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PATHOLOGY 2 > Oral cavity and GI tract > Flashcards

Oral cavity and GI tract Flashcards

1
Q
  1. Pathology of lips, oral cavity and pharynx:

MALFORMATIONS OF LIPS AND ORAL CAVITY

A
  1. cleft lip
  2. cleft palate
  3. cheilognathopalatoschisis
    ⇒ partial or complete lack of fusion of the maxillary prominence with the medial nasal prominences
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2
Q
  1. Pathology of lips, oral cavity and pharynx:

STOMATITIS

A 
= inflammation of the mucous linging of any structures in the mouth
RISK FACTORS:
 - poor oral hygiene
 - IDA
 - poorly fittend dentures
 - mouth burns
 - infections
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3
Q 
43. Pathology of lips, oral cavity and pharynx:
CANCER SORES (APHTHOUS ULCERS)
A 
- common small painful shallow ulcers
MORPHOLOGY:
 - rounded superficial erosions
 - covered by grey-white exudate + erythematous rim
 - single or in groups
TRIGGERS:
 - stress
 - fever
 - certain foods
 - activation on IBD
- autoimmune mechanism in immunocompetent
- self limited
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4
Q
  1. Pathology of lips, oral cavity and pharynx:

PEMPHIGUS

A
  • Autoantibodies against DESMOGLEIN
  • normally attaches epidermal cells in desmosomes
  • acantholysis (unglued)
  • cause blisters ⇒ sores
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5
Q
  1. Pathology of lips, oral cavity and pharynx:

HSV-1 INFECTION

A
  • causes labial herpes
  • transmission: person to person (kissing)
    PATHOGENESIS:
  • primary infection asymptomatic ⇒ virus remains latent in sensory ganglia
    ⇒ reactivation (sun, stress. fever, trauma) ⇒ vesicles ⇒ rupture ⇒ painful ulcer
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6
Q
  1. Pathology of lips, oral cavity and pharynx:

ORAL CANDIDASIS

A 
CAUSE: C.Albicans
MORPHOLOGY:
 - white, curdle, circumscribed plaque
RISK FACTORS:
 - DM
 - anemia
 - antibiotic or glucocorticoid treatment
 - immunodeficient state (HIV)
COMPLICATIONS: spread to esophagus or disseminate to blood
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7
Q
  1. Pathology of lips, oral cavity and pharynx:

TONSILLITIS

A

SYMPTOMS: sore throat and fever
CAUSATIVE AGENTS: common cold viruses, s.pyogenes
MORPHOLOGY:
- strawberry tonsils + purulent discharge

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8
Q
  1. Pathology of lips, oral cavity and pharynx:

PHARYNGITIS

A

SYMPTOMS: pain, sore throat

CAUSATIVE AGENTS: common cold viruses, EBV, s.pyogenes, c.diphteria

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9
Q
  1. Pathology of lips, oral cavity and pharynx:

NECROTIZING ULCERATIVE GINGIVITIS

A 
CLINICAL FEATURES:
 - necrosis, ulceration + pseudomembrane
CAUSATIVE AGENTS:
 - anaerobes
 - borrelia + troponema
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10
Q
  1. Pathology of lips, oral cavity and pharynx:

BENIGN NEOPLASMS OF ORAL CAVITY

A
  1. Fibromas
    - submucosal nodular fibrous tissue masses
    - chronic irritation ⇒ CT hyperplasia
    - treatment: surgery
  2. Pyogenic granulomas
    - gingiva of children, young adults and pregnant women
    - erythematous hemorrhagic exophytic masses ⇒ ulcer
    - can regress, mature or develop into peripheral ossifying fibroma
    - treatment: surgery
  3. Papilloma
    - finger like fronds
    - associated with HPV 6 and 11
    - treatment: surgery
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11
Q
  1. Pathology of lips, oral cavity and pharynx:

PRE-NEOPLASTIC LESIONS OF ORAL CAVITY

A
  1. Leukoplakia
    - white, well defined plaque
    - older men
    - 3-25% ⇒ squamous cell carcinoma
    - associated with tobacco
  2. Erythroplakia
    - red, velvety, granular circumscribed areas
    - epithelial dysplasia
    - 50% ⇒ malignant
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12
Q
  1. Pathology of lips, oral cavity and pharynx:

MALIGNANT NEOPLASMS OF ORAL CAVITY

A 
1. Squamous cell carcinoma
PATHOGENESIS:
 - tobacco, alcohol ⇒ mutation in p53, p63 and NOTCH 1
 - HPV16 ⇒ overexpress p16
MORPHOLOGY:
 - location: ventral surface of tongue, floor of mouth, lower lip, soft palate, gingiva
 - raised, firm, pearly plaque
 - metastasizes end up at cervical LN
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13
Q

44.Salivary gland diseases:

SIALADENITIS

A 
= inflammation of salivary glands
PATHOGENESIS + TYPES:
1. Traumatic:
 - blockage or rupture of duct ⇒ leakage of saliva
 - toddlers, young adults, elderly
 - appears as swelling of lower lip
 - treatment: excision of cyst
2. Viral:
 - mumps
 - swelling of all glands
3. Bacterial:
 - s.aureus or s.viridians
 - secondary to sialolothiasis obstruction
4. Autoimmune disease
 - Mikulics syndrome: sarcoidosis, lymphoma, Sjögren
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14
Q

