Brainscape's Knowledge GenomeTM

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


See full index

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. Pathology of lips, oral cavity and pharynx:

NECROTIZING ULCERATIVE GINGIVITIS

A 
CLINICAL FEATURES:
 - necrosis, ulceration + pseudomembrane
CAUSATIVE AGENTS:
 - anaerobes
 - borrelia + troponema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
  1. Pathology of esophagus:

BARRETT ESOPHAGUS

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
  1. Pathology of esophagus:

EOSINOPHILIC ESOPHAGITIS

A

SYMPTOMS:

  • food impaction
  • dysphagia
  • feeding intolerance
  • GERD-like symptoms
  • large number of eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q
  1. Pathology of esophagus:

MALIGNANT TUMORS

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

ACUTE GASTRITIS

A

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

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

CHRONIC GASTRITIS

A

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

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

DEFINITION

A

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

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

PATHOGENESIS

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q
  1. Peptic ulcers:

DEFENSES + DAMAGING FORCES

A 
DEFENSES:
 ⇒ mucus secretion
 ⇒ blood supply
 ⇒ bicarbonate
 ⇒ prostaglandin
 ⇒ regeneration
DAMAGING FORCES:
 ⇒ H.pylori
 ⇒ NSAIDs
 ⇒ smoking, alcohol
 ⇒ hyperacidity
 ⇒ GERD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q
  1. Peptic ulcers:

CLINICAL FEATURES

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q
  1. Peptic ulcers:

MORPHOLOGY

A
  • deep necrosis
  • mucosal folds (star-like)
  • CT proliferation
    HISTOLOGY:
  • epithelial slough on top
  • fibrinoid necrosis
  • granulation tissue
  • scarring on basolateral side
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
  1. Gastric tumors:

GASTRIC POLYPS

A 
= 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
  1. Gastric tumors:

GASTRIC CARCINOMA epidemiology

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q
  1. Gastric tumors:

GASTRIC CARCINOMA pathogenesis

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q
  1. Gastric tumors:

GASTRIC CARCINOMA histological types

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q
  1. Gastric tumors:

GASTRIC CARCINOMA morphology

A
  • mucosal flattening and thickening with erosions
  • diffuse thickening of gastric wall “linitis plastic”
  • large ulcers or polypoid fungating masses
  • exophytic / flat / depressed / excavated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q
  1. Gastric tumors:

GASTRIC CARCINOMA clinical features

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q
  1. Gastric tumors:

MALT LYMPHOMA

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q
  1. Gastric tumors:

GIST

A

= 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    ATRESIA
A
  • complete failure of development of intestinal lumen

- most common: duodenal atresia

44
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    STENOSIS
A
  • narrowing of the intestinal lumen with incomplete obstruction
45
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    DUPLICATION
A
  • well-formed saccular to tubular lytic structures, which may or may not communicate with the lumen of the small intestine
46
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    DIVERTICULOSIS OF THE COLON
A
  • 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
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    OMPHALOCELE
A
  • congenital defect of periumbilical abdominal musculature ⇒ membranous sac in peritoneal layer ⇒ intestines herniate
  • severe
48
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    MALROTATION
A
  • 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
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    HIRSCHSPRUNG DISEASE: CONGENITAL MEGACOLON
A 
= 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
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    MESENTERIC ARTERY THROMBOSIS/VENOUS THROMBOSIS
A
  • 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
51
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    ISCHEMIC BOWEL DISEASE
A 
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
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    ANGIODYSPLASIA
A

= 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
Q
  1. Developmental anomalies and vascular disorders of the GI tract:
    HEMORRHOIDS
A

= 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
Q
  1. Malabsorption:

MALABSORPTION SYNDROME

A

= 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
Q
  1. Malabsorption:

DEFECTS OF INTRALUMINAL DIGESTION

A
  • symptoms: osmotic diarrhea and steatorrhea
  • causes:
    • pancreatic insufficiency + chronic alcoholism
    • Crohn disease
    • intestinal bacterial overgrowth
    • cholestatic liver disease
56
Q
  1. Malabsorption:

LACTOSE INTOLERANCE

A
  • 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
Q
  1. Malabsorption:

DEFICIENCY OF APOLIPOPROTEIN-B

A
  • mucosal epithelial cells cannot export lipids
  • required for assembly of chylomicron ⇒ no chylomicron ⇒ lipid accumulates in enterocytes
  • symptoms: diarrhea, steatorrhea
58
Q
  1. Malabsorption:

CELIAC DISEASE

A

= 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
Q
  1. Malabsorption:

TROPICAL SPRUCE

A
  • 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
Q
  1. Malabsorption:

WHIPPLE DISEASE

A
  • 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
Q
  1. Malabsorption:

CONSEQUENCES OF MALABSORPTION

A
  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.
62
Q
  1. Malabsorption:

SPECIFIC DEFICIENCIES AND THEIR SYMPTOMS

A
  • 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)
63
Q
  1. Enterocolitis:

DIARRHEA

A

= 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
Q
  1. Enterocolitis:

VIRAL GASTROENTERITIS

A
  • 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
Q
  1. Enterocolitis:

BACTERIAL GASTROENTERITIS

A

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
Q
  1. Enterocolitis:

PARASITE GASTROENTERITIS

A
  • Entamoeba histolytica⇒ amoebic dysentery
    • ulcerating proctosigmoiditis and colitis
  • Trichuris trichuria, Ascaris lumbricoides, enterobius vermicularis, taenia saginata and solium
67
Q
  1. Colonic diverticulosis and bowel obstruction:

DIVERTICULUM

A

= 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
Q
  1. Colonic diverticulosis and bowel obstruction:

