Brainscape's Knowledge GenomeTM

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


See full index

Pathology 1 > GI 3 > Flashcards

GI 3 Flashcards

1
Q

IRRITABLE BOWEL SYNDROME (IBS)

A

Condition characterised by chronic, relapsing
abdominal pain, bloating, and changes in bowel
habits

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

IRRITABLE BOWEL SYNDROME (IBS)
Epidemiology

A

Peak incidence: 20-40 yrs.; F>M

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

IRRITABLE BOWEL SYNDROME (IBS)
Pathogenesis

A

Pathogenesis:
 Interplay between psychologic stressors,
diet and abnormal GI motility
 Impairment of signaling in the brain-gut
axis => Disturbances of intestinal motility and enteric sensory function
 In some cases, onset is related to a bout (attack) of infectious gastroenteritis

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

IRRITABLE BOWEL SYNDROME (IBS)
Clinical features

A

Occurrence of:
 Abdominal pain or discomfort at least
3 days per month over 3 months
 Improvement with defecation
 Change in stool frequency or form
.

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

IRRITABLE BOWEL SYNDROME (IBS)
Other manifestations

A

Other Manifestations: Fibromyalgia, visceral hyper-sensitivity, backache, headache, urinary symptoms, dyspareunia, lethargy, and depression

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

IRRITABLE BOWEL SYNDROME (IBS)

Diarrhoeic IBS cases:

A

Microscopic colitis, coeliac disease, giardiasis,
lactose intolerance, small bowel bacterial
overgrowth, bile salt malabsorption, colon
cancer, and inflammatory bowel disease

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

IRRITABLE BOWEL SYNDROME (IBS)
.Prognosis:

A

Related to symptom duration;
Longer duration and ongoing life stressors =
Reduced likelihood of improvement

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

IRRITABLE BOWEL SYNDROME (IBS)
Treatment:

A

 Psychotherapy
 Dietary fiber supplementation
 Tricyclic antidepressants
 Selective Serotonin Reuptake Inhibitors
(SSRIs)
 Probiotics
 Antibiotics
 Chloride channel agonist (cases with
constipation)

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

INFLAMMATORY BOWEL DISEASE

A

 Chronic condition resulting from inappropriate mucosal immune activation

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

Inflammatory Bowel Disease includes two disease entities:

A

 Ulcerative Colitis: Severe ulcerating inflam-
matory disease that is limited to the colon and
rectum and extends only into the mucosa and
submucosa
 Crohn’s Disease (synonym: Regional Enteritis): May involve any area of the GI tract and is typically transmural

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

INFLAMMATORY BOWEL DISEASE
Results from a combination of defects, including:

A

Results from a combination of defects, including:
 Host interactions with intestinal microbiota
 Intestinal epithelial dysfunction and
 Aberrant (different) mucosal immune responses

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

INFLAMMATORY BOWEL DISEASE
Genetics:

A

Concordance rate for monozygotic twins:

 Crohn Disease: Approximately 50% of cases  Ulcerative Colitis: 16% of cases
 Concordance rate for dizygotic twins: <10% for both Crohn Disease and Ulcerative Colitis

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

INFLAMMATORY BOWEL DISEASE
Crohn’s Disease associated genes:

A

 NOD2 (nucleotide oligomerisation binding
domain 2):
 Specific NOD2 polymorphisms: Four-fold
increase in Crohn Disease risk
 <10% of individuals with NOD2 mutations develop disease

 ATG16L1 (autophagy-related 16-like) and IRGM (immune-related GTPase M)
 Some polymorphisms of the IL-23 receptor gene: Susceptibility to Crohn’s Disease

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

CROHN’S DISEASE
Localisation:

A

 Small intestine alone: 40% of cases
 Small intestine and colon: 30% of cases
 Colon alone: 30% of cases

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

Macroscopic findings:
 Skip lesions (multiple, separate, sharply
delineated areas of disease)
 Aphthous ulcer (earliest Crohn’s Disease lesion); progression and coalescence of multiple lesions into elongated, serpentine ulcers, oriented along the axis of the bowel
 Oedema and loss of the normal mucosal
texture
 Sparing of interspersed mucosa =>.Coarsely textured, “cobblestone appearance”
 Fissures (between mucosal folds) => Deep
extension => Fistula tracts or sites of
perforation
 Thickened and rubbery intestinal wall;
as a consequence of transmural oedema, inflammation, submucosal fibrosis, and hypertrophy of the muscularis propria
 Stricture formation
 Cases with widespread transmural disease:
Extension of mesenteric fat around the serosal surface => “Creeping” fat

