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Pathway A > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What are the symptoms of Achalasia?

A

Dysphagia, return of undigested food, aspiration pneumonia, retrospective chest pain unresponsive to PPI’s, minor weight loss

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2
Q

What are the investigations for Achalasia?

A

Endoscopy, oesophageal manometry, the barium swallow

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3
Q

What are the differentials for Achalasia?

A

Oesophageal strictures, oesophageal spasms, GERD and rarely oesophageal malignancy

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4
Q

How is Achalasia treated?

A

Calcium channel blockers (Nifedipine to oesophageal dilation), botox, hellers myotomy to cut the LES and oesophageal dilation via endoscopy to disrupt the LES

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5
Q

What is Achalasia?

A

An inability of the LES to relax

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6
Q

What are the symptoms of acute pancreatitis?

A

Hypovolaemia, epigastric pain radiating to the flank, vomiting, nausea, possible guarding, pain relieved by moving into the fetal position. A fever is indicative of complications.

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7
Q

What are the investigations for acute pancreatitis?

A

You would do FBC’s (leukocytosis with necrotising pancreatitis), U’s and E’s, LFT’s (abnormal with gallstones), amylase & lipase (lipase more specific but amylase more readily available, 3x the normal limit when positive), US for gallstones, MRCP for obstructive pancreatitis, ERCP which can be therapeutic and CT at later stage to check for complications

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8
Q

How would you treat acute pancreatitis?

A

Fluid resuscitation, anti-emetics, strong analgesics (opioids) and catheterisation

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9
Q

What are acute porphyrias?

A

A defect in the synthesis of haem due to altered enzyme structure/function

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10
Q

How do patients with acute porphyrias present?

A

With nausea, confusion, hypertension and abdominal pain

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11
Q

How do you treat an acute porphyria?

A

Largely supportive but can also give haem arginate to increase amount of haem and reduce disease severity

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12
Q

What symptoms do alcohol withdrawal patients experience?

A

Typically nausea, vomiting, shaking, tremors, insomnia, anxiety, palpitations, agitation, hallucinations and in severe cases delirium tremens

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13
Q

How do you treat alcohol withdrawal?

A

Chlordiazepoxide in a reducing regime, 1 to 2 pabrinex capsules a day to prevent Wernicke’s Encephalopathy, benzodiazepenes for first time seizures, oral lorazepam for first time delirium

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14
Q

What two scoring systems determine alcohol withdrawal severity?

A

SADQ >30
AUDIT >20

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15
Q

What is alpha-1-antitrypsin deficiency?

A

A lack of alpha-1-antitrypsin which leaves the alveoli exposed to neutrophil elastase which cause emphysema and COPD in the 40’s particularly in smokers

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16
Q

What are the symptoms/signs of alpha-1-antitrypsin deficiency?

A

COPD in the 40’s, deranged LFT’s without cause, Hx neonatal jaundice

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17
Q

How do you treat alpha-1-antitrypsin deficiency?

A

Smoking cessation, liver transplant in severe cases

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18
Q

What is ascending cholangitis?

A

Acute inflammation of the biliary tree, usually in the 6th decade of life

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19
Q

What is charcot’s triad?

A

Symptoms of acute cholangitis: fever, RUQ pain, jaundice

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20
Q

What is reynold’s pentad

A

Symptoms of sever acute cholangitis, you have charcot’s triad (fever, RUQ pain, jaundice) plus mental confusion and hypotension

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21
Q

How would you treat ascending cholangitis?

A

US for stones, CT for anatomical view of stones (but less effective for radioluscent ones), MRCP and ERCP (which can be therapeutic

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22
Q

What is the treatment for Cholera?

A

Doxycycline or co-trimoxazole

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23
Q

What is the treatment for chronic alcoholism?

A

Chlordiazepoxide in a withdrawing regime, acamprosate and naltrexone to maintain abstinence. Give benzodiazepenes for first time seizures

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24
Q

What is chronic pancreatitis?

