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250 Cards in this Set
- Front
- Back
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What is the frequency of small intestine tumors in relation to all GI tumors?
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small intestine is an uncommon site for tumors
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What are the three benign lesions of the small intestine?
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Adenomas
gastrointestinal stomach tumors Puetz-Jeghers polyps |
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Adenomas in the Small Intestine
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Benign
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gastrointestinal stomach tumors in the small intestine
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Benign
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Puetz-Jeghers polyps in the small intestine
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Benign
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What is the malignant lesion of the small intestine?
what are the risk factors |
adenocarcinoma
Crohn disease FAP HNPCC Celiac disease |
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How are polyps classified (3 things)?
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Attachment to wall: pedunculated or sessile
Histology: hyperplastic or adenomatous neoplastic potential: benign or malignant |
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What are the four types of non-neoplastic polyps?
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inflammatory: solitary rectal ulcer syndrome: inflammatory lesion of anterior rectal wall: bleeds
hamartomatous (sporadic or syndromic) lymphoid hyperplastic |
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inflammatory polyp of the GI tract
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non-neoplastic
solitary rectal ulcer syndrome: inflammatory lesion of anterior rectal wall: bleeds |
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hamartomatous polyp of the GI tract
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non-neoplastic
Juvenile Polyposis Puetz Jeghers Cowden syndrome Babbayab-Ruvalcabe syndrome Cronkhite-Canada syndrome Using table 17-9 and notes describe the five GI polyposis syndromes with hamartomatous polyps |
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lymphoid polyp of the GI tract
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non-neoplastic
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hyperplastic polyp of the GI tract
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non-neoplastic
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Describe the morphology and malignant potential of a hyperplastic poylp
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decreased epithial turnover and delayed sheding = a pile of goblet cells
left colon <5mm. multiple esp in sigmoid & rectum. mature goblet and aabsorptive cells with serrated histologic surface architecture. no malignant potential must be distinguished from sessile serated adenomas on the right side of the colon--microsatellite instability, malignant potential |
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a pile of mature goblet cells with serrated histologic architecture near surface
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hyperplastic polyp
no malignant potential must be distinguished from sessile serated adenomas on the right side of the colon--microsatellite instability, malignant potential |
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What is the most common and clinically important neoplastic polyp in the colon?
Describe their morphology, clinical features and epidemiology |
colonic adenoma: precursors to colorectal cancer: screening colonoscopy at 50 yo.
ranfe form small pedunculated to large sessile. M=F. 50% of western adults have them by age 50. mostly tubular adenomas, low risk highest risk in sessile villous adenomas >4cm majority are clinically silent, but the frequency correlates to colorectal carcinoma |
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colonic adenoma
morphology, clinical features and epidemiology |
precursors to colorectal cancer: screening colonoscopy at 50 yo.
ranfe form small pedunculated to large sessile. M=F. 50% of western adults have them by age 50. mostly tubular adenomas, low risk highest risk in sessile villous adenomas >4cm majority are clinically silent, but the frequency correlates to colorectal carcinoma |
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Contrast the sessile serrated adenoma with a typical adenoma
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serrated architecture throughout full length of the glands, including the crypt base, vs in hyperplastic polyps wherein the serrated architecture confined to the surface
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Using Table 17-9 and 17-10 describe/compare and contrast the Familial Adenomatous Polyposis syndromes, Hereditary nonpolysposis colorectal cancer and the sporadic colon cancers
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have fun with that
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FAP:
pathways, inheirtance, dx, cancer prevention, prognosis |
APC/WNT is autosomal dominant
MUTYNH DNA mismatch repair gene is recessive 100 polyps required for diagnosis prophylactic coectomy ASAP 100% progress to cancer |
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HNPCC:
defect, aka, transmission, risk for |
Lynch syndrome
germ-line mutation of DNA mismatch repair MSH1, MSH2 results in microsatellite instability autosomal dominant: knud's 2 hit Patients are at increased risk for colorectal and extraintestinal cancer |
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epidemiology of adenocarcinoma of the colon
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usually devlops in people with prevelent adenomas a few years after adenoma dvlpt
Western diet: low unabsorbablevegatible fiber, high intake of refined CHO and fat. |
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What are the three molecular pathways for the development of colon cancer?
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APC/Beta-catenin pathway the adenoma carcinoma sequence
mismatch-repair/microsatellite instability pathway CpG island methylation pathway |
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How do cecal and right-sided lesions present?