A

CROHN’S DISEASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

 Microscopic features:
 Infiltration and damage of crypt epithelium
by neutrophils
 Formation of crypt abscesses (clusters of
neutrophils within a crypt)
 Commonly, ulcerations with abrupt transition
between ulcerated and adjacent normal
mucosa
 Distortion of mucosal architecture; bizarre
branching shapes of crypts and unusual
orientations to one another
 Pseudo-pyloric metaplasia (gastric antral-
appearing glands) and Paneth cell metaplasia (in the left colon)
 Non-caseating granulomas <=> Hallmark of
Crohn’s Disease (35% of cases)  Possible presence of granulomas in mesenteric
lymph nodes; Cutaneous granulomas form
nodules; referred to as metastatic Crohn’s
Disease

A

CROHN’S DISEASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

CROHN’S DISEASE
Clinical manifestations:

A

Variable:
 Onset with intermittent attacks of relatively
mild diarrhoea, fever, and abdominal pain
or
 Acute presentation, with right lower
quadrant pain, fever, and bloody diarrhoea
(about 20% of patients; mimics acute
appendicitis or bowel perforation)

 Alternating periods of active disease and
asymptomatic periods (last for weeks to many months)
 Disease re-activation = Association with a
variety of external triggers (e.g. physical or emotional stress, specific dietary items, and cigarette smoking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CROHN’S DISEASE
Complications:

A

Complications:
 Colonic disease cases => Iron-deficiency anaemia
 Extensive small bowel disease => Serum protein loss and hypoalbuminaemia, generalised nutrient malabsorption, or malabsorption of Vitamin B12 and bile salts
 Commonly, fibrosing strictures (particularly
of the terminal ileum)
 Recurrence at the site of anastomosis =>
Requirement of additional resections
 Fistulae formation between: i. loops of bowel (entero-enteric), ii. bowel and urinary
bladder (entero-vesical), iii. bowel and vagina
(entero-vaginal) or iv. bowel and skin (entero-cutaneous)
 Perforations and peritoneal abscesses

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

CROHN’S DISEASE
Extra-Intestinal manifestations:

A

 Uveitis (inflammation of the middle layer of the eye, called the uvea or uveal tract)
 Migratory polyarthritis
 Sacroiliitis
 Ankylosing spondylitis
 Erythema nodosum
 Clubbing of the fingertips
 Pericholangitis and Primary Sclerosing
Cholangitis (occurrence in Mb. Crohn, but more common in Ulcerative Colitis)
 Increased risk of Colonic Adenocarcinoma
development<=> Cases with long-standing colonic disease

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

ULCERATIVE COLITIS
Relapsing disorder, characterised by attacks of:

A

Relapsing disorder, characterised by attacks of:
 Bloody diarrhoea with stringy, mucoid material
 Lower abdominal pain
 Cramps (temporally relieved by pain)

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

ULCERATIVE COLITIS

A

Epidemiology:
 Persistence of symptoms for days, weeks to
months before they subside
 Occasionally, initial attack may be severe enough to constitute a medical or surgical emergency
 > 50% of cases, clinically mild disease
 Almost all patients experience at least one
relapse during a 10-year period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ULCERATIVE COLITIS
Clinical features (Extra-Intestinal):

A

Clinical features (Extra-Intestinal):
 Uveitis
 Migratory Polyarthritis
 Sacroiliitis
 Ankylosing Spondylitis
 Skin lesions (e.g. Pyoderma Gangrenosum,
Erythema Nodosum)
 5% of patients, Sclerosing Cholangitis; Increased risk for development of Cholangiocarcinoma

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

Macroscopic features:
 Always involvement of the rectum, and
extension proximally in a continuous fashion to involve other parts or all of the colon:
- Proctitis: 30% of patients
- Distal Colitis: 30% of patients
- Left-sided Colitis: 25%
- Total Colitis: 15%

 Affected mucosa may be: Slightly red and
granular or have extensive, broad-based ulcers  Abrupt transition between diseased and
uninvolved colonic mucosa

A

‘ULCERATIVE COLITIS

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

Macroscopic features (cont.):
 Isolated islands of regenerating mucosa=>
Bulging into the lumen => Pseudo-polyps => Fusion of the polyps’ tips => Mucosal bridges
 Ulcers aligned along the long axis of the colon
 Chronic disease: Mucosal atrophy with flat and smooth mucosal surface
 Inflammation and inflammatory mediators =>Damage of the muscularis propria and
disturbance of the neuro-muscular function =>
Colonic dilation and Toxic Megacolon =>
Increased risk of penetration

