in primary care if abdominal pain or discomfort has been present for at least 6 months and:
Is either relieved by defecation or associated with altered bowel frequency (increased or decreased), or stool form (hard, lumpy, loose, or watery) and:
Is accompanied by at least two of the following symptoms:
Altered stool passage (straining, urgency, incomplete evacuation).
Abdominal bloating (more common in women than men), distension, tension or hardness.
Made worse by eating.
Passage of mucus.
Alternative conditions with similar symptoms have been excluded.
14
Q
what is the pathophysiology of IBS?
A
However, the pathophysiology of IBS is not fully comprehended.
Pathogenic factors, such as genetic susceptibility, food intolerance, gut-brain axis dysfunction, or innate immunity and dysbiosis issues, possibly contribute to this disorder.
15
Q
management of IBS?
A
usually start with education around IBS and causes
lifestyle modifications initially
consider pharmacological intervention if needed
16
Q
pharmacological management of IBS?
A
Laxatives for constipation.
Loperamide for diarrhoea.
An antispasmodic drug for abdominal pain or spasm.
A low-dose tricyclic antidepressant (TCA) for refractory abdominal pain.
A selective serotonin reuptake inhibitor (SSRI) for refractory abdominal pain, if a TCA is ineffective, contraindicated, or not tolerated.
17
Q
what lifestyle advice should be given to a patient who has IBS?
A
A clear explanation of IBS in the context of the gut-brain axis, discussion on the aims of management and sign-posting to sources of information and support.
Advising the person to eat regular meals with a healthy, balanced diet, to adjust their fibre intake according to symptoms and to drink adequate fluid.
Advising people who choose to take over-the-counter probiotic supplements to continue for at least twelve weeks and discontinue if symptoms do not improve.
Encouraging regular physical activity.
Managing any associated stress, anxiety, and/or depression appropriately.
18
Q
which laxative should be avoided in IBS?
A
lactulose - increases the production of gas in the gut which can exacerbate symptoms
19
Q
what are the two different types of IBD?
A
ulcerative colitis
crohns
20
Q
difference between ulcerative colitis and crohns?
A
crohns - affects entire GI tract
UC - anus to small bowel
21
Q
symptoms of IBD?
A
bloody diarrhoea for more than 6 weeks
faceal urgency/incontinence
nocturnal defecation
tenesmus
pre-defecation pain
weight loss
fever
malaise
faltering growth / delayed puberty
abdo pain - LLQ
family hx of IBD/autoimmune conditions
22
Q
signs on examination of IBD?
A
pallor
clubbing
aothous ulcers
abdo distension / tenderness / mass
23
Q
symptoms of crohns disease?
A
unexplained persistent diarrhoea for 4-6 weeks
abdominal pain and distension
constitutional symptoms
mass in RLQ
24
Q
what are some complications of crohns?
A
bladder fistula
vaginal fistula
perianal fistula
bowl obstruction
25
management of suspected IBD?
consider urgent hospital admission if systemically unwell
urgent ref to gastro/paeds if not needing acute admission
DO NOT prescribe antidiarrhoeal medications - can precipitate toxic megacolon
26
management of confirmed IBD?
drug management
psychosocial support
crohns and colitis UK
encourage to stop smoking
management of flare ups
27
what medications are used to manage IBD?
Aminosalicylates — mesalazine and sulfasalazine may be considered for a mild-to-moderate first presentation or inflammatory exacerbation of ulcerative colitis. These drugs are also effective at maintaining remission. They are often prescribed topically (suppository or enema) initially, and orally if remission is not achieved. For extensive disease, topical and high-dose oral treatment may be offered first-line.
Corticosteroids — monotherapy with a time-limited course of corticosteroids may be used for induction of remission if aminosalicylates are ineffective or not tolerated, with the aim to gradually taper the dose according to disease severity and the person's response to treatment. They should not be used to maintain clinical remission due to the risk of multiple adverse effects with long-term use.
Ciclosporin — may be used for acute severe disease, especially if intravenous corticosteroids are not effective, contraindicated, or not tolerated.
Thiopurines — azathioprine or mercaptopurine may be considered to maintain remission in people using aminosalicylates who have required two or more courses of oral corticosteroids in the previous year or whose disease is steroid refractive or dependent.
28
what is diverticular disease?
Diverticula are sac-like protrusions of mucosa through the muscular wall of the colon, which occur in the sigmoid colon in about 80% of people over the age of 85.
The majority of people have symptoms in the left lower abdomen.
In a minority of people and in people of Asian origin, symptoms may be right-sided.
Diverticulum formation may be associated with a low-fibre diet.
29
how does diverticular disease present?
usually abo pain in LLQ
can sometimes present with bloody diarrhoea
usually asymptomatic finding
30
how does diverticulitis present?
Sudden change in bowel habit and significant rectal bleeding or passage of mucus from the rectum.
Tenderness in the left lower quadrant, a palpable abdominal mass or distention on abdominal examination, with a previous history of diverticulosis or diverticulitis
31
signs of complications of diverticulitis which may need referral to hospital as emergency?
Abdominal mass on examination or peri-rectal fullness on digital rectal examination — possible intra-abdominal abscess.
Abdominal rigidity, guarding, and rebound tenderness on examination — possible perforation and peritonitis.
Altered mental state, raised respiratory rate, low systolic blood pressure, raised heart rate, low tympanic temperature, no urine output or skin discolouration — possible sepsis.
Faecaluria, pneumaturia, pyuria or passage of faeces through the vagina — possible colovesical fistula.
Colicky abdominal pain, absolute constipation (passage of no flatus or stool), vomiting or abdominal distention — intestinal obstruction.
32
what conditions make acute obstruction more likely?
previous abdominal surgery
Ca
crohns / UC
diverticulitis
hernia
adhesions
gallstones
impacted stools
intersusseption
33
signs of abdominal perforation?
sudden and severe abdominal pain.
nausea and vomiting.
fever.
swelling and bloating of the abdomen.
34
which patients with diverticulitis should be admitted to hospital?
Has uncontrollable abdominal pain and any features that suggest complicated acute diverticulitis.
Is dehydrated or at risk of dehydration and is unable to take or tolerate oral fluids at home.
Is unable to take or tolerate oral antibiotics (if needed) at home.
Is aged over 65 years.
Has significant comorbidity or immunosuppression.
35
what is the management of suspected acute diverticulitis?
Co-amoxiclav 500/125 mg three times daily for 5 days — if the person is allergic to penicillin, or this is unsuitable:
Alternatives include cefalexin (500 mg twice or three times daily for 5 days [up to 1 to 1.5 g three or four times daily for severe infection]) plus metronidazole (400 mg three times daily for 5 days), or trimethoprim (200 mg twice daily for 5 days) plus metronidazole (400 mg three times daily for 5 days).
36
when is the risk of complicated diverticulitis the highest?
The course of acute diverticulitis and the likelihood of complicated disease or recurrent episodes — complicated diverticulitis is most often the first presentation of diverticulitis. The risk of complicated diverticulitis decreases with recurrences.
37
who should be referred routinely to the colorectal team with diverticulitis?
Consider arranging referral to a specialist in colorectal surgery if a person is managed in primary care and has frequent or severe recurrent episodes of acute diverticulitis.
38
what general advice should be given to a patient who has diverticulosis?
condition is asymptomatic and no treatment is usually needed
eat varied diet with lots of fruits and vegetables
to drink adequate fluid if they are increasing their fibre intake, especially if there is a risk of dehydration
about the benefits of exercise, and weight loss if they are overweight or obese, and stopping smoking, in reducing the risk of developing acute diverticulitis and symptomatic disease.
consider offering bulk-forming laxatives for people with constipation
39
what is diverticular disease vs diverticulosis?
Diverticulosis refers to the presence of diverticula—small, bulging pouches that can form in the walls of the colon. This is often a result of increased pressure in the colon, usually due to constipation or straining. Diverticulosis doesn’t typically cause symptoms, and many people with it don’t even know they have it. It's quite common, especially in people over 40.
