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GI Anatomy > Small + large intestine conditions > Flashcards

Small + large intestine conditions Flashcards

1
Q

Name 2 malabsorption disorders of the SI

A

Coeliac disease

Crohn’s (doesn’t just affect SI)

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2
Q

Define maldigestion v malabsorption

A

Maldigestion = Impaired breakdown of food in the intestinal lumen, e.g. lack of pancreatic enzymes, following gastric resection, bile acid deficiency

Malabsorption = Impaired absorption of digested food caused by alterations of the intestinal mucosa

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3
Q

Are Crohn’s disease and coeliac disease malabsorptive or maldigestive disorders

A

Malabsorptive

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4
Q

General symptoms (3) /signs (5) of malabsorption

A

Increased appetite
Bloating
Fatigue

Weight loss
Diarrhoea
Steatorrhoea (fat malabsorption --> fatty stool)
Clubbing
Apthous ulcers (crohn's)
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5
Q

Signs of iron deficiency (4)

A

Anaemia:

  • Fatigue
  • Pale skin
  • Dyspnoea on exertion
  • Koilonychia
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6
Q

Sign of vitamin A deficiency

A

Night vision impaired

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7
Q

Sign of vitamin K deficiency

A

Raised prothrombin time

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8
Q

Signs of vitamin
-B1
-B3
deficiency

A

Vitamin B1 (thiamine) deficiency –> memory loss

Vitamin B3 (niacin) deficiency –> dermatitis

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9
Q

Sign of vitamin C deficiency

A

Scurvy

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10
Q

Investigations of small intestine disorders (6)

A 
Endoscopy + biopsy
Barium follow through
Enteroscopy - longer version of endoscopy
CT
MRI enterography
Capsule enterography - pillcam
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11
Q

Investigations of bacterial overgrowth in SI (2)

A

H2 BREATH TEST (diagnostic of SI bacterial overgrowth and carbohydrate malabsorption)

Endoscopy + aspiration of duodenal/jejunal fluid –> then culture

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12
Q

What is coeliac disease

A

Autoimmune disease triggered by gluten (specifically gliadin component of gluten)

Sensitivity to gluten

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13
Q

Pathophysiology of coeliac disease

A

Immune activation –> inflammatory response to gliadin –> body produces anti-tissue transglutaminase) antibodies attacking the enzyme, tissue transglutaminase (tTG)), –> villous atrophy, hypertrophy of crypts and increased lymphocytes

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14
Q

Risk factors of coeliac disease (3)

A

Family history of coeliac
PMH or FH of autoimmune diseases - type 1 DM, thyroid disease
IgA deficiency

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15
Q

Symptoms (4) /signs (5) of coeliac disease

A

abdo pain
DIARRHOEA - most common
bloating,
fatigue

Steatorrhoea
Weight loss
Dermatitis herpetiformis (IgA deposit on skin)
IgA deficiency 
Anaemia
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16
Q

Investigations of coeliac disease (4)

  • serology (3)
  • gold standard
A 
Serology (test for antibodies):
-Total IgA - for IgA deficiency
-IgA-tTG antibody
-anti-endomysial IgA
(Some coeliacs are IgA deficient so ALWAYS measure total IgA)

Distal duodenal biopsy – GOLD STANDARD

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17
Q

Treatment of coeliac disease (2)

A

Gluten free diet

Nutritional support - calcium, vitamin D supplements

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18
Q

What is the characteristic histological finding of coeliac disease
+ other histological findings (3)

A

Villous atrophy

intraepithelial lymphocytes,
mucosal atrophy
crypt hyperplasia

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19
Q

What is the diagnostic investigation of coeliac disease

A

Distal duodenal biopsy

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20
Q

Other causes of small intestine malabsorption (4)

A

Infection, e.g. tropical sprue, HIV, giardiasis
Whipple’s disease
Iatrogenic - e.g. following gastric resection
Pancreas insufficiency

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21
Q

Treatment of small intestine bacterial overgrowth (3)

A

2 weeks each of:
Metronidazole
Tetracycline
Amoxycillin

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22
Q

What is IBD

A

A collective name for chronic inflammatory conditions of the bowel

Results from inappropriate and persistent activation of the mucosal immune system

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23
Q

Name the 3 types of IBDs

A

Crohn’s disease
Indeterminate colitis
Ulcerative colitis

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24
Q

Pathophysiology of IBD

A

Unknown activation of the immune system –> immune response against normal flora of the colon

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25
Q

Cause of IBD

A

Idiopathic

Thought to be due to combo of:

  • Environmental triggers
  • Immune dysfunction - possibly autoimmune
  • Genetic predisposition
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26
Q

What is ulcerative colitis + is it superficial/deep + where does the inflammation begin (3)

A

CONTINUOUS inflammation of the colon
Inflammation is SUPERFICIAL – limited to mucosa
Inflammation always starts from the rectum and moves proximally

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27
Q

Risk factors of UC (3)

A

Family history of UC
HLA-B27 gene
Infection

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28
Q

Symptoms (2) /signs (4) of UC

A 
Abdo pain (LLQ)
Diarrhoea

Abdo tenderness
Rectal bleeding
Blood in stool
Malnutrition –> vit deficiencies, inable to maintain ideal weight

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29
Q

Symptoms/signs of a flare up/relapse of UC (worsened or additional symptoms to usual) (4)

A

Arthritis
Mouth ulcers
Irritated red eyes
Painful red swollen skin

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30
Q

Signs (4) of a severe UC attack

A

Stool frequency >6 a day with blood
Fever
Tachycardia
Dyspnoea

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31
Q

Investigations of UC (6)

  • biochem
  • imaging (2)
A

Stool test - elevated calprotectin
FBC - high WBC, high platelets
ESR - elevated
CRP - elevated

Flexible sigmoidoscopy
Colonoscopy + biopsy - DEFINITIVE

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32
Q

Treatment of UC (4 medical, 2 surgical)

A

Medication:

  • 5ASA (aminosalicylates) - e.g. mesalazine, sulfasalazine
  • immunosuppressants
  • —–> steroids (prednisolone)
  • —–> azathioprine*
  • biologics (anti-TNFa antibodies - infliximab)**

Surgery

  • proctocolectomy (rectum + colon removal) + permanent ileostomy (stoma) - most standard
  • total colectomy + ileorectal anastomosis

*only used in refractory disease = if not responsive to normal treatment, i.e. 5ASA and steroids

**only used in refractory or severe disease

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33
Q

Pathological findings (i.e. if you were to look at it specimen physically) of UC (3)

A

Continuous pattern of inflammation
Inflamed RED granular mucosa
Pseudopolyps - projecting masses of scar tissue that have healed from ulceration (so old ulcer remnants)

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34
Q

Histological findings of UC (6)

A

Inflammatory infiltrates - high neutrophils

Mainly mucosal inflammation/ulcers + mucosal atrophy

CRYPT ABSCESSES/CRYPTITIS

NO GRANULOMAS

May get atypia (abnormal structure) of cells –> adenomatous change –> invasive cancer

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35
Q

Pathological findings (i.e. if you were to look at it physically) of Crohn’s disease (4)

A

GRANULAR serosa/dull grey
Mesentery - thickened and fibrotic
THICK COLON WALL –> NARROW lumen
‘Skip/cobblestone lesions’ - bits of normal colon then abnormal colon

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36
Q

Histological findings of Crohn’s (6)

A

NON-CASEATING GRANULOMAS

Cryptitis/ distortion of crypt cells

DEEP ulceration - TRANSMURAL inflammation

Fistula/stricture formation –> narrowing intestine

Fissuring ulcers

Lymphoid aggregates and neutrophil infiltrates

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37
Q

Is ulceration superficial/deep in UC vs crohn’s

A

UC - superficial

Crohn’s - deep

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38
Q

What is crohn’s disease

A

Disorder of unknown aetiology characterised by transmural inflammation (=all layers of bowel wall) of ANYWHERE in the GI) tract - from mouth to peri-anal area

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39
Q

Symptoms (3) /signs (4) of Crohn’s disease

A

Abdo pain/cramp - RLQ
CHRONIC diarrhoea - not usually bloody
Fatigue

Peri-anal lesions - skin tags/fistula/abscess
Blood in stool - more so microscopic, NOT GROSS BLEED
Oral lesions/ulcers
Weight loss

40
Q

Risk factors of Crohn’s disease (3)

A

White
Age 15-40 or 60-80
Family history of crohn’s

41
Q

Extra-intestinal manifestations of IBD (4)

A

Eyes - irritated, red eyes, e.g. uveitis
Joints - arthritis
Skin - painful red patches, often on legs
Liver - primary sclerosis cholangitis (risk of cholangiocarcinoma)

42
Q

Investigations of Crohn’s disease (7) + which of these is the definitive diagnosis

  • biochem (4)
  • imaging (3)
A

FBC - low Hb, high WBCs
CRP
ESR
Stool test - elevated faecal calprotectin only significant in UC

AXR
Abdo CT
Colonoscopy + biopsy - definitive diagnosis

43
Q

Treatment of Crohn’s disease

  • medical (6)
  • surgery indicated if
A

5ASA (aminosalicylates) - e.g. mesalazine, sulfasalazine

Immunosuppressants

  • Steroids (prednisolone/budesonide) - MORE USED
  • azathioprine, methotrexate

Manage extra-intestinal manifestations - uveitis, arthritis,

Biologics (anti-TNFa antibodies - infliximab) -

Antibiotics - only if septic complications suspected

Surgery - if no improvement with medical therapies

44
Q

Are antibiotics used for UC or crohn’s

A

Crohn’s

45
Q

Complications of Crohn’s disease (4)

A

Intestinal obstruction
Abscess formation
Fistulas
Extra-intestinal manifestations - uveitis, arthritis

46
Q

Complications of UC (5)

A 
Pseudopolyps
Toxic megacolon
Perforation
Stricture --> fistulas
Colonic adenocarcinoma
47
Q

Are immunosuppressants such as azathioprine and biologics (anti-TNFa antibodies) such as infliximab used more in crohn’s or UC

A

Crohn’s

Only used in UC if refractory disease = if not responsive to normal treatment, or severe disease

48
Q

Pathophysiology of acute appendicitis (4)

A

Obstruction of the lumen of the appendix usually by a calcified stone of faeces (faecolith) –> lumen distal to obstruction fills with mucus and swells –> increasing intraluminal pressure

Bacteria multiply rapidly and eventually leak out through the dying walls –> pus forms within and around appendix

49
Q

Histological features of appendicitis (3)

A

Fibrinopurulent exudate - pus + fibrin rich substance
Abscess
Full thickness necrosis of wall

50
Q

Risk factors of appendicitis (4)

A

Young adult
Smoking
Pre-existing infection spread to appendix
IBD

51
Q

Symptoms (3) /signs (3) in acute appendicitis

A

Abdominal pain (starts in umbilical region then moves to right lower quadrant)
Nausea
Anorexia

FEVER
RLQ tenderness (McBurney’s point)
Tachycardia

52
Q

Investigations of appendicitis (2)

  • bloods
  • imaging
A

FBC - elevated leukocytes (WBCs)

CT abdo/pelvis

53
Q

Treatment of appendicitis (3)

A

IV fluids
IV antibiotics
Appendectomy ASAP

+/- abscess drainage

54
Q

Complications of appendicitis (3)

A

Perforation
Peritonitis
Appendicular abscess

55
Q

What is dysplasia

A

Structural change of cells/ abnormal development of cells

56
Q

How is dysplasia related to colon cancer

A

Dysplasia can lead to formation of adenomas

57
Q

2 Types of dysplasia

A

Low grade or high grade

58
Q

Colorectal carcinoma is usually what type of tumour

A

Adenocarcinoma

59
Q

Risk factors of colorectal cancer (7)

A

Increasing age
APC mutation
Lynch syndrome (aka hereditary non-polyposis colorectal cancer (HNPCC))
IBD
Obesity
Family history of CRC
Previous history of colorectal adenoma or CRC

60
Q

Colorectal cancers are more often in the colon or rectum

A

Colon

61
Q

Symptoms (2) /signs (3) of colorectal cancer

A

Rectal bleeding - esp left sided CRC
Altered bowel habit - esp left sided CRC

Anaemia - esp right sided CRC
Rectal mass
Constitutional symptoms/signs - weight loss, anorexia - if advanced disease

62
Q

Common clinical features of a left sided CRC (3)

A

Altered bowel habit - more frequent, loss stools
Rectal bleeding - fresh blood
Annular shaped colon - apple core lesion

63
Q

Clinical features of a right sided CRC (3)

A

Tumour grows outwards like a polyp
ANAEMIA
Vague visceral pain

64
Q

Investigations of colorectal cancer (3 - imaging)

+ staging investigations (4)

A

Colonoscopy + biopsy
Barium enema
CT colonography (virtual colonoscopy)

CT chest/abdo/pelvis
Pelvic MRI
Rectal endoscopic ultrasound - better than CT for T staging
PET scan

65
Q

Are most CRCs sporadic or genetic

A

Sporadic

66
Q

Where does colorectal cancer spread to commonly (3)

A

Liver
Lungs
Lymph nodes

67
Q

Pathophysiology of CRC development (3)

A

High grade dysplasia of colonic/rectal epithelial cells –> adenomatous polyps –> carcinoma

68
Q

Colorectal polyps are…

A

Pre-malignant adenomas

69
Q

3 histological types of colorectal polyps

A

Tubular (majority)
Villous
Tubulovillous

70
Q

What do sessile polyps look like

A

Flat, blend in with lining

71
Q

What do pedunculate polyps look like

A

Raised growths

72
Q

Treatment of colorectal cancer

  • colon cancer (surgical (2) /non surgical candidate (1))
  • rectal cancer (surgical (2) /non surgical candidate (1))
  • may need removal of what organ with metastases
A

Colon cancer

  • if surgical candidate: surgical resection + chemotherapy
  • if non-surgical candidate: chemotherapy

Rectal cancer

  • if surgical candidate: surgical resection +/- neoadjuvant RADIOTHERAPY*/CHEMORADIOTHERAPY
  • if non-surgical candidate: chemotherapy

Partial hepatectomy if liver metastases

*radiotherapy for rectal cancer only

73
Q

Is neoadjuvant radiotherapy used in rectal or colon cancer

A

Rectal

74
Q

Staging systems used in colorectal cancer (2)

A

TNM

Dukes

75
Q

Name 2 inherited syndromes that can predispose you to colorectal cancer

A

FAP (Familial adenomatous polyposis)

HNPCC (hereditary non-polyposis colorectal cancer) aka Lynch syndrome

76
Q

Explain the Dukes staging system (4)

A

Dukes A - limited to mucosa and submucosa

Dukes B - invades through muscularis externa

Dukes C - regional lymph nodes involved

Dukes D - distant metastases

77
Q

Explain the TNM staging system

  • T (3)
  • N (3)
  • M (2)
A

T1 - involves mucosa/submucosa
T2 - involves muscularis externa
T3 - involves serosa

N0 - no lymph node metastases
N1 - 1-3 local lymph nodes
N2 - 4+ local lymph nodes involved

M0 - no distant metastases
M1 - distant metastases

78
Q

Name 2 screenings tests for CRC

A

Faecal occult blood test (FOBT)

Faecal immunochemical test (FIT)

79
Q

How does Faecal occult blood test (FOBT) work - to screen for CRC
+ how frequently is it done in Scottish bowel screening programme

A

Faecal sample placed on guaiac paper and hydrogen peroxide applied which, in the presence of blood, gives a blue reaction product

Every 2 years in Scottish bowel screening programme

80
Q

How does Faecal occult blood test (FOBT) work - to screen for CRC

A

Finds hidden blood in faeces

Uses specific antibodies that recognise human haemoglobin

81
Q

Faecal occult blood test has high … but low …

A

Specificity

Sensitivity

82
Q

Screening programme for CRC in people with FAP

A

annual colonoscopy from age 10-12

83
Q

Screening programme for CRC in people with HNPCC

A

from age 25, bi-annual colonoscopy

84
Q

What mutation occurs in FAP

A

APC gene mutation

85
Q

What mutation occurs in HNPCC

A

Mutation in DNA mismatch repair (MMR) genes

86
Q

Screening programme for people with family history of CRC

A

5 yearly colonoscopy from age 50 if high moderate risk

87
Q

Screening programme for CRC in people with IBD

A

colonoscopy 10 years post IBD diagnosis

88
Q

Screening programme for people with previous history of CRC

A

5 yearly colonoscopy

89
Q

Causes of small bowel/intestinal obstruction (7)

A 
Adhesions/scar tissue post surgery
Inguinal hernia
Foreign bodies
Intussusception (when part of the intestine slides into an adjacent part of the intestine
Tumour
Appendicitis
Crohn's disease
90
Q

Symptoms (3) /signs (2) of bowel obstruction

A 
Failure to pass wind/stool
Abdo pain
Nausea
Vomiting
Abdo distension
91
Q

Treatment of small bowel obstruction (5)

A

IV FLUIDS
NASOGASTRIC DECOMPRESSION - NG tube put in to decompress air/fluid

Analgesia
Anti-emetics
Correction of underlying cause, e.g. appendicitis, hernia, tumour

92
Q

Causes of large bowel obstruction (3)

A

Colorectal tumour - 90%
Colonic volvulus - loop of intestine twists around itself
Stricture

93
Q

Definitive treatment of large bowel obstruction (1)

+ acute treatment (6)

A

Surgery to correct the cause

Acute

  • Supplemental oxygen
  • IV fluids
  • electrolyte imbalances should be corrected
  • Blood transfusion/blood products may be required to correct anaemia or coagulopathy
  • Nasogastric decompression - to decompress the air/fluid in the intestinal tract
  • Pre-op antibiotics
94
Q

Low risk features of rectal bleeding (3)

A

Temp symptoms <6wks
Anal symptoms
<40yrs age = watch and wait for 6 wks, if symptoms persist/deteriorate –> refer for LI imaging

95
Q

High risk features of rectal bleeding (4)

A

Persistent change in bowel habit >6wks
Persistent bleeding WITHOUT anal symptoms
Rectal/abdominal mass
Unexplained iron deficiency anaemia

96
Q

Other causes of small intestine malabsorption apart from coeliac disease + crohn’s

A

Infection

  • tropical sprue
  • HIV
  • giardia lamblia
97
Q

Define a severe flare up of UC

A

> 6 bowel movements a day with lots of rectal bleeding

GI Anatomy (21 decks)

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