A

ULCERATIVE COLITIS

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

Microscopic findings:
 Inflammatory infiltrates, crypt abscesses, architectural crypt distortion, and epithelial metaplasia
 Inflammatory process: Diffuse but limited to the mucosa and superficial submucosa
 Severe cases: Extensive mucosal destruction
=> Ulcers => Deep extension into the submucosa (rare involvement of the muscularis propria)
 Residua of healed disease: i. Submucosal fibrosis, ii. Mucosal atrophy, and iii. Distorted mucosal architecture; after prolonged remission => Restoration of the normal histology
 Absent granulomas

A

ULCERATIVE COLITIS

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

Complications of long-standing Ulcerative
Colitis:

A

 Development of inflammatory polyps ‘ (“PseudoPolyps”):
- Composed of inflammatory tissue
- No dysplastic features (= No premalignant)
 Increased risk of ColorectalAdenocarcinoma; development through the process of Dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ULCERATIVE COLITIS
The risk of Dysplasia is related to several
Factors

A

 Increased risk, 8 to 10 years after disease
onset
 Greater risk for patients with Pancolitis
than those with only left-sided disease
 Higher risk, in cases with greater frequency
and severity of active inflammation

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

ULCERATIVE COLITIS
, Histological Classification of IBD-associated
Dysplasia: Low Grade Dysplasia:

A

Low Grade Dysplasia:
 Decreased intracellular mucin
 Nuclear enlargement
 Nuclear crowding
 Nuclear hyperchromasia
 Maintenance of the basilar orientation of
the nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ULCERATIVE COLITIS
Histological Classification of IBD-associated
Dysplasia:
High Grade Dysplasia:

A

High Grade Dysplasia:
 Irregular nuclear crowding
 Pleomorphic nuclei
 Variable nuclear hyperchromasia
 Markedly irregular external nuclear contours
 Increased nuclear stratification (many nuclei
located in the luminal half of the cell)

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

ULCERATIVE COLITIS
Management:

A

Management:
 Colectomy requirement in up to 30% of
patients within the first three years after presentation, because of uncontrollable symptoms
 Colectomy: Effective cure of intestinal
disease in Ulcerative Colitis, but persistence of extra-intestinal manifestations

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

-TOXIC MEGACOLON

Causes

A

‘Causes: Most commonly, a complication of IBD;
but also other aetiologic factors responsible (Table)

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

—TOXIC MEGACOLON

Pathogenesis

A

‘Pathogenesis:
 Association between inflammatory conditions
of the colon and decreased smooth muscle
contractility
.  Penetration of the muscularis propria by the
inflammatory process (in UC); Depth of inflam-
mation correlated with the extent of colonic
dilatation
 Detection of high iNOS levels in muscularis
propria of patients with Toxic Megacolon
 NO (non-adrenergic, non-cholinergic neuro-
transmitter) => Induction of colonic smooth
muscle relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

‘TOXIC MEGACOLON
. Clinical findings:

A

Clinical findings:
 Signs of systemic toxicity
 Abdominal tenderness
 Reduced bowel sounds
 Signs of Peritonitis <=> Indicative of colon
perforation
 Fever
 Tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

TOXIC MEGACOLON
. Laboratory studies:

A

‘Laboratory studies:
 Anaemia and Leukocytosis
 Increased ESR and Elevated CRP
 Hypokalaemia and Hypoalbuminaemia
 Toxin detection <=> C. difficile infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

TOXIC MEGACOLON
. Imaging studies:

A

Colonic dilatation in plain abdominal radiographs of >6cm; ascending and transverse colon, most dilated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

. TOXIC MEGACOLON
Management:

A

-Medical therapy:
 High-dose intravenous steroids <=> Patients
with Ulcerative Colitis
 Metronidazole or Vancomycin
 Gancyclovir (CMV cases)

-Surgery
‘

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

‘MICROSCOPIC COLITIS
. two entities:

A

-1. Collagenous Colitis
2. Lymphocytic Colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

-MICROSCOPIC COLITIS

Cause

A

Cause: Idiopathic diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

MICROSCOPIC COLITIS

Radiologic and Endoscopic Studies:

A

Radiologic and Endoscopic Studies: Normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

MICROSCOPIC COLITIS
1. Collagenous Colitis:

Epidemiology

A

-Epidemiology: Middle-aged and older women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Microscopic findings:
i. Dense sub-epithelial collagen layer
ii. Increased numbers of intra-epithelial lymphocytes iii. A mixed inflammatory infiltrate within the
lamina propria

