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CAM202 Pathology > Gastrointestinal II > Flashcards

Gastrointestinal II Flashcards

1
Q

DDx for appendicitis

A
  1. Mesenteric lymphadenitis, usually secondary to Yersinia or a virus
  2. Systemic viral infection
  3. Acute salpangitis
  4. Ectopic pregnancy
  5. Mittelschmerz
  6. Cystic fibrosis
  7. Meckel diverticulitis
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2
Q

Complications of acute appendicitis

A
  1. Perforation
  2. Abscess
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3
Q

Clinical presentation of acute appendicitis

A

This is a disease of adolescents, particularly young males. CHaracterised by:

  1. Periumbilican pain – RLF/RIF
  2. Nausea and vomiting
  3. Abdominal tenderness, esp. RLQ. McBurney’s point and McBurney’s sign.
  4. Mild fever
  5. Increased WCC

Note that variations in the positions of the appendix may lead to different presentations.

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4
Q

Pathogenesis of acute appendicitis

A

The lumen may become obstructed (e.g. faecalith, parasites, foreign body and bacteria within the lumen proliferate and attract neutrophils. Pururlent material in lumen leads to oeema and increased pressure leading to damage and bacterial invasion of the walls. Stretch receptors are activated, the appendix (midgut) visceral innervation, pain perceived in the center of the abdomen.

As there is an increased luminal pressure, venous drainage compressed ultimately leading to greater intraluminal pressures à vascular congestion and eventually arterial occlusion and ischaemic necrosis. At the time pain localizes to the RIF as local structures (somatic innervation) are innervated.

As disease progresses there is necrosis leading to decreased wall strength and risk of rupture. Appendiceal inflammation is associated with rupture in 50-80% of cases.

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5
Q

Staging of adenocarcinomas

A

There are three main methods of staging:

  1. Australian clinical pathological staging
  2. Dukes
  3. TNM (tumour, nodes metastasis)

Using the Australian clinical pathological staging to assess 5 year survival

  • Stage A (88%): confined to bowel wall submucosa and not beyond muscularis propria
  • Stage B (70%): confined to bowel wall, beyond muscularis propria.
  • Stage C (43%): regional nodal involvement
  • Stage D (7%): distant metastases
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6
Q

Clinical present of colonic adenocarcinomas

A

Can often be asymptomatic.

  • Caecal/right sided: fatigue, weakness, Fe deficiency anaemia.
  • Left side: occult bleeding, change in bowel habit, diarrhea, constipation, bowel obstruction. High suspicion in Fe anaemia in older men and women.
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7
Q

Pathogenesis of colorectal carcinoma

A

There are a well described set of genetic alterations that occur that ultimately leads to colorectal malignancy. There are two distinct pathways, but both include the stepwise accumulation of multiple mutations.

  1. Adenoma-carcinoma sequence: in 80% of sporadic colon tumours the APC gene is mutated/silenced by epigenetic events which lead to adenomas. Loss of this gene leads to an increase in beta-catenin which is part of the WNT signaling pathway. Beta-catenin activated transcription of genes which promote proliferation.
  2. Microsatellite instability pathway: microsatellite instability is seen in 90% of colorectal tumours from people with HNPCC, but is also seen in 10-15% sporadic carcinomas.
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8
Q

Risk factors for colorectal adenocarcinoma

A
  • Genetic: HNPCC, FAP, familial: family history
  • Environmental: increased calorific intact, a diet low in fibre, high content of refined carbohydrates, intake of red meat and fat, decreased intake of protective micronutrients (low A, C, E vitamins). NSAIDs and aspirin (COX-2) effects appear to be protective.
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9
Q

Peak incidence of adenocarcinoma

A

60-70 years of age. If in a younger person, must suspect pre-existing condition (including HNPCC).

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10
Q

What is colorectal adenocarcinoma?

A

This is referred to as sporadic colorectal cancer, unless associated with FAP or HNPCC. Most colorectal adenocarcinomas are sporadic.

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11
Q

What is the aetiology of hereditary non-polyposis colorectal cancer (Lynch Syndrome)?

