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Intestinal Pathology Flashcards

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1
Q

Where does intestinal obstruction most commonly occur? Why?

A
  • the small intestine

- because it is relatively narrow

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2
Q

What is Hirschprung Disease? What area of the intestines does it always affect? What morphology might result? What is it associated with?

A
  • a congenital defect in colonic innervation (ganglion cells fail to migrate into the bowel wall here), resulting in intestinal obstruction due to non-functional intrinsic plexuses (inability to relax)
  • ALWAYS affects the rectum (rectal constriction); may result in a dilated sigmoid colon as a result of the pressure build-up
  • associated with Down syndrome
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3
Q

How do patients with Hirschprung Disease present?

A
  • as neonates who are unable to pass meconium (the earliest stool of an infant) and who develop obstructive constipation
  • upon DRE, patients will also have an empty rectal vault (because no feces is entering this area due to the contraction)
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4
Q

What is a hernia? What may permit it to happen in the abdomen?

A
  • hernia: protrusion of peritoneum

- weakness/defect in the peritoneal wall may permit this to happen

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5
Q

Name three vascular disorders of the bowel.

A
  • ischemic bowel disease, angiodysplasia, and hemorrhoids
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6
Q

What is the range of damage in Ischemic Bowel Disease? What is each usually due to? What are the 2 phases? How can patients present?

A
  • damage can range from mucosal infarction (mucosa) –> mural infarction (mucosa + submucosa) –> transmural infarction (all 3 layers)
  • the first two are usually due to hypoperfusion/hypotension; the third is due to acute vascular obstruction (of SMA)
  • two phases: initial hypoxic phase + reperfusion injury phase (this one causes the most damage)
  • severe abdominal pain, bloody diarrhea, and decreased bowel sounds
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7
Q

What are some predispositions to Hemorrhoids?

A
  • constipation w/ heavy straining, pregnancy, and portal HTN
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8
Q

What are the top 3 causes of malabsorptive diarrhea in the US? What is another common cause?

A
  • pancreatic insufficiency, celiac disease, Crohn disease

- irritable bowel syndrome (IBS)

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9
Q

What occurs in malabsorptive diarrhea? What is the hallmark sign?

A
  • chronic diarrhea results from defective absorption of fats, vitamins, proteins, carbohydrates, electrolytes, and (therefore) water
  • the hallmark sign is steatorrhea
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10
Q

What is Celiac Disease also known as? What is the pathology involved? What do we use to diagnose it?

A
  • also known as gluten-sensitive enteropathy
  • it involves a T-cell immune-mediated enteropathy triggered by the ingestion of gluten that results in the blunting of villi (mainly in the terminal duodenum or proximal jejunum), leading to malabsorption and steatorrhea
  • diagnose with serology: antibodies against gliadin and tTG will be present (tTG antibodies are more specific for celiac than gliadin antibodies); in addition, serum levels may reflect micronutrient deficiencies due to malabsorption
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11
Q

What is Celiac Disease highly associated with? 10% of patients with Celiac Disease have what characteristic symptom/clinical sign? What are some other symptoms?

A
  • complete association with HLA-DQ2 and HLA-DQ8; 95% of patients have the former, the remaining 5% have the latter
  • dermatitis herpetiformis: a pruritic, blistering skin lesion due to IgA deposition at the tips of dermal papillae; also due to malabsorption of vit A
  • weight loss, weakness, chronic diarrhea, anemia, osteoporosis, osteomalacia, hormonal disorders (all due to malabsorption)
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12
Q

What is Irritable Bowel Syndrome (IBS)? How do we diagnose it? Is it more common in women or men?

A
  • chronic and relapsing abdominal pain, bloating, diarrhea, and constipation (changing bowel habits)
  • the diagnosis depends on these clinical symptoms, and all other pathology must be ruled out
  • (more common in females)
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13
Q

What intestinal disease is responsible for 1/2 of all worldwide deaths in children younger than 5?

A
  • infectious enterocolitis
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14
Q

Name 5 common bacterial causes of Infectious Enterocolotis and 2 viral causes.

A
  • bacteria: Cholera, Campylobacter enterocolitis, E. coli, Salmonellosis (and typhoid fever), Pseudomembranous Colitis
  • viral: norovirus and rotavirus (we have a rotavirus vaccine, but no norovirus vaccine)
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15
Q

What organism is responsible for Cholera? How is it transmitted? What is the pathologic mechanism? What percentage of untreated patients will die? How do we treat it?