A

’. MICROSCOPIC COLITIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

. 2. Lymphocytic Colitis:

A

 Strong association with Coeliac disease and auto-
immune diseases (e.g. Thyroiditis, Arthritis, and Autoimmune or Lymphocytic Gastritis)
 Similar histologic picture with Collagenous
Colitis, but
a. Normal thickness of sub-epithelial collagen
layer
b. Greater increase in intraepithelial lympho-
cytes; >1 T-lymphocyte per 5 colonocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

‘DIVERTICULAR DISEASE

A

Development of Diverticula, mainly in the
Sigmoid Colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

DIVERTICULAR DISEASE
Epidemiology:

A

Epidemiology:
 Common in Western world
 50% of people over 60 years; increased
incidence with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

DIVERTICULAR DISEASE

Diverticulum

A

-Diverticulum: Pouch of colonic mucosa
herniated through the muscularis propria and
found in sub-serosal (pericolic) fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

-DIVERTICULAR DISEASE
Important Factors for Diverticula formation:

A

 Area of weakness in colonic wall (natural defects
in circular muscle wall, where blood vessels pass through to supply the submucosa and mucosa)
 Raised intraluminal pressure, due to insufficient
dietary fibers:
- Binding of fibers to NaCl and H2O => Bulky,
moist faeces => Easily propelled through colon
- Low-fiber diet => Difficulty in the movement of
feces => Muscle hypertrophy and increased
intraluminal pressure
 Sigmoid Colon: Smallest diameter and highest
intraluminal pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Macroscopic Features:
 Small, flask-like out-pouchings (0.5-1.0 cm)
 Regular distribution in between the taeniae
coli of the Sigmoid Colon

Microscopic Findings:
Thin wall, composed of:
Flattened or atrophic mucosa
Compressed submucosa
Attenuated (or absent) muscularis propria

 Hypertrophy of the circular layer of the muscularis propria

A

DIVERTICULA & DIVERTICULOSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

DIVERTICULAR DISEASE
Clinical features: (+ acute diverticulitis)

A

.  Diverticulosis: Asymptomatic in 70-90% of
patients

Acute Diverticulitis:
Pathogenesis: Impaction and obstruction of
diverticulum’s neck with faecal matter =>
Rubbing to the mucosa by faecolith => Mucosal
injury => Acute inflammatory response
Clinical features: Abdominal pain in the left
iliac fossa, malaise, fever and localised
tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

PERICOLIC ABSCESS

A

Extension of acute inflammatory infiltrate
beyond the Diverticulum in the surrounding
subserosal tissue => ‘ Pericolic abscess
 Abscess: Localised collection of pus within a
newly formed cavity in a tissue
 Pus: Neutrophils, cellular debris, fibrin and
oedema fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

’ ‘PERFORATION -> PERITONITIS

A

 Perforation of a pericolic abscess into the abdominal cavity => Peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

‘DIVERTICULAR DISEASE
-Complications

A

‘ Stricture: Consequence of diverticular disease,
because of:
 Smooth muscle hypertrophy and hyperplasia
(due to low fiber diet)
 Fibrosis around Diverticula

 Consequence of the above conditions => Stricture
=> Reduction in lumen diameter => Clinically
manifested as bowel obstruction

 Lower GI tract bleeding: Painless and
spontaneous bleeding (small amount of blood)

52
Q

‘MECKEL DIVERTICULUM

A

‘Outpouching on the anti-mesenteric border of the
Terminal Ileum that represents the persistence of
the embryologic omphalo-mesenteric (vitelline) duct

53
Q

-MECKEL DIVERTICULUM

Localisation + epidemiology

A

Localisation: Approximately 20 cm from the
ileocaecal valve

, Epidemiology: Most common intestinal congenital
anomaly; 1% to 2% of the general population

54
Q

MECKEL DIVERTICULUM

Clinical manifestations:

A

‘Clinical manifestations: Intestinal obstruction,
ulcer with haemorrhage, perforation, or diverticulitis

55
Q

Microscopic findings:
 Small intestinal mucosa, in 50% to 70% of cases
 Ectopic gastric or pancreatic tissues; the rest

A

-MECKEL DIVERTICULUM

56
Q

HIRSCHSPRUNG DISEASE
. Synonym

A

Synonym: Congenital Aganglionic Megacolon

57
Q

HIRSCHSPRUNG DISEASE

  • Cause:
A

Cause: Heterozygous loss of function
mutations in receptor tyrosine kinase RET;
Congenital defect in colonic innervation