Diverticular disease is a broader term that can include diverticulosis, but it often refers to when those diverticula become symptomatic or cause complications. This can involve:
Diverticulitis: Inflammation or infection of one or more diverticula. It can cause pain (usually in the lower left side of the abdomen), fever, and digestive issues like nausea or constipation. Diverticulitis requires medical treatment and sometimes hospitalization.
Bleeding: Sometimes diverticula can bleed, leading to rectal bleeding, which can range from mild to severe.
40
what are the symptoms of diverticular disease?
Intermittent abdominal pain in the left lower quadrant (pain may be triggered by eating and may be relieved by the passage of stool or flatus).
Symptoms may overlap with conditions such as irritable bowel syndrome, colitis, and malignancy.
Tenderness in the left lower quadrant on abdominal examination.
In a minority of people and in people of Asian origin, pain and tenderness may be localized in the right lower quadrant.
41
when to suspect diverticulitis?
Constant abdominal pain (which is usually severe and starts in the hypogastrium before localizing in the left lower quadrant) with any of the following:
Fever.
Sudden change in bowel habit and significant rectal bleeding or passage of mucus from the rectum.
Tenderness in the left lower quadrant, a palpable abdominal mass or distention on abdominal examination, with a previous history of diverticulosis or diverticulitis.
42
what is meckels diverticulum?
Meckel's diverticulum is a congenital diverticulum of the small intestine. It is a remnant of the omphalomesenteric duct (also called the vitellointestinal duct) and contains ectopic ileal, gastric or pancreatic mucosa.
.
43
how common is meckels diverticulum?
2% of the population
44
how does meckels diverticulum usually present?
abdominal pain mimicking appendicitis
rectal bleeding
Meckel's diverticulum is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years
intestinal obstruction
secondary to an omphalomesenteric band (most commonly), volvulus and intussusception
45
what is the pathophysiology of crohns disease?
the cause is unknown but there is a strong genetic susceptibility
inflammation occurs in all layers, down to the serosa
this is why patients with Crohn's are prone to strictures, fistulas and adhesions
whilst it may cause inflammation anywhere in the gastrointestinal tract, the disease burden is not evenly distributed:
80% of patients have small bowel involvement, usually in the ileum, with around 30% of patients having ileitis exclusively
50% of patients have ileocolitis
20% of patients have colitis exclusively
30% of patients have perianal disease
46
symptoms suggestive of crohns disease?
presentation may be non-specific symptoms such as weight loss and lethargy
diarrhoea/ bloody diarrhoea
abdominal pain: the most prominent symptom in children
perianal disease: e.g. Skin tags or ulcers
extra-intestinal features are more common in patients with colitis or perianal disease
47
what investigations would you do for crohns diesease?
bloods- raised inflammatory markers, anaemia, low vitamin b12 and folate
faecal calprotectin-high
48
what are some of the extra intestinal manifestations of IBD?
Arthritis: pauciarticular, asymmetric
Erythema nodosum
Episcleritis
Osteoporosis
Uveitis
Pyoderma gangrenosum
Clubbing
Primary sclerosing cholangitis
49
which extra intestinal manifestations are more common in UC than in corhns?
Primary sclerosing cholangitis
Uveitis
50
what extra inestinal manifestations are more common in crohns than UC?
episcleritis
51
how common is surgery in crohns disease?
very common, around 80% of patients will go on to need surgery
52
what are patients who have crohns disease more at risk of?
small bowel cancer (standard incidence ratio = 40)
colorectal cancer (standard incidence ratio = 2, i.e. less than the risk associated with ulcerative colitis)
osteoporosis
53
when is the peak incidence of ulcerative colitis?
The peak incidence of ulcerative colitis is in people aged 15-25 years and in those aged 55-65 years.
54
what are the symptoms of ulcerative colitis?
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the left lower quadrant
55
how is mild to moderate ulcerative colitis treated?
proctitis-
topical (rectal) aminosalicylate: for distal colitis rectal mesalazine has been shown to be superior to rectal steroids and oral aminosalicylates
if remission is not achieved within 4 weeks, add an oral aminosalicylate
if remission still not achieved add topical or oral corticosteroid
proctosigmoiditis and left-sided ulcerative colitis-
topical (rectal) aminosalicylate
if remission is not achieved within 4 weeks, add a high-dose oral aminosalicylate OR switch to a high-dose oral aminosalicylate and a topical corticosteroid
if remission still not achieved stop topical treatments and offer an oral aminosalicylate and an oral corticosteroid
extensive disease
topical (rectal) aminosalicylate and a high-dose oral aminosalicylate:
if remission is not achieved within 4 weeks, stop topical treatments and offer a high-dose oral aminosalicylate and an oral corticosteroid
56
what medications are used to maintain remission in UC?
Following a mild-to-moderate ulcerative colitis flare
proctitis and proctosigmoiditis
topical (rectal) aminosalicylate alone (daily or intermittent) or
an oral aminosalicylate plus a topical (rectal) aminosalicylate (daily or intermittent) or
an oral aminosalicylate by itself: this may not be effective as the other two options
left-sided and extensive ulcerative colitis
low maintenance dose of an oral aminosalicylate
Following a severe relapse or >=2 exacerbations in the past year
oral azathioprine or oral mercaptopurine
57
what are the different classifications of UC?
The severity of UC is usually classified as being mild, moderate or severe:
mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
58
what are some common causes of flares of UC
stress
medications
NSAIDs
antibiotics
cessation of smoking
59
what is primary sclerosing cholangitis?
This is a chronic liver disease characterised by inflammation and fibrosis of the bile ducts, leading to cirrhosis and liver failure. It is strongly associated with ulcerative colitis (UC) but not Crohn's disease. The pathogenesis of primary sclerosing cholangitis (PSC) is not fully understood, but it is thought that immune-mediated damage occurs in the biliary epithelium, which can be triggered by gut-derived antigens in genetically susceptible individuals.
60
what are the differentials for dyspepsia?
Upper gastrointestinal malignancy
Gallbladder disease
Hepatobiliary disease
Pancreatic disease
Cardiac disease
Gastroenteritis
Coeliac disease
Lactose intolerance
Crohn's disease
Irritable bowel syndrome
Small intestine bacterial overgrowth
Abdominal aortic aneurysm
61
what is the hpylori eradication therapy?
NICE recommend the following PPI doses:
Lansoprazole 30 mg, omeprazole 20–40 mg, esomeprazole 20 mg, pantoprazole 40 mg, or rabeprazole 20 mg.
If a person tests postive for H. pylori, offer a 7-day triple therapy regimen of:
A PPI twice-daily and amoxicillin 1 g twice-daily and
Either clarithromycin 500 mg twice-daily or metronidazole 400 mg twice-daily.
62
what are the red flags for urgent referral for endoscopy?
All patients who've got dysphagia
All patients who've got an upper abdominal mass consistent with stomach cancer
Patients aged >= 55 years who've got weight loss, AND any of the following:
upper abdominal pain
reflux
dyspepsia
63
who should be referred for a non-urgent endoscopy?
Patients with haematemesis
Patients aged >= 55 years who've got:
treatment-resistant dyspepsia or
upper abdominal pain with low haemoglobin levels or
raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
64
what is autoimmune hepatitis?
Autoimmune hepatitis is condition of unknown aetiology which is most commonly seen in young females. Recognised associations include other autoimmune disorders, hypergammaglobulinaemia and HLA B8, DR3.
Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present
65
what are the three types of autoimmune hepatitis?
type 1 -Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA). Affects both adults and children.
type 2-Anti-liver/kidney microsomal type 1 antibodies (LKM1). Affects children only.
type 3- Soluble liver-kidney antigen. Affects adults in middle-age
66
what is the presentation of autoimmune hepatitis?
may present with signs of chronic liver disease
acute hepatitis: fever, jaundice etc (only 25% present in this way)
amenorrhoea (common)
67
what is the management of autoimmune hepatitis?
steroids, other immunosuppressants e.g. azathioprine
liver transplantation
68
where is ALT made?
INSIDE the hepatocytes
69
what causes ALT to be raised?
damage to the hepatocytes, causing them to break down and release ALT into the bloodstream.
