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Pathology > Pathology of the oral cavity and GI tract > Flashcards

Pathology of the oral cavity and GI tract Flashcards

1
Q

Malformations of the lips and oral cavity (3)

A
  1. Cleft lip
  2. Cleft palate
  3. Cheilognathopalatoschisis (cleft lip + jaw + palate)
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2
Q

Inflammatory + inflammatory lesions of the oral cavity, lips and pharynx

A
  • Stomatitis: inflammation of mucous linings
  • HSV-1 infections
  • Oral candidiasis
  • Follicular tonsillitis
  • Pemphigus vulgaris
  • Ulcerative, necrotizing gingivitis
  • Canker sores
  • HIV and Kaposi sarcoma
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3
Q

Pathomechanism of pemphigus vulgaris

A

Autoantibodies are formed against desmoglein (forms desmosomes). Cells become separated from each other, a process called acantholysis. This causes blisters which can turn into sores.

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4
Q

Most common neoplasms of the oral cavity

A

Benign: usually papillomas
- Related to HPV-6 and -11

Malignant: squamous cell cc

  • Associated with cigarette smoking and alcohol, causing mutations in the p53 gene
  • Related to HPV-16 infection
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5
Q

Relevance of xerostomia

A

= dry mouth

Seen in autoimmune disorders, i.e. Sjögren Syndrome

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6
Q

Etiology of sialadenitis

A
  • Traumatic: blockage of ducts causing mucocele (cyst-like pool of mucus lined by granulation tissue)
  • Viral: mumps, which causes swelling of all glands
  • Bacterial: usually S. aureus or Streptococcus
  • Autoimmune disease: causes chronic sialadenitis
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7
Q

Benign neoplasms of salivary glands

A
  • Pleiomorphic adenoma: arises in the superficial parotid; consists of ductal and myoepithelial cells
  • Warthin tumor (papillary cystadenoma lymphomatosum): only arises in the parotid
  • Onkocytoma
  • Monomorphic adenoma
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8
Q

Malignant neoplasms of salivary glands

A
  • Mucoepidermoid cc: mainly in the parotids
  • Adenoid cystic cc
  • Acinic cell cc
  • Adenocarcinoma
  • B cell non-Hodgkin lymphoma
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9
Q

Functional obstructions of the esophagus

A
  • Diverticula: outpouching involving all layers of the esophagus
  • Achalasia: triad incomplete LES relaxation, increased LES tone and esophageal aperistalsis
  • Hiatal hernia: stomach through the diaphragm; can be sliding (most common) or rolling (paraesophageal)
  • Laceration (Mallory-Weiss syndrome): tears in the esophagus at the esophagogastric junction; seen with vomiting related i.e. to alcholics and accompanied by hiatal hernia
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10
Q

Esophagitis: etiology

A
  • GERD
  • Infections: C. albicans, CMV
  • Uremia
  • Prolonged gastric intubation
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11
Q

Types of esophagitis

A
  • Reflux esophagitis
  • Eosinophilic esophagitis
  • Chemical (corrosive)
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12
Q

Malignant tumors of the esophagus

A
  • Adenocarcinoma (lower 1/3)

- Squamous cell cc (upper 2/3)

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13
Q

Complications of adenocarcinoma of the esophagus (3)

A
  1. Mechanical blockage
  2. Tracheo-esophageal fistula formation
  3. Ichorous mediastinitis: blockage of the esophageal wall by the tumor occurs within the mediastinum
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14
Q

Acute gastritis: pathogenesis

A
  • Use of NSAIDs
  • Excessive alcohol consumption
  • Smoking
  • Systemic infections
  • “Stress ulcers”
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15
Q

Acute gastritis: clinical features

A

Can be asymptomatic or cause epigastric pain with nausea and vomitting, or it may present as hematemesis and melena, causing fatal blood loss.

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16
Q

Type A gastritis

A

Autoimmune: production of autoantibodies against parietal cells.
Leads to loss of intrinsic factor, causing pernicious anemia.
Also causes atrophy and flattening of the mucosa.
Causes hyperchlorydia or achlorydia (loss of gastric HCl)

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17
Q

Type B gastritis

A

Bacterial, caused by H. pylori.
Antral type: high acid production, increasing the risk for duodenal ulcers.
Pangastritis: multifocal mucosal atrophy, with low acid production and increased risk for adenocarcinoma.

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18
Q

Mechanisms by which H. pylori causes peptic ulcers

A
  • Increases production of proinflammatory cytokines
  • CagA gene produces a vacuolating toxin, causing epithelial injury
  • Urease secretion breaks down urea, creating toxic compounds
  • Releases proteases and phospholipases, which break down the mucous layer and weakens the first line of defense
  • Decreases the luminal pH, favoring its own colonization
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19
Q

Complications of chronic peptic ulcers (5)

A
  1. Bleeding
  2. Perforation: thickness of the wall is destroyed; can cause peritonitis
  3. Penetration: necrosis of the wall enters surrounding tissues
  4. Stenosis
  5. Malignant transformation (NOT seen with duodenal ulcers)
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20
Q

Histologic layers of a chronic peptic ulcer (4)