58
Q

HIRSCHSPRUNG DISEASE

Epidemiology

A

Epidemiology:
 More common in males; More severe in
females

59
Q

‘HIRSCHSPRUNG DISEASE
. Pathogenesis

A

‘Pathogenesis:
 Disrupted neural crest cells migration from
Caecum to Rectum =>?Distal intestinal segment without both Meissner submucosal plexus and Auerbach myenteric plexus => Absent coordinated peristalsis=> Functional obstruction => Dilatation proximal to the affected segment

60
Q

Macroscopic features:
 Aganglionic region: Normal or contracted
appearance
-  Normal innervated proximal colon =>
Progressive dilatation, due to distal
obstruction

Microscopic findings:
 Absence of ganglion cells in the affected
segment

A

HIRSCHSPRUNG DISEASE

61
Q

‘HIRSCHSPRUNG DISEASE
Clinical manifestations

A

Clinical manifestations:
 Failure to pass meconium in immediate
postnatal period
 Obstructive constipation
 Fluid and electrolyte disturbances
 Perforation
 Peritonitis

62
Q

HIRSCHSPRUNG DISEASE

Management

A

-Management:
Surgical resection of the aganglionic segment,
with anastomosis of the proximal normal colon to the rectum

63
Q

NECROTISING ENTEROCOLITIS

A

Condition primarily affecting infants who
either are premature or have had exchange
transfusions

64
Q

NECROTISING ENTEROCOLITIS

Other causes

A

Other causes:
 Appearance of some cases, after thrombosis
of the abdominal aorta (suggestive of
ischaemia as an important risk factor)  Complication of Hirschprung Disease

65
Q

NECROTISING ENTEROCOLITIS
 Clinical manifestations (majority of cases,
onset in the first week of life):

A

 Abdominal distention
 Disappearance of bowel sounds
 Passage of small amounts of blood-stained
stool

66
Q

NECROTISING ENTEROCOLITIS

Localisation:

A

. Localisation: Terminal Ileum and Ascending
Colon

67
Q

-Microscopic findings:
 Necrotic mucosa that may partially slough off
 Small submucosal gas-filled cysts

A

’. NECROTISING ENTEROCOLITIS

68
Q

NECROTISING ENTEROCOLITIS

Diagnostic sign:

A

-Diagnostic sign: Radiographically observed
submucosal cysts

69
Q

NECROTISING ENTEROCOLITIS
Complication + management

A

-Complication: Bowel perforation =>
Management: Resection of the perforated and
necrotic bowel

70
Q

ACUTE APPENDICITIS

Epidemiology

A

Epidemiology: Most common in adolescents and
young adults; Lifetime risk: 7%

71
Q

ACUTE APPENDICITIS

Pathogenesis

A

 Progressive increases in intraluminal pressure=> Impairment of venous outflow
 50-80% of cases: Luminal obstruction (by
faecalith, gallstone, tumour, mass of worms)
 Ischaemic injury and stasis of luminal contents
=> Bacterial proliferation => Inflammatory
response (tissue oedema, neutrophilic
infiltration of the lumen, muscular wall and
peri-appendiceal soft tissues)

72
Q

Macroscopic Features:
 Dull, granular-appearing, erythematous surface

Microscopic Findings:
 Congested sub-serosal vessels
 Transmural, modest, perivasc. neutroph. infiltrate
 Neutrophilic infiltration of the muscularis propria
(key-point for the diagnosis)
 Formation of focal abscesses within the wall <=>
Acute suppurative appendicitis
 Haemorrhagic ulceration and gangrenous necrosis, extending to serosa => Acute gangrenous appendicitis => Rupture and suppurative peritonitis

A

ACUTE APPENDICITIS

73
Q

-ACUTE APPENDICITIS
Clinical Features:

A

, Clinical Features:
 Pain; Peri-umbilical region => Right lower
quadrant
 Nausea and Vomiting
 Low-grade Fever
 Mild elevation of WBC
 Characteristic McBurney’s sign (deep tender-
ness at a point located two thirds of the distance
from the umbilicus to the right anterior superior
iliac spine)

74
Q

ACUTE APPENDICITIS
. DD:

A

DD: Mesenteric lymphadenitis, acute salpingitis,
ectopic pregnancy, Meckel diverticulitis

75
Q

-INFLAMMATORY POLYPS

A

’. Polypoid mass made up of inflamed and
reactive mucosal tissue

Present as a part of the solitary rectal ulcer
syndrome

76
Q

INFLAMMATORY POLYPS

Cause/Pathogenesis:

A

Cause/Pathogenesis: Impaired relaxation of
the anorectal sphincter => Sharp angle at the
anterior rectal shelf => Recurrent abrasion and
ulceration of the overlying rectal mucosa =>
Chronic process of injury and repair =>
Inflammatory polyp

77
Q

INFLAMMATORY POLYPS
Patients with characteristic Clinical Triad:

A

-Patients with characteristic Clinical Triad:
1. Rectal bleeding
2. Mucus discharge
3. Inflammatory lesion of the anterior rectal
wall

78
Q

HAMARTOMATOUS POLYPS

A

 Sporadic occurrence

 Components of hereditary or acquired syndromes:
- Peutz-Jeghers syndrome
- Juvenile polyposis
- Cowden syn., Bannayan-Ruvalcaba-Riley syn.
- Cronkhite-Canada syndrome
- Tuberous sclerosis
- Familial Adenomatous Polyposis (FAP)

79
Q

HAMARTOMATOUS POLYPS

Hamartomas

A

Hamartomas: Disorganised, tumour-like growths
composed of mature cell types, normally present at the site of polyp’s development

80
Q

JUVENILE POLYPS

Epidemiology

A

 Most common type of hamartomatous polyps  Sporadic or syndromic type

Epidemiology: Children ≤ 5years

81
Q

JUVENILE POLYPS

Localisation

A

Localisation: Rectum
- Sporadic juvenile polyps <=> Solitary polyps
- Juvenile polyposis syndrome <=> 3-100 polyps

82
Q

JUVENILE POLYPS
Clinical manifestations:

A

Clinical manifestations:
 Rectal bleeding
 Rectal prolapse with polyp’s protrusion
through the anal sphincter

83
Q

JUVENILE POLYPS

Management

A

-Management: Colectomy; to limit haemorrhage
associated with polyp ulceration

84
Q

PEUTZ-JEGHERS SYNDROME

Synonym

A

Synonym: Intestinal Polyposis-Cutaneous
Pigmentation Syndrome
 Autosomal dominant disorder

85
Q

PEUTZ-JEGHERS SYNDROME

Causes:

A

Causes: Germline heterozygous mutations in
LKB1/STK11 gene

86
Q

PEUTZ-JEGHERS SYNDROME
Characterised by:

A

 Multiple gastro-intestinal hamartomatous polyps
and
 Muco-cutaneous hyperpigmentation

87
Q

. PEUTZ-JEGHERS SYNDROME

Localisation of Polyps:

A

Localisation of Polyps: Small intestine, stomach,
colon; rarely in bladder and lungs

88
Q

Macroscopic features:
 Large and pedunculated lesions
 Lobulated contour (outline)

Microscopic findings:
 Characteristic arborising network of
connective tissue, smooth muscle, lamina propria, and glands with normal intestinal- epithelium lining

A

PEUTZ-JEGHERS SYNDROME

89
Q

HYPERPLASTIC POLYPS

A

Common epithelial proliferations

90
Q

HYPERPLASTIC POLYPS
Hypothetical Pathogenetic mechanism:

A

Hypothetical Pathogenetic mechanism:
 Decreased epithelial cell turnover
 Delayed shedding of surface epithelial cells
=> “Pileup” of goblet cells

91
Q

HYPERPLASTIC POLYPS

Localisation:

A

Commonly, in the left colon

92
Q

Macroscopic features: Smooth nodular
protrusions of the mucosa (on crests of mucosal folds)
Microscopic Findings:
 Mature goblet and absorptive cells
 Irregular tufting (due to overcrowding) of
epithelial cells => Serrated architecture in cross-section

A

HYPERPLASTIC POLYPS

93
Q

‘HYPERPLASTIC POLYPS

Prognosis + DD

A

Prognosis: Benign lesions without malignant
potential
DD: Sessile serrated adenomas (with malignant
potential)

94
Q

COLONIC ADENOMAS

A

Dysplastic (pre-malignant) lesions that give rise to
majority of colorectal Adeno-CAs

95
Q

-COLONIC ADENOMAS

Epidemiology

A

‘Epidemiology:
 Most common neoplastic polyps
 50% of adult population, ≥ 50 years

96
Q

Macroscopic features:
 Pedunculated or sessile lesions; 0.3-10cm
 Surface: Velvet- or raspberry-like texture

Microscopic findings:
 Characteristics of epithelial Dysplasia:
 Nuclear hyperchromasia (Appreciated at Adenoma’s surface)
 Cellular elongation (“ “)
 Stratification (“”)