44.Salivary gland diseases:

NEOPLASMS OF SALIVARY GLANDS

A

LOCATION:
- 65-80% parotid gland (15-30% malignant)
- 10% submandibular gland (40% malignant)
- rest in sublingual + oral mucosal glands
ETIOLOGY:
- occurs in adults
- more in female

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15
Q

44.Salivary gland diseases:

BENIGN NEOPLASMS

A
  1. Pleiomorphic adenoma
    - slow growing, encapsulated
    - superficial parotid⇒ painless swelling in angle of jaw
    - ductal and myoepithelial cells, well differentiated
  2. Whartin tumor
    = papillary cystadenoma lymphomatosum
    - location: parotid
    - small, encapsulated, round
  3. Onkocytoma
  4. Monomorphic adenomas
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16
Q

44.Salivary gland diseases:

MALIGNANT NEOPLASMS

A
  1. Mucoepidermoid carcinoma
    - squamous cells, mucus-secreting cells, intermediate cells
    - location: parotid
    - mutation: MAML2
    - up to 8cm, no capsule, infiltrative
  2. Adenoid cystic carcinoma
    - infiltrate perineurial space
    - cause pain, slow growing, late metastasis
  3. Acinic cell carcinoma
  4. Adenocarcinoma
  5. B cell non-Hodgkin lymphoma
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17
Q
  1. Pathology of esophagus:

MECHANICAL OBSTRUCTION

A
  1. Agenesis
  2. Atresia
  3. Duplications
  4. Tracheo-esophageal fistula
  5. Stenosis ⇒ fibrosal thickening, due to inflammation + scarring due to GERD, irradiation, injury
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18
Q
  1. Pathology of esophagus:

DIVERTICULA

A
  • functional obstruction of the esophagus
    = outpouching of a hollow structure
    TYPES:
    1. Zenker diverticulum ⇒ of mucosa + submucosa, above UES
    2. Traction diverticulum ⇒ due to scarring from TB
    3. Epiphrenic diverticulum ⇒ due to dysfunction of LES, as in achalasia
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19
Q
  1. Pathology of esophagus:

ACHALASIA

A
  • functional obstruction of esophagus
    = incomplete LES relaxation, increased LES tone and esophageal aperistalsis
  • primary: failure of distal inhibitory neurons, idiopathic
  • secondary: e.g. Chagas disease
    CLINICAL FEATURES:
  • progressive distension of esophagus proximal to LES
  • stasis ⇒ mucosal inflam + ulceration
  • dysphagia, nocturnal regurgitation, aspiration of undigested food
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20
Q
  1. Pathology of esophagus:

HIATAL HERNIA

A
  • functional obstruction
    = protrusion of organ through tear of weakness (stomach through diaphragm)
    1. Sliding hernia ⇒ gastro-esophageal junction above diaphragm⇒ bell shaped dilation
    2. Rolling hernia ⇒ stomach though esophageal hiatus⇒ lies beside esophagus
    COMPLICATIONS: reflux, mucosal ulceration, bleeding, perforation
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21
Q
  1. Pathology of esophagus:

MALLORY WEISS SYNDROME

A

= longitudinal tear in esophagus
- in chronic alcoholics + acute illness due to vomiting
PATHOGENESIS:
- insufficient relaxation on LES ⇒ stretching + tearing
- Hiatal hernia can cause MW tears aswell

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22
Q
  1. Pathology of esophagus:

ESOPHAGEAL VARICES

A 
- porto-caval anastomosis
PATHOGENESIS:
 - obstructed liver ⇒ portal blood ⇒ stomach veins ⇒ esophageal veins ⇒ azygos vein ⇒ IVC
 - variceal rupture ⇒ massive hemorrhage ⇒ shock ⇒ death
CLINICAL FEATURES:
 - hematemesis + melena
 - 20-30% die first time 
 - reoccurence 70% within 1 year
TREATMENT:
 - coagulants + balloon tamponade
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23
Q
  1. Pathology of esophagus:

ESOPHAGITIS

A

CAUSE:

  • GERD ⇒ strictures, leukoplakia, Barrett
  • infections
  • ingestion of corrosive or irritant substances
  • prolonged gastric intubation
  • uremia
  • radiation
  • chemotherapy
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24
Q
  1. Pathology of esophagus:

GASTRO-ESOPHAGEAL REFLUX DISEASE

A

CAUSE:
- decreased efficiency of esophageal antireflux mechanism
- inadequate clearance of refluxed material
- presence of sliding hernia
- increased gastric volume, volume of refluxed materials
CLINICAL FEATURES:
- heartburn
- regurgitation of stomach content

