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500 SBA's > GI > Flashcards

GI Flashcards

1
Q

State some obstructive causes of dysphagia

A 
Oesophageal carcinoma
Peptic strictures
Oesphageal web/ring
Gastric carcinoma
Pharyngeal carcinoma
Extrinsic pressure from - lung carcinoma, restrosternal goitre
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2
Q

State some motility disorders which cause dysphagia

A 
Achalasia
Systemic sclerosis
Stroke
Myasthenia gravis
Neurological disorders - Motor neurone isease, Parkinson's
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3
Q

Which GI ulcers are the most common?

A

Duodenal

4x times fore than gastric

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4
Q

When are the different GI ulcers relived after eating?

A

o Gastric - pain is worse SOON after eating

o Duodenal - pain is worse SEVERAL HOURS after eating

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5
Q

Identify appropriate investigations for peptic ulcer disease and gastritis

A 
BLOODS 
o  FBC (for anaemia)  
o  Serum amylase (to exclude pancreatitis)  
o  U&Es  
o  Clotting screen  
o  LFT  
o  Cross-match if active bleeding  
o  Secretin test (if Zollinger-Ellison syndrome suspected) -  IV secretin causes a rise in serum gastrin in ZE patients but not in normal patients)

ENDOSCOPY
o Biopsies of gastric ulcers can be taken to rule out malignancy
o Duodenal ulcers do NOT need to be biopsied

• Testing for H. pylori:
o C13-urea breath test :
• Radio-labelled urea is given by mouth
• C13 is detected in the expelled air o Serology:
• IgG antibody against H. pylori confirms exposure to H. pylori but NOT eradication

o Campylobacter-like organism (CLO) test:
• Gastric biopsy is placed with a substrate of urea and a pH indicator
• If H. pylori is present, ammonia is produced from the urea and there is a colour change from yellow to red

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6
Q

What is the Rockall score? And what does it indicate.

A

• Rockall Scoring:
o Scores the severity after a GI bleed
o Score < 3 carries good prognosis
o Score > 8 carries high risk of mortality

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7
Q

Generate a management plan for peptic ulcer disease and gastritis

A

ACUTE
o Fluid resuscitation needed if the ulcer is perforated or bleeding (IV colloids/crystalloids)
o Close monitoring of vital signs

o Endoscopy
o Surgical treatment
o NOTE: patients with upper GI bleeding should be treated with IV PPIs at presentation until the cause of bleeding is identified

•  Endoscopy: 
o  If the ulcer is bleeding, haemostasis can be achieved with:  
•  Injection sclerotherapy  
•  Laser coagulation  
•  Electrocoagulation

• Surgery:
o Indicated if the ulcer has perforated or if the bleeding ulcer can’t be controlled

• Helicobacter pylori eradication:
o Triple therapy for 1-2 weeks
o Various combinations may be recommended M usually a combination of 2 antibiotics + PPI (e.g. clarithromycin + amoxicillin + omeprazole) **

• If peptic ulcer disease is NOT associated with H. pylori:
o Treat with PPIs or H2 antagonists
o Stop NSAID use
o Use misoprostol (prostoglandin E1 analogue) if NSAID use is necessary

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8
Q

Identify the possible complications of peptic ulcer disease and gastritis

A

• Rate of major complication = 1 % per year
• Major complications:
o Haemorrhage (haematemesis, melaena, iron-deficiency anaemia)
o Perforation
o Obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)

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9
Q

Summarise the prognosis for patients with peptic ulcer disease and gastritis

A
  • Overall lifetime risk = 10%

* Outlook is generally good because peptic ulcers associated with H. pylori can be cured by eradication

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10
Q

In triple therapy what AB can be used if the patient is allergic to penicillin?

A

Clarithromycin

Metronidazole

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11
Q

What’s the most common cause of duodenal ulcers?

A

H pylori (90%)

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12
Q

Whats the most appropriate investigation for a hiatal hernia?

A

Barium swollow

CXR - might show no abnormalities

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13
Q

What histological changes occur in barret’s?

A

The lower third of the oesophagus undergoes metaplasia of squamous cell to columnar
An adaptive mechanism in withstanding the erosive action of the stomach acid.
This metaplasia is described as premalignant state and increases the risk of adenocarcinoma of the oesophagus
IX - by OGD.

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14
Q

Which bacteria cause bloody diarrhoea?

A

Campylobacter
Salmonella
E Coli
Shigella

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15
Q

What is Budd-Chiari syndrome?

A

Hepatic vein outflow obstruction

Unkown cause in 50%

Triad:

  1. Acute abdominal pain
  2. Hepatomegaly
  3. Ascites

Can cause: liver failure, cirrhosis.

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16
Q

What is the most common cause of upper GI bleed?

A 
Peptic Ulcers (35-50%)
Mallory Weiss tears (15%)
oesophagitis
gastritis and gastric erosions
oesophageal varices
drugs - NSAID's
upper GI malignancy
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17
Q

Whats the prophylaxis for oesophageal varices?

A

Non-selective beta-blockers - reduces portal pressure and reduces risk of variceal bleeding

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18
Q

What is the most common cause of hepatitis?

A

Hep B & C

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19
Q

GI causes of ascites

A

Ascites secondary to venous hypertension: Cirrhosis, CHF, Constrictive pericarditis, Budd-Chiari syndrome, Portal vein thrombosis.

Ascites secondary to Hypoalbuminaemia: nephrotic syndrome, malnutrition

Ascites secondary to Malignant disease: 2’ mets of carcinomas of breast, ovary, colon.

Ascites secondary to Infections: TB

Ascites secondary to Others: pancreatic isease, ovarian disease, myxoedema.

20
Q

Whats the pattern of inheritence of a1-antitrypsin deficiency?

A

Autosomal recessive

21
Q

What is a1-antitrypsin a RF for?

A

Laz:
COPD
Liver cirrhosis (Portal hypertension)

500 SBA:
Emphysema
Chronic liver disease
Hepatocellular carcinoma
Asthma
Pancreatitis
Gallstones
Wegener's granulomatosis
22
Q

Most appropriate treatment for autoimmune hepatitis

A

Prednisolone

23
Q

What kindo f cancer does PSC predispose you to

A

Cholangiocarcinoma

24
Q

What are obstructive jaundice symptoms?

A

Yellow Sclera
Pale stools
Dark Urine
Pruritus

25
Q

State some benign liver tumors

A 
Hemangioma (most common)
Adenoma
Cyst
Focal nodular hyperplasia
Fibromas
Leiomyomas
26
Q

State some causes/risk factors of UC

A

Family History
pANCA
PSC

27
Q

Summarise the epidemiology of ulcerative colitis

A 
•  Higher prevalence in:  
o  Ashkenazi jews  
o  Caucasians 
•  Uncommon before the age of 10 yrs 
•  Peak onset: 20J40 yrs 
•  Equal sex ratio up to the age of 40 yrs (higher in males from then on)
28
Q

Recognise the presenting symptoms of ulcerative colitis

A
  • Bloody or mucous diarrhoea (stool frequency depends on severity of disease)
  • Tenesmus and urgency
  • Crampy abdominal pain before passing stool
  • Weight loss
  • Fever
  • Extra-GI manifestations (e.g. uveitis, scleritis, erythema nodosum, pyoderma gangrenosum)
29
Q

Recognise the signs of ulcerative colitis on physical examination

A 
•  Signs of iron deficiency anaemia (e.g.  conjunctival pallor)  
•  Dehydration 
•  Clubbing  
•  Abdominal tenderness  
•  Tachycardia  
•  Blood, mucus and tenderness on PR 
examination  
•  Extra-GI manifestations
30
Q

List some extra-GI manifestations of UC

A

Uveitis
Scleritis
Erythema nodosum
Pyoderma gangrenosum

31
Q

Identify appropriate investigations for ulcerative colitis

A 
BLOODS
o  FBC:  
•  Low Hb 
•  High WCC  
o  High ESR or CRP 
o  Low albumin 
o  NOTE: X-match if there is severe blood loss

STOOL
o Infectious colitis is a differential diagnosis so a stool culture maybe useful
o Faecal calprotectin* allows differentiation of IBS from IBD (raised in IBD not raised in IBS)

AXR
o Rule out toxic megacolon

FLEX SIG AND COLONOSCOPY
o Determines severity
o Histological confirmation
o Detection of dysplasia

BARIUM ENEMA
o Shows mucosal ulceration with granular appearance and filling defects (due to pseudopolyps)
o Narrowed colon
o Loss of haustral pattern - leadpipe* appearance (right)
o Colonoscopy and barium enema may be DANGEROUS
during an acute exacerbation - risk of perforation

32
Q

Markers of disease activity in UC

A

o Decreased Hb
o Decreased albumin
o Increased ESR and CRP

o Diarrhoea frequency:
• < 4 = mild
• 4M6 = moderate
• 6+ = severe

o Bleeding
o Fever

33
Q

What is the management of an Acute Exacerbation of UC

A 
o  IV rehydration  
o  IV corticosteroids  
o  Antibiotics  
o  Bowel rest  
o  Parenteral feeding may be necessary  
o  DVT prophylaxis  
o  If toxic megacolon - the patient is likely to need a proctocolectomy because toxic megacolon has a high mortality
34
Q