A

COLONIC ADENOMAS

97
Q

COLONIC ADENOMAS

A

-Invasion of Adenoma cells into submucosa <=>
Invasive Adeno-CA

98
Q

‘COLONIC ADENOMAS

Risk factors ( (for progression of an Adenoma to
Adeno-Ca):

A

Risk factors (for progression of an Adenoma to
Adeno-Ca):
 Increasing size
 High grade of Dysplasia
 Histological type (Villous > Tubular)

99
Q

Microscopic findings (cont.):
 Classification of Adenomas, depending on
morphology:
 Tubular: Small, pedunculated polyps with
small, rounded or tubular glands
 Villous: Large and sessile, covered by slender
villi (invasive growth more frequent than in
tubular adenoma)

A

COLONIC ADENOMAS

100
Q

Microscopic findings (cont.):

Classification of Adenomas, depending on
morphology:
 Tubulo-villous: Mixture of tubular and villous
elements
 Sessile serrated adenomas vs. Hyperplastic
polyps: Serrated architecture throughout
gland’s length (including crypt base)
 Size <=> Risk factor of malignant transformation

A

COLONIC ADENOMAS

101
Q

‘SERRATED PATHWAY

A

30% of cancers arise from serrated polyps
 Serrated polyps: Due to their microscopic
appearance
 Serrated adenomas can progress to carcinomas,
after mutations in specific genes:
 Activation of BRAF
 Silencing of mismatch repair genes (e.g. hMLH1,
hMSH2) due to promotor hypermethylation >
Microsatellite instability > Insertions or
deletions of nucleotides within repeated
sequences of DNA

102
Q

Microscopic features:
 Serrated epithelium at the surface and deep in
the crypts
- Saw-tooth appearance, epithelium has jagged appearing edge
 Crypt dilation at base with serrations
 “Boot”-shape or “L”-shaped glands
- Shape may be similar to a hockey stick
 Horizontal crypts = Crypt long axis parallel to
the muscularis mucosae
 Crypt branching

A

SESSILE SERRATED ADENOMAS

103
Q

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)

A

-Autosomal dominant disorder
- Characterised by the appearance of numerous
colorectal adenomas in teenagers

104
Q

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)

Causes

A

Causes: Mutations in Adenomatous Polyposis Coli
(APC) gene

105
Q

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)

Diagnosis

A

‘Diagnosis: A number of more than 100 polyps,
necessary for classic FAP

106
Q

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)
. Treatment

A

‘Treatment: Prophylactic colectomy (in individuals
with APC mutations); Untreated FAP > Colorectal
Adeno-CA (100% of patients, before 30 years of age)

107
Q

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)
Gardner syndrome:

A

Gardner syndrome:
 Variant of FAP
 Apart from intestinal polyps, also the following:
 Osteomas of mandible, skull and long bones  Epidermal cysts
 Desmoid and thyroid tumours
 Dental abnormalities (unerupted and
supernumerary teeth)

108
Q

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)
Turcot syndrome:

A

‘ Apart from intestinal adenomas, also tumours ‘
of the Central Nervous System
 2/3 of patients, APC gene mutations > Medulloblastomas
 1/3 of patients, Mutations in DNA repair genes
>Glioblastomas

109
Q

HEREDITARY NON-POLYPOSIS COLORECTAL CANCER (HNPCC)

+Synonym

A

‘Synonym: Lynch syndrome
Familial clustering of cancers at several sites
including the colorectum, endometrium, stomach,
ovary, ureters, brain, small bowel, hepatobiliary
tract, and skin

110
Q

-HEREDITARY NON-POLYPOSIS COLORECTAL CANCER (HNPCC)

Epidemiology

A

Epidemiology: Occurrence of colon cancers in
HNPCC patients, at younger ages than sporadic
colon cancers

111
Q

HEREDITARY NON-POLYPOSIS COLORECTAL CANCER (HNPCC)
, Localisation + causes

A

Localisation: Most often in the right colon

 Causes: Inherited mutations in genes, encoding
proteins responsible for the detection, excision, and
repair of errors that occur during DNA replication

112
Q

HEREDITARY NON-POLYPOSIS COLORECTAL CANCER (HNPCC)

Majority of HNPCC cases

A

Majority of HNPCC cases: Mutations in two
such mismatch repair genes, namely MSH2
and MLH1; Inheritance of one mutated DNA
repair gene and one normal allele > Loss of
the second copy through mutation or epigenetic
silencing > Defects in mismatch repair >
Accumulation of mutations at rates up to 1000
times higher than normal, mostly in regions
containing short repeating DNA sequences,
referred as microsatellite DNA (Microsatellite
instability)