70
what does raised ALT usually indicate?
Raised levels usually suggest acute liver injury or inflammation, such as in hepatitis (viral, alcoholic, or non-alcoholic fatty liver disease).
Markedly elevated ALT is a hallmark of liver cell injury.
71
where is AST generated?
inside the hepatocytes, and also in other tissues such as the heart, muscles and kidney.
72
what causes AST to be high?
What it indicates: Like ALT, AST is released when cells are damaged, but AST is not as liver-specific.
Raised AST can indicate liver injury, but because it's also present in the heart and muscles, high levels can also point to myocardial infarction (heart attack) or muscle damage.
73
where does ALP come from?
Source: Mainly from bile ducts, but also from the liver, bones, kidneys, and placenta.
74
what causes ALP to be raised?
What it indicates: ALP is raised when there is obstruction in the bile flow, such as with cholestasis or biliary obstruction.
75
what conditions can raise ALP?
Elevated ALP suggests obstructive liver disease (e.g., gallstones, bile duct obstruction, primary biliary cirrhosis), or it may indicate bone disease.
76
where does GGT come from?
hepatocytes and bile ducts
77
what causes GGT to be raised?
GGT is often raised in cases of cholestasis and can be a marker of alcohol abuse.
78
what causes GGT to be raised?
Raised GGT usually suggests liver disease (especially related to bile ducts) or alcohol-related liver injury.
It is sensitive to alcohol use, and often elevated in chronic alcoholics, even before other liver enzymes become elevated.
79
where does bilirubin come from?
Produced by the liver as a byproduct of red blood cell breakdown (from heme). Bilirubin is excreted into bile, but when liver function is impaired, bilirubin may accumulate in the bloodstream.
80
what causes bilirubin to be raised?
Raised bilirubin indicates impaired liver processing or obstruction of bile flow.
Pre-hepatic causes (hemolysis), hepatic causes (liver dysfunction like cirrhosis or hepatitis), or post-hepatic causes (obstruction like gallstones or tumors) can all lead to jaundice and raised bilirubin.
81
where does albumin come from?
Source: Synthesized by the hepatocytes.
What it indicates: Albumin is the main protein in blood and helps maintain oncotic pressure. Low levels of albumin suggest chronic liver disease, as the liver may not be able to produce it adequately.
82
what causes decreased albumin?
Decreased albumin is seen in cirrhosis or liver failure, where the liver’s synthetic function is impaired. Albumin has a 20 day half life - so will only be seen to be low in chronic disease.
83
where is PT/clotting factors produced?
Source: Hepatocytes synthesize clotting factors (like prothrombin, fibrinogen, etc.).
What it indicates: PT/INR measures the blood’s ability to clot. A prolonged PT/INR suggests impaired liver function, because the liver is not producing clotting factors properly. PT is low in acute and chronic disease.
84
what mechanisms cause autoimmune hepatitis to present with amenorrhoea?
Disrupted estrogen metabolism due to impaired liver function - oestrogen and progesterone are metabolised in the liver.
Systemic inflammation affecting the hypothalamic-pituitary-ovarian axis.
Possible effects from medications used to treat AIH.
85
what is the unit limit of alcohol per week?
men and women should drink no more than 14 units of alcohol per week
86
what are some examples of one unit of alcohol?
Examples of one unit of alcohol:
25ml single measure of spirits (ABV 40%)
a third of a pint of beer (ABV 5 to 6%)
half a 175ml 'standard' glass of red wine (ABV 12%)
87
how do you calculate the number of units per drink?
To calculate the number of units in a drink multiply the number of millilitres by the ABV and divide by 1,000. For example:
half a 175ml 'standard' glass of red wine = 87.5 * 12 / 1000 = 1.05 units
one bottle of wine = 750 * 12 / 1000 = 9 units
one pint of 5% beer or lager = 568 * 5 / 1000 = 2.8 units
88
what is primary biliary cholangitis?
The aetiology is not fully understood although it is thought to be an autoimmune condition. Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman
89
who is the classical PBC patient?
middle aged
itch + lethargy
woman
90
what is the M rule for primary biliary cholangitis?
Primary biliary cholangitis - the M rule
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females
91
what are the clinical features pf primary biliary cholangitis?
early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
around 10% of patients have right upper quadrant pain
xanthelasmas, xanthomata
also: clubbing, hepatosplenomegaly
late: may progress to liver failure
92
what investigations are carried out for primary biliary cholangitis?
anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients and are highly specific
smooth muscle antibodies in 30% of patients
raised serum IgM
imaging
required before diagnosis to exclude an extrahepatic biliary obstruction (typically a right upper quadrant ultrasound or magnetic resonance cholangiopancreatography (MRCP)
93
what is the management of primary biliary cholangitis?
first-line: ursodeoxycholic acid
slows disease progression and improves symptoms
pruritus: cholestyramine
fat-soluble vitamin supplementation
liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
recurrence in graft can occur but is not usually a problem
94
what are some complications of primary biliary cholangitis?
Complications
cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)
95
what is c.diff infection?
Clostridioides difficile is a Gram positive rod often encountered in hospital practice. It produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis. C. difficile develops when the normal gut flora are suppressed by broad-spectrum antibiotics.
96
what are the risk factors for c.diff infection?
antibiotic use (clindamycin)
PPI
97
what is the pathophysiology of c.diff infection?
anaerobic gram-positive, spore-forming, toxin-producing bacillus
transmission: via the faecal-oral route by ingestion of spores
releases two exotoxins (toxin A and toxin B) that act on intestinal epithelial cells and inflammatory cells resulting in colitis
98
what are the symptoms of c.diff?
diarrhoea
abdominal pain
a raised white blood cell count (WCC) is characteristic
if severe toxic megacolon may develop
99
what is the management of first infection with c.diff? (1st line, 2nd line and 3rd line)
first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy: oral vancomycin +/- IV metronidazole
100
what is the management of recurrent c.diff infection?
within 12 weeks of symptom resolution: oral fidaxomicin
after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin
faecal microbiota transplant
may be considered for patients who've had 2 or more previous episodes
101
what is H.pylori infection?
Helicobacter pylori is a Gram-negative bacteria associated with a variety of gastrointestinal problems, principally peptic ulcer disease.
102
what is the pathophysiology of H.pylori infection?
Helicobacter pylori releases bacterial cytotoxins (e.g. CagA toxin) → disruption of gastric mucosa
103
How is h.pylori infection spread?
oral - oral route
or oral -faecal route
person-person
poor hygeine
contaminated foods
104
what does Hpylori increase the risk of?
significantly increases risk of peptic and gastric ulcer disease (95%)
gastric cancer
B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
atrophic gastritis
105
what is the eradication therapy for Hpylori?
7 day course of amoxicillin + clarithromycin/metronidazole + high dose PPI
if pen allergic - Management
if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
106
what is IBS?
IBS (Irritable Bowel Syndrome) is a common, chronic digestive disorder characterized by abdominal pain, bloating, and changes in bowel habits (diarrhoea, constipation, or alternating between both). The exact cause is unclear but is thought to involve the gut-brain axis, stress, and digestive sensitivity. It’s not linked to serious diseases like cancer but can significantly affect quality of life.
107
what are the symptoms of IBS?
Abdominal pain: Crampy or sharp, often relieved by bowel movement.
Changes in bowel movements:
Diarrhoea (IBS-D): Frequent loose stools.
Constipation (IBS-C): Hard, infrequent stools.
Mixed (IBS-M): Alternating between diarrhoea and constipation.
Bloating and gas: Abdominal fullness, increased flatulence.
Mucus in stools: White or clear mucus may be present.
Urgency and incomplete evacuation: Sudden urge, feeling of not fully emptying bowels.
Other symptoms: Nausea, fatigue, backache, and mood disturbances (anxiety, stress, or depression).
108
how is IBS diangosed?
Diagnosis of exclusion
109
what is the lifestyle interventions of IBS?
Diet: Encourage regular meals with a balanced diet, adjust fibre intake depending on symptoms.
Hydration: Recommend adequate fluid intake.