A
  • Vibrio cholerae
  • transmitted mainly via contaminated drinking water (poor sanitation, natural disasters, etc.)
  • the cholera toxin causes Cl- release in the lumen, creating a large osmotic gradient that draws in water = diarrhea
  • 50-70% of untreated cases are fatal!
  • treating with simple fluid replacement save 99% of patients
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16
Q

What is the most common bacterial enteric pathogen of the developed world? What does it cause?

A
  • Campylobacter jejuni –> causes Campylobacter enterocolitis
  • patients usually present with water diarrhea (up to 50% of patients may present with dysentery)
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17
Q

There are two organisms responsible for Typhoid Fever - what are they? What is each associated with? What clinical sign may patients develop?

A
  • Salmonella typhi and Salmonella paratyphi
  • S. typhi: children and endemic areas
  • S. paratyphi: developed world and travelers
  • patients may develop “rose spots” (small, erythematous papular lesions on the chest and abdomen)
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18
Q

What is the most common organism involved with antibiotic-associated diarrhea? Which pathogen causes the most severe cases? What do we treat these patients with?

A
  • most times, the pathogen is unable to be identified
  • most severe: Clostridium dificile –> causes pseudomembranous colitis
  • treat C. dificile with metronidazole (mild to moderate cases) or vancomycin (severe cases); use both for complicated cases (shock, ileus, toxic colon, etc.)
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19
Q

How does the rotavirus cause diarrhea?

A
  • the virus destroys mature enterocytes, causing the villi surfaces to be replaced with immature secretory cells, leading to a loss of absorptive function = diarrhea
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20
Q

What is Inflammatory Bowel Disease (IBD)? What are the two major types?

A
  • a chronic condition resulting from inappropriate mucosal immune activation
  • two types: Chron disease and ulcerative colitis
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21
Q

Compare Chron Disease and Ulcerative Colitis.

A
  • Chron disease: can involve any area of the GIT (usually the terminal ileum and spares the rectum); transmural; ulcers are deep and linear; characterized by skip lesions; cobblestone appearance; creeping fat; bowel wall thickening (“string sign”; presence of fibrosing strictures and granulomas
  • ulcerative colitis: limited to the colon and rectum; extends only into the mucosa and submucosa; ulcers are superficial and broad; diffuse in nature; bloody diarrhea; loss of haustra (“lead pipe”); no strictures or granulomas
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22
Q

Chron Disease can occur anywhere along the GIT, but where is it most commonly found? As for Ulcerative Colitis, which part of the tract is always involved?

A
  • Chron disease is most common in the terminal ileum, the ileocecal valve, and the cecum
  • ulcerative colitis always involves the rectum, and may progress to some or all of the colon (full colon involvement = pancolitis)
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23
Q

What is Duodenal Atresia highly associated with? What are 3 of its clinical features?

A
  • highly associated with Down Syndrome
  • polyhydramnios (too much amniotic fluid because the baby is unable to digest the swallowed fluid = build up)
  • bilious vomiting (bile is present at this point)
  • “double-bubble” sign (distention of the stomach and of the duodenal blind loop w/ the pyloric sphincter in between yields a “double bubble”)
  • (meconium IS passed, but bowel movements do stop afterwards)
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24
Q

What is a diverticulum in the small bowel known as? Is it a true or false diverticulum? What is it due to?

A
  • Meckel’s diverticulum; it is a true diverticulum (out pouching of all 3 layers of the wall)
  • it is due the persistence of the vitelline duct, which is how the midgut gets its nutrients during embryogenesis
  • rule of 2’s: 2% of population, 2 inches long, w/in 2 feet of the ileocecal valve, presents w/in first 2 years of life, may contain 2 types of epithelia (gastric or pancreatic)
25
Q

What is a volvulus? What two things result from one? What is the most common site in a child? In an elderly patient? Whom is it more common in?

A
  • a volvulus is a twisting of the bowel along its mesentery
  • two things that result: infarction (due to the blood supply being cut off) and obstruction
  • child: cecum; elderly patient: sigmoid colon
  • classic patients: elderly; bedridden; constipation; patients on anti-cholinergics
26
Q

Intussusception is the telescoping of a proximal segment of bowel into a distal segment and requires a “leading edge” - what is meant by a leading edge? How do patients typically present?

A
  • it’s basically something that is protruding from the wall, allowing the wall to be “grabbed” by the movements along the tract, resulting in the telescoping effect
  • in children (most common), this is most commonly due to lymphoid hyperplasia
  • in adults (rare), it is most commonly due to cancer/tumor
  • patients are usually children with intermittent abdominal pain and “currant jelly” stool
27
Q

Which genotypes are genetically predisposed to Celiac Disease?