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Fatigue, weakness, iron deficiency anemia; bulky lesions which bleed easily
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How do left sided lesions present?
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occult bleeding, change in bowel habits, cramping
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occult bleeding, change in bowel habits, cramping
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left sided lesion
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Fatigue, weakness, iron deficiency anemia; bulky lesions which bleed easily
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right sided/cecal lesions
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iron-deficiency in an older male
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GI cancer until proven otherwise
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Colon cancer metastases sites?
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regional lymph nodes
liver, lungs, bones |
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What is the single most important prognostic indicator for colorectal carcinoma?
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depth of invasion, presence/absence of mets
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What staging system is in use for colorectal cancer?
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TNM
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What do carcinoid tumors arise from?
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neurendocrine cells responsible for secreting hormonal compounds
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What predicts aggressive behavior of carcinoid tumors?
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site of origin: ileal gastric & colonic worse,
depth of local penetration size of tumor |
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Carcinoids in what site infrequently metastasize?
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appendix and rectal rarely spread
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Where are carcinoid tumors most likely to arise
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appendix, ileum, rectum, stomach, colon
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What is the morphology of carcinoid tumors
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solid-yellow-tan appearance on cut section
cytology: monotonous without cytoplasm, form islands; can see granules on EM. |
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What is the carcinoid syndrome most likely due to?
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secrete hormone into portal system, eliminated in first pass by liver. carcinoid syndrome therefore strongly correlated with mets
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What three clinical features of the carcinoid syndrome are patients most likely to have?
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vasomotor cutaneous flushing, intestinal diarrhea and cramps, asthma..
vasomotor, GI, asthma. |
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cutaneous flushing, GI distress + asthma
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carcinoid sydrome
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What is the overall survival rate for carcinoids?
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not good. by the time you have sx you have mets. 8% at 5 years.
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Where do most GI lymphomas occur?
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Helicobacter gastritis, mediterranean natives and immunodeficient pts, and with sprue
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What are the three types of lymphomas in the GI tract?
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Enteropathy type intestinal T cell lymphoma: complicates celiac disease
Mediterranean Lymphoma: young low SE men in poor countries, assoc. w/ alpha heavy chain disease Western-type Lymphoma: adults over 40 and children under 10 |
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What does GIST stand for?
What mutations are present? How has the recognition of the mutation changed therapy? |
gastrointestinal stomach tumors
somatic mutation in c-KIT gene dvlpt of specific drugs Tyrosine kinase inhibitor imatinib mesylate used for CML, effective in GIST |
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What are the types of anal canal tumors?
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Basaloid pattern
Squamous cell pattern- HPV adenocarcinoma |
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What is the most common appendiceal tumor?
What is the prognosis? |
carcinoid
Very good, it rarely mets |
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A dilated appendix filled with mucin is called what?
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mucocele
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What are the three mucinous lesion of the appendix?
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benign mucocele, mucinous cystadenoma, mucinous cystadenocarcinoma
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What is pseudomyxoma peritoneii?
What cells are found in it? |
mucinous cystaednomcarcionma invasion through appendiceal wall with seeding. abdomen fils with semisolid mucin pseudomyxoma peritoneii
poorly differentiaed adenocarcinoma cells |
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The two primary types of primary peritoneal tumors
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mesotheliomas (asbestos)
desmoplastic small round cell tumor |
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which tumors commonly produce 2ndry perotinoeal tumors
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ovary and pancreas
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1) What are the most common types of malnutrition among patients who abuse alcohol?
