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patho > GI > Flashcards

GI Flashcards

1
Q

esophagus diseases

A

Congenital Anomalies
Achalasia
Hiatal Hernia
Diverticula
Tears
Varices
Reflux
Barretts
Esophagitis
Neoplasm: Benign, Sq. Cell Ca., Adenoca

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2
Q

esophagus anatomy

A

-25 cm
-Upper esophageal sphincter/Lower esophageal sphincter
-serosa when it becomes intraabdominal
-Mucosa/Submucosa/Muscularis/Adventitia*

-What type of mucosa on the inside -> Squamous cell

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3
Q

definitions

A

-Heartburn (GERD/Reflux)‏
-Dysphagia difficulty swallowing, a non-specific, generic term
-Hematemesis
-Esophagospasm (Achalasia)‏- esophageal motility disorderinvolving thesmoothlayer of theesophagusandlower esophageal sphincter (LES)

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4
Q

congenital anomalies: esophagus

A

-ECTOPIC TISSUE (gastric, sebaceous, pancreatic)‏
-Atresia/Fistula/Stenosis/”Webs”
-Schiatzki “Ring” in lower esophagus
-C in the picture is MC
-stomach inflate
-baby with vomit

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5
Q

motor disorders

A

-Achalasia -> barium swallow
-Hiatal Hernia (sliding [95%], paraesophageal)‏
-“ZENKER” diverticulum
-Esophagophrenic diverticulum
-Mallory-Weiss tear

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6
Q

achalasia

A

-Esophageal motility disorderinvolving thesmoothlayer of theesophagusandlower esophageal sphincter (LES)
-Characterized by incomplete LES relaxation, increased LES tone, andaperistalsisof esophagus (inability of smooth muscle to move food down the esophagus) - in the absence of any other etiology (e.g., cancer or fibrosis)
-Characterized bydifficulty swallowing,regurgitation, and sometimeschest pain

-Mostly UNCERTAIN etiology

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7
Q

hiatal hernia

A

-Diaphragmatic! muscular defect
-WIDENING of the space which the lower esophagus passes through
-IN ALL cases, STOMACH above diaphragm
-Usually associated with reflux
-Very common -> Increases with age
-Ulceration, bleeding, perforation, strangulation
-obesity, pregnancy, older age

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8
Q

genetic vs acquired thrombocilia

A

-test
-exposure to asbestosis - construction, any kind of building, ship building, wives of people who wash the clothes, prolonged period of time
-TB- granuloma
-leukemia/lymphoma -AML- aerlorods, middle aged
-Q- worst, heterogeneious
-acute APL- prognosis tx vitamin A, young, DIC, procoagulate
-CML- phildephic chromosome
-CLL- older person, chronic, smug cell
-ALL- childhood, lymphoblasts (not good) ->
-CRAB symtpoms of multiple myeloma
-reedsterngerg cell- hodgkins lymphoma

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9
Q

hiatal hernia with shatzki ring

A

(circular band of mucosal tissue that can form at the distal esophagus causing narrowing)

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10
Q

diverticula

A

-ZENKER (HIGH)‏
-TRACTION (MID)‏
-EPIPHRENIC (LOW)‏
-TRUE diverticula usually have all 4 layers in its wall: Muc/Submuc/Musc/Adventitia

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11
Q

tears

A

-tear are LONGITUDINAL (lower esophagus)
-usualy secondary to severe VOMITING
-usually in ALCOHOLICS
-usually MUCOSAL tears
-referred to as: MALLORY WEISS TEARS

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12
Q

varices

A

-THREE common areas of portal/caval anastomoses
-Esophageal
-Umbilical
-Hemorrhoidal

-Related to portal hypertension
-Found in 90% of cirrhotics
-MASSIVE, SUDDEN, FATAL hemorrhage may occur

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13
Q

esophagitis

A

-GERD/Reflux -> barrett’s
-barrett’s
-chemical
-infectious

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14
Q

reflex/GERD

A

-DECREASED LES tone
-Hiatal Hernia
-Slowed reflux clearing
-Delayed gastric emptying
-REDUCED reparative ability of gastric mucosa