• Management of Mild Disease of UC

A

o Oral or rectal 5-ASA derivatices (e.g. mesalazine, olsalazine, sulphasalazine)
o And/or rectal steroids

35
Q

• Management of Moderate to Severe Disease of UC

A

o Oral steroids
o Oral 5-ASA
o Immunosuppression (with azathioprine*, cyclosporine, 6-mercaptopurine or infliximab (anti-TNF monoclonal antibody))

36
Q

What is the surgical managment of UC and the advice fiven to patients.

A

• Advice
o Patient education and support
o Treat complications
o Regular colonoscopic surveillance

• Surgical
o If medical treatment fails, presence of complications or to prevent colonic carcinoma

o Procedures:
• Proctocolectomy with ileostomy
• Ileo-anal pouch formation (J pouch)

37
Q

Which part of the GI is mostly affected in Crohn’s and which deficiency is associated with this?

A

Terminal ileum

B12 deficiency

38
Q

Define coeliac disease

A

• An inflammatory disease caused by intolerance to GLUTEN, causing chronic intestinal
malabsorption.
• It leads to subtotal villous atrophy and crypt hyperplasia

39
Q

Explain the aetiology/risk factors of coeliac disease

A
  • Due to sensitivity to the GLIADIN* component of gluten
  • Exposure to gliadin triggers and immunological reaction in the small intestine leading to mucosal damage and loss of villi
40
Q

What are the genetic associations in coeliac disease?

A
  • 10% risk of first-degree relatives being affected

* Clear genetic susceptibility associated with HLA-B8, HLA-DR3 and HLA-DQW2 haplotypes

41
Q

Recognise the presenting symptoms of coeliac disease

A

Diarrhoea and abdominal bloating/distention/discomfort.

  • May be asymptomatic
  • Abdominal discomfort, pain and distention
  • Steatorrhoea (pale bulky stool, with offensive smell and difficult to flush away)
  • Diarrhoea
  • Tiredness, malaise, weight loss (despite normal diet)
  • Failure to ‘thrive’ in children
  • Amenorrhoea in young adults
42
Q

Recognise the signs of coeliac disease on physical examination

A

• Signs of anaemia: pallor

•  Signs of malnutrition:  
o  Short stature 
o  Abdominal distension 
o  Wasted buttocks in children  
o  Triceps skinfold thickness gives indication of fat stores
  • Signs of vitamin/mineral deficiencies: osteomalacia, easy bruising
  • Intense, itchy blisters on elbows, knees or buttocks (dermatitis herpetiformis)
43
Q

Identify appropriate investigations for coeliac disease

A 
•  Blood:  
o  FBC (low Hb, iron and folate)  
o  U&amp;E 
o  Albumin  
o  Calcium 
o  Phosphate

• Serology: **
o IgG anti-gliadin antibodies, IgA and IgG anti-endomysial tranglutaminase antibodies can be diagnostic
o NOTE: IgA deficiency is quite COMMON (1/50 with coeliac) so Ig levels should be measured to avoid false negatives

  • Stool: culture to exclude infection, faecal fat tests for steatorrhoea
  • D-xylose test: reduced urinary excretion after oral xylose indicates small bowel malabsorption

• Endoscopy: allows direct visualisation of villous atrophy in the small intestine (mucosa appears flat and smooth)
o Biopsy will show villous atrophy and crypt
hyperplasia in the duodenum
o The epithelium adopts a cuboidal appearance
- there is an inflammatory infiltrate of lymphocytes and plasma cells in the lamina propria

44
Q

Generate a management plan for coeliac disease

A
  • Advice: avoid gluten (wheat, rye and barley products)

* Medical: vitamin and mineral supplements. Oral corticosteroids if disease does not subside with avoidance of gluten

45
Q

Identify the possible complications of coeliac disease

A
  • Iron, folate and B12 deficiency**
  • Osteomalacia
  • Ulcerative jejunoileitis
  • GI lymphoma (particularly T cell)
  • Bacterial overgrowth
  • Cerebellar ataxia (rarely)
46
Q

Summarise the prognosis for patients with coeliac disease

A
  • FULL RECOVERY in most patients who strictly adhere to a gluten-free diet
  • Symptoms usually resolve within weeks though histological changes may take longer
  • Gluten-free diet must be followed for life

500 SBA's (12 decks)

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