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deficiencies of thiamine, pyridoxine, folate, vitamin A, vitamin C, PEM
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Marasmus:
Deficiency: Body Habitus: Serum Protein Level: Manifestations: Behavior: Severity: |
Deficiency: starvation: calories all nutrients
Body Habitus: decreased arm circuference, fat/muscle wasting Serum Protein Level: normal or slightly reduced Manifestations: anemia, infx, lymphocytopenia Behavior: dull, lethargic Severity: growth retardation, short stature |
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Kwarshiorkor:
Deficiency: Body Habitus: Serum Protein Level: Manifestations: Behavior: Severity: |
Deficiency: protein specifically
Body Habitus: spares fat and muscle, generalized edema Serum Protein Level: low Manifestations: fatty liver, flaky paint appearance of skin, flag sign Behavior: fussy Severity: more severe than marasmus |
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Anorexia Nervosa
age onset; weight, labs, menses, clinical and complications |
Onset w/in 7 years of menarche
Weight: Labs: low bone density, low wbc, anemia, hypokalemia, loss of brain tissue Menses: amenorrhea Clinical decreased T3, increased rT3, normal to low TSH; cold interlrance Complications: highest death rate of any pyshciatic disease; thined left venticle: sudden death from hypokalemia, osteoporosis |
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Bulemia
age onset; weight, labs, menses, clinical and complications |
Onset- late adolescence
Weight: normal/overweight Labs increased serum amylase Menses: generally normal Clinical Complications: metabolic alkalosis --> respiratory acidosis--> hypkalemia; pumonary aspiration. mallory weiss tears of eosphagus w/ potential rupture parotid gland hyperplasai, loss of dental enamel. russell sign |
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4) What are the causes and features of vitamin A deficiency?
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fat malabsorption, depletion during infxn, use of mineral oil laxtive, orlistat tx for obseity
nyctalopia: night blindess xerophthalmia, keratomalacia (corneal softening, scarring), bitot spots: build up of keratin debris keratotic squamous epithlial metaplasia (increasing turnover): increased respiratory infxn, kidney stones, acne like dermatitis |
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nyctalopia: xerophthalmia, keratomalacia, bigot spots: : increased respiratory infxn, kidney stones, acne like dermatitis
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features of vitamin A deficiency
nyctalopia: night blindess xerophthalmia, keratomalacia (corneal softening, scarring), bitot spots: build up of keratin debris keratotic squamous epithlial metaplasia (increasing turnover): increased respiratory infxn, kidney stones, acne like dermatitis |
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delerium and papilledema
jaundice like skin w/o icterus in eyes |
Acute Vitamin A toxicity
retinoid induced cerebral hypertension: delerium and papilledema carotemia: jaundice like skin w/o icterus in eyes |
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Acute Vitamin A toxicity
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retinoid induced cerebral hypertension: delerium and papilledema
carotemia: jaundice like skin w/o icterus in eyes |
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Chronic Vitamin A deficiency
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dryness of lips, epistaxis
hyperostosis = bone/joint pain, hepatomegaly w/ fibrosis, psychiatric manifestations |
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dryness of lips, epistaxis, bone/joint pain, hepatomegaly, mental disturbances
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Chronic Vitamin A deficiency
dryness of lips, epistaxis hyperostosis = bone/joint pain, hepatomegaly w/ fibrosis, psychiatric manifestations |
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What are the causes and features of vitamin D deficiency?
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causes: inadequate intake of calcium, vitamin D w/ limited sunlight expsoure; impaired fat absorption, renal or liver diseases, genetics
features: fracture risk, rickets in children, osteomalacia in adults, hypocalcemic tetany: trousseau's sign: carpal sams induced by BP cuff Chvostoc's sign: msucle cotnraxn of eye/mouth/nose by tapping on facial nerve |
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trousseau's sign:
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carpal sams induced by BP cuff: vitamin D deficiency (hypocalcemic tetany)
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Chvostoc's sign
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msucle cotnraxn of eye/mouth/nose by tapping on facial nerve: vitamin D deficiency (hypocalcemic tetany)
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vitamin D toxicity
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hypercalcemia-->
nephrolitiasis, metastatic calcifications/atherosclerosis, bone pain |
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What are the causes of and effects of Vitamin E deficiency?