-Inflammatory Cells:
-Eosinophils
-Neutrophils
-Lymphocytes

-Basal zone hyperplasia
-Lamina Propria papillae elongated and congested, due to regeneration

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15
Q

barrett’s esophagus

A

-Intestinal METAPLASIA of a normally SQUAMOUS esophageal mucosa.
-presence of GOBLET CELLS in the esophageal mucosa is DIAGNOSTIC (develop to protect from acid)
-SINGLE most common RISK FACTOR for esophageal adenocarcinoma
-INTESTINALIZED mucosa is AT RISK for glandular dysplasia
-Dysplasia may occur (0.2 – 2% of persons with Barrett’s per year)
-Screening
-MOST/ALL adenocarcinomas arising in the esophagus arise from previously existing BARRETT’s

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16
Q

esophagitis: chemical

A

-LYE (suicide attempts) with strictures
-Alcohol
-Extremely HOT drinks
-CHEMO ( harmful to ALL high turnover mucosas)

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17
Q

esophagitis: infectious

A

HSV, CMV, Fungal (especially CANDIDA)
-Candida esophagitis in a HIV positive patient often is indicative of “full blown” AIDS.
-Herpes esophagitis - ULCERS‏

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18
Q

esophageal tumors

A

-BENIGN
-MALIGNANT:
-Squamous cell carcinoma
-Adenocarcinoma

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19
Q

benign tumors

A

-LEIOMYOMAS
-FIBROVASCULAR POLYPS
-CONDYLOMAS (HPV)‏
-LIPOMAS
-“GRANULATION” TISSUE (PSEUDOTUMOR)‏

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20
Q

esophagus: squamous cell carcincoma

A

-Nitrites/Nitrosamines
-Betel (nut)
-Fungi in food (nitrosamines)
-Tobacco
-Alcohol
-DYSPLASIA -> IN-SITU -> INFILTRATION

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21
Q

esophagus: adenocarcinoma

A

-from barrett esophagus

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22
Q

stomach

A

-NORMAL: Anat., Histo, Physio.

-PATHOLOGY:
-CONGENITAL
-GASTRITIS
-PEPTIC ULCER
-“HYPERTROPHIC” GASTRITIS
-VARICES

-TUMORS
-BENIGN
-ADENOCARCINOMA
-OTHERS

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23
Q

stomach: congenital

A

-ECTOPIC PANCREAS (ectopic pancreas tissue -> stomach), common
ECTOPIC GASTRIC (ectopic gastric tissue -> pancreas), not rare
Diaphragmatic HERNIA -> Failure of diaphragm to close, not rare

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24
Q

pyloric stenosis

A

-CONGENITAL: Neonatal obstruction symptoms; pyloric splitting curative – projectile vomiting; palpation of the abdomen may reveal a mass in the epigastrium representing the enlarged pylorus (“olive”); risk factors include:
-Sex: seen more often in boys — especially firstborn children — than in girls.
-More common in whites of northern European ancestry, less common in African-Americans and rare in Asians.
-Premature birth
-Family history: develops in about 20% of male descendants and 10% of female descendants of mothers who had the condition
-Smoking during pregnancy

-ACQUIRED: Secondary to extensive scarring such as advanced peptic ulcer disease

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25
Q

gastritis

A

-ACUTE
-CHRONIC
-AUTOIMMUNE
-OTHER:
-EOSINOPHILIC
-ALLERGIC
-LYMPHOCYTIC
-GRANULOMATOUS
-GVH

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26
Q

acute gastritis

A

-hemorrhagic
-(NSAIDs), particularly aspirin
-Excessive alcohol consumption
-Heavy smoking
-CHEMO
-Uremia
-Salmonella, CMV
-Severe stress (e.g., trauma, burns, surgery)
-Ischemia and shock
-Suicidal attempts, as with acids and alkali
-Gastric irradiation or freezing
-Mechanical (e.g., nasogastric intubation)
-Distal gastrectomy

-histology- erosions, hemorrage
-neutrophils !!!!!!!!!!!!

