Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > Upper GI Diseases > Flashcards

Upper GI Diseases Flashcards

1
Q

Common upper GI pathology

A

Oral lesions.
GORD and PUD (dyspepsia).
Motility issues – achalasia, gastroparesis etc.
Upper GI bleed.
Cancer: oral, oesophageal, gastric, small bowel.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Exact division between upper and lower GI =

A

suspensory muscle of duodenum (attaches superior part of ascending duodenum to diaphragm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Angular cheilitis

A

Candida infection.
Red swollen patches on corner of mouth.
Due to iron deficient anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Aphthous stomatitis

A

i.e. Canker sores (mouth ulcers).
Erythematous macules develop into ulcers, well demarcated with a reddish ‘halo’ surrounding ulcer, should go away within a week.
Common in anaemia or haematinic (vit. B12) deficiency.
Linked to IBD (crohns), coeliac etc..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Acute pseudomembranous candidiasis

A

Oral thrush

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Oral cancer - causes

A

Alcohol and tobacco
HPV (16&18)
Candida
Low vitamin A, C and iron.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Oral cancer - common locations

A

High risk at soft sites (non-keratinizing squamous epithelium), ventral and lateral tongue, floor of mouth etc…
Rarely dorsal tongue and hard palate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Oral cancer - warnings

A

Red/white lesions, lump, irregular shape, increasing size, etc…
Persistent sores, dysphonia, dysphagia, double vision, facial palsy…
Systemic symptoms of cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute oesophagitis - causes

A

Rare.
Chemical ingestion.
Infection in immunocompromised (e.g. candidiasis, HSV, CMV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Chronic oesophagitis - causes

A

Reflux oesophagitis. (GORD)

Rarer causes like Crohn’s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Allergic oesophagitis - causes

A

Eosinophilic oesophagitis.

History of asthma/allergy or autoimmune disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Allergic oesophagitis presentation is similar to ——–

A

GORD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Allergic oesophagitis - investigation findings

A

pH probe negative for reflux.
Increased eosinophils in blood.
Failed course of PPIs.
Endoscopy: corrugated (feline) or spotty oesophagus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Allergic oesophagitis - treatment

A

Removal of suspected allergen, steroids, cromoglycate etc.

endoscopic dilation sometimes necessary in severe cases with strictures/narrowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Gastroesophageal reflux disease (GORD) - causes

A 
Incompetent LOS. (e.g. hiatus hernia). 
Poor esophageal clearance. (abnormal motility).  
Barrier function/visceral sensitivity.
Obesity/pregnancy. 
Stress.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

GORD - symptoms

A 
Heartburn. 
Reflux
Waterbrash. 
Dysphagia, odynophagia. 
Weight loss. 
Chest pain. 
Hoarseness. 
Coughing.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

GORD - investigations

A 
PPI trial. 
Endoscopy. 
Barium swallow. 
Oesophageal manometry (tests sphincters)
pH studies. 
Nuclear studies.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

GORD - complications

A

Ulceration.
Stricture.
Barrets.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

GORD - treatment

A

1) Lifestyle: smoking cessation, weight loss, avoid triggers (e.g. alcohol, spicy food), sit up in bed…
2) Antacids: PPIs, H2 Antagonists
3) Surgery: last resort - laparoscopic (Nissen fundoplication).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Barret’s oesophagus - mechanism of disease

A

Chronic acid reflux&raquo_space; chronic inflammation of stratified squamous epithelium due to acid&raquo_space; acid damages cells&raquo_space; induces intestinal metaplasia&raquo_space; change to simple columnar epithelium with interspersed goblet cells
(normally present in small intestine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Barret’s - signs/symptoms

A 
Chronic reflux. 
Dysphagia, odynophagia. 
Weight loss. 
Haematemesis.
Retrosternal pain.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Barret’s - diagnosis

A

Endoscopy and biopsy.
Normal tissue = pale.
Abnormal tissue = red and velvety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Barret’s is a precursor to ———

A

adenocarcinoma of the oesophagus

Barret’s = PREMALIGNANT condition, can become dysplasia&raquo_space; cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Barret’s – management

A

No dysplasia = surveillance
Low grade dysplasia = endoscopic radiofrequency ablation.
High grade dysplasia/cancer = oesophagectomy (for those unsuitable for surgery = ablation or endoscopic mucosal resection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Oesophageal cancer - types

A

1) squamous cell carcinoma.

2) adenocarcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Oesophageal squamous cell carcinoma - causes

A 
Smoking and alcohol. 
HPV (16,18)
Vit. A and zinc deficiency. 
Tannic acid/strong tea.
Oesophagitis. 
Genetic.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Oesophageal adenocarcinoma - causes

A

Commoner in white males.
Obesity.
Barret’s/GORD.
Commonest in lower 1/3 of oesophagus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Oesophageal cancer - symptoms

A 
Progressive dysphagia. 
Anaemia. 
Anorexia, weight loss. 
Malaise. 
Pain. 
Hoarse voice, cough. 
Haematemesis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Oesophageal cancer - common sites of metastasis

A

Direct invasion - laryngeal nerves.
Lymphatic spread.
Haematogenous spread (liver, lung, bone, brain).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Oesophageal cancer – management

A

Nutritional support.
Open/minimally invasive oesophagectomy, alongside chemoradiotherapy. Lymph node dissection.
Palliative = managing obstructions/dysphagia, stents, RT, chemo (metastatic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Gastritis - acute causes

A

Alcohol.
Irritant chemical injury.
Severe burns.
Shock/trauma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Gastritis - chronic causes

A

Chemical (alcohol, NSAIDS, bile reflux).
Bacterial (h.pylori assoc.)
Autoimmune (pernicious anaemia).

33
Q

Gastritis - other causes

do not fall under chronic or acute

A

Lymphocytic (assoc. h.pylori and coeliac).
Eosinophilic.
Granulomatous (infectious, non-infectious, idiopathic).

34
Q

PUD (peptic ulcer disease)

A

Breach in GI mucosa due to a failure of defence against acid and pepsin attack.
Gastric or duodenal ulcer.

35
Q

PUD - morphology

A

2-10 cm across.

Edges clear cut, punched out.

36
Q

PUD - causes

A 
** similar to gastritis
H. pylori and NSAIDS most commonly.
Gastric dysmotility.
Outflow obstruction.  
Stress/alcohol/smoking etc..
37
Q

PUD - complications

A 
Pain predominant dyspepsia. 
Perforation. 
Penetration. 
Haemorrhage.  
Stenosis. 
Intractable pain.
38
Q

Gastric ulcers vs duodenal ulcers

A 
Gastric = weight loss, pain 1hr after meals, vomiting, eating increases pain
Duodenal = most common, pain 3hrs after meals, food may decrease pain
39
Q

How does H. Pylori lead to duodenal PUD?

A

Bacteria between epithelial cell surface and mucous barrier&raquo_space; ammonia/proteases released by H. Pylori damage epithelium&raquo_space; presence of bacteria excites acute inflammatory response (can progress to chronic)

Ulcers occur when protective mechanisms (e.g. mucous membrane) break down&raquo_space; epithelium exposed to HCl/pepsin&raquo_space; ammonia increases pH, G cells release gastrin to compensate&raquo_space; excess acid production causes duodenal ulcer.

40
Q

How do NSAIDS lead to PUD?

A

They decrease prostaglandin formation via COX inhibition (PGE2 and PGI2 normally increase pH via decreased acid secretion and increased mucous/bicarbonate secretion).
So NSAIDs increase acid production and decrease protection.

41
Q

PUD - symptoms

A 
Pain predominant dyspepsia. 
Often nocturnal. 
Aggravated or relieved by eating. 
Relapsing and remitting. 
Nausea/vomiting. 
Weight loss. 
Reflux.
42
Q

PUD - investigations

A

1st line = carbon-13 urea breath test, faecal antigen test (FAT)
2nd line: re-test using urea breath test. serology (IgA antibodies)
Rarely, gastroscopy and biopsy.

43
Q

Most common cause of upper GI bleeding =

A

peptic ulcer

44
Q

Before conducting a urea breath test, ensure no —- has been taken in last 2 weeks, and no —– taken in last 4 weeks.

A

no PPI taken in last 2 weeks

no antibiotics in last 4 weeks

45
Q

H Pylori eradication therapy

A

Triple therapy for 7 days:

1) PPI
2) Amoxicillin
3) Clarithromycin/metronidazole

(PPI + metronidazole + clarithromycin if penicillin allergic)

46
Q

PUD - treatment

A

Full-dose PPI or H2RA therapy for 8 weeks.

  • *H Pylori eradication when needed (re-test after 6-8 weeks)
  • *If using NSAIDS, stop where possible.
47
Q

PUD - complications

A

Anaemia.
Bleeding (chronic or acute - coffee grounds)
Perforation.
Gastric outlet/duodenal obstruction (fibrotic scar).
Cancer.

48
Q

Dyspepsia = 2 syndromes =

A

1) Epigastric pain syndrome (bloating, epigastric pain/burning, reflux)
2) Post prandial distress syndrome (post-prandial fullness, early satiety, nausea/vomiting)

49
Q

Dyspepsia – causes
Strongly associated with ——– (bacteria)
More common with use of ——— (drug group)
Overlaps with ———- (other GI conditions)

A

Strongly associated with H. pylori.
More common with use of NSAIDs.
Overlaps with GORD, PUD, IBS.

50
Q

Dyspepsia – causes

A

25% organic = PUD, GORD, drugs (NSAIDs, COX-2 inhibitor), gastric cancer
75% functional = assoc. with functional gut disorders e.g. IBS (no evidence of structural disease)

51
Q

ALARMS - symptoms

A 
A – Anaemia. 
L – Loss of weight. 
A – Anorexia. 
R – Recent onset of progressive symptoms. 
M – Masses and Melena/Haematemesis. 
S – Swallowing difficulty.

