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Clinical Pathology > GI > Flashcards

GI Flashcards

1
Q

Summary of GI pathology?

A

Upper GI: Oesophageal/Stomach/SI pathology

Lower GI: Diverticular/IBD, Polyps, Adenoma, CRC,

Infective GE
Intra-abdominal infections
Nutritional support in trauma

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2
Q

What is the most common cause of oesophagitis?

A

Gastro-oesophageal reflux

infection if immunocomp/ corrosives

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3
Q

State 5 risk factors for reflex oesophagitis.

A 
Male
Caucasion
Overweight
Defective LES
Hiatus heria
Increased intra-abdo pressure
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4
Q

Ulceration/Haemorrhage/Perforation/Strictures are possible complications of long-standing reflux oesophagitis.

What is another one which is a pre-malignant condition?

A

BARRETT’S OESOPHAGUS

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5
Q

What are the risk factors for Barrett’s oesophagus?

A

Same as reflex oesophagitis

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6
Q

State the histiological changes in Barrett’s oesophagus.

A

Glandular metaplasia

sq –> columnar

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7
Q

Those wth Barrett’s oesophagus require regular endoscopic surviellance. For what?

A

ADENOCARCINOMA

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8
Q

What are the 2 types of Oesophageal cancer?

A

Adenocarcinoma - from Barrett’s

Squamous Carcinoma - from native cells (middle/lower 1/3)

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9
Q

Which Oesophageal cancer has the same risk factors as Barrett’s/reflex oesophagitis?

A

Adenocarcinoma

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10
Q

Risk factors for Squamous carcinoma?

A 
Smoking
Alcohol
Thermal injury
HPV
Male
Black
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11
Q

The 2 oesophageal cancers have the same macroscopic appearence. Describe these.

A

Strictures
Ulcerated
Fungating
Polypoidal

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12
Q

Causes of Chronic gastritis?

A

ABC: Autoimmune, Bacterial (H.pylori), Chemical injury

NSAIDs
Bile reflux

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13
Q

H.pylori is associated with which 2 cancers?

A

Gastric cancer

MALT Lymphoma

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14
Q

What effects does H.pylori have on the stomach?

A

Chronic inflammation (mucosa)

Glandular atrophy (fibrosis, intestinal metaplasia)

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15
Q

What is defined as a localised defect extending to the submucosa +

A

Peptic ulcer

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16
Q

Name 5 causes of peptic ulcers

A 
H.PYLORI
Smoking
NSAIDs
Hyperacidity
Duodenl-gastro reflux
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17
Q

Is duodenal or gastric ulcer more common?

What is it always almost caused by?

A

Duodenal

H.PYLORI

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18
Q

Complications of peptic ulcers?

A

Haemorrhage
Perforation
Penetrate adjacent organs
Stricturing (hour-glass deforming –> reflux)

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19
Q

The most common type of gastric cancer is MALT lymphoma. T/F?

A

F

ADENOCARCINOMA

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20
Q

Adenocarcinoma of the GOJ has the same risk factors as Reflux oesophagitis.

What are the risk factors for Adenocarcinoma of body/antrum?

A

H.Pylori
Diet
Hypochlrohydria
Bile reflux

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21
Q

Gastric cancer in

A

HDGC

Hereditary diffuse-type

(scattered growth)

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22
Q

Other uncommon forms of gastric cancer?

A

Endocrine tumours
GIST
MALT lymphoma

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23
Q

Coeliac D is autoimmune and gliadin induces IL-15 expression –> CD8 IEL activation –> villi atrophy.

T/F?

A

T

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24
Q

Give 4 symptoms of Coeliac D.

A

Anaemia

Chronic diarrhoea

Bloating (bacteria)

Chronic fatigue (malabsorption)

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25
Q

How would you investigate for Coeliac D?

A

Antibodies

Biopsy

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26
Q

If got symptoms despite gluten-free diet, what would this suggest?

A

Cancer

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27
Q

Are diverticula are inward or outward protrusion of mucosa and submucosa?

A

OUTWARD

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28
Q

Diverticula are associated with…?

A

West
Urban
Elderly
Low fibre

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29
Q

Most diverticula present as…?

Other presentations?

A

Asymptomatic (90%)

Abdo pain
Alternating diarrhoea/constipation

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30
Q

Diverticulosis, Perforation, Haemorrhage are examples of what?

A

Acute complications of diverticula

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31
Q

Intestinal obstruction, Fistula, Colitis, Polypoid prolapsing mucosa folds are examples of what?

A

Chronic complications of diverticulosis

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32
Q

IBD is a form of chronic colitis. T/F?

A

T

33
Q

3 Risk factors for IBD?

A

Smoking
Oral contraceptive
FH

34
Q

The longer you have UC, the more likely you are to develop CRC. What is neccessary after 10yrs of UC?

A

Colonoscopy

35
Q

The following features are indicative of which IBD?

  • muscoal inflamm
  • affects colon- starts in rectum
  • continuous disease
  • inflammatory polyps
A

UC

36
Q

Clinical presentation of UC? (4)

A

Diarrhoea – urgency
Rectal bleeding
Anorexia –> weight loss
Abdo pain

37
Q

The complications of UC include…? CRC was already mentioned

A

Toxic megacolon

Haemorrhage

CRC

38
Q

The complication of Crohns are the same as UC. What other ones are there that are not seen in UC?

A

Fistula
Stricture
Small bowel syndrome –> malabsorption

39
Q

Crohns is transmural/affects any part of GI/ pathcy/ cobblestone appearence. T/F?

A

T

40
Q

State 5 ways Crohns way present.

