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Gastroenterology Flashcards

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1
Q

if someone has an autoimmune condition, what are they more likely to have?

A

another autoimmune condition e.g.
T1DM and coeliac’s disease, thyroid disease, autoimmune hepatitis

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2
Q

pathophysiology of coeliac disease

A

autoantibodies created in response to gluten that target the epithelial cells of the small intestine, leading to inflammation

particularly of the jejunum, leading to villus atrophy = malabsorption of nutrients & symptoms of disease

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3
Q

investigations for coeliac disease

A

need to be eating gluten for at least 6 weeks

anti-TTG and anti-EMA (endomysial) both IgA
** need to check for IgA deficiency beforehand

endoscopic intestinal biopsy (gold standard - duodenal)
-villous atrophy
-crypt hyperplasia

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4
Q

presentation of coeliac disease

A

failure to thrive in children
diarrhoea
abdominal pain/bloating
weight loss
fatigue
anaemia
mouth ulcers
dermatitis herpetiformis (itchy blistering skin rash typically on the abdomen)

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5
Q

complications of coeliac disease

A

hyposplenism
anaemia: iron, folate, B12 (folate more common than b12)
osteoporosis
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility
non-hodgkin lymphoma
oesophageal cancer

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6
Q

what are all new cases of T1DM tested for

A

coeliac disease

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7
Q

what is haemochromatosis

A

an autosomal recessive condition
iron storage disorder that results in excessive total body iron and deposition in tissues

mutation in HFE gene on chromosome 6

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8
Q

presentation of haemochromatosis

A

early symptoms: fatigue, arthralgia, erectile dysfunction
bronze skin pigmentation
diabetes mellitus
liver: chronic liver disease, hepatomegaly, cirrhosis
cardiac failure
amenorrhoea, infertility, reduced libido

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9
Q

reversible vs irreversible complications of haemochromatosis

A

reversible: cardiomyopathy, skin pigmentation
irreversible: diabetes, cirrhosis, arthropathy, hypogonadotrophic hypogonadism

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10
Q

significance of HBsAg in interpreting hepatitis B serology

A

if positive, ongoing infection
1-6 months = acute
>6 months = chronic

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11
Q

significance of anti-HBs and anti-HBc in interpreting hepatitis B serology

A

anti-HBs = implies immunity (either exposure/vaccination), negative in chronic disease

anti-HBc = negative if immunised
IgM anti-HBc appears during acute/recent HB infection and lasts for around 6 months
IgG persists

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12
Q

symptoms of scurvy

A

follicular hyperkeratosis & perifollicular haemorrhages
easy bruising
poor wound healing
Gingivitis with bleeding and receding gums
Sjogren’s syndrome
generalised symptoms = weakness, malaise, anorexia, depression

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13
Q

what is pseudomembranous colitis

A

inflammation of the colon due to overgrowth of c.diff bacteria
develops when the normal gut flora are suppressed
due to broad spectrum antibiotics

risk factors: PPIs, clindamycin, 2nd and 3rd generation cephalosporins

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14
Q

side effects of PPIs

A

hyponatremia, hypomagnasaemia
increased risk of osteoporosis
microscopic colitis
increased risk of c.diff infections

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15
Q

causes of vitamin b12 deficiency

A

pernicious anaemia
Diphyllobothrium latum infection
Crohn’s disease
atrophic gastritis (Secondary to h.pylori infection)
gastrectomy
malnutrition e.g. alcoholism

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16
Q

Ulcerative colitis - CLOSE UP

A

continuous inflammation
limited to colon & rectum
only superficial mucosa affected
smoking is protective
excrete blood & mucus
use aminosalicylates
primary sclerosing cholangitis

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17
Q

different types of autoimmune hepatitis

A

type 1 = affects women in lates 40s/50s, fatigue & features of liver disease, less acute

type 2 = affects teenagers/early twenties, more acute picture of raised transaminases & jaundice

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18
Q

autoantibodies involved in autoimmune hepatitis

A

type 1 - ANA, SMA

type 2 - Anti-liver/kidney microsomal type 1 antibodies (LKM1)

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19
Q

features of autoimmune hepatitis

A

may present with signs of chronic liver disease
acute hepatitis: fever, jaundice
amenorrhoea
ANA/SMA/LKM1 antibodies, raised IgG levels

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20
Q

management of autoimmune hepatitis

A

steroids e.g. prednisolone, azathioprine
liver transplantation

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21
Q

scoring systems used for liver cirrhosis

A

Child-Pugh classification: albumin, bilirubin, prothrombin time, encephalopathy, ascites

Model for End-Stage Liver Disease (MELD): bilirubin, creatinine, INR

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22
Q

pathophysiology of pernicious anaemia

A

antibodies against intrinsic factor/parietal cells
parietal cells release intrinsic factor, essential for the absorption of vitamin b12 in the ileum