Probiotics: Suggest a 12-week trial if the person wants to try over-the-counter probiotics.
Physical Activity: Promote regular exercise (30 minutes at least 5 days/week).
Mental Wellbeing: Address stress, anxiety, and depression (refer to mental health services if necessary).
Dietary Adjustments Based on Symptoms:
Diarrhoea/Bloating: Reduce insoluble fibre (e.g., whole grains, high-fiber cereals) and foods that may trigger symptoms (e.g., caffeine, alcohol, carbonated drinks).
Constipation: Recommend soluble fibre supplements (e.g., ispaghula) or foods like oats, linseed, and gradually increase fibre intake.
110
what medical interventions can be used for IBS?
Constipation: Prescribe a bulk-forming laxative, review after 3 months.
Diarrhoea: Prescribe loperamide for symptom control, review after 3 months.
Abdominal pain/spasms: Consider antispasmodics (mebeverine, alverine, peppermint oil). If ineffective, consider low-dose TCAs (e.g., amitriptyline) or SSRIs (e.g., citalopram), reviewing efficacy every 4–6 weeks.
111
what are the different tests for h.pylori?
Stool antigen test
sensitivity 90%, specificity 95% - most commonly used
Urea breath test
CLO test
serum antibody
culture of gastric biopsy
112
how is a urea breath test performed?
patients consume a drink containing carbon isotope 13 (13C) enriched urea
urea is broken down by H. pylori urease
after 30 mins patient exhale into a glass tube
mass spectrometry analysis calculates the amount of 13C CO2
should not be performed within 4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)
sensitivity 95-98%, specificity 97-98%
may be used to check for H. pylori eradication
113
what is the main function of the liver?
metabolism - maintains blood glucose levels by storing glycogen or breaking it down
synthesises proteins (albumin) and clotting factors
Fats - produces bile to emulsify fats + aid digestion
Detoxification - removes toxins, drugs and alcohol - cytochrome p450 system
Immune function - contains kupffer cells that filter pathogens and debris from the blood
hormone regulation - regulates hormones such as insulin, glucagon and sex hormones
114
what is the main function of bile?1
emulsification of fats - bile contains bile salts which break down large fat globules into smaller micelles + aids absorption of fatty acids.
excretion of waste products - elimination of bilirubin (byproduct of RBC breakdown) via the intestines for secretion
eliminates cholesterol
neutralises stomach acid as it enters the small intestine, providing optimum pH for intestinal enzymes
115
what is bile acid malabsorption?
Bile acid malabsorption (BAM) is a condition where bile acids, which are normally reabsorbed in the ileum (the last part of the small intestine), are not efficiently absorbed. This leads to an excess of bile acids entering the colon, causing diarrhea and other gastrointestinal symptoms.
116
what are the two different types of bile acid malabsorption?
primary - cause is unknown
secondary - i.e. ileal disease or resection, cholecystectomy, SIBO, radiation enteritis, other diseases - chronic pancreatitis or coeliac
117
symptoms of bile acid malabsorption?
chronic diarrhoea
cramping pain
frequent flatulence
diarrhoea can be grey/pale in colour and greasy
118
investigations for bile acid malabsorption?
refer to gastro
the test of choice is SeHCAT
nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT
119
what is the management of bile acid malabsorption?
usually bile acid sequestrants - colestyramine and colestipol - have a high affinity for bile acidws so will come and mop them up in the small intestine
120
disadvantage of colestyramine and colestipol?
unpleasant taste - leads to poor adherence
can cause constipation, nausea, flatulence, abdo pain
121
what causes gallstone formation?
gallstones are solid deposits that form within the gallbladder or biliary tree - they are usually formed due to an imbalance in bile composition leading to the precipitation of its components. This usually results from too much cholesterol in the formation of the bile acids or impaired gallbladder motility.
122
what are some risk factors for gallstones?
Crohns disease, diabetes mellitus, obesity, prolonged fasting or weight loss
diet high in triglycerdies/refined carbohydrates
female sex
increasing age
medications
NAFLD
HRT
123
what are the symptoms of gallstones?
typically RUQ pain
colicky in nature
worse after fatty meal
can be acute
124
what are the most common complications of gallstones?
acute cholecystitis - most common, other two are rarer
cholangitis
pancreatitis
125
which investigations should be organised in primary care for gallstones
abdo USS
LFT's
126
what is the management of asymptomatic gallstones?
no treatment needed usually
refer for bile duct clearance if stones are visible in the CBD
127
what is the management of symptomatic gallstones?
referral to upper GI team for consideration of laparoscopic cholecystectomy
128
what pain management should be advised for patients with symptomatic gallstones?
para/nsaids
diclofenac / opiods if severe
129
what are the symptoms of acute cholecystitis?
RUQ pain
fever
nausea and vomiting
murphys sign on examination
130
what is acute cholecystits?
inflammation of the gallbladder - typically due to obstruction of the cystic duct with gallstones, leading to increased intraluminal pressure and bacterial overgrowth. Can happen without obstruction.
131
what are some complications of acute cholecystitis if not treated?
perforation
abscess
132
which investigations should be done for acute cholecystitis?
Ultrasound: First-line imaging; may show gallstones, thickened gallbladder wall, and pericholecystic fluid.
CT scan: Useful if complications are suspected.
Liver function tests: May show elevated bilirubin or transaminases in cases of common bile duct involvement.
133
management of acute cholecystitis?
Needs admission -
Initial management includes fasting, IV fluids, and analgesia.
Antibiotics targeting Gram-negative and anaerobic bacteria (e.g., piperacillin-tazobactam).
Surgical intervention (cholecystectomy) is usually performed within 24-48 hours of diagnosis.
134
how does a gallbladder abscess present?
prodromal illness - malaise, nausea, vomiting prior to the onset of more severe pain
RUQ pain
swinging pyrexia
systemically unwell
generalised peritonism not present
135
what is cholangitis?
inflammation and infection of the bile DUCTS, often caused by obstruction leading to infection
136
how do cholangitis and acute cholecystitis differ?
Cholangitis: Inflammation of THE BILE DUCTS, often caused by obstruction (e.g., gallstones, strictures, or tumors) that leads to infection.
Cholecystitis: Inflammation of THE GALLBLADDER, typically caused by obstruction of the cystic duct by gallstones.
137
What are the signs of cholangitis?
Charcot's triad: fever, right upper quadrant pain, and jaundice. In severe cases, it may progress to Reynolds' pentad, which includes hypotension and altered mental status.
138
what causes jaundice during cholangitis?
bilirubin (yellow pigment from break down of RBC) - usually excreted into the bile and eliminated through the stool, due to cholestasis there is a back up of the bilirubin leading to hyperbilirubinaemia
139
what is the management of suspected cholangitis?
urgent admission
IV abx
urgent biliary decompression via ERCP
140
what is gallstone ileus?
rare complication of cholelithiasis, occurring when a gallstone passes into the small intestine causing obstruction - this typically happens after a stone erodes through the gallbladder wall into the adjacent duodenum.
141
symptoms of gallstone ileus?
Patients typically present with signs of bowel obstruction: abdominal pain, distension, vomiting, and constipation. There may be a history of biliary colic or acute cholecystitis preceding the ileus.
142
management of gallstone ileus?
needs admission to hospital
surgical intervention usually required
143
what is acalculus cholecystits?
inflammation of gallbladder that occurs without presence of gallstones - often due to biliary stasis, ischaemia and infection. Tends to happen in those who are critically unwell or have multiple comorbidities.
144
what are risks of ERCP?
bleeding
duodenal perforation
cholangitis
pancreatitis
145
what is cholangiocarcinoma?
malignancy that arises from the epithelial cells of the bile ducts. Two main types - intrahepatic and extrahepatic.
146
what is the prognosis of cholangiocarcinoma?
prognosis is poor - 5 yr survival rate below 20% due to late presentation
147
what are some risk factors of cholangiocarcinoma?