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45. Pathology of esophagus: | BARRETT ESOPHAGUS
- complication of GERD - males more affected, 40-60 yo MORPHOLOGY: - patches of red, velvety mucosa extending upward from gastroesophageal junction - gastric metaplasia (columnar epithelium) - risk for adenocarcinoma
26
45. Pathology of esophagus: | EOSINOPHILIC ESOPHAGITIS
SYMPTOMS: - food impaction - dysphagia - feeding intolerance - GERD-like symptoms - large number of eosinophils
27
45. Pathology of esophagus: | MALIGNANT TUMORS
1. Adenocarcinoma RISK FACTORS: - Barrett esophagus / GERD - tobacco, alcohol, obesity, radiation therapy MORPHOLOGY: - distal third - flat patch ⇒ large exophytic masses ⇒ infiltrate, ulcerate, invade deeply CLINICAL FEATURES: - cachexia, tracheo-esophageal fistula, ichorous mediastinitis 2. Squamous cell carcinoma RISK FACTORS: tobacco, alcohol MORPHOLOGY: - middle third - in situ lesion of small grey plaque ⇒ large mass ⇒ ulcerate, infiltrate - can invade respiratory tree, aorta, mediastinum, pericardium
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46. Gastritis: | ACUTE GASTRITIS
CAUSE: - NSAIDS, alcohol, smoking, chemotherapy, uremia, systemic infection, stress, ischemia, shock, mechanical trauma MORPHOLOGY: - localized or diffuse inflammation with hemorrhage and focal erosions - mucosal edema, neutrophilic infiltration, petechiae, epithelial regeneration in neck of glands CLINICAL FEATURES: - asymptomatic - epigastric pain, nausea, vomiting - hematemesis, melena, fatal blood loss
29
46. Gastritis: | CHRONIC GASTRITIS
CAUSE: - H.pylori infection, autoimmune, radiation injury, chronic bile reflux PATHOGENESIS: -TYPE A: H.pylori ⇒ bacterial enzymes + toxins ⇒ antral type or pangastritis - TYPE B: autoimmune: autoantibodies against gastric gland parietal cells ⇒ gland destruction + mucosal atrophy ⇒ loss of acid production and intrinsic factor ⇒ pernicious anemia CLINICAL FEATURES: - upper abdominal discomfort, nausea, vomiting - hypochlorhydria or achlorhydria + hypergastrinemia - peptic ulcer and gastric carcinoma, MALT lymphoma
30
47. Peptic ulcers: | DEFINITION
ULCER: breach in mucosa, can extend deep. Take long time to heal. Anywhere in GI tract, mostly in duodenum and stomach. PEPTIC ULCER: chronic, solitary lesion exposed to peptic juices
31
47. Peptic ulcers: | PATHOGENESIS
1. H.pylori infection: - bacteria induces inflammatory and immune response⇒ pro inflammatory cytokines - produces toxins ⇒ epithelial injury - secrete urease ⇒ form ammonium-chloride - increases phospholipase ⇒ damage surface epithelial cells ⇒ weakening of mucosal defense - enhances gastric acid secretion + impairs duodenal bicarbonate production ⇒ lower pH in duodenum 2. Mucosal exposure to gastric acid and pepsin - NSAIDs ⇒ suppress prostaglandin synthesis ⇒ increased HCl, decreased bicarbonate
32
47. Peptic ulcers: | DEFENSES + DAMAGING FORCES
``` DEFENSES: ⇒ mucus secretion ⇒ blood supply ⇒ bicarbonate ⇒ prostaglandin ⇒ regeneration DAMAGING FORCES: ⇒ H.pylori ⇒ NSAIDs ⇒ smoking, alcohol ⇒ hyperacidity ⇒ GERD ```
33
47. Peptic ulcers: | CLINICAL FEATURES
- epigastric pain (worse at night and after meals) - nausea, vomiting, bloating, belching, weight loss COMPLICATIONS: - hemorrhage - perforation - penetration into adjacent organs - carcinoma - stenosis TREATMENT: - antibiotics, PPIs, hydrogen receptor antagonists
34
47. Peptic ulcers: | MORPHOLOGY
- deep necrosis - mucosal folds (star-like) - CT proliferation HISTOLOGY: - epithelial slough on top - fibrinoid necrosis - granulation tissue - scarring on basolateral side
35
48. Gastric tumors: | GASTRIC POLYPS
``` = mass projecting above level of surrounding mucosa TYPES: 1. Hyperplastic polyp - hyper plastic epithelia, edematous stroma 2. Fundic gland polyp 3. Adenomatous polyp - dysplastic epithalia, preneoplastic - arise in setting of chronic gastritis ```
36
48. Gastric tumors: | GASTRIC CARCINOMA epidemiology
- geographic incidence LOCATION: - lesser curvature, antrum, corpus, fundus CLASSIFICATION: 1. protruding nodular or polypoid lesion 2. sligthly elevated or depressed flat lesion 3. excavated or ulcerated lesion
37
48. Gastric tumors: | GASTRIC CARCINOMA pathogenesis
1. Nutritional factors - smoked fish, pickled vegetables, salted food, little fruits 2. Infections - H.pylori 3. Genetic factors - blood group A - changes in p53, germline mutations, genetic mismatch repair 4. Other factors
38
48. Gastric tumors: | GASTRIC CARCINOMA histological types
1. Intestinal type adenoocarcinoma: - arise from gastric mucous cells ⇒ metaplasia due to chronic gastritis - better differentiated - tubular glands - male >50yrs 2. Diffuse adenocarcinoma: - arise de novo from native gastric mucous cells - not associated with chronic gastritis - poorly differentiated - extensive mucus production + signet ring cells - risk factor: mutation in E-cadherin
39
48. Gastric tumors: | GASTRIC CARCINOMA morphology
- mucosal flattening and thickening with erosions - diffuse thickening of gastric wall "linitis plastic" - large ulcers or polypoid fungating masses - exophytic / flat / depressed / excavated
40
48. Gastric tumors: | GASTRIC CARCINOMA clinical features