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fat malabsorption
immature gut of low birth weight infants abetalipoproteinemia genetic impairment of metabolism spinocerebellar degeneration: decreased DTR's Ataxia, analgesia, impaired vision |
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decreased DTR's Ataxia, analgesia, impaired vision
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spinocerebellar degeneration from vitamin E deficiency
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What are the causes and consequences of vitamin K deficiency
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fat malabsportion
diffuse liver disease warfarin therapy broad spectrum antibiotics (synthesyzed by endogenous bacteria) neonatal: no intestinal flora, low in breast milk Vitamin K dependent factors 7, 9, X, 2, anticoagulant proteins S and C prolonged PT, bleeding diseases |
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prolonged PT, bleeding diseases
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Vitamin K deficiency
fat malabsportion diffuse liver disease warfarin therapy broad spectrum antibiotics (synthesyzed by endogenous bacteria) neonatal: no intestinal flora, low in breast milk Vitamin K dependent factors 7, 9, X, 2, anticoagulant proteins S and C |
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thiamine deficiency
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Alcoholics
dry beriberi: polyneuropathy: demyelination of peripehral nerves: weakness, sensory loss wet beriberi: cardiovascular disease: high output cardiac failure, peripheral edema Wernicke-Korsackoff syndrome: CNS disease Wernickei is stumbling, nystagmus Korsakoff is confabulation, amnesia |
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dry beriberi:
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thiamine deficiency (Alcoholics )
polyneuropathy: demyelination of peripehral nerves: weakness, sensory loss |
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wet beriberi
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thiamine deficiency (Alcoholics )
cardiovascular disease: high output cardiac failure, peripheral edema |
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Wernicke-Korsackoff syndrome
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thiamine deficiency (Alcoholics )
Wernickei is stumbling, nystagmus Korsakoff is confabulation, amnesia |
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What are the causes of and effects of riboflavin deficiency
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Alcoholism, Advanced Cancer, Anorexia, Milk Avoidance
Cheilosis: cracks at angles of mouth glossitis: atrophy of tongue muslce eye: intersitital keratitis scaling dermatitis at nasolabial fold bone marrow hypoplasia |
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cracks at angles of mouth, atrophy of tongue muslce, intersitital keratitis
scaling dermatitis at nasolabial fold, anemia |
riboflavin deficiency?
Alcoholism, Advanced Cancer, Anorexia, Milk Avoidance Cheilosis: cracks at angles of mouth glossitis: atrophy of tongue muslce eye: intersitital keratitis scaling dermatitis at nasolabial fold bone marrow hypoplasia |
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Cheilosis
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indicative of riboflavin or pyridoxine deficiency
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What are the causes of and effects of niacin (B3) deficiency?
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Malnutrition in general
CORN based diets administration of isoniazid and 6 mercaptopurine pellegra: 4 d's dermatitis: sloughing off of skin diarrhea from intestinal atrophy demetentia from spinal cord degeneration death if prolonged |
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CORN based diets
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niacin (B3) deficiency
pellegra: 4 d's dermatitis: sloughing off of skin diarrhea from intestinal atrophy demetentia from spinal cord degeneration death if prolonged |
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isoniazid
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niacin and pyridoxine defieincies
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sloughing off of skin, diarrhea, demetentia
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3 of 4 ds of pellegra
dermatitis: sloughing off of skin diarrhea from intestinal atrophy demetentia from spinal cord degeneration death if prolonged from niacin deficiency Malnutrition in general CORN based diets administration of isoniazid and 6 mercaptopurine |
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What are the causes of and effects of pyridoxine deficiency?
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long term use of isoniazid and estrogen
suberrheic dermatitis cheilosis glossitis peripheral neuropathy, convulsions sideroblastic anemia increased plasma homocysteine |
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Vitamin C Deficiency
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ascorbic acid, scavenges free radicals directly
accelerates hydroxilation: activates prolyl and lysyl hydroxylases Poor diet, dialysis, milk-fed infants blood vessel hemorrhages: into joints and into CNS "scorbutic rickets" bowing bones, widened epiphyses, depressed sternum loose teeth, rash, impaired wound healing, anemia |
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causes of and effects of folate deficiency
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smoking, oral contraceptives, anticonvulsants, chronic disease
neural tube defects in fetus megaloblastic anemia hyperhomocyesteinemia w/ increased risk for coronary thrombosis/stroke |
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causes of and effects of B12 deficiency
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vegan diet
pernicious anemia intestinal malabsorption tapeworm, blind loop bacteiral overgrwowth (competition) hyperhomocysteinemia with increased risk for coronary thrombosis/stroke megalobalstic anemia subacuted combined dengeration of spinal cord meylin glossitis |
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consequences of zinc deficiency
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acrodermatitis eneropathica: rash about eyes nose mouth, distal extremities
anorexia, diarrhea growth retardation: hypogonadism-infertility impaired wound healing altered imunity impaired night vision malformations in infant of deficient mother |
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What are the associations, including complications, of periodontitis?