PSC
chronic liver disease
cirrhosis
congenital biliary abnormalities
exposure to certain chemicals
148
symptoms of cholangiocarcinoma?
jaundice
pruritis
abdo pain
weight loss
dark urine and pale stools
149
what investigations should be organised for suspected cholangiocarcinoma?
should be referred via 2ww - jaundice over the age of 40 yrs
investigations:
ultrasound - detects tumour mass, dilated ducts
ERCP - shows abrupt or irregular obstruction to contrast, usually at hilum; brush cytology may be taken for histology
percutaneous transhepatic cholangiogram (PTC) - defines extent of tumour
CT / MRI - shows site of main bulk of tumour
angiography and venography - defines nature and extent of vascular involvement
150
what is primary biliary cholangitis?
autoimmune condition associated with inflammation of the bile ducts, caused bu anti-mitochondrial antibodies (which are present in 98% of the patients)
151
who does primary biliary cholangitis most typically effect?
women - ratio of 9:1
152
what are the features of primary biliary cholangitis?
can be asymptomatic if early
cholestatic jaundice
fatigue
pruritis
RUQ pain
xanthelasma, xanthoma
clubbing
hepatosplenomegaly
153
management of primary biliary cholangitis?
first-line: ursodeoxycholic acid
slows disease progression and improves symptoms
pruritus: cholestyramine
fat-soluble vitamin supplementation
liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
recurrence in graft can occur but is not usually a problem
154
complications of primary biliary cholangitis?
cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)
155
what is primary sclerosing cholangitis?
unknown aetiology - characterised by inflammation and FIBROSIS/scarring of the intra and extra-hepatic bile ducts.
156
what is primary sclerosing cholangitis associated with?
UC
HIV
crohns - but the least of the three
157
symptoms of primary sclerosing cholangitis?
jaundice
pruritis
RUQ pain
fatigue
158
what are the investigations for primary sclerosing cholangitis?
Diagnosis is typically made via MRCP or ERCP, which reveal bile duct strictures and beading. Liver function tests often show elevated alkaline phosphatase levels. A liver biopsy may show ductopenia and fibrosis.
159
what is the management of primary sclerosing cholangitis?
There is no effective medical treatment; management focuses on symptomatic relief. Ursodeoxycholic acid may improve liver biochemistry but does not alter disease progression. Endoscopic interventions can relieve biliary obstruction.
160
how common is NAFLD?
25%
161
what are the stages of NAFLD?
Non-alcoholic fatty liver
Non-alcoholic steatohepatitis
Fibrosis
Cirrhosis
162
risk factors for NAFLD?
middle age, older
obesity
poor diet
low activity level
t2DM
hypercholesterolaemia
HTN
smoking
163
what invesitgations may indicate NAFLD?
derranged LFT, usully raised ALT
USS - hepatic steatosis
enhanced liver fibrosis
164
what is the enhanced fibrosis test?
blood test - assesses likelihood of advanced fibrosis
measures three markers within the blood
10.51 or above indicates advanced fibrosis
if below this, should be re-checked every 3 years
165
what score should be calculated for NAFLD?
NAFLD Fibrosis score - takes into account age, BMI, liver enzymes (ALT/AST), platelets, albumin and diabetes
OR
Fib-4 score -
Age
liver enzymes
platelet count
166
what are the symptoms of NAFLD?
can be asymptomatic usually
can have fatigue, nausea, abdominal discomfort
167
what are the next steps if NAFLD is suspected?
Blood tests should be arranged to exclude alternative causes of liver disease and possible metabolic complications.
The risk of advanced liver fibrosis should be assessed using a non-invasive scoring system, such as the NAFLD Fibrosis Score (NFS), Fibrosis (FIB)-4 score or the Enhanced Liver Fibrosis (ELF) test.
The risk of cardiovascular disease should be assessed using a validated tool.
168
what score on the NAFLD score indicates advanced liver cirrhosis?
intermediate or high score - greater than -1.455
169
what score on the fibrosis 4 score indicated advanced liver fibrosis?
score of greater than > 2.67
170
what should be done if there is a fibrosis 4 score of 2.75?
any score > 2,67 refer to hepatology for specialist assessment
171
what score on the ELF test suggests advanced liver fibrosis?
10.51
172
what is usually organised for patients with NAFLD who have possible advanced liver fibrosis based on the fibrosis 4 scoring?
refer to hepatology
usually they organise a fibroscan
173
what lifestyle advice should be given for patients with NAFLD in primary care?
A recommended target of 5-10% weight loss over 6 months may be helpful with a target calorie deficit of 600kcal/day.
EASL recommends a Mediterranean diet which can reduce liver fat even without weight loss.
EASL promotes water rather than sugar sweetened beverages.
Aim for moderate intensity exercise training for 150-200 minutes per week in 3-5 sessions. Aerobic exercise plus diet is the most effective method of managing NAFLD.
Reduce ETOH intake
Manage all comorbidities - particularly HTN/T2DM etc
174
when should I refer a patient with NAFLD to secondary care?
high risk of advanced fibrosis
signs of advanced liver disease on examination
uncertainty about the diagnosis
175
how should a patient with NAFLD be followed up in general practice?
yearly blood test
yearly assessment for cardiovascular risk
three year risk of advanced liver fibrosis
176
what is alpha-1 anti trypsin disease?
Common inherited conditio - lack of protease inhibitor usually produced by the liver.
Alpha-1 antitrypsin (AAT) is a serine protease inhibitor primarily produced in the liver, playing a crucial role in protecting tissues from enzymes of inflammatory cells, particularly neutrophil elastase. Deficiency in AAT can lead to various clinical manifestations, predominantly affecting the lungs and liver. Insufficient AAT allows unchecked activity of neutrophil elastase, leading to lung tissue damage and liver damage.
177
where is alpha 1 antitrypsin gene located?
chromosome 14
178
hwo is A1AT deficiency inherited?
autosomal recessice / co-dominant fashion
179
what are the manifestations of A1AT?
emphysema in young patients
liver cirrhosis and hepatocarcinoma in young patients
cholestasis in children
180
how is A1AT diagnosed?
blood test - A1AT concentration in blood
181
management of A1AT?
IV A1AT protein concetrates can be given
lung transplant
no smoking
supportive
182
what is wilsons disease?
autosomal recessive disorder characterised by excessive copper deposition in the tissues.
183
what gene is affected in wilsons disease?
ATP7B gene - chromosome 13
184
what is the pathophysiology of wilsons disease?
Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion. Wilson's disease is caused by a defect in the ATP7B gene located on chromosome 13.
185
when do the symptoms of wilsons disease typically start?
ages 10-25 years
186
what are the features of wilsons disease?
liver: hepatitis, cirrhosis
neurological:
basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism
Kayser-Fleischer rings
green-brown rings in the periphery of the iris
due to copper accumulation in Descemet membrane
present in around 50% of patients with isolated hepatic Wilson's disease and 90% who have neurological involvement
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
187
investigations for wilsons disease?
reduced serum caeruloplasmin
reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
free (non-ceruloplasmin-bound) serum copper is increased
increased 24hr urinary copper excretion
the diagnosis is confirmed by genetic analysis of the ATP7B gene
188
management of wilsons disease?
penicillamine (chelates copper) has been the traditional first-line treatment
trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
189
what are the symptoms of hep A?
flu like prodrome
icertic phase -
jaundice then develops - usually lasts 1-3 weeks
itching
abdo pain - typically RUQ
tender hepatomegaly
derranged LFTs
fever not usually typically during this phase
convalescent period - symptoms resolve
190
what is the incubation period for hep A?
2-4 weeks
191
how is hep A transmitted?
faecal-oral route - poor hygeine, contaminated foods, sexual intercourse, injecting drug use also
virus is thought to be excreted into the bile and shed into the stools
192
does hep A lead to chronic hepatitis?
no - it is acute only then cleared
193
management of hep A?
supportive only - no specific treatment
adequate rest and nutrition
advice given to families to limit spread - i..e hand washing, disposal of sanitary waste, avoid unprotected intercourse
notify local authority - it is a notifiable disease
194
when should a patient with hep A be admitted to hospital?
severe attack with vomiting
dehydration
signs of hepatic decompensation
195
how long should a patient with hep A stay away from work?