A
  1. Epithelial slough: necrotic material, PMNs, fungi, fibrin
  2. Fibrinoid necrosis
  3. Granulation tissue: PMNs and proliferating capillaries
  4. Scarring
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21
Q

Zollinger-Ellison syndrome

A

A tumor, usually located in the pancreas, which secretes gastrin. Too much acid produced leads to development of peptic ulcers.
Symptoms: abdominal pain and diarrhea

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22
Q

Etiology of gastric erosions (acute ulcers) (5)

A
  1. Stress-induced
  2. Zollinger-Ellison syndrome
  3. H.pylori
  4. NSAIDs
  5. CMV
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23
Q

Histologic classification of gastric carcinomas

A
  1. Intestinal type adenocarcinoma: malignant cells form neoplastic intestinal glands; associated with gastritis; better differentiated
  2. Diffuse adenocarcinoma: arises de novo from native gastric mucous cells; not associated with gastritis; poorly differentiated
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24
Q

Metastatic properties of gastric carcinomas

A
  1. To regional lymph nodes
  2. Liver
  3. Peritoneum (peritoneal carcinosis)
  4. Ovaries (Krukenberg tumor)
25
Q

Pathogenesis of GIST

A

Gain-of-function mutation in the gene encoding c-KIT, a receptor for stem cell factor with tyrosine kinase activity. c-KIT is expressed by interstitial cells of Cajal.

26
Q

Treatment of GIST

A

Imatinib: inhibits the tyrosine kinase activity of c-KIT.

27
Q

Developmental abnormalities of the GI tract

A
  • Atresia: complete blockage
  • Stenosis: narrowing of lumen
  • Meckel diverticulum
  • Omphalocele: intestines herniate into the umbilicus
  • Hirschprung disease (congenital megacolon): results in formation of an aganglionic segment
28
Q

Predisposing conditions for ischemic bowel disease

A
  • Arterial thrombosis
  • Arterial embolism
  • Venous thrombosis
  • Nonocclusive ischemia: cardiac failure, shock, dehydration
29
Q

Angiodysplasia

A

Tortuous dilations of the submucosal and mucosal blood vessels, usually in the cecum and ascending colon. Causes severe anemia.

30
Q

Possible complications of hemorrhoids

A
  • Frequent bleed
  • Can become thrombosed
  • May prolapse and become trapped by the compressive anal sphincter, leading to edematous hemorrhagic enlargement or strangulation
31
Q

Causes of malabsorption syndrome

A

Disturbance of the following:

  • Intraluminal digestion
  • Mucosal absorption
  • Nutrient delivery
32
Q

Features and causes of defective intraluminal digestion

A

Features: osmotic diarrhea and steatorrhea

Causes:

  • Pancreatic insufficiency
  • Chronic alcoholism
  • Crohn disease
33
Q

Defects of mucosal absorption in malabsorption syndrome

A
  • Lactose intolerance: acquired or inherited
  • Deficiency of apolipoprotein-B: mucosal epithelial cells cannot longer export lipids, thus they aren’t absorbed
  • Celiac disease: reduction in small intestine absorption area as the mucosa atrophies; loss of villi
  • Tropical spure and Whipple disease: associated with intestinal infections
34
Q

Organ manifestations of malabsorption syndrome

A
  • Weight loss, anorexia, steatorrhea
  • Anema: iron, folate, vitamin B12 deficiencies
  • Bleeding: vitamin K deficiency
  • Osteopenia and tetany: defective calcium, magnesium, vitamin D and protein absorption
  • Amenorrhea
  • Hyperparathyroidism
  • Purpura and petechia: vitamin K deficinecy
  • Peripheral neuropathy: vitamin A and B12 deficiencies
35
Q

Major forms of diarrhea

A
  • Secretory diarrhea: persist during fasting
  • Osmotic diarrhea: subside with fasting
  • Exudative diarrhea: purulent, bloody stool
  • Malabsorption diarrhea: increased osmolarity
  • Deranged motility diarrhea
36
Q

Viral gastroenteritis: mechanism and viruses causing it

A

Destroys the epithelium and their absorptive function. Villi are repopulated with immature enterocytes.

  • Rotavirus
  • Calicivirus
  • Adenovirus
37
Q

Mechanisms causing bacterial gastroenteritis

A

Ingestion of either:

  • Preformed toxin: in contaminated foods
  • Toxigenic organisms
  • Enteroinvasive organisms: destroy mucosal epithelial cells
38
Q

Bacterial gastroenteritis: morphology

A
  • Damage to surface epithelium
  • Increased mitotic rate
  • Hyperemia
  • Neutrophilic infiltration
39
Q

Bacterial gastroenteritis: complications

A

More severe than the viral form!