- prognosis: 5yr survival ⇒ <20% - abdominal discomfort + weight loss - dysphagia METASTASIS: - LN at lesser/greater curvature, subpyloric region and porta hepatis - Virchow node - lungs - bone marrow - ovaries "krukenberg tumor" - peritoneum - liver
41
48. Gastric tumors: | MALT LYMPHOMA
- 1-4% of GI malignancies - originates in B cells - adults affected - Location: stomach(50-60%), small intestine(25-30%), colon(10-15%) - HP associated chronic gastritis ⇒ activation of B and T cells ⇒ polyclonal B cell hyperplasia ⇒ monoclonal B cell neoplasm
42
48. Gastric tumors: | GIST
= Gastro-intestinal stromal tumor - mutation in cKIT (CD117) - derive from Cajal cells - ligand binds ⇒ dimerization ⇒ signal transduction ⇒ cell survival ⇒ uncontrolled growth - evaluation: mitotic number + size of tumor - target therapy
43
49. Developmental anomalies and vascular disorders of the GI tract: ATRESIA
- complete failure of development of intestinal lumen | - most common: duodenal atresia
44
49. Developmental anomalies and vascular disorders of the GI tract: STENOSIS
- narrowing of the intestinal lumen with incomplete obstruction
45
49. Developmental anomalies and vascular disorders of the GI tract: DUPLICATION
- well-formed saccular to tubular lytic structures, which may or may not communicate with the lumen of the small intestine
46
49. Developmental anomalies and vascular disorders of the GI tract: DIVERTICULOSIS OF THE COLON
- herniation of the colonic mucosa or submucosa through intestinal muscular wall ⇒ cystic expansion in adventitial tissue - people over 60 yrs affected - location: sigmoid colon ( can be anywhere) - develops at sites of weakness in muscle wall due to increased colonic pressure due to low fiber diet COMPLICATIONS: - hemorrhage - stasis of feces in diverticula ⇒ recurrent inflammation - perforation ⇒ fecal peritonitis
47
49. Developmental anomalies and vascular disorders of the GI tract: OMPHALOCELE
- congenital defect of periumbilical abdominal musculature ⇒ membranous sac in peritoneal layer ⇒ intestines herniate - severe
48
49. Developmental anomalies and vascular disorders of the GI tract: MALROTATION
- malrotation of developing bowel ⇒ prevent intestines from assuming normal intra-abdominal position - problem: appendicitis if colon misplaced ⇒ pain in upper quadrant instead of McBurney point
49
49. Developmental anomalies and vascular disorders of the GI tract: HIRSCHSPRUNG DISEASE: CONGENITAL MEGACOLON
``` = dissension of colon to greater than 6-7 cm in diameter - congenital/acquired - Hirschsprung disease (congenital) results when neural crest derived cells migrate along alimentary tract arrests at some point before reaching anus - Aquired causes: * Chagas disease (trypanosoma) * Obstruction * toxic megacolon (IBD) CONSEQUENCES: - aganglionic segments ⇒ functional obstruction + progressive distension CLINICAL FEATURES: - delayed passage of meconium - vomiting in 48-72h - superimposed enterocolitis ```
50
49. Developmental anomalies and vascular disorders of the GI tract: MESENTERIC ARTERY THROMBOSIS/VENOUS THROMBOSIS
- produce hemorrhagic infarction of intestines - arterial thrombosis causes: * atherosclerosis * systemic vasculitis * dissecting aneurysm - venous thrombosis causes: * abdominal trauma or surgery * sepsis * hypercoagulation state - occlusion ⇒ 18 h ⇒ ischemic injury ⇒ hyperemia, hemorrhage, progressive necrosis ⇒ gangrenous enteritis + peritonitis + bowel perforation
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49. Developmental anomalies and vascular disorders of the GI tract: ISCHEMIC BOWEL DISEASE
``` CLASSIFICATION OF SEVERITY: 1. Mucosal infarct 2. Mural infarct (mucosa + submucosa) 3. Transmural infarct PREDISPOSING FACTORS: 1. Arterial thrombosis 2. Arterial embolism (cardiac vegetation, MI jnfarction, aortic atheroembolism) 3. Venous thrombosis CLINICAL FEATURES: - common in later years - transmural: sudden onset abdominal pain, blood in stool, may progress to shock + vascular collapse - mural and mucosal: abdominal distension, GI hemorrhage, abdominal pain ```
52
49. Developmental anomalies and vascular disorders of the GI tract: ANGIODYSPLASIA
= tortuous dilations of submucosal and mucosal blood vessels - after 60yrs old - location: cecum, ascending colon - prone to rupture - hemorrhage is chronic and intermittent ⇒ anemia - isolated lesion or after systemic disorder ⇒ hereditary hemorrhagic teleangiectasia or CREST syndrome
53
49. Developmental anomalies and vascular disorders of the GI tract: HEMORRHOIDS
= variceal dilation of anal and perianal submucosal plexuses - common after 50yrs old - develop in setting of elevated venous pressure PREDISPOSING FACTORS: - straining with defecation - chronic constipation - venous stasis of pregnancy CLASSIFICATION: 1. Internal hemorrhoids: - inside rectum - varicosities of superior and middle hemorrhoidal veins above anorectal line - risk of prolapse ⇒ strangulated by anal sphincter 2. External hemorrhoids: - outside the distal end of anal canal - varicosities of inferior plexuses - covered by anal mucosa
54
50. Malabsorption: | MALABSORPTION SYNDROME