The infected person (source) should stay away from work, school or nursery until 7 days after the onset of jaundice (if there is no history of jaundice then 7 days after symptom onset)
196
what are some possible complications of hepatitis A?
prolonged jaundice/relapses
cholestatic hepatitis
acute liver failure
in pregnancy - increased risk of miscarriage and prematurity
197
is there a vaccination for hep A?
yes - not routinely offered in the uk, only recommended if travelling to a high risk area or are at high risk of complications , can be offered to anyone over 1 years
monovalent vaccine - 2 dose, 6-12 months apart
also can be offered as part of occupational health assessment ie. healthcare workers
people who inject drugs
people with chronic liver disease
men who have sex with men
sewage workers
workers with primates
people recieving plasma derived clotting factors to treat haemophilia
198
what virus causes hep A?
RNA picornavirus
199
what virus causes hep B?
double stranded DNA hepadnavirus
200
how is hep B spread?
exposure to infected blood or bodily fluids
vertical transmission from mother to child
most infections in the uk are due to needle injury/drug use or sexual transmission
201
what is the incubation period for hep B?
6-20 weeks
202
how can hep B present?
fever
jaundice
derranged LFT's
can be acute and chronic
203
how many people have symptoms during the acute phase of hep B?
1/3 of adults
90% children have no symptoms
204
how long do symptoms last in acute phase of hep B?
1-6 weeks
205
how many people go on to have chronic hep B?
90% of children will go on to have chronic
25% of adults will go on to have chornic hep B
206
what are the complications associated wtih chronic hep B?
high risk of cirrhosis and hepatocellular carcinoma
polyartertitis nodosa
cryoglobulinaemia
207
who is vaccinated against hep B?
all children born in the UK - vaccinated at 2,3 and 4 months
high risk individuals - helathworkers, IV drug users, sex workers, close family contacts of hep B positive, prisoners, CKD + those who recieve RRT or blood transfusions
208
what is the management of hep B?
in acute phase - supportive
refer to hepatology team if stable
can use pegylated interferon alpha - this is only treatment available and reduces viral replication in up to 30% of chronic carriers
209
what type of virus is hep C?
single stranded RNA virus
210
how is hepatitis C transmitted?
through blood to blood contact - i.e. needlestick injury + blood transfusions received prior to 1990's
211
what is the pathogenesis of hep C?
after entering the bloodstream, HCV infects hepatocytes, leading to chronic inflammation and potential progression to cirrhosis or hepatocellular carcinoma over decades.
212
is hep C chronic or acute?
both -
acute infection can occur immediately following incubation to within 6 months of acquiring infection
chronic follows acute infection in about 55-85% of people
213
how many people go on to have chronic hep C?
55-85%
214
who should be tested for hep c?
those who have risk fctors for hep C
clinical features of hep C
abnromal liver function tests
215
what are the risk factors for hep C infection?
high risk activities - drug users
healthcare workers with needlestick injury
those who recieved blood transfusion before 1990's
216
is breastfeeding contraindicated in women with hep C?
no - only contraindicated in HIV
217
symptoms of possible hep C?
fatigue
arthalgia
transient rise if LFT's
jaundice
218
what investigations are done to confirm hep C?
HCV RNA - to diagnose acute infection
219
what are some of the complications of chronic hep C infection?
rheumatological problems: arthalgia, arthritis
Sjogrens syndrome
cirrhosis - 5-20%
Hepatocellular cancer
glomerulonephritis
220
what is the management of chronic hep C?
refer urgently for specialist care
treatment usually depends on genotype
currently combination therapies of protease inhibitors are used
221
what lifestyle advice is given in general practice to patients with hep C?
Ensuring the person is attending specialist appointments.
Offering sources of information and support.
Advising on measures to reduce the risk of disease progression, such as reducing alcohol consumption and stopping smoking.
Advising on measures to prevent the spread of the infection, such as not sharing razors, toothbrushes, toiletries, or other items that may be contaminated with blood.
Advising on the risk of sexual transmission, which is greater in people with multiple partners, in people co-infected with HIV, and with risky sexual practices (for example anal sex).
Encouraging the person to inform injecting or sexual contacts, so that they can be tested for hepatitis C.
Monitoring for adverse effects of specialist drug treatment (for example hypoglycaemia).
222
who does hep D infect?
only people with co-current hep C infection
Hepatitis D virus (HDV) is a defective virus that cannot propagate without the presence of hepatitis B virus (HBV) surface antigen
causes most severe form of hepatitis and highest risk for cirrhosis/hepatocellular CA
223
what type of virus is hep E?
RNA hepevrius
224
how is hep E spread?
faceal-oral route
225
what is the incubation period of hep E?
3-8 weeks
226
where is hep E most common?
central and south east Asia
north and west africa
mexico
227
what symptoms does hep E cause?
similar disease to hep A - prodromal flu like symptoms, then jaundice + RUQ pain
228
does hep E increase risk of cirrhosis and hepatocellular carcinoma?
no
229
what are some examples of liver viruses?
hepatoviruses - hep A-E
leptospirosis
hydatid disease
CMV
adenovirus
230
what is leptospirosis?
infection caused by the spirochaete Leptospira interrogans
231
how is leptospirosis spread?
classically spread by infected rat urine
232
who is at risk of leptospirosis?
sewage workers
farmers
vets
people workin gin abattoir
233
what are the phases of leptospirosis?
early phase - lasts 1 week - flu like symptoms, fever
latent phase - weils disease
AKI
hepatitis - jaundice, hepatomegaly
meningitis
234
investigations for leptospirosis?
serology - leptospira antibodies - develop after 7 days
PCR
culture
235
management of leptospirosis?
mild-moderate - doxycycline + axithromycin
severe disease - IV benpen
236
what can cause liver cysts?
hydatid disease - infection with tapeworm parastie
237
where are hydatid cysts common?
mediterranean and middle eastern countries
238
where do most cysts occur in hydatid disease?
90% of cysts occur in the liver and the lungs
239
how do hydatid cysts present
abdo pain
cough and chest pain
jaundice
240
how are hydatid cysts diagnosed?
ultrasound- first line to identify cysts
CT
241
wht is the management of hydatid cysts?
if symptomatic or complex - surgical intervention
medial tx - albendazole or mebendazole
242
what is autoimmune hepatitis?
condition of unknown aetiology - autoimmune destruction of the liver
243
who is usually most affected by autoimmune hepatitis?
young women
244
how many different types of autoimmune hepatitis are there?
type 1 - ANA / SMA antibodies
type 2 - LKM1 antobodies
type 3
245
signs of autoimmune hepatitis?
signs of chronic liver disease - jaundice, acscites, pain, n+v
25% of patients present acutely with short history of fever, jaundice, RUQ pain
246
test for autoimmune hepatitis
usually part of liver screen - testing for ANA antibodies
definitive diagnosis is liver biopsy
247
management of autoimmune hepatitis?
steroids + immunosupressants
liver transplant
248
what are the most common causes of liver cirrhosis?
alcohol induced
viral hep B and C
fatty liver disease - related to diabetes and obesity
249
what are the symptoms of liver cirrhosis?
jaundice
ascites
variceal haemorrhage
hepatic encephalopthay
250
how is liver cirrhosis diagnosed?
fibroscan - measures transient elastography
251
who should be offered regular fibroscan for screening of cirrhosis?
people with hep C
menn who drink over 50 units a week , women who drink over 35 units a week
anyone with alcohol related liver disease
252
what should patients with cirrhosis be offered for screening for hepatoceullar carcinoma?
fibroscan every 6 months as high risk
regular upper endoscopy to check for varicies
253
what are the two scoring systems for liver cirrhosis severity?
child-pugh classification
MELD score (Moderate to end stage liver disease score)
254
what does the child pugh score take into consideration?
bilirubin
albumin
PT
encephalopathy
ascites
255
what are varices?
Oesophageal varices are dilated veins in the submucosa of the lower oesophagus, resulting from portal hypertension, commonly due to liver cirrhosis. They pose a significant risk of bleeding, termed variceal haemorrhage, which can be life-threatening.