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23
Q

role of vitamin b12

A

production of blood cells & myelination of nerve cells

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24
Q

features of pernicious anaemia

A

anaemia features: fatigue, pallor, dyspnoea
peripheral neuropathy
glossitis
neuropsychiatric: depression, memory loss, confusion, poor concentration, irritability

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25
management of pernicious anaemia
no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections (1mg of intramuscular hydroxycobalamin) more frequent doses are given for patients with neurological features
26
complications of pernicious anaemia
subacute combined degeneration of the spinal cord gastric malignancy
27
symptoms that should suggest IBS
functional bowel disorder, symptoms present for 6 months not common after 60yrs abdominal pain/discomfort: relieved on opening bowels associated with a change in bowel habit and 2 of the following: abnormal stool passage (urgency, incomplete stool evacuation, straining) bloating worse after eating mucus lethargy, nausea, backache and bladder symptoms may also support the diagnosis
28
symptoms that should suggest IBS
abdominal pain/discomfort: relieved on opening bowels associated with a change in bowel habit and 2 of the following: abnormal stool passage bloating worse after eating mucus
29
pathology to rule out with IBS
faecal calprotectin (IBD) coeliac disease malignancy
30
management of IBS
first line: loperamide for diarrhoea laxatives for constipation (avoid lactulose, linaclotide is used 2nd line) Antispasmodics for cramps e.g. hyoscine butylbromide (Buscopan) 2nd line: tricyclic antidepressants (better for diarrhoea) psychological interventions e.g. CBT, psychologically manage condition & reduce distress regular small meals adequate fluid intake avoid caffeine & alcohol low FODMAP diet (FODMAPs are short-chain carbohydrates that are poorly absorbed in the small intestine, they then encourage the intake of water into the small intestine causing diarrhoea or when reaching the large bowel they are prone to fermentation by bacteria causing bloating)
31
what causes flares of UC
stress NSAIDs, antibiotics stopping smoking
32
flare severity criteria for UC
mild: <4 stools a day, with or without blood no systemic upset moderate: 4-6 stools a day, with blood, minimal systemic upset severe: >6 bloody stools, systemic upset (fever, tachycardia, abdominal tenderness)
33
urgent referral for endoscopy criteria
dysphagia upper abdominal mass consistent with stomach cancer >55, weight loss AND: upper abdominal pain dyspepsia reflux
34
non-urgent referral for endoscopy criteria
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
35
pathophysiology of h.pylori
gram negative aerobic bacteria forces its way into gastric mucosa, the break it makes exposes gastric epithelium to acidic environment produces ammonia to neutralise acid, which also directly damages epithelial cells results in gastritis, ulcers, malignancy
35
what is essential before a h.pylori test (urea breath test)
no antibiotics for 4 weeks no PPIs for 2 weeks used as test of eradication after therapy
36
stages of non-alcoholic fatty liver disease
steatosis steatohepatitis Fibrosis Cirrhosis
37
associated features of non-alcoholic fatty liver disease
T2DM obesity hyperlipidaemia low activity levels high cholesterol jejunoileal bypass sudden weight loss/starvation
38
differentials for abnormal liver function tests
USS (non-alcoholic fatty liver disease) Hepatitis B & C serology Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis) caeruloplasmin (Wilson's) Alpha 1 Anti-trypsin levels transferrin & ferritin (haemochromatosis)
39
presentation of NAFLD
asymptomatic hepatomegaly ALT is typically greater than AST increased echogenicity on ultrasound
40
investigation in NAFLD
enhanced liver fibrosis blood test
41
management of NAFLD
Weight loss Exercise Stop smoking Control of diabetes, blood pressure and cholesterol Avoid alcohol
42
what drugs tend to cause cholestasis
COCP antibiotics e.g. flucloxacillin, co-amoxiclav, erythromycin sulfonylureas anabolic steroids, testosterones raised ALP, GGT
43
what should happen to males drinking >50 units a week & females >35 with normal LFTs
should be referred for ELF test or fibroscan, even if liver function tests are normal
44
investigations for haemochromatosis
general population: transferrin saturation family members: HFE mutation **ferritin is an acute phase reactant, transferrin will indicate if ferritin is high due to inflammation/NAFLD or iron overload Liver biopsy with Perl’s stain can be used to establish the iron concentration in the parenchymal cells
45
management of haemochromatosis
venesection - transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l desferrioxamine may be used second-line
46
complications of haemochromatosis
chronic liver disease/carcinoma cardiomyopathy T1DM hypothyroidism Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)
47