A

Germline mutation in DNA mismatch repair genes leads to microsatellite instability. Associated with colorectal adenocarcinoma, endometrial carcinoma, stomach, over, small intestine, hepatobiliary, ureter, renal pelvis and brain. Colon adenocarcinomas tend to occur at younger ages then sporadic and often located on the right side of the colon. Adenomas occur in low numbers but earlier in the general adult population.

The ‘first hit’ is when a person inherits germ line mutations of one of the five DNA mismatch repair genes involved in DNA repair: 90% involve MSH2, MLH1. The ‘second hit’ occurs in somatic cells – the normal allele is either lost through mutation or epigenetic silencing.

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12
Q

Aetiology and clinical presentation of FAP

A

Mutations of the adenomatous polyposis coli gene (APC) on chromosome 5q2. There are several different clinical presentations:

  1. Classic: at least 100 adenomas carpeting the mucosal surface, mostly tubular, occasionally villous. 100% will develop adenomcarcinomas, often by the age of 30 if untrated.
  2. Attenuated: fewer polyps around 30, located in proximal colon, develop adenocarcinoma later.
  3. Gardner: like classic FAP + oesteomas of mandible, skull, long bones etc.
  4. Turcot syndromes
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13
Q

Familial adenomatosis polyposis syndrome

A

Adenomatous polyps are present throughout the bowel and will progress to adenocarcinoma.

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14
Q
  1. What familial syndromes increase the risk of colorectal cancer?
A
  1. Familial anenomatous polyposis (FAP) syndrome
  2. Hereditary non-polyposis colorectal cancer (Lynch syndrome/ HNPCC)
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15
Q

What is the clinical presentation of adenamotous polyps?

A

Adenomatous polyps may be asymptomatic or cause anaemia if there is blood loss. Rarely, they secrete mucoid material.

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16
Q

What are the malignant risks of adenocarcinomas being present in an adenomatous polyp?

A

Maligannt risk correlates with three independent features:

  1. Size
  2. Architecture
  3. Severity of epithelial dysplasia
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17
Q

What are adenomatous polyps?

A

These are benign neoplasms arising as a result of epithelial proliferation and dysplasia (low grade to carcinoma in situ). They are precursors to invasive colorectal carcinoma.

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18
Q

Describe the classification of hamartomatous polyps.

A

These is general have no malignant potential. Hamartomatous polyps include:

  1. Juvenile polyps: occurs in <5 years of age, the majority occur in the rectum.
  2. Juvenile polyposis syndrome: autosomal dominant. Some of these cases attributed to SMAD/DZPC4. There are 50-100 juvenile polyps. Increased risk of adenocarcinoma.
  3. Peutrz-Jeghers polyps: rare AD syndrome (mutations of the gene LKB1/STK11 gene located on chromosome 19). Polyps scattered throughout entire GIT and melanotic mucosal and cutaneous pigmentation around the lips, oral mucosa, face, genitalia, palmar surfaces of the hands.
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19
Q

Describe the classification system for intestinal polyps

A

Polyps are either:

  1. Non-neoplastic have no malignant potential per say.
    1. Inflammatory polyp: may form from chronic cycles of injury and healing
    2. Hyperplastic polyp: associated with changes in cell turnover – 90% of polyps, very common.
    3. Hamartomatous polyp: tumour like growths composed of mature tissues that are normally present at the site in which they develop: Juvenile polyp (sporadic or syndromic) or Peutz-Jeghers polyp (rare autosomal dominant syndrome).
  2. Neoplastic. The common neoplastic poly is the adenoma (adenomatous) polyp.
20
Q

Presentation of bowel obstruction

A
  1. Abdominal pain
  2. Abdominal distension
  3. Vomiting
  4. Constipation (faeces and flatus if complete bowel obstruction)
21
Q

Describe the common aetiologies of bowel obstruction.

A
  1. Within the lumen: tumour, strictures, atresias, bands, faecaliths, foreign bodies, gallstones.
  2. Within the wall: intussuscepition, inflammatory strictures, tumours.
  3. Outside the wall: adhesions (post surgical, peritonitis, endometriosis), hernias, volvulus
  4. Pseudo-obstruction: paralytic ileus, vascular-bowel infarction, myopathies, Hirschsprungs disease.
22
Q

Pathogenesis of diverticular disease

A

Focal weakness in colonic wall and increased intraluminal pressure. Weakness when nerves and arteries penetrate the inner circular muscle coat along side the taenia.