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27
Q

chronic gastritis

A

-NO EROSIONS, NO HEMORRHAGE
-Chronic infection by H PYLORI!!!!
-Immunologic (autoimmune), e.g., PA
-Toxic, as with alcohol and cigarette smoking
-Postsurgical, reflux of bile
-Motor and mechanical, including obstruction, bezoars (luminal concretions), and gastric atony
-Radiation
-Granulomatous conditions (e.g., Crohn disease)
-GVH, uremia

-Few neutrophils
-Lymphocytes, lymphoid follicles
-REGENERATIVE CHANGES:
-METAPLASIA, intestinal
-ATROPHY, mucosal hypoplasia, “thinning”
-DYSPLASIA

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28
Q

AUTOIMMUNE GASTRITIS

A

-10%
-ANTIBODIES AGAINST-> :
-acid producing enzyme H+
-K+ -ATPase
-gastrin receptor
-intrinsic factor -> pernicious anemia -> low B12

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29
Q

other gastritis

A

-EOSINOPHILIC, middle aged women
-ALLERGIC, children (also eosinophils)
-LYMPHOCYTIC, T-Cells, body, DIFFUSE
-GRANULOMATOUS, Crohn’s, other granulomas
-GVH, in bone marrow transplants

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30
Q

peptic ulcers

A

-Ulcer on lining of stomach or duodenum
-“PEPTIC” implies acid cause/aggravation
-ULCER (all layers are compromised) vs. EROSION (muscularis mucosa intact)
-MUC -> SUBMUC -> MUSCULARIS -> SEROSA
-Chronic, solitary (usually), adults
-Most caused by H. pylori
-NSAIDS
-“STRESS”

-Gnawing, burning, aching pain, epigastric
-Fe deficiency anemia
-Acute hemorrhage
-Penetration, perforation:
-Pain in BACK
-Pain in CHEST
-Pain in LUQ

-Not felt to develop into malignancy

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31
Q

peptic ulcers: bleeding, perforation, obstruction from edema or scarring

A

-Bleeding:
-Occurs in 15% to 20% of patients
-Most frequent complication
-May be life-threatening
-Accounts for 25% of ulcer deaths
-May be the first indication of an ulcer

-Perforation:
-Occurs in about 5% of patients
-Accounts for two thirds of ulcer deaths
-Rarely, is the first indication of an ulcer

-Obstruction from edema or scarring:
-Occurs in about 2% of patients
-Most often due to pyloric channel ulcers
-May also occur with duodenal ulcers
-Causes incapacitating, crampy abdominal pain
-Rarely, may lead to total obstruction with intractable vomiting

32
Q

helicobacter pylori

A

-!!!!!!!!!!!low grade lymphoma, chronic gastritis, adenocarcinoma !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
-Responsible for majority of peptic ulcers, as well as chronic gastritis and potentially gastric cancer/lymphoma
-Present in about 20 percent of people < 40 years old and half of those over 60 years; most infected people do not develop ulcers; unknown why
-H. pylori weakens protective mucous coating of stomach and duodenum, allowing acid to reach mucosa; acid and bacteria irritate mucosa, cause ulcer
-H. pylori able to survive in stomach acid because it secretes enzymes that neutralize the acid
-Causes 80% of gastric peptic ulcers
-Causes almost all duodenal peptic ulcers
-Causes chronic gastritis
-Causes gastric adenocarcinomas
-Causes MALT lymphomas

33
Q

acute ulcers

A

-NSAIDS
-“STRESS” ULCERS

-ENDOGENOUS STEROIDS:
-SHOCK
-BURNS
-MASSIVE TRAUMA
-Intracranial trauma, Intracranial surgery
-SEPSIS