= defective absorption of fats, fat-soluble + other vitamins, proteins, carbohydrates, electrolytes, minerals, water - presents as chronic diarrhea ⇒ steatorrhea - defects in: 1. intraluminal digestion 2. mucosal absorption 3. nutrient delivery EXAMPLES: pancreatic insufficiency, celiac disease, Crohns disease
55
50. Malabsorption: | DEFECTS OF INTRALUMINAL DIGESTION
- symptoms: osmotic diarrhea and steatorrhea - causes: * pancreatic insufficiency + chronic alcoholism * Crohn disease * intestinal bacterial overgrowth * cholestatic liver disease
56
50. Malabsorption: | LACTOSE INTOLERANCE
- caused by deficiency in lactase enzyme - inherited form ⇒ infants have milk intolerance ⇒ diarrhea, weight loss, failure to thrive - acquired form⇒ common among adults DIAGNOSIS: hydrogen breath test
57
50. Malabsorption: | DEFICIENCY OF APOLIPOPROTEIN-B
- mucosal epithelial cells cannot export lipids - required for assembly of chylomicron ⇒ no chylomicron ⇒ lipid accumulates in enterocytes - symptoms: diarrhea, steatorrhea
58
50. Malabsorption: | CELIAC DISEASE
= gluten sensitive enteropathy - resulting from reduction in small intestine absorptive surface area PATHOGENESIS: - associated with HLA-DQ2 - gliadin AGs presented by APCs in lamina propria to helper T cells ⇒ immune response - the mucosa accumulates with intraepithelial killer T cells ⇒ CD8+ T cell mediated destruction of intestinal epithelial cells ⇒ loss of villi - higher risk for malignancy
59
50. Malabsorption: | TROPICAL SPRUCE
- associated with intestinal infections - resemble celiac disease - injury in whole small intestine - acute diarrhea ⇒ malabsorption - steatorrhea, weight loss, anorexia, abdominal distension, flatus, muscle wasting
60
50. Malabsorption: | WHIPPLE DISEASE
- systemic infection - intestine, CNS, joints - cause: Tropheryma whippelii - PAS + macrophages - males >40yrs - symptoms: * startorrhea, anorexia, abdominal distension, flatus, muscle wasting * lymphadenopathy * hyperpigmentation * polyarthritis * CNS complaints
61
50. Malabsorption: | CONSEQUENCES OF MALABSORPTION
1. General symptoms: - weight loss, anorexia, abdominal dissension, steatorrhea 2. Hematopoietic system: - anemia ⇒ iron, folate, vitamin b12 deficiency - bleeding ⇒ vitamin K deficiency 3. Musculoskeletal system: - osteopenia, tetany ⇒ defective calcium, magnesium, vitamin D, protein absorption 4. Endocine system: - amenorrhea, impotense, infertility - hyperparathyroidism ⇒ calcium + vitamin K def. 5. Skin: - purpura, petechia ⇒ vitamin K - dermatitis, hyperkeratosis ⇒ vitamin A, zinc, FAs, niacin 6. Nervous system: - peripheral neuropathy ⇒ vitamin A, B12 def.
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50. Malabsorption: | SPECIFIC DEFICIENCIES AND THEIR SYMPTOMS
- vitamin B12 + folic acid (megaloblastic anemia) - vitamin K (bleeding with petechia) - Vitamin D and calcium (osteomalacia, tetany) - Vitamin A (hyperkeratosis, dermatitis) - protein (edema, malnutrition) - zinc (dermatitis, immune defects)
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51. Enterocolitis: | DIARRHEA
= increased stool mass, frequency + fluidity, accompanied with pain, urgency, perianal discomfort, incontinence - Dysentery= low-volume, painful, bloody diarrhea (shigella, amoeba, dysenteriformic colitis) TYPES: 1. Secretory diarrhea: - net intestinal fluid secretion - isotonic with plasma and persist during fasting 2. Osmotic diarrhea: - excessive osmotic forces excreted by luminal solutes that subside with fasting 3. Exudative diarrhea: - purulent, bloody stool- persist on fasting. Frequent stools 4. Malabsorption diarrhea: - voluminous, bulky stools - increased osmolarity - subside with fasting 5. Deranged motility diarrhea: - variable features
64
51. Enterocolitis: | VIRAL GASTROENTERITIS
- infection of superficial epithelium in small intestine ⇒ destroy epithelium + absorptive function - repopulation of vili with immature enterocytes + preservation of crypt secretory cells ⇒ net secretion of water and electrolytes + osmotic diarrhea CAUSES: rotavirus, caliciviruses
65
51. Enterocolitis: | BACTERIAL GASTROENTERITIS
MECHANISM: 1. ingestion of preformed toxin (e.g. s.aureus, vibrio, c.perfringens) 2. infection by toxigenic organisms ⇒ proliferate in lumen ⇒ elaborate an enterotoxin 3. infection of enteroinvasive organisms ⇒ proliferate, invade, destroy mucosal epithelial cells (e.g. EIEC) ⇒ ability to adhere to mucosal epithelial cells ⇒ ability to elaborate enterotoxins ⇒ capacity to invade, IC proliferation, cell-cell spread MORPHOLOGY: - increased mitotic rate in crypts + decreased maturation on surface epithelium - hyperemia, edemia in lamina propria - neutrophilic infiltrate COMPLICATIONS: - dehydration - sepsis - perforation NECROTIZING ENTEROCOLITIS= necrotizing inflammation of small and large intestines in neonates
66
51. Enterocolitis: | PARASITE GASTROENTERITIS
- Entamoeba histolytica⇒ amoebic dysentery * ulcerating proctosigmoiditis and colitis - Trichuris trichuria, Ascaris lumbricoides, enterobius vermicularis, taenia saginata and solium
67
52. Colonic diverticulosis and bowel obstruction: | DIVERTICULUM