A

Inflammation & fibrosis of the pancreatic tissue

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25
Q

What are the symptoms of chronic pancreatitis?

A

steatorrhea, epigastric pain, malabsorption, symptoms of diabetes mellitus

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26
Q

Are serum amylase and lipase typically raised in chronic pancreatitis?

A

No not in chronic pancreatitis

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27
Q

What investigations would you do for chronic pancreatitis?

A

Abdominal x-ray to detect calcifications and CT to show pancreatic calcifications, faecal elastase to show exocrine dysfunction, fasting glucose/ OGTT to show endocrine dysfunction

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28
Q

Management for chronic pancreatitis?

A

Healthy diet and abstinence from alcohol, analgesia, help the endocrine dysfunction with insulin and the exocrine with pancreatic enzyme replacement therapy

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29
Q

What type of bacteria is clostridium difficile?

A

Gram positive, causes a pseudomembranous colitis

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30
Q

What are the symptoms of C diff?

A

watery diarrhoea, dehydration, fever, loss of appetite, weight loss and confusion

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31
Q

How is C diff diagnosed?

A

stool culture or enzyme immunoassay

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32
Q

What tends to cause C diff?

A

Broad spectrum antibiotics like clindamycin, ciprofloxacin, carbapenams, ceftriaxone, penicillins like tazocin, being in a care home for a long time, PPI’s, HIV

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33
Q

How do you manage C diff?

A

Move to side room + barrier nurse. Look for toxic megacolon and colitis, antidiarrhoeal agents and narcotic use minimised. Replace fluid and electrolyte loss, first line is PO vancomycin, then second line fidaxomicin. In recurrent disease you may do a faecal transplant

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34
Q

What are the symptoms of coeliac disease?

A

Weight loss, fatigue and failure to thrive

35
Q

What are the symptoms/signs of coeliac disease?

A

Presence of HLA-DQ2, abdominal distention, failure to thrive, nausea and vomiting, short stature and wasted buttocks, bruising secondary to vitamin K deficiency, dermatitis herpetiformis, steatorrhea, diarrhoea, pallor

36
Q

What would histology reveal in coeliac disease?

A

Villous atrophy, crypt hyperplasia and intra-epithelial lymphocytes. You would do anti TTG IgA antibody and anti-endomyseal antibody

37
Q

Complications of coeliac disease

A

Anemia, hyposplenism, osteoporosis, enteropathy-associated T cell lymphoma

38
Q

What are the symptoms of a peptic ulcer?

A

Epigastric pain, fullness, bloating, nausea and intolerance of fatty foods, duodenal ulcers are common and are worse before eating meals and revealed by food and drink where as gastric ulcers are worse upon eating and there is a risk of malignancy

39
Q

What does ALARMS stand for?

A

Anemia, loss of weight, anorexia, recent onset of symptoms, melaena/haematemesis, and dysphagia

40
Q

Indications for urgent endoscopy RE dyspepsia?

A

gastric mass or persistent vomiting

41
Q

How do you treat a patient with a peptic ulcer, positive for H. pylori via breath test or stool antigen?

A

PPI, clarithromycin and amoxicillin, if they test negative they are usually prescribed PPI or H2 receptor antagonist

42
Q

salmonella and shigella are treated with

A

ciprofloxacin

43
Q

Campylobacter is treated with a macrolide such as

A

erythromycin

44
Q

Cholera is treated with

A

tetracycline to reduce transmission

45
Q

What are the potential complications of GORD?

A

Transition of the tissue in the oesophagus from squamous epithelium to metaplastic columnar epithelium
Adenocarcinoma
Oesophageal strictures
Oesophageal ulcers

46
Q

Typical vs atypical symptoms of GORD

A

Typical are dyspepsia and a feeling of acid reflux, atypical would be tooth erosion, laryngitis, globus, belting, bloating, nausea, epigastric pain plus any ALARMS - warrants OGD

47
Q

How do you treat GORD?