A 
Bloody diarrhoea
Colicky abdo pain
Palpable abdo mass
Mouth ulcers
Anorexia

Peri-anal D
Fever

41
Q

Name systems in the body which may show extra IBD-mainfestations.

(inflammatory)

A 
Hepatic
Renal
Skeletal
Haematological
Mucocutaneous
42
Q

Colorectal polyps are an outward mucosal protrusion. T/F?

A

F

INWARD

43
Q

What is the term for the common non-neoplastic polyps that are benign unless LARGE & RIGHT-SIDED?

A

Hyperplastic

44
Q

Name the 2 non-neoplastic polyps that present in youth and ass with cancers

A

Juvenille polyps (malignanrt potential)

Peutz-Jeghers syndrome (predisposes to many cancers)

45
Q

The neoplastic benign polyp is called adenoma. Is it a precursor of CRC?

A

YES

46
Q

What type of cancer is CRC generally?

A

Adenocarcinoma ~95%

47
Q

Risk factors for CRC?

A 
Diet
Obesity
IBD
Alcohol
NSAIDs
HRT
FH
Adenoma
pelvic radiation
Schistosomiasis
48
Q

Are most CRC related to FH or sporadic?

A

Sporadic ~ 75%

FH ~20%

49
Q

Which inhertied conditions increase your risk of CRC?

Which one also increases risk for other cancers?

A

HNPCC*

FAP 100%

50
Q

Where does CRC tend to spread to?

A

Liver

Lung

51
Q

State the staging system for CRC.

A 
Dukes
A: confined to wall
B: invading wall
C: regional LN
D: distant mets
52
Q

What mode of infection is common in Infectious Gastroenteritis (GE)

A

Food/water-bourne

53
Q

Common viral causes of GE include Rotavirus/Norovirus. What about bacteria?

A 
Salmonella
E.Coli
Campylobactera
V.cholerae
C.dif
54
Q

Presenting complaint of GE are SUDDEN non-specific GI symptoms. Complications?

A 
Dehydration
Renal dysfunction
Toxic megacolon
GBS
HUS
55
Q

What SHOULDN’T you give to treat GE?

A

ANTIBIOTICS
(except in young/old/immunocomp)

bacteria dying will release toxins –> worse

56
Q

The Winter-vomiting disease = Norovirus. What is the classic presentation?

Treatment?

A

Diarrhoea
Projectile vomiting
24-48hr illness

Supportive

57
Q

Which strain of E.Coli releases shinga toxin causing diarrhoea + dehydration?

A

E.Coli 0157

58
Q

Complication of E.Col 0157 GE?

A

HUS

Shinga toxin acts on RBC

59
Q

Antibiotic-associated diarrhoea can occur up to how long after treatment?

A

2 months

60
Q

C.dif is common in >60s / taken borad spectrum antibiotics.

Whats the treatment?

A

Oral Metronidazole/Vancomycin!

Faecal transplants

61
Q

State 2 sources of intra-abdominal infections.

A

GI tract

Blood

62
Q

What are the 3 mechanisms of how an intra-abdo infection can occur?

A
  1. Translocation across wall
    (Perforated Appendix/Diverticulum)
  2. Translocation across lumen
    (hepatobiliary)
  3. Translocation from extra-intestinal source
    (blood, trauma)
63
Q

Cholecystitis = ?

Causes?

A

= inflammation of GB wall

Obstruction of cystic duct (GALL STONES, malignancy, worms, ERCP)

64
Q

How does cholecystitis present?

A

RUQ pain
Fever
Mild jaundice

65
Q

Complication and treatment of cholecystitis?

A

Empyema of GB

Remove pus

66
Q

Cholangitis = ?

Causes?
Presentation?

A

= Inflammation of biliary tree

Same as cholecystitis

67
Q

Intraperitoneal abscesses can be caused by…?

A 
Perforation
Cholecystitis/Cholangitis
Ischaemia
Pancreatitis
Anastomatic leak
68
Q

Is the presentation oof intra-peritoneal abscesses specific or non-specific?

A

Non-specific

Sweating
Anorexia
High fever

69
Q

State the locations where intra-peritoneal abscesses occur.

A

Subphrenic
Subheaptic
Paracolic
Pelvic

70
Q

How would you investigate intra-abdominal infections?

A

Bloods: FBC, CRP, LFTs

Imaging: CXR, USS, Abdo CT

Microbiological: microscopy, culture, sensitivity testing

71
Q

Intra-abdominal infections are treated diff for > 65s and

A

Start:

Cefuroxime + Metronidazole 65s

72
Q

What are the 3 phases post-trauma?

A

Phase 1: Clinical shock

Phase 2: Catabolic state

Phase 3: Anabolic state

73
Q

What is the amrker for tissue hypoxia?

A

LACTATE

74
Q

When is a patient most vulnerable of refeeding syndrome?

What is it?

A

IN ANABOLIC PHASE

If feed too quickly from malnourishment –> increased uptake into cells –> ions decrease in blood (when already low) –> CARDIAC ARREST

75
Q

Manifestation of refeeding syndrome after tests?

A

Decreased K/Mg/Pi, Thiame

Salt/H20 retetion –> oedema

76
Q

The term for inflammation of the large intestine due to C.dif overgrowth?

Complication of antibitoic therapy.

A

Pseudomembranous colitis

77
Q

What is the term for inflammation of the ascites fluid?

A

Spontaneous Bacterial Peritonitis

78
Q

~10 days post-trauma patients are at risk of what respiratory syndrome?

A

ARDS

Clinical Pathology (13 decks)

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