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Final Med > gastrointestinal > Flashcards

gastrointestinal Flashcards

1
Q

treatment for H. Pylori

A 
triple therapy PAC500 
proton pump inhibitor 
amoxicillin 1g
clarithromyocin 500 
or 
PMC250 full dose PPI metronidazole 400mg, clarithromycin 250 mg
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2
Q

risk factors for peptic ulcer

A 
H. pylori
smoking
alcohol 
NSAIDS and aspirin 
group O
hypercalcaemia 
physiological stress
burns (curling’s ulcers) or brain trauma (cushings ulcers)
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3
Q

different types of portosystemic shunts

A 
caput medusae (umbilicus) 
oesophageal varices 
rectal varices 
diaphragm 
retropertineum
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4
Q

what is the child-Pugh score used for

A

liver cirrhosis
score 5-6 100% one year survival
10-15 points 45%

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5
Q

clotting cascade simplify

A 
intrinsic APTT (34 sec) heparin prolongation caused by von willebrand disease haemophilias 
extrinsic PT (14 sec) Warfarin and liver disease
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6
Q

liver produces which clotting factors

A

II, VII, IX, X

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7
Q

treatment for achalasia

A
  1. pneumatic balloon dilatation 60% free at 5 years
  2. surgical (Heller’s) myotomy longitudinal incision of the muscle fibres of the distal oesophagus risk of GORd so sometimes occurs with funoplication
  3. botox injection
  4. drugs like ca channel blockers and nitrates but these are last and not very effective
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8
Q

risk factors for squamous cell carcinoma

A 
drinking smoking 
nitrosamines (pickled moldy foods) and nitrates 
aflatoxins 
achalasia 
plummer vinson syndrome 
hereditary tylosis 
coeliac disease
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9
Q

risk factors for adenocarcinoma

A

barrett’s oesophagus

smoking and alcohol but not as imp as school

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10
Q

plummer vinson syndrome

A 
strophic glossitis (smooth tongue) 
cheilosis (cracks at the mouth)
koilonychia 
dysphagia 
post cricoid web of hyperkeratinization 
may require balloon dilatation and it is premalignant to cricopharyngeal carcinoma
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11
Q

what is the pathophysiology of achalasia?

A

absence of ganglion cells in the myenteric plexus which leads to failure of the relaxation of the lower esophageal sphincter and aperistalsis in the oesophageal body. ddx chagas disease or met carcinoma

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12
Q

vomit with undigested foods

A

oesophageal disorders achalasia, pharyngeal pouch

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13
Q

partially digested vomit

A

gastric outlet obstruction, gastroparesis

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14
Q

bile in the vomit

A

small bowel obstruction distal to the ampulla of vater

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15
Q

foul looking vomiting

A

distal intestinal or colonic obstruction

NB the only time you will see true faeces in the vomit is if there is a gastocolonic fistula or coprophagia

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16
Q

blood or coffee ground appearance

A

heamatemsis

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17
Q

long duration of vomiting

A

less likely it is a small bowel obstruction rules out acute pathologies

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18
Q

why should you always ask about constipation and flatus?

A

because an absolute constipation and flatus is a serious sign suggesting bowel obstruction

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19
Q

management of cholecystitis

A

nonoperative
clear fluids- avoiding food in the duodenum symptomatic relief to keep the gallbladder from contraction and also to prepare her for surgery.
IV fluids- vomiting
analgesics- WHO paracetamol and opioids given regular intervals.
antibiotics- according to local hospital guidelines gram neg
operative
laparoscopic cholecystectomy
urgent within 72 hours
or treating the acute episode and cholecystectomy 6-12 weeks later.

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20
Q

complications of cholecystitis

A

empyema
cholecystodoudenal fistula
gallbladder carcinoma
ascending cholangitis

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21
Q

what are the sings of ascending cholangitis?

A 
charcots triad:
RUQ pain 
jaundice 
fever with rigors 
swinging fever
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22
Q

management of ascending cholangitis

A 
surgical emergency- 
blood culture 
fluids 
oxygen
broad spectrum antibiotics 
lactate serum 
 urine output 
endoscopic retrograde cholangiopancreatography drainage 
endoscope is placed in the esophagus through to the duodenum sphincter of oddi a fine catheter placed there pus drained and sent for culture. small basket collect any obstructing stone or sludge sphincterotomy
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23
Q

post drainage of CBD management

A

nil by mouth
monitoring and abx
definition mgx is cholecystectomy

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24
Q

bile is made up of what?

