Pathology flashcards

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92 Terms

1
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What characterizes endoinfectious processes of the digestive system?
Disorders with inflammatory manifestations caused by a biological imbalance between the host and its gut microorganisms
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What percentage of fecal solids is made up of bacteria?
Around 60%
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How many different bacterial species typically inhabit the human gut?
Approximately 300–500 or more species
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How does the number of microbial cells in the gut lumen compare to the body’s eukaryotic cells?
It is about ten times greater
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What congenital anomalies can predispose to digestive‐system endoinfections?
Enterocyte membrane dysfunction, cellular or humoral immunity failure, and tract dysplasias such as megacolon, dolichosigma, and diverticula
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What is congenital small intestinal atresia?
A birth defect in which a segment of the small intestine is completely blocked or missing
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How is purulent inflammation defined?
Production of pus containing dead neutrophils, necrotic cells, and edema fluid
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How do microorganisms trigger appendiceal inflammation?
Following epithelial damage from luminal obstruction, dyskinesia, coprostasis, coproliths or helminths, plus intravascular stasis and thrombosis
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What is superficial (catarrhal) appendicitis?
Early inflammation limited to mucosa and submucosa with hyperemia, edema, increased mucus secretion, and neutrophil infiltration
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What defines ulcerative appendicitis?
Destructive focal mucosal erosion forming small ulcers with neutrophils extending into the submucosa
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What is ulcerative-phlegmonous (suppurative) appendicitis?
Ulcers extending through the muscularis into the wall, diffuse pus formation, and serosal fibrinous exudate
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What characterizes abscedent appendicitis?
A walled‐off abscess within or around the appendix, with central necrosis and fibrous capsule formation
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What occurs in gangrenous appendicitis?
Severe inflammation causes vascular compromise, full‐thickness wall necrosis (gray‐green to black), and high perforation risk
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What is a microperforation complication of appendicitis?
Minute wall breaches allowing small leaks of bacteria or fluid into surrounding tissues
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What is a macroperforation complication?
A larger rupture of the appendix wall with frank leakage of pus and bowel contents into the peritoneum
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What is periappendicitis with localized fibrino‐purulent peritonitis?
Spread of inflammation from the appendix serosa to adjacent peritoneum, producing a focal zone of fibrin and pus
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What defines diffuse purulent peritonitis?
Generalized peritoneal infection by pus after appendix rupture, leading to widespread exudate
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How can appendicitis lead to intestinal adhesions and obstruction?
Inflammation and healing deposit fibrous bands between bowel loops that can tether or kink the intestine
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What is purulent thrombophlebitis as an appendicitis complication?
Septic thrombosis of veins draining the appendix that spreads to portal branches, causing liver abscesses and sepsis
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What is appendix empyema?
Accumulation of purulent exudate (pus) confined within the appendiceal lumen
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What is hydrops of the appendix (muco‐hydrops)?
Noninfectious distension of the appendix by a clear, mucus‐like fluid due to luminal obstruction
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What is an appendiceal mucocele?
Dilatation of the appendix from intraluminal accumulation of mucinous material, which may arise from mucosal hyperplasia or mucinous neoplasm
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What is gastrointestinal candidiasis?
Fungal infection of mucosal surfaces (mouth, esophagus) by Candida albicans, especially in newborns or immunocompromised patients
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Where does Candida albicans normally reside without causing disease?
On skin, in the mouth, GI tract, and vagina as a benign commensal
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What protects healthy individuals from Candida overgrowth?
Intact normal bacterial flora and robust immune defenses
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What is thrush?
A superficial Candida infection of the oral mucosa
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What are complications of gastrointestinal candidiasis?
Ulceration leading to perforation, postinflammatory scarring and strictures, and systemic dissemination (generalisation)
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What is a gastric ulcer?
An ulcer of the stomach mucosa (ulcus ventriculi).
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What is a duodenal ulcer?
An ulcer of the duodenal mucosa (ulcus duodeni) with defects deeper than half the mucosal thickness.
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What are erosions?
Mucosal defects that involve less than half of the mucosal thickness.
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What are the main damaging forces in peptic ulcer pathogenesis?
Gastric acidity and peptic enzymes.
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What are the normal mucosal defensive forces against ulceration?
Surface mucus secretion
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What causes peptic ulcer disease to develop?
An increase in damaging forces and/or impairment of the mucosal defenses.
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List common causes of peptic ulcers.
Helicobacter pylori infection
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Where are peptic ulcers most commonly located?
In the gastric pylorus and the proximal duodenum.
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What proportion of peptic ulcers are solitary?
About 80%.
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Describe the typical shape and size of peptic ulcers.
Round or oval lesions, 0.5–3 cm in diameter.
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How deep can peptic ulcers extend?
They can vary in depth and may penetrate through the wall to reach the pancreas or liver.
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What complications can arise from peptic ulcers?
Bleeding
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What defines a precancerous condition?
A lesion or state with increased cancer risk if left untreated.
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Give examples of precancerous conditions in the GI tract.
Chronic inflammation with ulceration
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What is chronic inflammation with ulceration?
Persistent immune-mediated mucosal injury causing ulcers that may bleed or scar.
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What is leukoplakia?
A white, well-defined hyperkeratotic mucosal patch that cannot be scraped off and is often premalignant.
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What are GI polyps?
Localized mucosal overgrowths—whether inflammatory, hyperplastic, or neoplastic—that protrude into the lumen and may harbor dysplasia.
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What is atrophic gastritis?
Thinning of the gastric mucosa with loss of glands and parietal cells, resulting in decreased acid and intrinsic factor production.
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What is Barrett’s esophagus?
Replacement of normal squamous epithelium in the distal esophagus by intestinal-type columnar epithelium due to chronic acid reflux.
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What is intraepithelial dysplasia (carcinoma in situ)?
Full-thickness epithelial atypia without invasion past the basement membrane—the final premalignant stage.
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What are the hallmarks of cancerous tumors?
Abnormally large, partly autonomous masses with genetic changes, continuous growth after carcinogen removal, and parasitic consumption of host resources.
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What GI tract complications can lead to death?
Lumen obstruction
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Congenital small intestinal atresia with enlargement, purulent inflammation and necrosis