23
Q

Clinical presentation of diverticular disease

A

Typically presents on the left side of the colon, but can occur on either side – the majority are in the sigmoid colon. 50% of people are over 60, and it is rare under 40 years. This may be an incidental finding on colonoscopy, otherwise may present with complications:

  1. Haemorrhage (diverticular bleed)
  2. Infection (diverticulitis)
  3. Abscess
  4. Sinus tracts
  5. Perforation and peritonitis
24
Q

What is diverticular disease?

A

Diverticular disease refers ot an acquired outpouching of colonic mucosa and submucosa that communicated with the colonic lumen.

25
Q

Complications of haemorrhoids

A
  1. Thrombosed
  2. Recanalised
  3. Superficial ulceration fissure formation
  4. Infarction and strangulation
26
Q

Pathogenesis of haemorrhoids

A

They occur secondary to constitently higher pressures in the haemorrhoidal plexus due to:

  1. Constipation and straining
  2. Pregnancy
  3. Portal hypertension
27
Q

What are haemorrhoids?

A

Haemorrhoids are variceal dillatations of the anal and perianal venous plexuses. External (inferior haemrrhoidal plexuses) occur below the anorectal line. Internal (superior haemorrhoidal plexus).

28
Q

What can cause chronic ischaemia of the gut?

A
  1. Atherosclerosis
  2. Vasculitis (PAN)
  3. Henoch-Schonlein and Wegner granulomatosis
  4. Amyloidosis
29
Q

Clinical features of ischaemic colitis

A

This has a very high mortality

  1. Older adults
  2. Severe abdominal tenderness
  3. Sometimes nausea and vomiting
  4. Sometimes bloody diarrhea
30
Q

Describe the pathogenesis of ischaemic colitis

A

Ischaemic colitis is caused by a disrupted blood supply, this can have several causes:

  1. Arterial: almost always is caused by a compromise (thrombosis or embolus) of one of the major mesenteric vessels (most often the superior mesenteric artery) that leads to transmural infarction.
  2. Hypoperfusion of the intestine either acute of chronic leading to:
    • Mural infarction: mucosa and submucosa
    • Mucosal infarction: where the lesion extends no deeper than muscularis mucosa.
  3. Venous thrombosis: rarely.

There are two phases of injury: an initial hypoxia and then secondary reperfusion injury when the blood supply is restored. Restoration of the blood and oxygen supply leads to oxygen free radical formation, neutrophil infiltration and inflammatory mediator release.

31
Q

Complications of ulcerative colitis

A
  1. In the most severe cases (UC and CD) does toxic damage to muscularis propria and neural plexus lead to compete shut down of neuromuscular function, causes swelling and becomes gangrenous (toxic megacolon).
  2. Tendency of dysplasia to occur in multiple sites.
32
Q

Describe the presentation of ulcerative colitis

A

This is a relapsing disorder. Patients are typically white females, with the peak age being between 20-25. Pts may have only one attack, but they are often precipitated by emotional distress.

  1. Bloody mucousy diarrhea
  2. Lower abdominal pain relieved by defecation

Extraintestinal symptoms include

  1. Migratory polyarthritis
  2. Sacroiliitis
  3. Anklylosing spondylitis
  4. Uveitis
  5. Skin lesions
  6. Pericholangitis
  7. Primary sclerosing cholangitis
33
Q

Extraintestinal manifestations of Crohn’s disease

A
  1. Migratory polyarthritis
  2. Sacroilitis
  3. Ankylosing spondylitis
  4. Erythema nodosum
  5. Clubbing
  6. Hepatic sclerosing cholangitis (stronger association with UC)
  7. Systemic amyloidosis
34
Q

Complications of Crohn’s disease

A
  1. Fibrosing strictures (terminal ileum especially)
  2. Fistulas (viscus and skin)
  3. Malabsorption (albumin, B12, bile salts) with terminal ileal disease
  4. Anaemia (B12 or Fe deficiency)
  5. Increased risk of GIT cancer in those with long standing CD (5-6x risk, even greater in those with UC)
35
Q

What is Crohn’s disease characterised by pathologically?