= blind pouch that communicates with lumen of GI tract - Congenital diverticulum: all three layers of bowel ⇒ Meckel diverticulum - Aquired diverticulum ⇒ diet low in fiber ⇒ reduced bulky stool ⇒ increased luminal pressure ⇒ herniation of bowel wall through weak points CAUSES: exaggerated peristaltic contractions, focal defects CLINICAL FEATURES: - asymptomatic - intermittent cramping - diverticulitis ⇒ inflammed ⇒ tenderness, fever - hematochezia, perforation, fistula formation TREATMENT: high fiber diet
68
52. Colonic diverticulosis and bowel obstruction: | HERNIAS
= weakness in wall of peritoneal cavity permit protrusion of pouch like series lined sac of peritoneum - locations: umbilicus, inguinal and femoral canal, surgical scars - pressure at neck of such ⇒ impair venous drainage ⇒ stasis and edema ⇒ incarceration ⇒ further compromise blood supply ⇒ infarction
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52. Colonic diverticulosis and bowel obstruction: | INTESTINAL ADHESIONS
- surgical procedures, infection, endometriosis ⇒ localized or general peritoneal inflammation - with healing ⇒ adhesions may develop between bowel segments
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52. Colonic diverticulosis and bowel obstruction: | INTUSSUSCEPTION
- denotes telescoping of proximal segment of bowel into immediately distal segment - children: excessive peristaltic activity - adults: intraluminal mass - cause obstruction + compromised vascular supply ⇒ infarction
71
52. Colonic diverticulosis and bowel obstruction: | VOLVUS
- twisting of a loop of bowel (or other structure) around its base of attachment ⇒ constricting venous outflow⇒ intestinal obstruction + infarction - mostly small intestine, rarely sigmoid
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53. Inflammatory bowel disease: | IBD general + pathogenesis
=group of diseases characterized by exaggerated and destructive mucosal immune response of colon and small intestine - Crohn disease + UC ⇒ chronic relapsing inflammatory disorders of unknown origin - result from abnormal immune response against normal flora of gut PATHOGENESIS: - loss of balance between factors that activate host immune system and host defense that down-regulate inflammation ⇒ IBD - genetic susceptibility, failure of immune regulation, triggering by microbial flora
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53. Inflammatory bowel disease: | IBD genetic predisposition + immunological factors
GENETIC PREDISPOSITION: - specific MHC-II alleles 1. Crohns disease: - mutation in gene NOD2 ⇒ defective response to bacteria + promote excessive host response 2. CD and UC: - mutation in IL-23 receptor gene ⇒ IL23 promotes production of IL-17 by T cells IMMUNOLOGICAL FACTORS: - primary damaging agents: helper T cells - inflammation due to IL17
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53. Inflammatory bowel disease: | IBD consequenses
- impaired integrity of mucosal epithelial barrier - loss of surface epithelium - intermittent bloody diarrhea
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53. Inflammatory bowel disease: | CROHN DISEASE general + morphology
- location: anywhere, mostly terminal ileum - systemic inflammatory disease - accompanied with extra-intestinal complications: uveitis, sacroiliitis, migratory polyarthritis, erythema nodosum etc. MORPHOLOGY: - sharply limited transmural involvement ⇒ mucosal damage - transmural edema + fibrosis - nodular and follicular lymphocytic infiltrates - non-caseating granulomas - fistula formation
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53. Inflammatory bowel disease: | CROHN DISEASE clinical features + consequences
``` CLINICAL FEATURES: - any age, peak at 20-30yrs - more in women - recurrent episodes of diarrhea - cramping abdominal pain - fever - malabsorption - melena - remitting-relapsing CONSEQUENCES: - fistula formation - abdominal abscesses and peritonitis - intestinal stricture or obstruction ```
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53. Inflammatory bowel disease: | ULCERATIVE COLITIS general + epidemiology
- affecting colon, mucosa and submucosa - begins in rectum and extends proximally - systemic disorder, associated with: polyarthritis, ankylosing spondylitis, uveitis etc. EPIDEMIOLOGY: - any age, peak at 20-25 yrs - more common in whites - equal between sexes - familiar association
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53. Inflammatory bowel disease: | ULCERATIVE COLITIS morphology + clinical features
``` MORPHOLOGY: - no well-formed granulomas - no skip lesions - mucosal ulcers + little fibrosis - serosal surface normal - high risk of cancer development - formation of pseudo polyp CLINICAL FEATURES: - attacks of bloody mucoid diarrhea - slow onset ⇒ cramps, tenesmus, colicky lower abdominal pain COMPLICATIONS: - severe diarrhea - massive hemorrhage - severe colonic dilation - rupture - cancer ```
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54. Pathology of the appendix and peritoneum: | ACUTE APPENDICITIS pathogenesis
- peak incidence: 20-30yrs - male predominance 5:1 - associated with obstruction due to fecalith, gallstone, tumor, worms ⇒ buildup of pressure ⇒ collapse of draining veins ⇒ favor bacterial proliferation + edema and exudate STAGES: 1. acute early 2. acute suppurative 3. acute gangrenous 4. rupture ⇒ peritonitis