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Epithelium is intact and no inflammatory cells intraepithelial

<p><span>Epithelium is intact and no inflammatory cells intraepithelial</span></p>
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Inflammation started due to large coprolith → ischemia, epithelium disclamation and inflammation in deep layers of appendix

<p><span>Inflammation started due to large coprolith → ischemia, epithelium disclamation and inflammation in deep layers of appendix</span></p>
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Enterobiosis vermicularis penetrate through mucosa into deep layers → cause inflammation

<p><span>Enterobiosis vermicularis penetrate through mucosa into deep layers → cause inflammation</span></p>
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Hyperaemic vessels

<p><span>Hyperaemic vessels</span></p>
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Purulent exudate on surface of appendix + inflammation

<p><span>Purulent exudate on surface of appendix + inflammation</span></p>
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Discoloration of appendix and purulent exudate around and inside appendix.

No muscular or submucosal layer is visible → only necrosis

<p><span>Discoloration of appendix</span> and purulent exudate around and inside appendix.</p><p><span>No muscular or submucosal layer is visible → only necrosis</span></p>
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Adenomas – tubular structure of neoplasm

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<p></p>

Tubular papillary carcinoma

Tubular and papillary structures formed from neoplastic epithelial cells from GI tract

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<p>Explain all three pictures</p>

Explain all three pictures

Cyanate ring carcinoma

Ø  Formed of neoplastic cells from GI tract.

Ø  Alcion blue in the middle where we see mucus inside cells.

Ø  Immunohistochemical reaction (right) – positive for cytokeratin’s → shows that they are carcinoma epithelial origin.