113
Q

COLON ADENOCARCINOMA

Epidemiology

A

Epidemiology: ‘’
 Most common malignancy of GI tract
 15% of cancer-related deaths; Second to lung CA
 Dietary factors responsible for the development
of colorectal cancer: i. Low intake of unabsorbable vegetable fiber and ii. High intake of refined carbohydrates and fat

114
Q

COLON ADENOCARCINOMA

Pathogenesis

A

Pathogenesis:
 Two genetic pathways involved in colorectal
carcinogenesis:
1. APC β-Catenin/WNT signaling
pathway
2. Microsatellite instability pathway

Epigenetic events: Most common,
methylation-induced gene silencing

115
Q

COLON ADENOCARCINOMA
 Pathogenesis (cont.):
1. APC/β-Catenin pathway

A
  1. APC/β-Catenin pathway
     80% of sporadic colon tumours
     Early event: Mutation of APC
     Prerequisite for Adenoma development:
    Functional inactivation of both APC gene copies,
    either by mutation or epigenetic events
     APC: Negative regulator of β-Catenin
     Normally, APC binds to β-Catenin and promotes
    its degradation
     Loss of APC function > Accumulation and
    translocation of β-Catenin to the nucleus > Activation of gene transcription (MYC, Cyclin D1)
     Additional mutations in KRAS gene (promotes
    growth and prevents apoptosis)
     Mutations in other tumour suppressor genes
    (SMAD2 and SMAD4)
     Loss of TP53 (either through chromosomal
    deletions or silencing by methylation of CpG
    islands)
116
Q

COLON ADENOCARCINOMA
Pathogenesis (cont.):
2. Microsatellite instability pathway

A
  1. Microsatellite instability pathway
    • Germline (inherited) or somatic (acquired)
    mutations of mismatch-repair genes >
    • > Mutations in microsatellite repeats
    (Microsatellite instability)
    • Mutations located in coding or promoter regions of
    genes involved in cell growth (TGFβRII and BAX)
    • Mutations in BRAF oncogene
    • NO Mutations in KRAS and TP53
117
Q

Macroscopic Features:
 Proximal Colon (Caecum & Ascending Colon):
Polypoid, exophytic lesions; Rarely lumen obstruction
 Distal Colon: Annular lesions (“napkin ring”) > Constrictions and luminal narrowing

A

-COLON ADENOCARCINOMA

118
Q

–Microscopic findings:
 Tall columnar cells
 Invasive growth with intense desmoplastic
reaction
 Amount and morphology of glandular
structures, depending on grade of
differentiation (Grade I-III)
 Some tumours characterised by abundant
mucin production <=> Mucinous Adeno-CAs
 Others with presence of “signet ring” cells

A

COLON ADENOCARCINOMA

119
Q

COLON ADENOCARCINOMA
Clinical features:

A

 Right-sided colon cancers:
 Fatigue and weakness (iron-deficiency anaemia)

 Left-sided colorectal Adeno-CAs:
- Occult bleeding
- Changes in bowel habits
- Cramping

 Complications related to metastases (most
commonly, liver)

120
Q

COLON ADENOCARCINOMA
 Prognostic factors:

A

 Mucinous & poorly differentiated histologic
patterns (Grading of tumour)
 Depth of wall invasion (T staging)
 Presence or absence of lymph node
metastases (N staging)

121
Q

-HAEMORRHOIDS

A

.  Definition: Dilated anal and perianal colateral
vessels that connect the portal and caval
venous systems, to relieve elevated venous
pressure within the haemorrhoid plexus

122
Q

, HAEMORRHOIDS
Causes:

A

Causes:
 Constipation > Straining during defecation
> Increase in intra-abdominal and venous
pressures
 Venous stasis of pregnancy
 Portal hypertension

123
Q

Macroscopic features:
 Collateral vessels within inferior haemorrhoidal
plexus <=> External haemorrhoids (below anorectal line)
 Dilated vessels of superior haemorrhoidal plexus
<=> Internal haemorrhoids (distal rectum)

Microscopic findings:
 Thin-walled, dilated, sub-mucosal vessels that
protrude beneath the anal or rectal mucosa
 Inflammatory infiltrates
 Thrombosis with recanalisation
 Superficial ulceration

A

HAEMORRHOIDS

124
Q

HAEMORRHOIDS
 Clinical features:

A

Pain and Rectal bleeding (bright red blood)

125
Q

‘HAEMORRHOIDS
Management:

A

Management:
 Sclerotherapy
 Rubber band ligation
 Infrared coagulation
 Haemorrhoidectomy

Pathology 1 (4 decks)

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