A
  • HLA-DQ2 (95%) and HLA-DQ8 (5%)
28
Q

What is the pathogenic component of gluten? In what form is is presented to the APCs?

A
  • gliadin is the pathogenic component

- it is presented in its deamidated form (it gets deamidated by tissue transglutaminase/tTG)

29
Q

Celiac Disease is similar to Tropical Sprue - how can we tell them apart?

A
  • celiac disease: doesn’t respond to antibiotics and the damage is mainly in the duodenum
  • tropical sprue: does respond to antibiotics (its due to an infectious agent), occurs only in tropical regions, and the damage is more in the jejunum and ileum
30
Q

Damage to the jejunum results in decreased absorption of what nutrient? What about damage to the ileum?

A
  • jejunum: folic acid
  • ileum: vitamin B12 and bile salts (also some folic acid)
  • (also, iron is mainly absorbed in the duodenum)
31
Q

What does the diagnosis of Hirschprung Disease require?

A
  • a rectal suction biopsy
  • (normal biopsy is just of the mucosa, but we need to check for the absence of the ganglia, so suction is required to get a biopsy of the submucosa)
32
Q

What happens in a colonic diverticula? Is it a true or false diverticulum? Where is it most commonly found?

A
  • outpouchings of mucosa and submucosa through the muscularis externa/propria
  • it is a false diverticulum
  • most common location = the sigmoid colon (left colon)
33
Q

3 possible complications of a colonic diverticula? How common is complicated diverticular disease?

A
  • rectal bleeding from rupture of adjacent vasa recta, diverticulitis, fistula (w/ bladder, ureter, vagina, uterus, abdominal wall, etc.)
  • complications are relatively uncommon; 90% of cases of diverticulosis are uncomplicated
34
Q

What is hematochezia?

A
  • the passage of fresh (bright red) blood through the anus

- associated with ruptured diverticula and angiodysplasia (among other things)

35
Q

What is Angiodysplasia? Where does it most commonly occur?

A
  • an acquired malformation of the mucosal and submucosal vessels due to high wall tension (occurs in elderly patients)
  • usually occurs in the cecum/right colon
  • hematochezia results
36
Q

Dilated, thin-walled blood vessels in the nasopharynx and the GIT due to a genetic defect is known as:

A
  • hereditary hemorrhagic telangiectasia

- (it’s autosomal dominant)

37
Q

What is the most common cause of ischemic colitis?

A
  • atherosclerosis of the superior mesenteric artery

- (most commonly occurs at the splenic flexure because this is the last thing fed by the SMA)

38
Q

Colonic polyps are raised protrusion of the colonic _______; what are the two most common types? Are either pre-cancerous?

A
  • protrusions of the colonic mucosa
  • most common types = hyperplastic polyps followed by adenomatous polyps; both are benign, but adenomatous polyps have the potential to become malignany
39
Q

Describe the Adenoma-Carcinoma Sequence.

A
  • this is the sequence involved in an adenomatous polyp becoming a carcinoma
  • APC loss-of-function mutations result in an increased risk for polyp formation –> KRAS mutation results in polyp formation and an increased risk for mutations –> p53 loss-of-function and an increase in COX results in carcinoma
40
Q

Which chromosome is the APC gene found on?

A
  • it’s a TSG on chromosome 5q

- APC = adenomatous polyposis coli

41
Q

What can act as a prophylaxis against colorectal carcinoma? Why?

A
  • aspirin; because it inhibits COX (and an increase in COX is associated with progression from adenomatous polyp to carcinoma)
42
Q

What is FAP? In a patient with FAP, what prophylaxis is given to reduce the risk of developing colorectal carcinoma?

A
  • familial adenomatous polyposis; an inherited genetic knockout of APC leading to 100’s and 1000’s of adenomatous polyps
  • nearly all patients with FAP have their colons and rectums removed as prophylaxis (without this, nearly all patients develop carcinoma by 40)
43
Q

Gardener Syndrome

A
  • FAP + osteomas (benign tumors in the bone - usually the skull) + fibromatosis (non-neoplastic proliferation of fibroblasts)
44
Q

Turcot Syndrome

A
  • FAP + CNS tumors (medulla blastomas)
45
Q

Peutz-Jeghers Syndrome

A
  • hamartomatous polyps throughout the GIT + hyperpigmentation of the lips, oral mucosa, and genital skin
  • results in an increased risk for colorectal, breast, and gynecologic cancers
46
Q

What are some of the more common extraintestinal manifestations and complications of IBD?