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Ø  Whitish region near coronary artery – metastasis:

1.     Caused obstruction of BV → infarction.

<p><span>Ø</span><span style="font-size: 7pt; font-family: &quot;Times New Roman&quot;">&nbsp; </span><span>Whitish region near coronary artery – metastasis:</span></p><p class="MsoListParagraphCxSpLast"><span>1.</span><span style="font-size: 7pt; font-family: &quot;Times New Roman&quot;">&nbsp;&nbsp;&nbsp;&nbsp; </span><span>Caused obstruction of BV → infarction.</span></p>
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<p></p>

Ø  Congenital outpouching in the small intestine.

1.     Usually located in the ileum, that results from a failure of the omphalomesenteric duct (also known as the vitelline duct) to fully close during foetal development.

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Mucosa is red, ulcerated due to UC

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Ulcerative colitis

1.     Architecture of mucous gland is distorted, branched, deformed.

2.     Infiltration of leukocytes.

3.     Centre with ulceration.

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Pseudomembranous colitis:

Damaged mucosa covered with exudate with greenish colour.

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Pseudomembranous colitis:

1.    Green – rest of mucous glands.

  1. Other regions with necrotic debris due to inflammation and exudate

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What is Meckel’s diverticulum?
A congenital outpouching of the small intestine, usually in the ileum, resulting from failure of the omphalomesenteric (vitelline) duct to close during fetal development.
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What is tonsillitis?
Inflammation of the tonsils and pharynx, often viral in origin with possible secondary bacterial infection (e.g., Streptococcus, Staphylococcus).
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What factors predispose to tonsillitis?
Common cold, immune system failure, vitamin deficiency, and other underlying diseases.
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How is tonsillitis classified by clinical course?
As acute or chronic.
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How is tonsillitis classified by exudate type?
Serous, fibrinous, purulent, or necrotizing.
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What are complications of tonsillitis?
Peritonsillar abscess, retropharyngeal abscess, purulent otitis media, phlegmon, thrombophlebitis, sepsis, and scarring.
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What is enteritis?
Inflammation of the small intestine leading to impaired nutrient absorption, malnutrition, and diarrhea with water and salt loss.
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How is enteritis classified by location?
Duodenitis, jejunitis, or ileitis.
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How is enteritis classified by course?
Acute or chronic.
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How is enteritis classified by etiology?
Infectious, toxic, immune‐mediated, or nutritional.
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What are the morphological types of acute enteritis?
Catarrhal, fibrinous, purulent, and ulcerative‐necrotizing.
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What are the histologic features of chronic enteritis?
Loss of epithelial brush border, cell vacuolation and death, and lamina propria infiltration by lymphocytes, plasma cells, and eosinophils.
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What complications can result from enteritis?
Bleeding, perforation, dehydration, and—if chronic—cachexia, hypoproteinemia, anemia, and vitamin deficiencies.
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What is typhlitis (caecitis)?
A necrotizing inflammatory condition of the caecum that can extend into the ascending colon or terminal ileum.
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What are other segment‐specific colitis terms?
Transversitis (transverse colon), sigmoiditis (sigmoid colon), proctitis (rectum), proctosigmoiditis (rectum + sigmoid), pancolitis (entire colon), enterocolitis (small + large intestine), and gastroenterocolitis (stomach + small + large intestine).
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How do the causes and complications of colitis compare to enteritis?
They mirror enteritis in etiology, pathogenesis, morphology, and complications such as bleeding, perforation, and systemic effects.
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What is ulcerative colitis?
A chronic idiopathic inflammatory bowel disease beginning in the rectum, progressing proximally, with a relapsing (undulating) course and diffuse mucosal and submucosal inflammation.
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Which layers of the bowel are affected in ulcerative colitis?
The mucosa and submucosa.
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What factors may trigger ulcerative colitis?
Commensal gut bacteria, dietary and environmental factors, primary immunological defects, mucus secretion disorders, genetic predisposition, psychological stress, or combinations.
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What are complications of ulcerative colitis?
Cachexia, anemia, sepsis, secondary amyloidosis, toxic megacolon, pseudopolyps, and intraepithelial neoplasia progressing to carcinoma.