features of c.diff infection
diarrhoea abdominal pain raised WCC if severe, toxic megacolon can develop
48
criteria for varying severities of c.diff infection
mild: normal WCC moderate: raised WCC 3-5 loose stools a day severe: raised WCC temp >38.5, evidence of severe colitis (abdominal/radiological signs) life-threatening: hypotension partial/complete ileus toxic megacolon
49
diagnosis of c.diff infection
Clostridium difficile toxin (CDT) in the stool
50
management of c.diff infection
first-line therapy is oral vancomycin for 10 days second-line therapy: oral fidaxomicin third-line therapy: oral vancomycin +/- IV metronidazole recurrent episode: within 12 weeks of symptom resolution: oral fidaxomicin after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin Life-threatening Clostridium difficile infection: oral vancomycin AND IV metronidazole specialist advice - surgery may be considered
51
criteria for same day admission for someone presenting with jaundice
acutely unwell fever encephalopathy (confusion, ataxia) cholangitis dehydrated bilirubin >100 abnormal coagulation abnormal kidney function suspected paracetamol overdose frail/significant co-morbidities
52
differentials for dysphagia
oesophageal cancer oesphagitis oesophageal candidiasis achalasia pharyngeal pouch systemic sclerosis myasthenia gravis globus hystericus
53
what is primary sclerosing cholangitis
biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts
54
associations of primary sclerosing cholangitis
UC crohn's HIV
55
presentation of PSC
cholestasis: jaundice, raised ALP, bilirubin, pruritus RUQ pain fatigue
56
investigation for PSC
ERCP/MRCP - beaded appearance
57
complications of PSC
cholangiocarcinoma increased risk of colorectal cancer
58
what is Peutz Jeghers syndrome
autosomal dominant condition characterised by numerous hamartomatous polyps in the GI tract (mainly small bowel) & pigmentation of lips, face, palms & soles **can present with small bowel obstruction often due to intussusception GI bleeding
59
management of Peutz Jeghers syndrome
conservative unless complications develop
60
what to think with T2DM and abnormal LFTs
non alcoholic fatty liver disease
61
symptoms of oesphageal cancer
dysphagia weight loss anorexia vomiting odynophagia, hoarse voice, cough, melaena
62
features of cyclical vomiting syndrome
severe nausea and vomiting lasting hours to days Prodromal intense sweating and nausea Well in between episodes might have: weight loss reduced appetite abdominal pain diarrhoea photophobia headache
63
what is cyclical vomiting syndrome
rare seen in children more than adults seen in females more than males associated with migraines
64
investigations of cyclical vomiting syndrome
clinical diagnosis pregnancy test to exclude in women routine blood tests to identify any underlying condition
65
management of cyclical vomiting syndrome
avoidance of triggers Prophylactic treatments include amitriptyline, propranolol and topiramate. Ondansetron, prochlorperazine and triptans in acute episodes
66
management of GORD
endoscopically negative: full dose PPI for one month if response = offer low dose treatment no response = offer H2RA e.g. ranitidine endoscopically proven oesphagitis: full dose PPI 1-2 months if response: lower dose no response: double dose PPI for 1 month lifestyle: weight loss smaller, lighter meals avoid heavy meals before bed sit upright after eating stop smoking reduce tea, coffee, caffeine
67
complications of GORD
oesphagitis ulcers anaemia benign strictures Barrett's oesphagus carcinoma
68
what can often be used to test for H.pylori
stool test
69
management of patients with a raised ALT
all patients should be investigated with a raised ALT with a liver screen including USS
70
presentation of UC
bloody diarrhoea urgency tenesmus abdominal pain, particularly in the LLQ
71
investigations for UC
colonoscopy + biopsy ** if severe colitis use flexible sigmoidoscopy to prevent perforation findings: red, raw mucosa that bleeds easily no inflammation beyond submucosa pseudopolyps barium enema: loss of haustrations narrowing of colon if long standing disease
71
investigations for UC
colonoscopy + biopsy ** if severe colitis use flexible sigmoidoscopy to prevent perforation findings: red, raw mucosa that bleeds easily no inflammation beyond submucosa pseudopolyps barium enema: loss of haustrations narrowing of colon if long standing disease
72
what is melanosis coli
disorder of pigmentation of the bowel wall histology shows pigment laden macrophages associated with laxative abuse
72
what is melanosis coli
disorder of pigmentation of the bowel wall histology shows pigment laden macrophages associated with laxative abuse
73
presentation of crohn's
non-specific e.g. fatigue, weight loss diarrhoea abdominal pain perianal disease e.g skin tags, ulcers
74
Is small bowel or large bowel obstruction more common
Small bowel
75
Pathophysiology of bowel obstruction