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inflammation in periodontal ligaments, alveolar bone and cementum resulting in loss of teeth
assoc. AIDS, acute leukemia, crohn's disease, diabetes mellitus, down syndrome, agranulocytosois, or defects in granulocytic fnx complications: infective endocarditis, brain abscess, adverse pregnancy outcomes, increased risks of many cancers, including non-oral |
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Irritation fibroma:
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buccal mucosa along bite line
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Pyogenic granuloma:
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gingiva of children and pregnant women; may grow rapidly, bleeds readily; red/purple pedunculated, granulation tissue
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Peripheral ossifying fibroma
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: may arise form pyogenic granuloma or de novo. young teenage females; prone to recurrence.
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giant cell epulus
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gingiva at site of inflammation
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aphthous ulcer.
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cancer sores; unknown cause; assoc: familial, behcet syndrome (oral/genital ulcers & uveitis), autoimmune, dietary chagnes, HIV
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Define glossitis. List associations
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beefy red tongue/inflammed tongue
due to deficiencies of: plummer-vinson/paterson-kelly syndromes: iron deficiency, glossitis, esophageal webbs, risk for squamous CA B12, riboflavin, niacin, pyridoxine assoc w/ sprue |
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What is the cause, morphology and spectrum of oral disease due to herpes simplex
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recurrent herpetic stomatitis "cold sore" reactivated by trauma, allergies, UV light, URI
located anywhere in oral/nasal area. Dx: Tsank smear for Cowdry bodies |
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Recognize causes of deep fungal infections. What are the associations and morphology of thrush?
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immunosuppressed: HIV, transplants, cancer therapy\
aspergillus, zygomycosis (Mucor and Rizopus) histoplasmosis, coccidiomycosis, blastomycosis |
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What are the associations and morphology of thrush?
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Thrush: candida albicans in immunocompromized, or antibiotic regimen; it can be scraped off (pseudomembrane)
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What are the cause and clinical course of Lugwig’s angina?
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oral infection of molars; infectious process spreading through submental, sublingual and submandibular spaces, progresses rapidly to hemodynamic instability and airway obstruction: fatal. immediate surgical debridement and antimicrobials.
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rasberry tonuge
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Scarlet fever: rasberry tonuge = fiery red: white coated with hyperemic papillae = strawberry tongue.
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strawberry tongue
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Scarlet fever: rasberry tonuge = fiery red: white coated with hyperemic papillae = strawberry tongue.
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koplik spots about stensen duct:
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Measles
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oral manifestation of Diphtheria:
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dirty white fibrinosuppurative membrane over tonsils, retropharynx
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oral manifestation of Infectious Mono
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pharyngitis, tonsillitis with gray white exudate, cervical LN's enlarged
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oral manifestation of HIV
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HSV, Candida, aphthous ulcers, cheilosis, kaposi sarcoma, hairy leukoplakia
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Describe and recognize morphology of hairy leukoplakia. What is the cause?
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Immunosuppression --> white confluent patches of fluffy thickenings on lateral border of the tongue.
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white confluent patches of fluffy thickenings on lateral border of the tongue.
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hairy leukopenia from immunosuppression
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white plaque on oral mucosa that cannot be scraped off and cannot be classified as another disease entity
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leukoplakia.
1/4 may be precancerous for squamous cell CA. from thickening to carcinoma in situ. |
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Leukoplakia
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white plaque on oral mucosa that cannot be scraped off and cannot be classified as another disease entity. 1/4 may be precancerous for squamous cell CA. from thickening to carcinoma in situ.
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erythroplakia-
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red, velvety eroded oral mucosa: high risk of malignancy at site and elsewhere.
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red, velvety eroded oral mucosa
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erythroplakia
high risk of malignancy at site and elsewhere. |
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What are the causes, gross and microscopic morphology and clinical behavior of oral squamous cell carcinoma? Correlate prognosis with location
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Tobacco smoke plus alcohol; HPV infection: progressive genomic changes
gross morphology: leukoplakia, erythroplakia, nodular/ulcerated lesions micro morphology: invasive sheets of polygonal (multisided) cells with eosinophilic cytoplasm, enlarged hyperchromiatc nuclei. keratin (squamous) perls swirling cell clusters lip: best prognosis floor of mouth: poor prognosis posterior tonuge: very poor prognosis local invasion with late mets to regional LN's. |
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associations of Dentigerous cyst
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impacted molars, crown of unerupted teeth.
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associations of Odontogenic keratocyst
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locally aggressive, recurrant. multiple nevoid basal line "Gorlin" syndrome. AD: tumor suppressor gene PTCH defect. cyst lined by squamous prominent basal cells.