A
  • (these are all largely immune-mediated)
  • skin: erythema nodosum (painful red nodes), pyoderma gangrenosum (large, gangrenous skin ulcers that are amazingly NOT painful)
  • joints: seronegative arthritis, ankylosing spondylitis (inflammation of the spine and large joints)
  • eyes: episcleritis (most common), uveitis
  • CD: calcium oxalate nephrolithiasis (inflammation increases oxalate absorption), migratory polyarthritis; strictures, fistulas
  • UC: primary sclerosing cholangitis; toxic megacolon, CRC
47
Q

What is toxic megacolon? What disease is it a potential complication of?

A
  • a dilated, paralyzed colon that can be infected, necrotic, and is prone to rupture
  • a complication of ulcerative colitis (especially when attempting to treat with antispasmodics)
48
Q

Which two types of tissue can be found in a Meckel diverticulum? What can each result in?

A
  • gastric tissue and/or pancreatic tissue

- the gastric tissue may be acid-secreting and result in ulceration

49
Q

What organism is responsible in Whipple disease? What is the pathophysiology? What symptoms can patients present with?

A
  • Tropheryma whipplei gets ingested by macrophages, which are unable to completely clear them and become foamy macrophages that classically accumulate in the lamina propria
  • this results in an inability to absorb fats (due to physical blockage), leading to fat malabsorption and steatorrhea
  • accumulation in mainly small bowel (diarrhea), heart (Cardiac symptoms), joints (Arthralgias) and CNS (Neurologic symptoms)
  • “foamy whipped cream in a C.A.N.”
50
Q

Which polyps have the greatest risk of becoming malignant?

A
  • polyps larger than 2 cm
  • polyps that are sessile (not pedunculated)
  • polyps with a villous histology (rather than tubular)
51
Q

Risk Factors for CRC

A
  • FAP, Peutz-Jeghers, juvenile poplyposis syndrome, IBD (especially ulcerative colitis), HNPCC, tobacco use, large villous sessile adenomas
52
Q

Where does colorectal cancer most likely hit? Compare CRC of the left colon to that of the right colon.

A
  • rectosigmoid > ascending > descending
  • left colon: tendency for obstruction, “napkin-ring” / “apple-core” lesion, associated with adenoma-carcinoma sequence and FAP
  • right colon: tendency to bleed, iron deficiency anemia, associated with microsatellite instability and HNPCC
53
Q

What can colorectal cancer rarely present as? Men with what clinical finding are deemed to have CRC until proven otherwise?

A
  • can rarely present as Strep. bovis bacteremia and endocarditis (make sure to check these patients for CRC!)
  • men (over 50) with iron deficiency anemia have CRC until proven otherwise
54
Q

What are the two pathways of colorectal carcinoma development?

A
  • 1) adenoma-carcinoma sequence (most common; 85%)
  • 2) microsatellite instability pathway (15%): mutation in microsatellite segments suggests mutations in other genes due to mutations in DNA mismatch repair genes; associated with HNPCC
55
Q

Hereditary Nonpolyposis Colorectal Carcinoma

A
  • HNPCC (AKA Lynch syndrome)
  • associated with microsatellite instability; increases risk for colorectal, ovarian, and endometrial carcinomas
  • right sided CRC
  • “nonpolyposis” = no polyp precursor to the carcinoma
56
Q

What are the two broad causes of bowel obstruction? Which is more common? Which is more serious? How can we tell them apart clinically?

A
  • 1) mechanical obstruction: less common; a medical emergency; increased bowel sounds, diffuse
  • 2) adynamic ileus: more common; usually self-limiting; decreased/absent bowel sounds, more localized
57
Q

What is the most common cause of small bowel obstruction? What about large bowel obstruction? What are other causes?

A
  • SBO: adhesions after abdominal surgery; incarcerated hernias
  • LBO: neoplasms; diverticular disease, sigmoid volvulus (rarely caused by adhesions and hernias)
58
Q

What can ulcerative colitis present as? In terms of general IBD, what marker can we use to help rule in/rule out this disease?

A
  • UC can present as acute severe colitis: at least 6 bloody stool motions a day + fever + inflammatory markers + anemia
  • to help diagnose IBD, the patient’s FC (fecal calprotectin) levels can be looked; calprotectin is a neutrophil protein and a patient with IBD will have elevated FC levels

GIT (14 decks)

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