  • Dehydration
  • Sepsis
  • Perforation
40
Q

Protozoal gastroenteritis: examples

A

Entamoeba histolytica: protozoal parasite; can cause abscess formation in the liver

Giardia lamblia: intestinal protozoa; causes malabsorptive diarrhea due to mucosal cell injury

41
Q

Complications of colonic diverticulitis

A
  • Collection of stool in the diverticula –> irritation of mucosa –> bleeding (hematochesia)
  • Inflammation (diverticulitis)
42
Q

Entities causing bowel obstruction (4)

A
  1. Hernias: usually in the small bowel; can lead to permanent trapping (incarceration) or infarction of the trapped segment (strangulation)
  2. Intestinal adhesions: follows peritonitis, after healing of this small bowel segments can adhere to one another
  3. Intussusception: part of the intestine invaginates into the another section of the intestine; in adults it is related to tumors; can cause obstruction of vascular supply and subsequent infarction
  4. Volvus: twisting of a loop of bowel, which further constricts the venous flow
43
Q

Genetic background of Crohn’s disease

A

Mutation in the gene encoding NOD2, an intracellular receptor for a peptide component of the bacterial cell walls. This receptor is expressed in Paneth cells. The mutated form 1. cannot respond properly to bacteria or 2. promotes excessive host responses.

44
Q

Direct consequences of inflammation related to IBD

A
  1. Impaired integrity of the mucosal epithelial barrier
  2. Loss of surface epithelium
  3. Bloody diarrhea
45
Q

Crohn’s disease: morphology and consequences

A
  • Transmural involvement (all segments of the tract, but usually the ileum): edema with subsequent fibrosis
  • Nodular and follicular lymphocytic infiltrates
  • Non-caseating granulomas
  • Fistula formation (internal-external): can further cause abscess formation
  • Intestinal stricture or obstruction
  • Conglomerates

With long-standing disease, there’s a risk for dysplasia that increases the risk for carcinomas.

46
Q

Crohn’s disease: clinical features

A

Recurrent episodes of diarrhea, cramping abdominal pain and fever, as well as malabsorption.
Melena.

47
Q

How does Ulcerative Colitis differ from Crohn’s disease?

A
  • UC is limited to the colon
  • No granuloma formation
  • No skip lesions
  • Mucosal ulcers rarely extend below the submucosa, and there’s little fibrosis
  • There’s no mural thickening
  • The serosal surface is normal
  • Higher risk for cancer development
48
Q

Complications of Ulcerative Colitis

A
  • Bleeding, causing anemia
  • Regeneration of the mucosa, forming pseudopolyps
  • Mucosal atrophy
  • Toxic megacolon
  • Sclerosing cholangitis: ducts narrow, which can lead to icterus (jaundice)
  • Dysplasia (preneoplastic condition)
49
Q

Acute appendicitis: pathogenesis

A

Usually associated with obstruction due to fecalith (less commonly: gallstone, tumor or worms).

Obstruction increases the intraluminal pressure, causing collapse of draining veins.

Obstruction and ischemic injury favors bacterial proliferation with edema and exudate formation.

50
Q

Acute appendicitis: symptoms

A
  • Periumbilical discomfort
  • Anorexia
  • Right lower quadrant tenderness
  • Constant pain at McBurney’s point
51
Q

Tumors of the appendix

A
  • Carcinoids: most common; arise from neuroendocrine cells (enterochromaffin cells); some secrete serotonin
  • Mucinous neoplasms: range from benign mucinous cystadenoma to malignant mucinous cystadenocarcinoma
  • Mucocele (not a neoplasm): dilation of the lumen by mucinous secretion; caused by obstruction due to i.e. fecolith
52
Q

Stages of acute appendicitis

A
  1. Acute early appendicits: serosal vessels are congested; neutrophil infiltrate
  2. Acute supporative appendicitis: abscess formation in the wall, together with ulceration and foci of necrosis
  3. Acute gangrenous appendicitis
  4. Rupture and supporative peritonitis
53
Q

Pneumoperitoneum: definition and causes

A

Accumulation of air or gas in the abdominal cavity.

Caused by i.e.:

  • Perforated abdominal organ (perforated peptic ulcer)
  • Bowel obstruction
  • Rupture diverticulum
  • Necrotizing enterocolitis
54
Q

Ascites: pathogenesis

A
  • Sinusoidal HTN: alteration of Starling forces drives fluid into the space of Disse, which is removed by hepatic lymphatics
  • Leakage of hepatic lymph into the abdominal cavity
  • Renal retention of sodium and water (i.e. due to secondary hyperaldosteronism)
55
Q

Peritonitis: causes

A
  • Perforation of abdominal organs
  • Acute pancreatitis
  • Spontaneous bacterial peritonitis (seen with liver cirrhosis)
  • Ascending from the genitourinary tract
56
Q

Peritonitis: consequences

A
  • Adhesions
  • Intraintestinal abscesses
  • Subphrenic, subhepatic abscesses
  • Shock, death
57
Q

Neoplasms of the peritoneum

A

Rare: mesothelioma (associated with asbestos exposure) and carcinoma

More common: metastasis from ovaries, stomach or pancreas

58
Q

Pathogentical pathways (2) involved in the development of colorectal adenocarcinomas

A

APC/beta-catenin pathway

  • Chromosomal instability
  • Stepwise acquirement of mutations

DNA mismatch repair pathway

  • Causes microsatellite instability
  • Genes: TGF-beta (inhibits growth of colonic epithelial cells) and BAX

Pathology (14 decks)

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