HERNIAS

A

= 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

69
Q
  1. Colonic diverticulosis and bowel obstruction:

INTESTINAL ADHESIONS

A
  • surgical procedures, infection, endometriosis ⇒ localized or general peritoneal inflammation
  • with healing ⇒ adhesions may develop between bowel segments
70
Q
  1. Colonic diverticulosis and bowel obstruction:

INTUSSUSCEPTION

A
  • 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
Q
  1. Colonic diverticulosis and bowel obstruction:

VOLVUS

A
  • 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
72
Q
  1. Inflammatory bowel disease:

IBD general + pathogenesis

A

=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

73
Q
  1. Inflammatory bowel disease:

IBD genetic predisposition + immunological factors

A

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

74
Q
  1. Inflammatory bowel disease:

IBD consequenses

A
  • impaired integrity of mucosal epithelial barrier
  • loss of surface epithelium
  • intermittent bloody diarrhea
75
Q
  1. Inflammatory bowel disease:

CROHN DISEASE general + morphology

A
  • 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
76
Q
  1. Inflammatory bowel disease:

CROHN DISEASE clinical features + consequences

A 
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
77
Q
  1. Inflammatory bowel disease:

ULCERATIVE COLITIS general + epidemiology

A
  • 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
78
Q
  1. Inflammatory bowel disease:

ULCERATIVE COLITIS morphology + clinical features

A 
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
79
Q
  1. Pathology of the appendix and peritoneum:

ACUTE APPENDICITIS pathogenesis

A
  • 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
80
Q
  1. Pathology of the appendix and peritoneum:

ACUTE APPENDICITIS clinical features

A
  • 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
81
Q
  1. Pathology of the appendix and peritoneum:

APPENDIX CARCINOIDS

A
  • slow growing neuroendocrine tumor
  • arise from enterochromaffin cells
  • asymptomatic
  • solid, yellow tan color
  • almost never metastasize
82
Q
  1. Pathology of the appendix and peritoneum:

APPENDIX MUCINOUS NEOPLASM

A
  • benign mucinous cystadenoma ⇒ malignant mucinous cystadenocarcinoma
  • malignant ⇒ invade wall ⇒ pseudomyxoma peritonei
83
Q
  1. Pathology of the appendix and peritoneum:

APPENDIX MUCOCELE

A
  • dilation of the lumen by mucinous secretion

- cause: non-neoplastic obstruction associated with fecalith

84
Q
  1. Pathology of the appendix and peritoneum:

ACUTE PERITONITIS

A

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

85
Q
  1. Pathology of the appendix and peritoneum:

PNEUMOPERITONEUM

A 
= 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
86
Q
  1. Pathology of the appendix and peritoneum:

ASCITES

A

= 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

87
Q
  1. Pathology of the appendix and peritoneum:

NEOPLASMS OF PERITONEUM

A
  • primary neoplasms rare, but aggressive ⇒ survival 6 months
    1. Mesothelioma
    • asbestos exposure
      2. Carcinoma
    • resemble ovarian carcinoma
    • masses on omentum and peritoneum
88
Q
  1. Pathology of the appendix and peritoneum:

METASTATIC CARCINOMA

A

FROM:

  • ovary
  • stomach
  • pancreas
  • intra-abdominal carcinoma (colon, GIST)
89
Q
  1. Tumors of the small and large intestines:

POLYP

A

= 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
90
Q
  1. Tumors of the small and large intestines:

NON-NEOPLASTIC POLYPS

A
  • 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
91
Q
  1. Tumors of the small and large intestines:

ADENOMAS

A
  • 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
92
Q
  1. Tumors of the small and large intestines:

FAMILIAL POLYPOSIS SYNDROMES

A
  • 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
93
Q
  1. Tumors of the small and large intestines:

COLORECTAL CARCINOMA epidemiology + pathogenesis

A 
EPIDEMIOLOGY:
  - peak incidence: 60-70yrs
  - male predominance
PATHOGENESIS:
  - presursor adenoma 
  - environmental factors: diet
  - genetic factors ⇒ HNPCCS, UC
94
Q
  1. Tumors of the small and large intestines:

COLORECTAL CARCINOMA APC/B-catenin pathway

A 
- chromosomal instability + accumulation of mutations
STAGES:
 1. localized epithelial proliferation
 2. formation of small adenoma
 3. these become dysplastic
 4. develop into invasive cancer
95
Q
  1. Tumors of the small and large intestines:

STEPS OF APC/B-CATENIN PATHWAY

A
  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
96
Q
  1. Tumors of the small and large intestines:

DNA MISMATCH REPAIR PATHWAY

A
  • 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
97
Q
  1. Tumors of the small and large intestines:

COLORECTAL CARCINOMA morphology + clinical features

A 
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
98
Q
  1. Tumors of the small and large intestines:

MOST FREQUENT BENIGN TUMORS

A
  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
99
Q
  1. Tumors of the small and large intestines:

ADENOCARCINOMA OF SMALL INTESTINE

A
  • 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%
100
Q
  1. Tumors of the small and large intestines:

GIST

A

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
101
Q
  1. Tumors of the small and large intestines:

GASTROINTESTINAL LYMPHOMA

A
  • 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
102
Q
  1. Tumors of the small and large intestines:

MEDITERRANEAN-TYPE LYMPHOMA

A
  • immunoproliferative small intestinal disease
  • in underdeveloped countries
  • infection related
  • proliferation of IgA plasma B cells + malabsorption
103
Q
  1. Tumors of the small and large intestines:

WESTERN-TYPE MALIGNANT NHL

A
  • 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
104
Q
  1. Tumors of the small and large intestines:

CARCINOID TUMORS

A

= 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

105
Q
  1. Tumors of the small and large intestines:

NEOPLASMS OF SMALL AND LARGE INTESTINE

A
  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)

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