-EXOGENOUS STEROIDS
-CUSHING ULCER

-usually small (<1cm), superficial, multiple

34
Q

hypertrophic* gastropathy

A

-RUGAL PROMINENCE (cerebriform)
-NO INFLAMMATION
-HYPERPLASIA of MUCOSA

-dont focus on diseases:
-Ménétrier disease, resulting from profound hyperplasia of the surface mucous cells with accompanying glandular atrophy, ass. w. CMV, H. Pylori, ↑TGF-α
-Hypertrophic-hypersecretory gastropathy, associated with hyperplasia of the parietal and chief cells within gastric glands (NORMAL gastrin)
-Gastric gland hyperplasia secondary to EXCESSIVE gastrin secretion, in the setting of a gastrinoma (Zollinger-Ellison syndrome)

35
Q

gastric tumors

A

-BENIGN:
-“POLYPS” (HYPERPLASTIC vs. ADENOMATOUS)
-LEIOMYOMAS (Same gross and micro as smooth muscle)
-LIPOMAS (Same gross and micro as adipose tissue)

-MALIGNANT
-ADENOCarcinoma
-LYMPHOMA

-POTENTIALLY MALIGNANT
-G.I.S.T. (Gastro-Intestinal “Stromal” Tumor)
-CARCINOID (NEUROENDOCRINE)

36
Q

adenocarcinoma : stomach

A

-MC malignant tumor of stomach
-H. pylori associated
-Japan, Chile, Costa Rica, Colombia, China, Portugal, Russia, and Bulgaria
-M»F
-Socioeconomically related

-RISK FACTORS:
-H. pylori
-Nitrites, smoked meats, pickled, salted, chili peppers, socioeconomic, tobacco
-Chronic gastritis, Barrett’s, adenomas
-Family history

37
Q

linitis plastica

A

-adenocarcinoma of stomach
-grows diffusely through all layers of stomach
-thickened wall
-leather bottle appearance
-poor prognosis
-SIGNET RING CELLS

38
Q

gastric lymphoma

A

-Lymphoid origin; 6th decade of life
-Grossly indistinguishable from adenocarcinoma
-5% of gastric malignancies are primary lymphomas
-Most common is B Cell Type (MALTomas, diffuse large B-cell lymphoma)
-!MALTomas (lymphomas of mucosa-associated lymphoid tissue) are the majority (extranodal marginal B-cell lymphomas)
-MALT Tx: H. Pylori eradication (antibiotics) -> basically puts pt into remission

39
Q

gastrointestinal stromal tumors (GIST)

A

-Solitary, circumscribed, fleshy mass, whorled cut surface – may be ulcerated
-can be up to 30 cm
-Mesenchymal neoplasms - arise from interstitial cells of Cajal (innervated network of intestinal pacemaker cells for gut peristalsis), located in muscularis propria (“spindle” cells)
-Rare; > 1/2 arise in stomach (can happen anywhere)
-not common < 40 years
-!!! IHC for c-KIT (aka CD117) usually positive, useful diagnostic marker
-Prognosis depends on size, mitotic index, and location – gastric GISTs somewhat less aggressive than those in small intestine
-Recurrence or metastasis rare if < 5 cm; common if > 10 cm
-GISTs with mutations in KIT or PDGFRA respond to imatinib, a tyrosine kinase inhibitor, especially used in patients with unresectable, recurrent or metastastic disease

40
Q

small/large intestine

A

-NORMAL: Anat., Vasc., Mucosa, Endocr., Immune, Neuromuscular
-PATHOLOGY:
-CONGENITAL
-ENTEROCOLITIS: DIARRHEA, INFECTIOUS, OTHER
-MALABSORPTION: INTRALUMINAL, CELL SURFACE, INTRACELL.
-(I)IBD: CROHN DISEASE and ULCERATIVE COLITIS
-VASCULAR: ISCHEMIC, ANGIODYSPLASIA, HEMORRHAGIC
-DIVERTICULOSIS/-ITIS
-OBSTRUCTION: MECHANICAL, PARALYTIC (ILEUS) (PSEUDO)
-TUMORS: BENIGN, MALIGNANT, EPITHELIAL, STROMAL