A

water
fats cholesterol and phospholipids
bile salts (help stabilise fats to ease digestion)
conjugated bilirubin (stool brown colour)
bile salts are reabsorbed in the terminal ileum

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25
Q

Give parental vitamin K due to what type of jaundice

A

if PT time is prolonged you can give vit K in obstructive jaundice

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26
Q

types of gallstone

A

bile pigment: heamolytic anaemia pictureor long term parental nutrition
cholesterol stone: the five fs fat, fair, fertile, female of forty.

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27
Q

complications of gallstones

A

anatomically
gallbladder ciliary colic, cholecystitis,mucocoele, empyema, cancer of gallbladder of CBD (cholangiocarcinoma)
CBD- obstructive jaundice, ascending cholangitis
acute pancreatitis
gallstones ileus

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28
Q

how do fatty foods cause pain in biliary colic and cholecystitis

A

CCK released in duodenum in response to fatty foods stimulating the gallbladder to contract.

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29
Q

what is calots triangle

A

top liver
inferior is cystic duct
medial side is common bile duct and right hepatic duct
cystic artery is a branch of the right hepatic artery which passes behind the common bile duct.

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30
Q

what is Mirizzi syndrome

A

stone in hartmann’s pouch pressing on the common bile duct

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31
Q

courvoisier’s law

A

if the gallbladder is palpable in the presence of jaundice then the jaundice is unlikely to be due to stones…
if stone in the CBD gallbladder thickened and fibrotic *shrivelled
CBD is obstructed due to carcinoma gallbladder is likely to be normal.

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32
Q

what is ERCP and how does it differ from MRCP

A

ERCP can be therapeutic and diagnostic
therapeutic * dormia basket and endoscopic sphinctectomy
MRCP purely diagnostic
risks of ERCP is bleeding, perforation of biliary tree, cholangitis, and pancreatitis.

33
Q

if you think that your patient has pancreatitis what blood tests would you order?

A

FBC- leucocytosis and neutrophillia
LFT= hepatic involvement or obstructive picture (primary cause)
serum amylase- greater than 1000 Amylase or greater than 300 Lipase
modified Glasgow score for pancreatitis severity FBcm calcium, urea, liver enzymes, LDH, albumin, glucose, and arterial blood gas)

34
Q

what can result in protienuria

A

UTI and appendicitis irritating the bladder

35
Q

how should patient be follow up after acute diverticulitis

A

offered colonscopy 2-6 weeks after resolution of episode
extent and strictures
high fibre diet

36
Q

when would surgery be considered in this patient

A 
advise 1/3 remain well without symptoms 
1/3 ocasional cramps 
1.3 require hospital admission 
2 episodes of hospital admission 
associated obstructive symptoms
contrast leak during CT abdomen
37
Q

emergency management of a perforated diverticulitis

A
  1. resus (fluids titrated in response to BP, HR, and urinary output)
    oxygen keeping it greater than 94 Nil by mouth
  2. blood tests: VBG, FBC, U&E, cross match
  3. analgesia
  4. antibiotics
  5. CT
    emergency laparoscopy - normally Hartmanns procedure
38
Q

when should a patient with renal stones (nephrolithiasis) be admitted?

A

evidence of an upper UTI
renal impairment (high creatinine, urea, high k)
refractory pain
bilateral obstructing stones
patient is elderly, child or systemically unwell

39
Q

management for kidney stone

A
  1. regular multimodal analgesia (NSAIDS and paracetamol)
  2. encourage fluid intake
  3. tamsulosin (alpha blocker) or nifedipine (ca channel blockers)
    both relax smooth muscle
  4. active stone removal
    stones less than 5mm can spontaneously 50% of time (keep the stone for analysis)
  5. KUB x-ray before discharge to see if stone appears
  6. stones greater than 5 mm are unlikely to pass discuss with urology
40
Q

methods of kidney stone removal

A

lithotripsy extracorporeal shock wave if stones are less than 2 cm
ureterorenoscopic removal = dormia basket, holmium laser and mechanical lithotripsy may require a post op ureteric stent

percutaneous nephrolithotomy= rarely
stenting or percutaneous nephrostomy may be performed in order to prevent hydronephrosis
antibiotic cover- given if their are invasive procedure.

41
Q

what are the different causes of kidney stones

A

calcium- investigate for hyperparathyroidism
struvite- ammonium magnesium phosphate proteus infection, pseudomonas
urate- tx with potassium citrate
cystine

42
Q

RF fro developing kidney stones

A 
metabolic:
hypercaliuria 
hyperuricosuria 
hypocitraturia 
hyperoxaluria 
gout (G6PDH deficiency, malignancy)
cystinuria 
primary hyperparathyriodism
crohn’s 
chronic urinary tract 
medullary sponge or polycystic kidneys 
sarcoidosis
43
Q

jelly like or mucous stool what species?