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54. Pathology of the appendix and peritoneum: | ACUTE APPENDICITIS clinical features
- mild periumbilical discomfort - anorexia - RLQ tenderness - deep contract pain - fever, nausea, vomiting, constipation, diarrhea, leukocytosis DIFFERENTIAL DIAGNOSIS: - mesenteric lymphadenitis after viral infection - gastroenteritis with mesenteric adenitis - PID - rupture of ovarian follicle - ectopic pregnancy - meckel diverticulitis TREATMENT: surgical removal
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54. Pathology of the appendix and peritoneum: | APPENDIX CARCINOIDS
- slow growing neuroendocrine tumor - arise from enterochromaffin cells - asymptomatic - solid, yellow tan color - almost never metastasize
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54. Pathology of the appendix and peritoneum: | APPENDIX MUCINOUS NEOPLASM
- benign mucinous cystadenoma ⇒ malignant mucinous cystadenocarcinoma - malignant ⇒ invade wall ⇒ pseudomyxoma peritonei
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54. Pathology of the appendix and peritoneum: | APPENDIX MUCOCELE
- dilation of the lumen by mucinous secretion | - cause: non-neoplastic obstruction associated with fecalith
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54. Pathology of the appendix and peritoneum: | ACUTE PERITONITIS
PATHOGENESIS: - bacterial infection - chemical irritation ⇒ pancreatic juice, gastric juice, bile, blood - usually a complication of perforation of intraabdominal organs, abdominal surgery or peritoneal dialysis MORPHOLOGY: - fibrinopurulent, gangrenous or fecal inflammation with fibrous adhesions CLINICAL FEATURES: - nausea, vomiting - abdominal tenderness and pain - abdominal distension - reduction of intestinal motility - paralytic ileus - high fever - septic shock TREATMENT: antibiotics, surgical drainage, supportive therapy
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54. Pathology of the appendix and peritoneum: | PNEUMOPERITONEUM
``` = accumulation of air or gas in abdominal cavity CAUSES: - perforated peptic ulcer - bowel obstruction - ruptured diverticulum - penetrating trauma - ruptured IBD - necrotizing enterocolitis - bowel cancer - ischemic bowel - colonic or peritoneal infection - from chest ⇒ bronchopleural fistula ```
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54. Pathology of the appendix and peritoneum: | ASCITES
= accumulation of fluid in peritoneal cavity - serous fluid - 3mg/dL protein + solutes - may contain mesothelial cells and mononuclear leukocytes ⇒ neutrophils ⇒ infection ⇒ RBCs ⇒ cancer - long standing ascites ⇒ hydrothorax CAUSES: - liver cirrhosis - severe liver disease - HF ⇒ increased venous pressure ⇒ portal HT ⇒ ascites
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54. Pathology of the appendix and peritoneum: | NEOPLASMS OF PERITONEUM
- primary neoplasms rare, but aggressive ⇒ survival 6 months 1. Mesothelioma - asbestos exposure 2. Carcinoma - resemble ovarian carcinoma - masses on omentum and peritoneum
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54. Pathology of the appendix and peritoneum: | METASTATIC CARCINOMA
FROM: - ovary - stomach - pancreas - intra-abdominal carcinoma (colon, GIST)
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55. Tumors of the small and large intestines: | POLYP
= mass protruding into lumen of gut - pedunculate or sessile - formed due to: * abdominal mucosal maturation, architecture or inflammation ⇒ non-neoplastic polyp * epithelial proliferation, dysplasia ⇒ adenoma - Hyperplastic polyp= most common of colon and rectum
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55. Tumors of the small and large intestines: | NON-NEOPLASTIC POLYPS
- people >60 yrs - occurs sporadically, increase with age HYPERPLASTIC POLYP: - small, nipple-like, hemispherical, smooth protrusion of mucosa - single/ multiple - mostly in rectosigmoid region - Histo: abundant crypts, goblet cells or absorptive epithelial cells - not malignant (except sessile serrated adenomas) JUVENILE POLYP: - hamartomas ⇒ proliferations of lamina propria - in children <5yrs + adults (retention polyp) - no malignant potential - source of rectal bleeding + twisting⇒ infarction
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55. Tumors of the small and large intestines: | ADENOMAS
- prevalence increasing with age - arise as result of epithelial proliferation and dysplasia ⇒ mild to severe range SUBTYPES: 1. tubular adenomas 2. villous adenoma 3. tubulovillous adenomas 4. sessile serrated adenomas MALIGNANT RISK: - polyp size - histological architecture - severity of dysplasia CLINICAL FEATURES: - asymptomatic - bleeding ⇒ IDA
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55. Tumors of the small and large intestines: | FAMILIAL POLYPOSIS SYNDROMES
- AD disorder - potential for malignancy FAMILIAL ADENOMATOUS POLYPOSIS: - APC mutation - 500-2500 colonic tubular adenomas + duodenum - high colon cancer risk - associated with: Gardner syndrome + Turcot syndrome PEUTZ-JEGHERS POLYP: - hamartomas polyp - increased risk for intestinal and extra intestinal malignancies - LKB1 gene inactivation mutation (chr 19p) - complication: bleeding, anemia, intussusception