41
Q

congenital intestine problems (didnt read this slide)

A

-DUPLICATION
-MALROTATION
-OMPHALOCELE- abdominal wall defect: intestines, liver, and occasionally other organs remain outside of abdomen in a sac because of a defect in the development of muscles of abdominal wall
-GASTROSCHISIS-birth defect: infant’s intestines protrude out of the body through a defect on one side of the umbilical cord.
-ATRESIA/STENOSIS SPECTRUM
-MECKEL
-AGANGLIONIC MEGACOLON (HIRSCHSPRUNG DISEASE) - cant defecate

42
Q

congenital intestines: meckel**

A

-meckel (terminal ileum, “vitelline” duct) diverticulum
-Most common true diverticulum, most common congenital anomaly of GI tract, occurs in ileum due to failed involution of vitelline duct (connects lumen of developing gut to yolk sac)
-Solitary diverticulum extends from the antimesenteric side of the bowel
-“rule of 2’s”: Occurs in approximately 2% of the population, generally present within 2 feet (60 cm) of ileocecal valve, approximately 2 inches (5 cm) long, twice as common in males, most often symptomatic by age 2 (only approximately 4% symptomatic)

43
Q

aganglionic megacolon: congenital intestines

A

-HIRSCHSPRUNG DISEASE
-absence of ganglion cells in a segment of the bowel in an infant; leads to aperistalsis
-Failure to pass a first stool for 24-48 hours is suggestive of HS -> meconium
-distention
-aperistalsis
-Infants with HS often have abdominal distention, abdominal pain, and vomiting; constipation, poor weight gain, and slow growth

44
Q

celiac disease

A

-Small intestine, duodenal bx
-also called SPRUE or NON-tropical sprue
-Also called GLUTEN-SENSITIVE ENTEROPATHY:
-Sensitivity to GLUTEN, a wheat protein, gliadin
-Immobilizes T-cells
-Also in oat, barley, rye
-Progressive mucosal “atrophy”, i.e. villous flattening!
-Relieved by gluten withdrawal
-bloating
-chronic diarrhea
-flatulence, greasy, bulky, and bad–smelling stools
-nausea or vomiting
abdominal
-pain

-Increased risk of malignancy; most common cancer is enteropathy-associated T-cell lymphoma, an aggressive lymphoma of intraepithelial T lymphocytes

45
Q

tropical sprue

A

-Prevalent in tropical regions of the Caribbean, India, South Africa, and Southeast Asia
-Affected patients often suffer from malabsorption, malnutrition, and stunted growth
-Epidemic forms
-NOT related to gluten
-Exact cause not known; acquired disorder, may be related to environmental and nutritional factors, or related to an infectious organism (viral or bacterial), dietary toxin, parasitic infestation, or nutritional deficiency
-Tropical Sprue causes damage to mucosal lining of the intestine resulting in impaired absorption of food, minerals, and water

46
Q

whipple’s disease

A

-Rare, multi-orgam chronic disease caused by Tropheryma whipplei
-Bacteria-laden macrophages accumulate within small intestinal lamina propria and mesenteric lymph nodes, causing lymphatic obstruction (malabsorptive diarrhea of Whipple disease due to impaired lymph drainage)
-Bacteria-laden macrophages can accumulate within mesenteric lymph nodes, synovial membranes, cardiac valves, brain, and other sites
-Most common in Caucasian men, particularly farmers and others with occupational exposure to soil or animals; genetic risk factors may exist
-Triad of diarrhea, weight loss, and arthralgia
-Extraintestinal symptoms may precede malabsorption by months or years and include arthritis; arthralgia; fever; lymphadenopathy; and neurologic, cardiac, or pulmonary disease
-a rare, systemic infectious disease caused by the bacterium Tropheryma whipplei