A

weight loss, dietary changes, elevation of the head of the bed
PPI, <40, typical symptoms, standard dose PPI 8 weeks w/ lifestyle changes
Antacids for symptomatic relief
Anti-reflux surgery for refractory cases

48
Q

How do you treat ulcerative colitis?

A

aminosalicylates - mesalazine and sulfasalazine for mild-moderate disease (left sided, proctitis, proctosigmoiditis), topical then high dose oral

Corticosteroids, monotherapy and time-limited to induce remission

Calcineurin inhibitors - tacrolimus or ciclosporin plus oral corticosteroids to induce remission

Immunosuppresion - thiopurines (first line) methotrexate (second)

Biological therapy - anti TNF factor monoclonal antibody agents e/g/ IV infliximab and sc adalimumab and gloimumab

49
Q

What is gastroparesis?

A

Delayed gastric emptying, commonly associated with diabetes mellitus (neuropathy plus high glucose)

50
Q

What are the symptoms of gastroparesis?

A

nausea, vomiting, early satiety, abdominal pain, and bloating

51
Q

How would you diagnose gastroparesis?

A

solid meal gastric scintigraphy e.g. radionucleotide images of gastric emptying

52
Q

How do you treat gastroparesis?

A

low fibre diet, frequent, smaller meals, mashed or pureed food
Domperidone (dopamine receptor antagonist), motility agents metoclopramide and erythromycin for symptomatic relief

53
Q

What is giardiasis? What are the key symptoms?

A

caused by giardia lamblia, explosive watery diarrhoea (non-bloody), bloating, flatulence, nausea, weight loss, anorexia

54
Q

How would you test for giardiasis?

A

stool microscopy/stool antigen tests and stool pcr

55
Q

How do you treat giardiasis?

A

metronidazole (abx treatment) and managing any new onset lactose intolerance

56
Q

What is gilbert’s syndrome?

A

autosomal recessive condition that causes decreased activity of the enzyme that conjugates bilirubin with glucuronic acid due to mutation in UGT1A1

mildly elevated bilirubin with normal FBC, patients often see this during periods of stress, fasting, exercise and infection

57
Q

What is Henoch Schonlein Purpura?

A

Most common vasculitis in children 3-15, post URTI, small vessel leukocytoclastic vasculitis characterised by deposition of IgA complexes in the affected organs

58
Q

What are the symptoms of HSP?

A

palpable purpura, abdominal pain, arthralgia/arthritis, renal disease

59
Q

How do you manage HSP?

A

Analgesia and supportive measures
Corticosteroids for symptom control
Severe abdominal pain may require surgical review to assess for infarction or intussusception

59
Q

What is hepatitis and what are the symptoms?

A

Inflammation of the liver caused by variety of infectious disease, most common causes in the UK are A, B and C

60
Q

What are the symptoms of hepatitis?

A

fatigue, nausea, vomiting, jaundice

61
Q

What are the differentials for hepatitis?

A

drugs, toxins, alcohol, CMV, EBV, hep E, leptospirosis and malaria

62
Q

What type of virus is hepatitis A?

A

RNA picornavirus, transmitted by faecal-oral route

63
Q

Epidemiology of Hep A

A

High prevalence in developing countries
Increasing age is the only real indicator of mortality and morbidity in those over 50
Travelers and at risk can be offered immunisation

64
Q

Presentation of Hep A

A

Flu-like symptoms, jaundice (sometimes), pale stools, dark urine and abdominal pain
2-6 weeks incubation
Possible 6m recovery

65
Q

Investigations and management of hep A?

A

IgM and IgG antibodies to HAV and supportive

66
Q

How do you treat Hep B (and who do you treat)?

A

Only adults who are HBsAG-positive, have compensated liver disease, are pregnant or of young age get treatment

Peginterferon alfa-2a is first line with tenofovir and entecavir as second-line

67
Q

What is the serology of hep B?