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55. Tumors of the small and large intestines: | COLORECTAL CARCINOMA epidemiology + pathogenesis
``` EPIDEMIOLOGY: - peak incidence: 60-70yrs - male predominance PATHOGENESIS: - presursor adenoma - environmental factors: diet - genetic factors ⇒ HNPCCS, UC ```
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55. Tumors of the small and large intestines: | COLORECTAL CARCINOMA APC/B-catenin pathway
``` - chromosomal instability + accumulation of mutations STAGES: 1. localized epithelial proliferation 2. formation of small adenoma 3. these become dysplastic 4. develop into invasive cancer ```
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55. Tumors of the small and large intestines: | STEPS OF APC/B-CATENIN PATHWAY
1. Loss of APC gene- tumor suppressor gene: - b-catenin accumulates ⇒ translocates into nucleus ⇒ activates transcription ⇒ cell proliferation 2. Mutation of K-RAS: - trapped in activated state ⇒ delivers mitotic signals ⇒ prevents apoptosis 3. 18q21 deletion: - genes DCC,SMAD2,SMAD4 ⇒ uncontrolled cell growth 4. Loss of p53: - no apoptosis
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55. Tumors of the small and large intestines: | DNA MISMATCH REPAIR PATHWAY
- genetic lesion in DNA mismatch repair genes - leads to hypermutable state ⇒ micro satellites are unstable during DNA replication ⇒ widespread alteration in genes that regulate growth, differentiation, apoptosis - accumulation of mutations
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55. Tumors of the small and large intestines: | COLORECTAL CARCINOMA morphology + clinical features
``` MORPHOLOGY: - polyploid and ulcerating - well-differentiated with mucus secretion CLINICAL FEATURES: - asymptomatic for years - cecal + right colonic cancer ⇒ fatigue, weakness, IDA - left colonic cancer ⇒ hemorrhages, bowel habit changes, cramps LLQ discomfort METASTASIS: - direct excision - regional LN - liver - lungs - bones DIAGNOSIS: - rectal examination for blood - fecal testing for blood - barium enema - sigmoidoscopy and colonoscopy - CT ```
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55. Tumors of the small and large intestines: | MOST FREQUENT BENIGN TUMORS
1. stromal tumors of smooth muscle origin 2. adenomas and polyps 3. lipomas 4. various neurogenic, vascular, hamartomatous epithelial lesions 5. adenocarcinoma and carcinoid tumors
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55. Tumors of the small and large intestines: | ADENOCARCINOMA OF SMALL INTESTINE
- grow in napkin-ring encircling pattern or polyploid fungating masses - arise in duodenum⇒ obstructive jaundice, pancreatitis - risk factor: chronic inflammatory disease - types: acinar, medullary, undifferentiated - symptoms: cramping pain, vomiting, weight loss - 5yr survival ⇒ 70%
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55. Tumors of the small and large intestines: | GIST
TYPES: - tumor show smooth muscle differentiation - tumors with neural differentiation - tumors with smooth muscle/ neural dual differentiation - tumors lacking differentiation - somatic mutation in cKIT (CD117) - treatment: imatinib mesylate
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55. Tumors of the small and large intestines: | GASTROINTESTINAL LYMPHOMA
- systemic dissemination of NHL - primary GI lymphomas ⇒ regional LN involvement - B or T cell origin TYPES: 1. mediterranean type lymphoma 2. western type malignant NHL
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55. Tumors of the small and large intestines: | MEDITERRANEAN-TYPE LYMPHOMA
- immunoproliferative small intestinal disease - in underdeveloped countries - infection related - proliferation of IgA plasma B cells + malabsorption
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55. Tumors of the small and large intestines: | WESTERN-TYPE MALIGNANT NHL
- develop in ileum as plaque like infiltration or intraluminal fungating mass ⇒ bleeding or obstruction - known as MALT lymphoma - adults - location: stomach, small intestine, proximal colon, distal colon - gastric MALT ⇒ H.pylori - MALT cells are CD5 and CD10 negative - t(11;18) BCL2/MLT
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55. Tumors of the small and large intestines: | CARCINOID TUMORS
= tumors arising from endocrine cells - Kulchitsky cells - in pancreas, peripancreatic tissue, lungs, biliary tree, liver - potentially malignant - may synthesize and secrete bioactive products + hormones ⇒ serotonin ⇒ carcinoid syndrome: diarrhea, flushing, bronchospasm, cyanosis, skin teleangiectasis - paraneoplastic syndromes
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55. Tumors of the small and large intestines: | NEOPLASMS OF SMALL AND LARGE INTESTINE
1. polyps 2. colorectal carcinoma 3. adenocarcinoma of small intestine 4. gastrointestinal stromal tumor 5. gastrointestinal lymphoma 6. carcinoids 7. squamous cell carcinoma of anus

PATHOLOGY 2 (11 decks)

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