47
Q

enterocolitis

A

-DEFINITION of diarrhea: INCREASE in MASS, FLUIDITY, and/or FREQUENCY
-DIARRHEA is a SYMPTOM: 1) SECRETORY, 2) OSMOTIC, 3) EXUDATIVE, 4) MALABSORPTION, 5) MOTILITY

-INFECTIOUS (Viral, Bacterial, Parasitic)
-NECROTIZING
-COLLAGENOUS
-LYMPHOCYTIC
-AIDS
-DRUG INDUCED
-RADIATION
-“SOLITARY” RECTAL ULCER

48
Q

diarrhea: secretory, osmotic, exudative, malabsorptive (dont need to know specifics)

A

-Secretory:
-Viral damage to mucosal epithelium
-Entero-toxins, bacterial
-Tumors secreting GI hormones
-Excessive laxatives

-Osmotic
-Disaccharidase deficiencies
-Bowel preps
-Antacids, e.g., MgSO4
-“osmotic” diarrhea means there are too many solutes in the lumen and therefore absorption is impaired

-Exudative
-BACTERIAL DAMAGE to GI MUCOSA; increased damage to intestinal mucosa epithelium can result in exudate from mucosa into lumen – usually caused by gram positive gut flora
-Inflammatory bowel disease

-Malabsorption -
-characterized by defective absorption of fats, fat- and water-soluble vitamins, proteins, carbohydrates, electrolytes and minerals, and water; excessive loss of nonabsorbed substances in stool
-Steatorrhea: excessive (large volumes) fecal fat and bulky, frothy, greasy, yellow or clay-colored stools
-chronic malabsorptive disorders most common in US are pancreatic insufficiency, celiac disease, and Crohn disease

49
Q

infectious entercolitis

A

-VIRAL
-Rotavirus (69%), Calciviruses, Norwalk-like, Sapporo-like, Enteric adenoviruses, Astroviruses

-BACTERIAL
-E. coli, Salmonella, Shigella, Campylobacter, Yersinia, Vibrio, Clostridium difficile, Clostridium perfringens, TB
-Bacterial “overgrowth”

-PARASITIC
-Ascaris, Strongyloides, Necator, Enterobius, Tricuris
-Diphyllobothrium, Taenia, Hymenolepsis
-Amebiasis (Entamoeba histolytica)
-Giardia

50
Q

viral entercolitis

A

-Rotavirus most common
-Selectively infects and destroys mature enterocytes in the small intestine
-Crypts spared

-Most have a 3-5 day course
-Person to person, food, water

51
Q

bacterial enterocolitis

A

-Ingestion of bacterial toxins
-Staph
-Vibrio
-Clostridium

-Ingestion of bacteria which produce toxins
-Traveller’s diarrhea, E.coli

-Infection by enteroinvasive bacteria
-Enteroinvasive E. coli (EIEC)
-Shigella
-Clostridium difficile

-E. coli:
-Toxin, invasion, many subtypes
-Food, water, person-to-person
-Usually watery, some hemorrhagic
-INFANTS often

-SALMONELA - food, non-hermorrhagic
-SHIGELLA - person-to-person, invasive, often bloody diarrhea
-CAMPYLOBACTER – Toxins, invasion, food spread
-VIBRIO cholera - Water, fish, person-to-person; epidemics, no invasion (watery diarrhea), enterotoxin

52
Q

costridium difficile

A

-CYTOTOXIN (lab test readily available)
-NOSOCOMIAL
-PSEUDOMEMBRANOUS (ANTIBIOTIC ASSOCIATED) COLITIS

53
Q

parasites

A

-NEMATODES (ROUNDWORMS)
-Ascaris, Strongyloides, Hookworms (Necator & Anklyostoma), Enterobius, Trichuris

-CESTODES (TAPEWORMS)
-FISH (DIPHYLLOBOTHRIUM latum)
-PORK (TAENIA solium)
-DWARF (HYMENOLEPSIS nana)

-PROTOZOANS: AMOEBA (ENTAMOEBA histolytica), Giardia lamblia- Giardiasisin humans - caused by infection of small intestine by the CYST of a single-celled organismGiardia lamblia; occurs worldwide with prevalence of 20–30% in developing countries