OR

OVER 55

52
Q

Anyone with dyspepsia/GORD that fits any of the ALARMS criteria receives ———–

A

Upper GI endoscopy

53
Q

Management of dyspepsia

in the absence of ALARMS symptoms

A

1) Lifestyle measures (weight loss, trigger foods, smoking cessation, alcohol reduction, stress)
2) Assess medication
3) Medical treatment (1 month PPI, test for H Pylori - eradication if positive)

54
Q

Gastric cancer - risk factors

A

Infections: H. pylori in up to 85% gastric cancers.
Smoking.
Diet: processed meats.
Obesity.

55
Q

Gastric cancer histopathology:
90% are ———-
5% are ———-

A

90% are adenocarcinomas (intestinal or diffuse)
5% are lymphomas (MALT lymphomas, stomach lymphomas)
** carcinoid and stromal tumours may also occur.

56
Q

Gastric cancer - symptoms

A

Dyspepsia

ALARMS or > 55 yrs

57
Q

Gastric cancer - investigations

A

Endoscopy and biopsy.

CT scan.

58
Q

Gastric cancer - treatment

A

Definitive treatment = surgery.

**For MALT lymphoma, treatment of underlying H Pylori infection results in remission in 80% of cases

59
Q

Achalasia

A

Oesophageal motility disorder

60
Q

Achalasia - pathogenesis

A

Failure of smooth muscle relaxation of LOS&raquo_space; increased LOS tone&raquo_space; lack of peristalsis due to degeneration of the myenteric plexus
(failure of distal inhibitory neurons – no known cause, can be cancer)

61
Q

Achalasia - symptoms

A

Dysphagia – difficulty with both liquids and solids.
Regurgitation of undigested food.
Chest pain.
Weight loss.

62
Q

Achalasia - investigations

A

Barium swallow study will show a BIRD BEAK APPEARANCE
X-ray may show dilated oesophagus.
Oesophageal manometry.
Endoscopy to rule out cancer.

63
Q

Achalasia - management

A

CCB’s + nitrates relax the sphincter while waiting for more definitive surgery.
Young people get a Heller’s myotomy (cardiomyotomy)
Old people get balloon dilation.

64
Q

Manometry

A

Test that evaluates the motility and muscle contractions of the oesophagus via catheter insertion

65
Q

Gastroparesis

A

Delayed gastric emptying that IS NOT due to an obstruction

66
Q

Gastroparesis - causes

A

Diabetes (diabetic autonomic neuropathy).
Chemotherapy induced neuropathy.
Smoking weed.

67
Q

Gastroparesis - symptoms

A 
Feeling of fullness.
Bloating.
Weight loss caused by ‘food fear’.
Nausea/vomiting after meals (usually lunch and dinner).
Abdo pain.
68
Q

Gastroparesis - investigations

A

Gastric emptying studies.

Manometry

69
Q

Gastroparesis - management

A

Nutritional support.
Metoclopramide.
Implantable gastric stimulation.
Vertical sleeve gastrectomy.

70
Q

Haematemesis

A

blood in vomit

71
Q

Melena

A

black, extremely foul smelling stool (old blood)

72
Q

Acute upper GI haemorrhage - causes

A 
Ruptured ulcers. 
Ruptured varices (19-40% bleed < 2 years). 	
Mallory-Weiss tear. 
Oesophagitis and erosive duodenitis. 
Neoplasm.
Other e.g. trauma.
73
Q

Acute upper GI haemorrhage - assessment of severity

A

100 RULE
Systolic BP < 100
Pulse > 100
Hb < 100g/l

Also
Age > 60
Comorbid disease.
Postural BP drop.

74
Q

Acute upper GI haemorrhage - management

A

Resuscitate (ABCDE).

Then facilitate prompt endoscopy&raquo_space; find cause&raquo_space; therapeutic manoeuvres&raquo_space; assess risk of rebleed

75
Q

Bleeding peptic ulcer - management

A

Endoscopy + adrenaline injection/heater probe thermo-coagulation/clips/haemospray. (NEW)
Omeprazole 80mg IV (acid suppression)
UNABLE TO STOP&raquo_space; surgery

76
Q

Why is omeprazole important in management of a bleeding peptic ulcer?

A

Acid suppression

acid and pepsin can cause clot dissolution

77
Q

Acute variceal bleed - risk factors

A 
Portal pressure > 12
Varices > 25% oesophageal lumen. 
Wale mark (red wale sign - suggesting recent haemorrhage)
Degree of liver failure. 
Known history of cirrhosis. 
Chronic viral hepatitis.
78
Q

Acute variceal bleed - treatment

A

1st line: Terlipressin
2nd line: SB balloon, EVL, scleropathy
3rd line: TIPSS

79
Q

How does terlipressin treat an acute variceal bleed?

A

ADH analogue

causes vasoconstriction of splanchnic vessels&raquo_space; reduces blood flow to portal vein&raquo_space; reduces portal pressure

GI (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions