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Gastroenterology > Intestinal disorders > Flashcards

Intestinal disorders Flashcards

1
Q

Pancreas : Name the different cells found in the pancreas and their function?

A

The pancreas consists of
1. Alpha cells : produce glucagon
2. Beta cells : produce insulin
3. Acinar cells : produce digestive enzymes into the duodenum to help break down macromolecules.
* Acinar cells manufacture inactive form of enzymes called proenzymes or zymogens
* Zymogens are activated by trypsin a pancreatic enzymes whose inactive form in trypsinogen

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2
Q

Pancreatitis : Definition

A

Sudden inflammation and haemorrhaging of the pancreas due to destruction by its own digestive enzymes.

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3
Q

Pancreatitis : Pathophysiology

A
  1. Acinar cells : produce digestive enzymes into the duodenum to help break down macromolecules.
  2. Acinar cells manufacture inactive form of enzymes called proenzymes or zymogens
  3. Zymogens are activated by trypsin a pancreatic enzymes whose inactive form in trypsinogen
  4. Trypsinogen is activated into trypsin by enteropeptidase enzyme which is found in the duodenum
  5. If trypsinogen or other digestive enzymes become activated whilst still in the pancreas - they can break down pancreatic tissue resulting in pancreatitis
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4
Q

Pancreatitis : Risk factors

A

Alcohol abuse -
1. Increases zymogen secretion and reduces fluid and bicarbonate release from epithelial cells
2. Making pancreatic fluid very viscous which blocks the pancreatic duct,
3. Increases pressure - damages acinar cells which release zymogens which then can get into contact with digestive enzymes thus becoming pre maturing activated.

Gall stone blockage of the pancreatic duct -
1. Increase in pressure and damage to acinar cells resulting in hydrolysis of the digestive enzymes and hence the pancreatic tissue

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5
Q

Pancreatitis : Causes

A

G E T S M A S H E D
-Gallstone, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion venom, High cholesterol/Hypercalcaemia, hypothermia, ERCP, Drugs

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6
Q

Pancreatitis : Precipitant drugs

A
  1. Azathioprine,
  2. Thiazide, furosemide,
  3. Steroid,
  4. Sodium valproate
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7
Q

Pancreatitis : Complications

A

Pancreatic pseudocyst

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8
Q

Pancreatitis : Clinical features

A
  1. Epigastric pain - radiating to the back assoc with vomiting
  2. Severe epigastric tenderness
  3. Cullen’s sign - periumbilical discolouration
  4. Grey-turner’s sign - flank discolouration
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9
Q

Pancreatitis : Investigations for diagnosis

A

Lab results;
1. Serum amylase levels >3 x upper limit, does not correlate with disease severity
Not specific - also be due to pseudocyst, cholecystitis
2. Serum lipase - higher sensitivity and specificity and has a higher half life for later presentation
3. CT scan - to confirm diagnosis

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10
Q

Pancreatitis : How is severity graded?

A

GLASGOW scoring system - to identify severity of pancreatitis; factors in severe pancreatitis include;
* age>55, hypocalcaemia, hyperglycaemia, hypoxia, neutrophilia, elevated LDH and AST

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11
Q

Chronic pancreatitis : Definition

A

Long term inflammation of the pancreas leading to irreversible damage to the pancreatic tissue.

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12
Q

Chronic pancreatitis : Clinical features

A
  • Chronic abdominal pain
  • Steatorrhea
  • Diabetes
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13
Q

Chronic pancreatitis : Investigations for diagnosis

A
  1. Abdominal X-ray - shows pancreatic calcification
  2. CT abdomen - higher sensitivity
  3. Faecal elastase - a human pancreas specific enzyme, can diagnosis pancreatic exocrine insufficiency
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14
Q

Chronic pancreatitis : Management

A

Pancreatic enzyme supplementation

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15
Q

Chronic pancreatitis : HIV and Pancreatitis

A

Pancreatitis in a patient with HIV may be due to;
* Antiretroviral therapy - esp didanosine
* Opputurnistic infection such as CMV

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16
Q

Pancreatic cancer : Risk factors

A
  1. Genetic predisposition - BRCA2 gene is the most common genetic cause
  2. Smoking - increases risk by 2-5x
  3. Obesity
  4. Diabetes, chronic pancreatitis and liver cirrhosis which also have a link to alcohol excess
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17
Q

Pancreatic cancer : definition

A
  1. Pancreatic adenocarcinoma account for 90% of pancreatic cancer
  2. They arise in the pancreas’s exocrine tissue within its epithelial cell lining
  3. Typically found at the head or neck of the pancreas
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18
Q

Pancreatic cancer : Clinical features

A
  1. Anorexia, weight loss
  2. Epigastric pain radiating the back - worse on lying down
  3. Steatorrhea - dysfunctional release of pancreatic enzyme prevent fat in food from being broken down fully
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19
Q

Pancreatic cancer : Clinical signs

A
  1. Trousseau sign - blood clots visible under the skin
  2. Courvoisier sign - gall bladder is enlarged, palpable but non tender
    -occurs when common bile duct is blocked by the tumor
    -indicating tumor likely to be at the head of the pancreas
    * If blocking the common bile duct } leading to obstructive jaundice - can cause pruritus from leak of bile salts.
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20
Q

Pancreatic cancer : Labs and tumor markers

A
  1. Serum amylase and lipase elevated
  2. CA 19-9 antigen
  3. CEA
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21
Q

Pancreatic cancer : Management

A

Chemotherapy and Whipple’s procedure

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22
Q

Coeliac disease : Definition

A
  • Autoimmune condition caused by sensitivity to gluten
  • Repeated exposure leads to villous atrophy which in turn leads to malabsorption.
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23
Q

Coeliac disease : Other disease association

A
  • Dermatitis herpetiformis : a vesicular pruritic skin eruption
  • Autoimmune disorders : type 1 DM, autoimmune hepatitis
  • HLA-DQ2, HLA-DQ8
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24
Q

Coeliac disease : Clinical features

A
  1. Chronic or intermittent diarrhoea
  2. Failure to thrive
  3. N+V
  4. Recurrent abdominal pain, cramping
  5. Unexpected weight loss
  6. Unexplained iron deficiency anaemia
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25
Q

Coeliac disease : Serology for diagnosis

A
  1. Tissue transglutaminase IgA + IgA levels are } FIRST LINE
  2. Endomyseal antibody IgA
  3. Anti-gliadin antibody
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26
Q

Coeliac disease : Investigation for diagnosis

A
  1. Endoscopic intestinal biopsy - Gold standard, - - gluten should remain in the diet for at least 6 week prior to testing
    Coeliac disease;
  2. Villous atrophy
  3. Crypt hyperplasia
  4. Increase in intraepithelial lymphocytes
  5. Lamia propia infiltration with lymphocytes
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27
Q

Coeliac disease : management

A
  1. Gluten free diet - TTG antibodies can be checked to confirm compliance with gluten-free diet
  2. Pneumococcal vaccine once every 5 years - patient have a degree of functional hyposplenism
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28
Q

Whipple’s disease : Definition

A

Rare malabsorbtive infectious disease caused by bacteria Tropheryma whipplei

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29
Q

Whipple’s disease : Pathophysiology

A
  1. G+ bacteria which spreads through out body causing multi-system effect, evade immune system so bacilli accumulates in body tissues.
  2. Transmission : Faecal - oral route
  3. Genetic assoc : HLA - B27
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30
Q

Whipple’s disease : Risk factors

A
  1. Immunosupression
  2. middle aged caucasian males, exposure to faecal matter (sewage workers, farmers)
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31
Q

Whipple’s disease : Clinical features

A
  1. W - weightloss,
  2. Hyperpigmentation,
  3. Infection with tropheryma whippelii,
  4. Pas positive granules in macrophages,
  5. Polyarterisis
  6. Lymphadenopathy
  7. Enteric involvement
  8. Steatorrhea
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32
Q

Whipple’s disease : Clinical signs

A

Skin
* Lymphadenopathy
* Hyperpigmentation
* Photosensitivity

Systemic
* Endocarditis
* Pericarditis

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33
Q

Whipple’s disease : Investigations for diagnosis

A
  1. Colonoscopy + jejunal biopsy - deposition of macrophages containing Periodic acid-Schiff granules
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34
Q

Whipple’s disease : Management

A

Oral co-trimoxazole for 1 year - lowest relapse rate

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35
Q

Ulcerative colitis : Definition

A

inflammatory bowel disease originating at the rectum and does not spread beyond the ileocaecal valve.

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36
Q

Ulcerative colitis : Incidence

A

Peak incidence : 15-25 years and 55-65 years

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37
Q

Ulcerative colitis : Clinical features

A

Bloody diarrhoea
Urgency
Tensesmus
Abdominal pain - lower left quadrant

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38
Q

Ulcerative colitis : Extraintestinal clinical features

A
  • Arthritis
  • Primary sclerosing cholangitis,
  • Uveitis
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39
Q

Ulcerative colitis : Investigations for diagnosis - Colonoscopy

A
  • Colonoscopy + biopsy -
    -In severe colitis - a flexible sigmoidoscopy is preferred

*Typical findings
1. No inflammation beyond submucosa
2. Widespread ulceration with preservation of adjacent mucosa - appearance of polyps also known as ‘pseudopolyps’
3. Inflammatory cell infiltrate in lamina propia
4. Crypt abscess caused by neutrophil migration
5. Fewer goblet cells and mucin in the gland epithelium

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40
Q

Ulcerative colitis : Investigations for diagnosis - Barium enema

A
  1. Loss of haustrations
  2. Superficial ulceration, pseudopolyps
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41
Q

Ulcerative colitis : what are the results seen in barium enema in long-standing disease

A

In long-standing disease; colon is narrow and short - ‘Drain pipe colon’

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42
Q

Ulcerative colitis : Main complication

A

Ulcerative colitis causes chronic inflammation significantly increases the risk of colorectal cancer.

43
Q

Ulcerative colitis : Colonoscopy surveillance

A

Colonoscopy surveillance in inflammatory bowel disease patients decided on the basis of risk stratification

  1. Low risk (5 yearly colonoscopy) : Left sided colitis or Crohn’s colitis of <50% of colon
  2. Intermediate risk (3 yearly colonoscopy) : extensive colitis or post inflammatory polyps or family hx of colorectal cancer in first degree relative >50 years
  3. High risk (1 year colonoscopy) : extensive colitis with moderate to severe inflammation, stricture or dysplasia, primary sclerosis cholangitis, FH of colorectal cancer in first degree relatively aged <50 years.
44
Q

Ulcerative colitis : Flare triggers

A
  1. Stress
  2. Medication : NSAIDs, antibiotics
  3. Cessation of the smoking
45
Q

Ulcerative colitis : Classification of Flares

A
  1. Mild
    * < 4 stools daily with small amount or no blood
    * No systemic disturbance
    * Normal ESR and CRP
  2. Moderate
    * 4-6 stool a day with blood
  3. Severe (needs hospital admission)
    * >6 stool a day with blood
    * Systemic disturbance : fever,tachycardia, abdominal tenderness, anaemia, raised inflammatory markers
46
Q

Ulcerative colitis : Management of mild-moderate flares

A

Proctitis/distal colitis/proctosigmoiditis
1. Proctiti/Proctosigmoiditis : Topical/Rectal Mesalazine
2. Extensive or left sired ulcerative colitis : Oral Mesalazine
3. Oral mesalazine + Prednisolone : short term for inducing remission that has not responded to topical treatments or oral mesalazine

47
Q

Ulcerative colitis : Management extensive disease

A
  1. Extensive or left sired ulcerative colitis : Oral Mesalazine
  2. Oral mesalazine + Prednisolone : short term for inducing remission that has not responded to topical treatments or oral mesalazine
  3. Topical rectal aminosalicyclate and a high dose oral aminosalicyclate if not achieved remission in 4 weeks
  4. SWITCH : High dose oral aminosalicyclate and oral corticosteroid
48
Q

Ulcerative colitis : Management of severe colitis

A

For treatment in hospital
1. IV steroids
2. IV ciclosporin

49
Q

Ulcerative colitis : Management of maintaining remission

A

Mild to moderate UC: Proctitis and proctosigmoiditis/Left sided UC
1. Proctitis : Topical aminosalicyclate daily
2. topical aminosalicylate + oral aminosalicyclate

50
Q

Ulcerative colitis : Maintaining remission in left sided and extensive ulcerative colitis

A

Low maintainance dose of aminosalicyclate

51
Q

Severe relapse or >2 exacerbations in the past year

A
  1. Oral azathioprine or oral mercaptopurine
52
Q

Aminosalicyclate drugs : Mechanism of action

A

MOA - releases 5-aminosalicyclic acid in the colon but is not absorbed, acts as a local anti-inflammatory by inhibiting prostaglandin synthesis

53
Q

Amino salicyclate drugs : Name two drugs and common side effects

A
  1. Sulphasalazine - combination of sulphapyridine and 5-ASA
    * SE specific to Sulphasalazine : rashes, anaemia, lung fibrosis
  2. Mesalazine - modified release of 5-ASA
    * GI upset, pancreatitis (more common in mesalazine, agranulocytosis, interstitial nephritis
  • Common side effects;
    GI upset, pancreatitis (more common in mesalazine, agranulocytosis, interstitial nephritis
54
Q

Crohn’s disease : Definition

A
  1. Inflammatory bowel diseases that affects anywhere from the mouth to the anus, commonly affects the terminal ileum and colon.
  2. Presents in early adulthood
  3. Inflammation penetrates across all layer down to the serosa - thus prone to strictures, fistulas and adhesions.
55
Q

Crohn’s disease : Clinical features

A
  1. Weight loss and lethargy
  2. Diarrhea - most prominant
  3. Abdominal pain
  4. Perianal disease e.g. skin tags or ulcers
56
Q

Crohn’s disease : Extraintestinal features

A
  • Arthritis
  • Episcleritis
57
Q

What is the most common extraintestinal manifestation of Crohn’s disease?

A

Arthritis

58
Q

What is the first line investigation for coeliac’s disease?

A

Serum IgA and tTGA antibody levels

59
Q

Which extraintestinal manifestation of Crohn’s disease related to disease activity?

A

Erythema nodosum - inflammation of the subcutaneous fat

  • Correlates with disease activity as it appears or worsens during a flare up
60
Q

Crohn’s disease : Complication

A
  1. Small bowel ca,
  2. Colorectal ca,
  3. Osteoporosis
  4. Perianal fistula / abscess
  5. Terminal ideal disease } may require ileocaecal resection
61
Q

Crohn’s disease : Investigations for diagnosis

A
  1. Labs
  2. Colonoscopy with biopsy
  3. Small bowel enema
62
Q

Crohn’s disease : Investigations for diagnosis - Labs results

A

Labs : raised inflammatory markers, faecal calprotectin, anaemia, low vitamin B12/D

63
Q

Crohn’s disease : Investigations for diagnosis - Colonoscopy results

A

Colonoscopy with biopsy : deep ulcers, skip lesions
Histology - inflammation extending through the serosa, goblet cells, granulomas

64
Q

Crohn’s disease : Investigations for diagnosis - Small bowel enema results

A

-High sensitivity and specificity for examining the terminal ileum
-Strictures showing ‘Kantor’s strain sign’, proximal bowel dilatation

65
Q

Crohn’s disease : Management - Inducing remission

A
  1. Lifestyle advice - stop smoking, avoid NSAIDs or COCP
    Inducing remission
  2. First line : Glucocorticoids (oral, topical or IV)
  3. Second line : 5-ASA drugs such as Mesalazine can be added
  4. Third line : Azathioprine/Mercaptopurine or Methotrexate can be added
  5. Fourth line : Infliximab - can be used in refractory disease and fistulating Crohn’s disease
66
Q

Crohn’s disease : Management - Maintaining remission

A
  1. First line. : Azathioprine or Mercaptopurine : assess to ensure sufficient +TPMT activity an enzyme which processes and breaks down thioprine drugs
  2. Second line : Methotrexate
67
Q

Crohn’s disease : refractory and fistulating disease management

A
  1. Infliximab
  2. Continue azathiprine or methotrexate
68
Q

Crohn’s disease : Isolated perianal disease management

A

Metronidazole

69
Q

Crhohn’s disease : Perianal fistula - Definition and types

A

Definition : inflammatory tract or connection between anal canal and perianal skin
* Simple fistula
* Complex/High fistula - passed through or abovve muscle layers

70
Q

Crohn’s disease : Perianal fistula - Investigation

A

MRI : exclude abscess and identify type of fistula

71
Q

Crohn’s disease : Perianal fistula - Management

A
  1. Symptomatic fistulae - Oral metronidazole
  2. Anti-TNF alpha agents e.g. infliximab - effective in closing and maintaining closure of fistula
  3. Draining seton (surgical threat left in fistula to leep it open) : prevents abscess formation in persistent fistula tracts
72
Q

Crohn’s disease : Perianal abscess- Management

A
  1. Incision and drainage +/- antibiotic therapy
  2. Draining seton if fistula tract is identified
73
Q

Bowel obstruction : Definition

A

when normal flow of contents moving through the intestines is interrupted
1. Partial bowel obstruction - gas or liquid stool can pass through the narrowed intestine
2. Complete bowel obstruction - nothing is able to pass though

74
Q

Bowel obstruction : Pathophsyiology

A
  1. Bowel obstruction causes bowel contents distal to the obstruction to get passed
  2. Proximally - gas and stool start to accumulate, causing the bowel to dilate - distending the overall abdominal cavity
  3. Pressure compresses arteries, lymph nodes leading to ischaemia of the intestinal wall
  4. This can result in perforation and sepsis
75
Q

Bowel obstruction : Mechanical causes

A

Small intestine
1. Perioperative adhesions
2. Hernia
Large intestine
1. Volculus - loop of intestine twists upon itself
2. Inflammatory bowel disease can cause strictures which can occlude the bowel

76
Q

Bowel obstruction : Functional causes

A

Anything which decreases smooth muscle contractility
1. Post-operative ileus - transient paralysis of smooth muscles in the intestinal wall usually caused by trauma during surgery
2. Infection or inflammation e.g. appendicitis, peritonitis
3. Endocrine dysfunction - hypothyroidism, hyperaemia, hypercalcaemia
4. Drugs - excess opioids such as morphine

77
Q

Bowel obstruction : Investigations for diagnosis

A

X-ray - dilated loops of bowel
CT abdomen

78
Q

Bowel obstruction : Clinical features

A
  1. Abdominal discomfort
  2. Constipation
  3. Vomiting
79
Q

Colorectal cancer : Genetic association

A
  1. Hereditary non-polyposis colorectal carcinoma - HNPCC (Lynch syndrome)
    * Autosomal dominant condition - most common genetic cause of colorectal cancer
    * Most commonly occurs in the proximal colon
    * Also increases the risk of endometrial cancer
    • Familial adenomatous polyposis (FAP)*
      * Rare autosomal dominant condition - leads to the formation of hundred of polyps by the age of 30-40 years
      * Genes : APC gene ( a mutation within this tutor suppressor gene)
80
Q

Colorectal cancer : Screening

A
  1. Public screening every 2 years for people 60- 94 years; sent Faecal Immunochemical Test through the post to detect blood in stool
    -If abnormal - to be offered a colonoscopy
81
Q

Colorectal cancer : Clinical features

A
  1. Right sided carcinomas : features of chronic disease such as malaise, weightloss and anaemia
    * Obstruct ileocaecal valve and cause bowel obstruction
  2. Left sided carcinomas : changes in bowel habits, large bowel obstrction and rectal bleeding
82
Q

Colorectal cancer : Two week wait pathway criteria

A
  1. Patients of any ages with rectal or abdominal mass
  2. Patients of any ages with rectal bleeding AND; abdominal pain ; change in bowel habit ; weight loss ; iron deficiency anaemia
  3. Unexplained weightloss AND abdominal pain if > 40 years
  4. Unexplained rectal bleeding - >50years
  5. Iron deficiency anaemia OR Changes in bowel habits - >60 year
83
Q

Colorectal cancer : if patient develops new bowel symptoms but does not meet 2WW criteria?

A

If patients develop new symptoms but do not meet the 2 week criteria - offer a FIT test

84
Q

Irritable bowel syndrome : Diagnosis criteria

A

Minimum 6 months of abdominal pain relieved by defecation or associated with altered bowel frequency in addition of at least 2 symptoms below;
* Abdominal bloating
* Altered stool passage - straining, urgency
* Symptoms may exacerbated by eating
* Passage of mucus

85
Q

Irritable bowel syndrome : Management of abdominal pain

A

Antispasmodic agents : peppermint oil, meberverine, hyoscine butyl bromide

86
Q

Irritable bowel syndrome : Management of Constipation

A
  1. Laxatives but avoid lactulose,
  2. If conventional laxatives are not helpful and constipation on going >12 months - trail Lincaclotide
87
Q

Irritable bowel syndrome : of mixed diarrhea and constipation

A
  1. First line : adjust diet and antispasmodics
88
Q

Irritable bowel syndrome : Management of Diarrhoea

A

Diarrhoea - Loperamide

89
Q

Irritable bowel syndrome : MOA and examples of Osmotic laxatives

A
  • Osmotic laxatives - draw water to soften faeces
    Lactulose
    Macrogol
90
Q

Irritable bowel syndrome : MOA and examples of Bulk-forming laxatives

A
  • Bulk-forming laxatives - increase bulk of faeces to stimulate bowel peristalsis
    Fubogel (Ispaghula husk)
91
Q

Irritable bowel syndrome : MOA and examples of Stimulant laxatives

A
  • Stimulant laxatives - stimulate muscles in the bowel to excrete
    Bisacodyl
    Senna
    Glycerol
92
Q

Irritable bowel syndrome : MOA and examples of Stool softening

A

laxatives
Arachis oil enema, docussate sodium

93
Q

Diverticulosis / Diverticulitis : Definition

A
  1. Outpouching of the bowel wall, most commonly in the sigmoid colon
  2. Diverticular disease - patients with symptoms associated with the presence of diverticulosis of the colon
  3. Diverticulitis : Infection of diverticulosis present
94
Q

Diverticulosis : Clinical features

A

Altered bowel habit
Left sided abdominal pain

95
Q

Diverticulitis : Clinical features

A
  1. Left sided iliac fossa pain and tenderness
  2. N+V
  3. Pyrexia, raised inflammatory markers
96
Q

Diverticulitis : Management

A

Mild episode - oral antibiotics
Severe episode : IV Abu and hospital admission

97
Q

Diverticulitis : Complications

A

Abscess formation, peritonitis, perforation

98
Q

Appendicitis : Incidence

A

Most common acute abdominal condition requiring surgery - occurs most frequency in ages 10-20 years

99
Q

Appendicitis : Pathophysiology

A

Lymphoid hyperplasia or faecolith obstructs the appendices lumen - gut organisms invade the appendix wall -> cause oedema, ischaemia or perforation of the appendix

100
Q

Appendicitis : Clinical features

A
  1. Periumbilical pain radiating then migrating to the right iliac fossa
  2. 1-2 x episodes of vomitting
  3. Mild pyrexia
  4. Anorexia - off food
101
Q

Appendicitis : Clinical signs

A
  1. Generalised peritonitis - rebound tenderness, guarding and rigidity
  2. Rovsing’s sign - palpation of LIF causes pain in RIF
  3. Psoas sign - pain on extending hip if retrocaecal appendix
102
Q

Appendicitis : Investigations for diagnosis

A
  1. Raised inflammatory marker, high leukocytes and neutrophils
  2. Urine analysis - leucocytosis, excl pregnancy in women
  3. CT scan
103
Q

Appendicitis : Management

A

Appendectomy and IV Abx

Gastroenterology (5 decks)

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