54
Q

miscellaneous colitis

A

-NECROTIZING ENTEROCOLITIS (neonate) (Cause unclear)
-COLLAGENOUS (Cause unclear)
-LYMPHOCYTIC (Cause unclear)
-AIDS
-GVHD after BMT, as in stomach
-DRUGS (NSAIDS, etc., etc., etc.)
-RADIATION, CHEMO
-NEUTROPENIC (TYPHLITIS), (cecal, caecitis)
-“DIVERSION” (like overgrowth)
-“SOLITARY” RECTAL ULCER (anterior, motor dysfunction)

55
Q

disaccharidase deficiency

A

-LACTASE by far MOST COMMON
-ACQUIRED, NOT CONGENITAL
-LACTOSE -> GLUCOSE + GALACTOSE
-OSMOTIC DIARRHEA

56
Q

IBD

A

-CROHN DISEASE (granulomatous colitis)
-ULCERATIVE COLITIS

-COMMON FEATURES
-IDIOPATHIC
-DEVELOPED COUNTRIES
-COLONIC INFLAMMATION
-SIMILAR Rx
-BOTH have CANCER RISK UC>CD

57
Q

crohns disease

A

-TRANSMURAL, THICK WALL
-NOT LIMITED to COLON
-GRANULOMAS
-FISTULAE COMMON
-TERMINAL ILEUM OFTEN
-SKIP AREAS
-“CRYPT” ABSCESSES NOT COMMON
-NO PSEUDOPOLYPS
-MALABSORPTION

58
Q

ulcerative colitis

A

-MUCOSAL, THICK MUCOSA
-LIMITED to COLON
-NO GRANULOMAS
-FISTULAE RARE
-TERMINAL ILEUM NEVER
-NO SKIP AREAS
-“CRYPT” ABSCESSES COMMON
-PSEUDOPOLYPS
-NO MALABSORPTION
-granulomas are NOT found
-mucosal pseudopolyps are found

59
Q

vascular diseases

A

-ISCHEMIA/INFARCTION
-ANGIODYSPLASIA – not true dysplasia
-HEMORRHOIDS

60
Q

ischemia/infarction

A

-HEMORRHAGE is the main HALLMARK of ischemic bowel disease
-ARTERIAL THROMBUS
-ARTERIAL EMBOLISM
-VENOUS THROMBUS
-CHF, SHOCK
-INFILTRATIVE, MECHANICAL

-MUCOSAL -> TRANSMURAL

-Especially seen in elderly with cardiovascular problems
-Severe pain, rigid abdomen

61
Q

angiodysplasia

A

-not really dysplasia
-NOT neoplastic
-twisted, dilated submucosal vessels, can rupture

62
Q

hemorrhoids

A

-INCREASED INTRABDOMINAL PRESSURE
-i.e., VALSALVA
-INTERNAL vs. EXTERNAL
-Like varices, ultimate cause is chronically elevated increased submucosal venous pressure, either from portal hypertension (much less likely), or ANYTHING which commonly causes chronically increased abdominal pressure

63
Q

diverticulosis/itis

A

-FULL THICKNESS BOWEL OUTPOCKETING
-Assoc. w.:
-INCREASED LUMINAL PRESSURE, ↑transit time
-AGE
-L -> R (decreased liquidity)
-Decreased dietary FIBER
-Weakening of wall

-IMPACTION
-INFLAMMATION
-PERFORATION -> Peritonitis, local, diffuse
-BLEED, silently, even fatally
-OBSTRUCT
-COMMON
-NOT assoc. w. neoplasm, but may mimic carcinomas clinically, radiologically, surgically, and grossly

-Diverticuli resemble hernias of the colonic wall in that they occur @ sites of entry of mucosal arteries as they pass through the muscularis – represents weak spot that leads to a diverticulum if the individual generates high colonic intraluminal pressure (low fiber diet)
-True v. Pseudo diverticulum