256
what medication can be given to prevent oesophageal ruputre?
propranolol
257
what are some of the complications of liver cirrhosis?
malnutrition
frailty
osteoporosis
infection/sepsis
ascites
jaundice
hepatic encephalopathy
variceal bleeding
AKI
hepatorenal syndrome
HCC
258
what are the risk factors for hepatocellular carcinoma?
hep B - most common cause worldwide
hep c - most common cause in Europe
alcohol
haemochromatosis
primary biliary cirrhosis
alpha 1 antitypsin deficiency
NAFLD
drugs: COCP, anabolic steroids
259
what are the symptoms of possible hepatocellular carcinoma?
RUQ pain
weight loss
jaundice
malaise
fatigue
pruritis
ascites
hepatomegaly/splenomegaly
260
investigations for hepatocellular carcinoma?
Consider an urgent direct access ultrasound scan (to be performed within 2 weeks) to assess for liver cancer in people with an upper abdominal mass consistent with an enlarged liver.
261
management options for hepatocellular carcinoma?
early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation
sorafenib: a multikinase inhibitor
262
which cancers commonly metastasise to the liver?
Colorectal Cancer: The most common primary malignancy that spreads to the liver, often presenting with multiple lesions.
Lung Cancer: Particularly non-small cell lung cancer (NSCLC), which can lead to solitary or multiple liver metastases.
Breast Cancer: Often metastasises to the liver, especially in advanced stages, and may present as multiple lesions.
Pancreatic Cancer: Known for aggressive behaviour, it frequently spreads to the liver at diagnosis.
Melanoma: This skin cancer has a high propensity for distant metastasis, including the liver.
Gastric Cancer: Can metastasise to the liver, particularly in advanced disease.
Esophageal Cancer: Also associated with hepatic metastases, especially in later stages.
263
causes of acute pancreatitis?
gallstones - most common cause (40-70% of all cases)
alcohol consumption - both most common
GET SMASHED:
Gallstones
Ethanol
Trauma
Scorpion bite
Mumps
Autoimmune
Scorpion venom
Hypertriglycerides/hypothermia/hypercalcaemia
ERCP
Drugs
264
what are the most common drugs to cause acute pancreatitis?
azathioprine
mesalazine
didanosine
bendroflumethiazide
furosemide
steroids
sodium valproate
265
what are the 4 categories of acute pancreatitis?
Mild — characterized by the absence of local or systemic complications or organ failure. It usually has an uneventful recovery and resolves in the first week. This is the most common form of acute pancreatitis.
Moderately severe — characterized by local complications and/or transient organ failure which resolves within 48 hours.
Severe — characterized by persistent single or multiorgan failure for more than 48 hours.
Recurrent acute pancreatitis — describes acute pancreatitis which occurs on more than one occasion, with full recovery between episodes.
266
what are some complications of acute pancreatitis?
necrosis
abscess formation
fisutale
thrombosis
haemorrhage
267
what are the symptoms of acute pancreatitis?
acute sudden onset upper or generalised abdominal pain - often increases over time
nausea and vomiting
classical features - pain is worse when lying down and radiates to the back
268
what findings on examination could suggest acute pancreatitis?
localised epigastric tenderness/ abdominal tenderness
if gaurding/peritonitic - could be a sign of acute tetroperitoneal haemorrhage
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what analgesia should be avoided in acute pancreatitis?
morphine - can induce spasm of the sphincter of Oddi
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management of acute pancreatitis?
refer to hospital as acute surgical emergency
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what advice should be given to patients to prevent further attacks of acute pancreatitis
low fat diet
avoid triggers - alcohol / fatty foods / medications
treat reversible causes ie. gallstones
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what is chronic pancreatitis?
progressive ad irreversiible inflammation and/or fibrosis of the pancreas - often characterised by severe pain and progressive loss of endocrine and exocrine function
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what is the pathophyisiology of loss of endocrine function in chronic pancreatitis?
damage to the iselts of langerhans, characterised by a deficiency of insulin, leading to non-diabetic hyperglycaemia and pancreatogentic diabetes
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what is the pathophysiology of loss of exocrine function in chronic pancreatitis?
pancreatic exocrine function leads to damage to the acinar cells, leading to decreased secretion of digestive enzymes by the pancreas, causing maldigestion and malabsroption
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what are some causes of chronic pancreatitis?
alcohol is the major cause - 70-80%
more rare: haematomachrosis, pancreatic duct obstruction, hyperparathyroidism
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symptoms of chronic pancreatitis?
constant or episodic epigastric pain - radiates to the back, relieved by sitting forwards
vomiting
weight loss
weakness
jaundice
new DM
chronic poor health
steatorrhoea
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management of patient with chronic pancreatitis?
urgent ref if acute is suspected
urgent ref if complication suspected
routine referral to gastroenterology for everyone else
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what is the major cause of pancreatic insufficiency in children?
cystic fibrosis
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what is the management of chronic pancreatitis?
low fat, high protein diet
fat soluble supplements - dietician input
pancreatic enzyme supplmentation - creon
alcohol abstinence
pain control
surgery - pancreatectomy
diabetes management
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what is the most common type of pancreatic cancer
90% of pancreatic cancers are adenocarcinoma's - usually developing from the head of the pancreas.
Vast majority develop from the exocrine function - in the acinar cells, and affect the head of the pancreas.
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what is an adenocarcinoma?
cancer originating from the glandular epithelial cells which are responsible for producing and secreting substances such as mucous / enzymes and hormones
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what are the risk factors for pancreatic cancer?
smoking - accounts for 25-30%
chronic pancreatitis
T2DM
obestiy - increases risk by 19%
genetics
occupation
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where does pancreatic cancer typically spread?
commonly to LN, peritoneum, liver and further to the lungs - this is common at diangosis
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what are the signs and symptoms of pancreatic cancer?
painless jaundice
weight loss
can also sometimes have pain - radiating to back, can be relieved by sitting forwards
nausea
vomiting
general malaise/fatigue
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what is the criteria for 2ww ref for pancreatic cancer
Refer people using a suspected cancer pathway referral (for an appointment within 2 weeks) for pancreatic cancer if they are aged 40 years and over and have jaundice.
Consider an urgent direct access CT scan (to be performed within 2 weeks), or an urgent ultrasound scan if CT is not available, to assess for pancreatic cancer in people aged 60 years and over with weight loss and any of the following:
Diarrhoea.
Back pain.
Abdominal pain.
Nausea.
Vomiting.
Constipation.
New-onset diabetes.
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management of pancreatic cancer?
usually spread at diagnosis
< 15% suitable for surgery
whipples procedure is surgical option - pancreaticodudodenectomy
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what is the prognosis for pancreatic cancer?
2-6 months if spread at diagnosis
6-11 months if advanced local disease
5 year survival rate of 5-25% for those who have had surgical resection
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what palliative treatments are offered for pancreatic cancer?
surgical intervention for bypass of the CBD/dudoodenal obstruction in order to provide symptomatic relief
refer for palliative intervention early
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what are the endocrine tumours of the pancreas?
glucagonoma - islet cell tumour of pancreas
insulinoma - tumour specifically of the cells in the iselt of langerhans that produce insulin
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how does a glucagonoma present?
attacks of hypoglycaemia
skin changes - sores
weight loss
thrombosis
aneamia
diarrhoea
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what is the prognosis of glucagonoma?
poor - 90% have LN and liver mets at presentation
292
what are the differentials for dysphagia?
oesophageal cancer
oesophagitis
oesophageal candidiasis
achalasia
pharyngeal pouch
systemic sclerosis
MG
globus hystericus
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what is achalasia?
primary motility disorder of the oesphagus, characterised by the failure of the lower oesophageal sphincter to relax and impaired peristalsis in the distal oesophagus.