A

salmonella or villious polyps

44
Q

How do you diagnose IBS

A

ROME III
at least 3 months with onset at least 6 months previously of recurrent abdominal pain or discomfort associated with two or more of the following:
improvement with defecation
onset associated with a change is stool consistency
and also frequency of stooling

45
Q

what is the definition of inflammatory bowel disease?

A

this is a spectrum of diseases including pouchititis and also have extraintestinal effects of the disease.

46
Q

risk factors for IBD

A

white, european ancestry and jewish populations

47
Q

prevalece

A

1: 500
1: 1000

48
Q

which IBD is less likely in smokers

A

ulcerative colitis

49
Q

which is more common in smokers?

A

crohns

50
Q

what is the genetic component of IBD?

A

5-10% in siblings

50% in monozygotic twins

51
Q

What are the gene variants that associated with Chrons?

A

NOD2

52
Q

IBD pathogenesis

A

dysfunction of the bowel immune system.
pathology- acute (neutrophils) and chronic inflammation
gut flora- take away gut improves

53
Q

Ulcerative colitis presentation

A

frequency
tenesmus
rectal bleeding

54
Q

endoscopy UC

A 
ulcers
friability 
pseudopolyps 
variable extension proximal 
continous
55
Q

histology hallmark UC

A

lumen of the crypt is lined with neutrophils

56
Q

what is the differential for UC

A 
crohn’s disease
shingella 
salmonella 
e. coli
campylobacter 
pseudomembranous colitis (severe C DIFF) 
non-steroidal anti-inflammatory drugs
57
Q

How do you diagnose IBD- UC?

A

no gold standard- clinical ddx
diarrhoea and rectal bleeding for a couple weeks or months
neg. stool culture
neg C diff
colonoscopy showing continuous colitis from anal verge proximally absence of small bowel involvement
histology shows chronic inflammation with crypt abcesses.

58
Q

extra-enteric manifestations

A

Uveitis
enteropathic arteritis
oligioartheritis = large joint single joint
ankolsing spondylitis - morning stiffness and back involvement
primary scelerosing cholangitis- irregular, narrow bile ducts greatly increased risk of cholangiocarcinoma. No effective treatment.
obstructive picture.
pyoderma gangrenosum
erythmatous nodusum= painful bumps on shins

59
Q

UC treatment

A

aminosalicylates- mesalazine mild disease
corticosteroids= severe disease
azathioprine=
anti- TNF

60
Q

UC complications

A

toxic megacolon- higher risk of perforation
if flare up= IV fluids and corticosteroids
normal X ray of colon even if symptomatic
2 daily physical examination for abdominal tenderness- peritonitis

61
Q

toxic megacolon

A

indication for emergency surgery.

62
Q

surgery ulcerative colitis

A

permanent illiotosmy
permanent J pouch= works well in young people but not older people= anal
6 bowel movements a day

63
Q

crohn’s disease associated with which which gene change

A

NOD2 or CARD15

the more alleles the greater the risk
1= 3X risk
2= 40X

64
Q

what are some of the traits associated with Crohns

A

mouth to anus
transmural disease
skip lesions

65
Q

crohn’s presentation

A

diarrhoea
crampy pain
rectal
perianal disease

66
Q

endoscopic chrons

A

deep ulcers

67
Q

surgical chrons

A

fat proliferation

producing proinflammatory cytokines

68
Q

perianal disease in crohns

A

abcess and fistula

69
Q

How can you tell the air fluid level in a CT?

A

look up on radio pedía

70
Q

treatment of crohn’s disease

A

do not use amiosalicyates
use coritcosteriods
immunosuppressants
inflixamab and other biologics

71
Q

treatment of fistula and abcess

A

surgical drainage

metronidazole

72
Q

should you do surgery in Crohns

A

recurrence in the illuim just above anastomosis
most patients don’t have granuloma
crypt abcess is the most

73
Q

complications of Crohns

A

abcess and fistula and stricture formation

74
Q

biologics

A

inflixamab- 1/5 of patients in remission
placebo = 10%
patients needed to treat- 13 patients

active crohns - combination of inflix and azothioprine is better

75
Q

anti drug antibodies

A

trough inflixamab

can amount immune response against it.

76
Q

vedolizumab

A

gut specific
anti intergrin= MS and UC
prevent rolling

77
Q

historical treatment vs current treatment of crohns

A

currently based on severity of the disease and going with a strong therapy.

78
Q

fecal calportectin

A

neg good for saying they don’t have the disease

also monitoring disease activity

Final Med (35 decks)

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