64
Q

obstruction

A

-ADHESIONS (post-surgical)
-IMPACTION
-HERNIAS
-VOLVULUS
-INTUSSUSCEPTION
-TUMORS
-INFLAMMATION, such as IBD (Crohn) or divertics
-STRICTURES/ATRESIAS
-STONES, FECALITHS, FOREIGN BODIES
-CONGENITAL BANDS, MECOMIUM, INPERF. ANUS

-ILEUS, esp. postsurgical
-INFARCTION
-MOTILITY DISEASES, esp., HIRSCHSPRUNG DISEASE

65
Q

ileus

A

-disruption of normal propulsive gastrointestinal motor activity from NON-mechanical mechanisms
-Motility disorders that result from structural abnormalities are termed mechanical bowel obstruction

66
Q

tumors : intestine

A

-NON-NEOPLASTIC (POLYPS)
-EPITHELIAL
-MESENCHYMAL (STROMAL)
-LYMPHOID
-BENIGN
-MALIGNANT

67
Q

intestines: polyps

A

-HYPERPLASTIC (NON-NEOPLASTIC)
-ADENOMATOUS (TRUE NEOPLASM, and regarded by many as PRE-MALIGNANT)

-SESSILE vs. PEDUNCULATED
-TUBULAR vs. VILLOUS

-Villous adenomas behave more aggressively than tubular adenomas; HIGHER rate of developing into adenocarcinomas than the “tubular” patterns.

68
Q

familial neoplasms of intestine

A

-1) POLYPOSIS (NON-NEOPLASTIC, hamartomatous)
-2) POLYPOSIS (NEOPLASTIC, i.e., cancer risk)
-3) HNPCC: (Hereditary Non Polyposis Colorectal Cancer)

69
Q

cancer genetics

A

-Loss of APC gene
-Mutation of K-RAS
-Loss of SMADs (regulate transcription) SMADsare intracellularproteinsthat transduce extracellular signals fromTGF beta ligandsto the nucleus where they activate downstream TGF-ß gene transcription
-Loss of p53
-Activation of TELOMERASE

-cancer risk factors:
-Family history
-Age (rare <50)
-LOW fiber, HIGH meat, LONG transit time, refined carbs

70
Q

intestine cancer pathogenesis

A

-From existing ADENOMATOUS POLYPS
-DE-NOVO

-DYSPLASIA -> INFILTRATION -> METASTASIS

71
Q

growth patterns of cancer

A

-POLYPOID
-ANNULAR, CONSTRICTING
-DIFFUSE

72
Q

other tumors of intestine

A

-CARCINOID, with or without syndrome
-LYMPHOMA (MALTOMAS, B-Cell)
-LEIOMYOMA/-SARCOMA
-LIPOMA/-SARCOMA

73
Q

anal canal carcinoma

A

-MORE LIKELY TO BE SQUAMOUS, or “basaloid”
-WORSE IN PROGNOSIS
-HPV RELATED

74
Q

appendix

A

-Junction of 3 tenia coli, variable in location
-All 4 layers, true serosa
-Thickest layer is submucosal lymphoid tissue

-APPENDICITIS (ACUTE)
-MUCOCELE
-MUCUS CYSTADENOMA
-MUCUS CYSTADENOCARCINOMA

75
Q

acute appendicitis

A

-GENERALLY, a disease of YOUNGER people
-OBSTRUCTION by FECALITH the classic cause but fecaliths present only about half the time
-EARLY APPENDICITIS: NEUTROPHILSMucosa, submucosa
-NEED NEUTROPHILS in the MUSCULARIS to confirm the DIAGNOSIS
-25% normal rate, usually
-Perforation -> peritonitis the rule, if no surgery

76
Q

mucus tumors

A

-Mucocele (common) - CYST on APPENDIX filled with MUCIN; Can RUPTURE to become:
-PSEUDOMYXOMA PERITONEII

-Mucinous Cystadenoma (rare)
-Mucinous Cystadenocarcinoma (rare)

patho (11 decks)

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