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what is a defining feature of achalasia?
difficulty swallowing both solids and liquids
other symptoms include - progressive dysphagia usually over years, heartburn, regurgitation of undigested food and weight loss due to poor oral intake
295
what is the pathophysiology of achalasia?
degeneration of ganglion cells in the myenteric plexus, leading to loss of inhibitory neurotransmitters - disrupting peristalsis
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how do you diagnose achalasia?
barium swallow - bird beak appearance
CXR
endoscopy
297
management of achalasia?
surgical intervention
or medication such as nitrates/CCB
298
does achalasis increase the risk of oesophageal Ca?
yes
299
what is a pharyngeal pouch?
posteromedial herniation between the thyropharyngeus and cricopharyngeus muscles
more common in older men
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symptoms of pharyngeal pouch?
first swallow is easy as the pouch is empty then is filled, then after that swallowing becomes more difficult, regurgitation of food, palpable swelling 2/3rds of cases
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diagnosis of pharyngeal pouch?
barium swallow
302
management of pharyngeal pouch?
Management options include dietary modifications, endoscopic techniques (e.g., diverticulotomy), or surgical intervention (e.g., excision of the diverticulum) depending on severity and patient factors.
303
what is a benign oeosphageal stricture?
benign narrowing of the oesphageal lumen - secondary to severe oephagitis which can cause fibrosis and narrowing of the lumen
304
how does a benign oesophageal stricture present?
presents as a long history of reflux, followed by more recent dysphagia - may be associated with night time coughing
305
investigations of benign oesophageal stricture?
should be referred for urgent endoscopy or usually via 2ww due to new dysphagia to rule out cancer
306
what is a globus pharyngis?
sensation of lump in throat or discomfort, but no concerning or benign cause- can be caused by reflux, discomfort is usually relieved by eating, and there is no interference with swallowing
307
management of globus pharyngis?
usually reassurance, treat possible underlying reflux
can refer to ENT routinely to exclude organic cause
308
what is the pathophysiology of barretts oesophagus?
metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium
309
risk factors for barretts oesopahgus
gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity
310
management of barretts oesophagus?
high dose PPI
endoscopic surveillance every 3-5 years
if dysplaisa of any grade is identified - endoscopic intervention is offered - radiofrequency ablation is first line
311
management of uncomplicated gord with no red flag symptoms?
trial of PPI for 1 month
if no improvement - test and treat ofr h.pylori
if no improvement - trial of ranitidine / h2 receptor antagonist 1 month
if no improvement - refer for endoscopy
312
what is the most common type of oesophageal cancer?
adenocarcinoma
313
where are adenocarcinomas of the oesophagus most commonly found?
lower third - near the gastrooesophageal junction
314
where are squamous cell carcinomas most commonly found?
upper 2/3
315
risk factors for oesphageal Ca?
GORD
barretts oesophagus
smoking
obestiy
alcohol
achalasia
316
symptoms of oesophageal Ca??
dysphagia
anorexia
weight loss
hoarse voice
cough
317
referral criteria for 2ww ref for oesophageal ca?
Offer urgent direct access upper gastrointestinal endoscopy (to be performed within 2 weeks) to assess for oesophageal cancer in people:
With dysphagia, or
Aged 55 years and over with weight loss and any of the following:
Upper abdominal pain.
Reflux.
Dyspepsia.
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what is the most common type of stomach cancer?
adenocarcinoma
319
what are the symptoms of stomach cancer?
vague symptoms - abdo pain, anorexia, weight loss, reflux, early satiety, vomiting, anaemia, GI bleeding
320
criteria to refer for 2ww for stomach cancer?
upper abdo mass
anyone with dysphagia
> 55 years with weight loss + upper abdo pain/reflux/dyspepsia
321
what are the symptoms of gastric ulcer?
epigastric pain worsened by food, and helped with antacids or lying flat
can be associated with weight loss
322
who does gastric ulcer typically present in?
middle aged/elderly
323
risk factors for gastric ulcer?
h.pylori infection
NSAID use
smoking
324
management of gastric ulcer?
usually has been confirmed on endoscopy
high dose PPI
treat any hpylori
needs repeat endoscopy in 6-8 weeks to ensure healing
can use PPI at lowest possible dose moving forwards if long term management needed
325
who is duodenal ulcer most common in?
younger adults
326
risk factors for duoedenal ulcer?
h.pylori infection - 90%
smoking
stress
nsaid use
327
presentation of duodenal ulcer?
pain relieved by food, worse at night
328
what is peutz-jeghers syndrome?
Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles.
329
management of anal fissue?
lifestyle advice - improve diet, stool softeners
Simple analgesia
lubricants such as petroleum jelly can be used before defecation
topical anaesthetics such as lidocaine 5% ointment for few days
if no improvement after 1 week, consider GTN ointment for 6-8 weeks, twice daily - warn can cause headache, avoid in children and breastfeeding/pregnancy
330
management of haemorrhoids?
lifestyle
laxatives
topical - anusol Anusol HC Plus®/Anusol HC® ointment/suppositories: contains a corticosteroid (hydrocortisone acetate) and astringent(s) - 7 days
If bothersome, frequent flares - can refer for consideration of rubber band ligation/haemorrhoidectomy
331
management of suspected rectal cancer?
Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for anal cancer in people with an unexplained anal mass or unexplained anal ulceration.
331
what is the most common type of rectal cancer?
squamous cell carcinoma
331
risk factors for rectal carcinoma?
HPV infectino
immunosuppression
hx of anal warts
smoking
331
what are the three types of colorectal cancer?
sporadic - 95%
hereditary non-polyposis colorectal carcinoma
familial adenomatous polyposis
332
what is HNPCC?
autosomal dominant condition - leading to gene mutations which increase the risk of colon cancer + other cancers such as endometrial cancer
333
what is the crtieria used to diagnose HNPCC?
amsterdam criteria -
- 3 members of family with colorectal Ca
cases span at least 2 generations
at least one case diagnosed < 50 years
334
what is familial adenomatous polyposis?
autosomal dominant condition that leads to the formation of hundreds of polyps by the age of 30-40 years, due to mutation of APC gene on chromosome 5
335
what screening is offered for colorectal cancer?
FIT test - for anyone 50 - 74 years, offered stool sample test every 2 years, patients over the age of 74 years can request FIT testing
336
what are carcinoid tumours?
neuroendocrine neoplasms that arise from the enterochromaffin cells in the GI tract
337
how do carcinoid tumours behave?
they secrete various bioactive substances, including serotonin , histamine and bradykinin, This leads to carcinoid syndrome and typically occurs when there are hepatic metastasis.
338
what are symptoms of carcinoid syndrome?
flushing
diarrhoea
wheezing
R sided heart valvular lesions - due to fibrosis
339
treatment of carcinoid syndrome?
Surgical resection is the primary treatment for localised tumours. For metastatic disease, somatostatin analogues (e.g., octreotide) are used to manage symptoms and inhibit hormone secretion. Targeted therapies like everolimus may be considered for advanced cases.
340
what are some adverse effects of PPI use?
hyponatraemia
hypomagnasaemia
increases risk of osteoporosis
microsocpic colitis
increased risk of c. diff
341
how does lincaclotide work?
increases fluid in the intestinal lumen - therefore speeds up transit time and makes stool looser
342
which questionnaire is recommended for screening of alcohol misuse?
AUDIT - C
343
which is the single most common LFT derangement in NAFLD?
Relatively greater rise in alanine aminotransferase (ALT) than aspartate aminotransferase (AST)
344
what do LFT's show in NAFLD once this has progressed to cirrhosis?
Once significant fibrosis or cirrhosis develops, the AST/ALT ratio flips (AST > ALT), which is a sign of worsening liver disease.
345
what are the symptoms of vitamin b12 deficiency?
poor balance, fatigue, clumsiness, irritability, angular stomatitis
pallor - anaemia
346
what mass can be found inferior and lateral to the pubic tubercle?
femoral hernia
347
what mass can be found medial and inferior to the pubic tubercle?
inguinal hernia
348
management of femoral hernia?
referral urgently for surgical repair as the risk of strangulation is > 50%
349
which medications can worsen dyspepsia?
NSAIDs
CCB
nitrates - ISM
heophyllines
bisphosphonates
steroids
350
what are the symptoms of opioid induced bowel dysfunction?
dry mouth, gastro-oesophageal reflux, vomiting, bloating, abdominal pain, anorexia, hard stool and delayed digestion.
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