Obstruction of food, fluids and gas results in a build up proximal to the obstruction, resulting in back pressure which causes vomiting & dilatation of intestines proximal to the obstruction GI tract secretes fluid later absorbed in the colon, when there is an obstruction & fluid can’t be absorbed, fluid loss from intravascular space leads to hypovolaemia and shock = third spacing The higher up the intestine the obstruction, the greater the fluid loss as there is less bowel for fluid to be reabsorbed
76
Causes of bowel obstruction
Adhesions and hernias (small bowel) Malignancy (large bowel) Other causes: intussusception, strictures, diverticular disease, volvulus
77
What causes adhesions
Abdominal or pelvic surgery Peritonitis Endometriosis Abdominal or pelvic infections e.g. PID Can be congenital or secondary to radiotherapy
78
What is closed loop obstruction
Two points of obstruction along the bowel, middle section sandwiched between 2 points of obstruction E.g. adhesions Hernias Volvulus Single point of obstruction with competent ileocaecal valve (does not allow any movement back into ileum)
79
Consequences of a closed loop obstruction
Do not have an open end where they can drain and decompress Will continue to expand, leading to ischaemia and perforation EMERGENCY SURGERY
80
Presentation of bowel obstruction
Vomiting (green bilious vomiting) Abdominal distension Diffuse abdominal pain Constipation and lack of flatulence Tinkling bowel sounds in early bowel obstruction
81
How to tell the difference between small and large bowel on X-ray
Small bowel = valvulae conniventes Mucosal folds extending full width of the bowel Large bowel = haustra Pouches formed by muscles in walls of large bowel, do not extend full width of bowel
82
Investigation for bowel obstruction
Abdominal X-RAY = initial >3cm diameter small bowel >6cm colon >9cm caecum Free intraperitoneal gas might indicate perforation Erect CXR can demonstrate air under the diaphragm if intra-abdominal perforation Contrast abdominal CT scan
83
Initial management of bowel obstruction
ABCDE approach: May be haemodynamically unstable if hypovolaemic shock, bowel ischaemia or perforation, or sepsis Nil by mouth IV fluids to hydrate and correct any electrolyte abnormalities NG tube with free drainage (reduce risk of vomiting and aspiration)
84
Key blood findings in bowel obstruction
U&Es Metabolic alkalosis (vomiting) Bowel ischaemia (raised lactate)
85
Further management of bowel obstruction
Conservative management if patient stable and secondary to adhesions/volvulus If this fails, definitive management anyway is surgery Exploratory surgery Adhesiolysis Hernia repair Emergency resection of tumour Stents may be inserted during colonoscopy
86
When will IV ABx be started during bowel obstruction
Perforation suspected or surgery planned
87
Role of mesentery
Membranous peritoneal tissue that creates a connection between the bowel and posterior abdominal wall Bowel gets its blood supply via the mesentery through the mesenteric arteries
88
What is a volvulus
Condition where the bowel twists around itself and the mesentery it is attached to Leads to a closed bowel obstruction Bowel vessels might be involved, leading to ischaemia, necrosis and bowel perforation
89
What are the 2 types of volvulus
Sigmoid Caecal
90
Associations of sigmoid volvulus
More common (80%), affects older individuals Associated with chronic constipation (becomes overloaded with faeces, sinks downwards and causes a twist) Chagas’ disease Neurological conditions e.g. Parkinson’s, duchenne muscular dystrophy Psychiatric e.g. scizhophrenia
91
Associations of caecal volvulus
All ages Pregnancy Adhesions
92
Presentation of volvulus
Same as bowel obstruction
93
Investigations of volvulus
Abdominal X-ray - coffee bean sign Contrast CT to confirm
94
what type of peptic ulcer are more common
duodenal > gastric
95
pathophysiology of peptic ulcers
stomach mucosa is prone to ulceration from breakdown of the protective layer of the stomach/duodenum or an increase in the production of stomach acid protective layer can be broken down due to: medications (steroids/NSAIDs) or H.pylori increase in production of stomach acid: caffeine, stress, alcohol, smoking, spicy foods
96
presentation of peptic ulcers
epigastric pain nausea and vomiting dyspepsia haematemesis, coffee ground vomit, melaena iron deficiency anaemia *** eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.
97
investigations for peptic ulcers
endoscopy - rapid urease test (CLO) can be performed to check for H.pylori - biopsy should be considered to check for malignancy
98
management for peptic ulcers
high dose PPIs endoscopy can be used for monitoring
99
complications of peptic ulcers
bleeding - most common complication, with the gastroduodenal artery being a source of significant GI bleeding perforation - epigastric pain that becomes generalised due to peritonitis can be diagnosed with an erect CXR indicating air under the diaphragm scarring and strictures of the muscle and mucosa, which can lead to pyloric stenosis

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