A

HbsAg is detected 3-5w after infection, carrier status = >6m
HBeAG positive more infections

Antibody to HBsAG indicate vaccination
Anti-HBx indicates past infection

Patients with chronic infection who are HBeAG negative may get immune scape phase where virus mutates despite antibodies present, these are the main spread in UK so all chronically infected need yearly screen

Acute infection have raised IgM to HBcAg but negative in chronic

68
Q

What is the epidemiology of hep B?

A

Most common globally
sub-saharan africa, asia and pacific islands
routine vaccination is declining disease
incubation 60-90 days

69
Q

How is hep B transmitted

A

vaginal/anal intercourse
transfusion
vertical transmission (90% of pregnancies where mother is HBeAg positive)
Developing countries it’s childhood vertical or horizontal transmission, in UK it’s normally adulthood

70
Q

How is Hep C transmitted?

A

IV drug use
Blood transfusion
Hemodialysis (rare in the UK)
Sexual transmission (less than 1% per year of relationship but higher rate with HIV co-infection)
Needlestick injuries in healthcare facilities, 3% risk
Perinatal infection from infected mother
Incubation 6-9 weeks

71
Q

Acute and chronic hep C infection features

A

Most are asymptomatic, 15-25% will clear the virus, 75% will have chronic infection
Pts with chronic infection will have high LFTs and cirrhosis in 20-30%%
1-4% of those with cirrhosis develop hepatocellular carcinoma and 2-5% liver failure

72
Q

How do you investigate hep C?

A

Anti-HCV serology - 90% positive 3 months after infection but many months for others
HCV RNA - if pos for more than 2 months needs treatment

73
Q

Management of Hep C

A

Symptomatic treatment in early disease

Drug therapy for all depends on genotype of the virus - nucleoside analogs are generally preferred e.g. sofosbuvir and often lead to undetectable viral loads

Antivirals of proven benefit in basically every patient irrespective of cirrhosis and fibrosis

74
Q

Loperamide indications

A

Acute diarrhoea, chronic diarrhoea, faecal incontinence, pain of bowel colic in palliative care

75
Q

Loperamide common side effects

A

Headache, nausea, dizziness, drowsiness, dry mouth, GI discomfort, skin reaction, vomiting

76
Q

Loperamide contraindication

A

UC, antibiotic colitis, bacterial enterocolitis, conditions with abdominal distention, conditions where inhibition of peristalsis should be avoided

77
Q

Hyoscine butlybromide indication (anti-muscaranic)

A

Symptomatic relief of gastro-intestinal or genito-urinary disorders characterised by smooth muscles spasm e.g. IBS, spasm in diagnostic procedures, excessive respiratory secretion in palliative care, bowel colic

78
Q

Side effects of hyoscine butylbromide

A

constipation, dizziness, drowsiness, dry mouth, dyspepsia, flushing, headache, nausea, palpitation, skin reaction, tachycardia, urinary disorder, vision disorder, vomiting

79
Q

Contrindications to hyoscine butylbromide

A

angle-closure glaucoma, gi obstruction, intestinal atony, mg, paralytic ileus, pyloric stenosis, severe UC, significant bladder outflow obstruction, toxic megacolon, urinary retention

80
Q

What are the two different types of hiatus hernia?

A

80% are sliding so the gastro-oesophageal junction slides into the chest, less competent sphincter and treatment similar to GORD
20% are rolling so the gastro-oesophageal junction stays in

81
Q

What is the conservative management of hiatus hernia?

A

weight loss, elevating the head of the bed, avoidance of large meals and eating 3-4 hours before bed time, also avoidance of alcohol and acidic foods, smoking cessation (nicotine relaxes the LES), also avoidance of chocolate, peppermint, caffeine, fatty foods and meds e.g. calcium-channel blockers, nitrates, beta blockers

82
Q

Medical management of hiatus hernia

A

PPI’s 4-8 weeks before assessing response

83
Q
A

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