A
  1. Sharply deliminated and typically transmural involvement of the bowel by an inflammatory process with mucosa damage – skip lesions
  2. The presence of non-caseating granulomas; and
  3. Fissuring with the formation of fistula
36
Q

Presentation of Crohn’s disease

A

Occurs at any age but peaks 20-30s, and a minor peak in the 60s to 70s. Smoking increases the risk of Crohn disease.

  1. Intermittent attacks of diarrhea, fever, and abdominal pain
  2. Often precipitated by periods of stress.
  3. Chronic blood loss may lead to anaemia.
37
Q

How is the diagnosis of IBD made?

A

History, examination, laboratory findings and examination of bowel biopsy.

38
Q

What is the aetiology and pathognesis of idiopathic inflammatory bowel disease?

A
  1. Hygeine hypothesis
  2. Defects in host interactions with intestinal mibrobiota
  3. Intestinal epithelial dysfunction
  4. Abherrent immune mucosal immune response

The NOD-2 gene is associated with CD. NOD-2 encodes a protein that binds intracellular bacterial peptidoglycans. Some variants of the gene may lead to less effective binding allowing the microbes to get into the lamina propria to incite an inflammatory response or NOD-2 variants may be important in regulation of immune responses to prevent excessive immune activation by luminal flora.

39
Q

Main differences between Crohn’s disease and UC

A

Crohn disease may affect any portion of the GIT from the oesophagus to the anus, but most often involves the distal SI and colon and is typically transmural.
UC is a chronic inflammatory disease limited to the colon and rectum and typically extends only into the mucosa and submucosa.

40
Q

Complications of coeliac disease

A
  1. Malabsorption
  2. Long term risk of T cell lymphoma
  3. SI adenocarcinoma
  4. SCC of the oesophagus
41
Q

Laboratory examinations for coeliac disease

A
  1. Anti-tissue transglutaminase (IgA) and anti-deamidated gliadin peptide (IgA and IgG) are commonly used to screen.
  2. Further testing: IgA tissue transglutaminase, IgA deficiency is also common, so anti0deamidated gliadin IgG is also used to assist in the diagnosis. Check for IgA deficiency.
42
Q

Clinical features of coeliac disease

A

In adults it commonly presents at age 30-60, and in children 6-24 months of age, however this is highly variable.

  1. Diarrhoea
  2. Failure to thrivem
  3. Flatulence
  4. Weight loss and fatigue
  5. Up to 10% of patients have dermatitis herpetiformis – itchy, skin blistening lesions.

With the reduction in surface for absorption there is difficulty absorbing nutrients including vitamins and minerals and often iron deficiency anaemia results.

43
Q

Pathogenesis of coeliac disease

A

Gluten is broken down into many substances, one of which is gliadin. Gliadin causes activation of the epithelial cells, causing them to express cytokine IL-15, which activates CD8+ T cells. These proliferate, become cytotoxic and destroy the enterocytes (they are not gliadin specific). This leads to damaged absorptive surface that gliadin can cross. Once across, the gliadin can be deaminated by tissue transflutaminase. The deaminated gliadin is presented to the CD4+ T cells on MHC-II (HLA-DQ2 or HLA-DQ8). These CD4+ T cells are gliadin specific. These activated CD4+ T cells produce cytokines that damage the mucosa further and also drive antibody production. This imflammation destroys the absorptive surface of the small intestine (the villi) which is demonstrated on biopsy. Those suffering from coeliac disease produce antibodies against gliadin (anti-gliadin Ab and deaminated gliadin Ab) and the bowel wall itself (endomysial Ab and anti-tissue transflutaminase Ab).

44
Q

Aetiology of coeliac disease

A

The aetiology is largely unknown. It is known that there is a strong familial component – HLA-DQ2/DQ8 (remember this MHC-II) but other regulatory genes are involved.

45
Q

What is coeliac disease?

A

Coeliac disease is a chronic disease of the small intestine, which is characterized by diffuse enteritis and marked atrophy and loss of villi, secondary to sensitivity to gluten, which improved on withdrawal of gluten containing cereals.

CAM202 Pathology (3 decks)

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