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associations of Periapical cyst
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inflammatory origin; associated with carrries
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associations of Ameloblastoma-
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cystic, indolent tumor of odontogenic (squamous) epithlium; both benign and malignant.
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associations of Odontoma
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hamartoma, enamel, dentin, epithelium.
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What are the defining morphologic features andcause of nasal polyps?
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these people have allergies, but not atopy, take aspirin and get nasal polyps.
glistening protrusions of edematous mucosa: recurrent rhinitis and sinusitis. defining morphologic feature is eosinophils. |
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What are causes and complications of sinusitis?
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viral is most common
bacterial freq follows URI can come from bad teeth, allergies/asthma kartagener's syndrome atypically: deep fungal infections mucormycosis, fungi in diabetes complications: spread into the orbit, osteomyelities septic thrombophlebitis of dural venous sinus |
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Develop a differential diagnosis of necrotizing lesions of the nose.
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spreading fungal infections (mucormycosis)
wegener's granulomatosis extranodal NK/T cell lymphoma |
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Angiofibroma of the nose
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adolescent males; a vascular tumor which bleeds profusely
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Inverted papilloma (nose)
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benign squamous proliferation, may be exophytic or inward (inverted growth). ivnerted papillomas prone to recurrence, extension to the cranium.
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Olfactory neuroblastoma-
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aggressive malignancy of neuroendocrine cells: positive for NSE, synaptophysin, chromagranin
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Solitary plasmacytoma
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clonal proliferation of plasma cells curable by plasma resection. unlikely to progress to multiple myeloma.
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Describe the associations and behavior of nasopharyngeal carcinoma.
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epstein barr virus in genetically predisopsed indivials.
african childrena nd asian adutls grows silently, often resectable. mets to cervical LN's & distant sties. 50-50 cure with radiation. |
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What are the complications of Streptococcal pharyngitis
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quinsy: paratonsillar/retropharyngeal abscess
poststreptococcal glomerulonephritis, rheumatic fever, ludwigs' angina. |
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Associations of Laryngitis
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usually tobacco smoke. part of URI, seeding by pulmonary TB.
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Associations of Laryngoepiglottis
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life theatening edema of epiglottis/cords; in small children usually due to H influenzae.
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Associations of Laryngotracheobronchitis
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croup: airway narrowed by spasm in cihldren. usually viral: inspiratory stridor.
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What are the causes and behavior of laryngeal nodules (know synonyms) and squamous papillomas?
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Laryngeal nodules; sx: hoarsenss. Causes: tobacco smoke, vocal strain
squamous papilloma: HPV 6 & 11. not malignant, but may be fatal due to airway obstrx. |
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What are the causes, morphology and clinical features of laryngeal carcinoma?
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strong association with tobacco and EtOH.
in true vocal cords good prognosis: (caught early via hoarseness, no vaculature. supra/subglottic: worse tx: surgery, radiation late sx: pain, dysphagai, hemoptysis pets to local LN's, death from local disease (compression) |
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) What are the causes and complications of acute otitis media?
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the best test for acute otitis media is bulging eardrum
complciation: ruptured eardrum (stops hurting sudeenly) squamous eptihelium incorporaed into resealed eardrum--scar called cholesteatomas mastoiditis, labrynthitis, temproal cerebritis or abscess, destrx of ossicles (hearing loss) |
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What is the complication of Pseudomonas otitis in diabetics?
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necortizing infection
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Define cholesteatoma of the ear drum, including cause and effects.
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cystic lesiosn of ear drum lined by epithelium, squamous or metaplastic glands. arises from healed perforation, may contain cholesterol.
progressive enlargement w/ erosion of surrounding strx: destroys bones and lymph produces neck mass. |
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Describe the most common cause of conductive hearing loss in adults? Describe pathology. What is the etiology of conductive loss in young and middle aged adults
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otosclerosis: slowly progressive fibrous aknylosis of footplate at oval window with ossification, immobilization. If inherited AD moderate disease in adults, AR severe disease.
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Recognize causes of deep fungal infections.
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Immunosuppression: HIV transplants, chemotx. organisms: aspergillus, zygomycosis (mucor/rizopus) histoplasmosis, coccy, blastomycosis
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. What are the associations and morphology of thrush?
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thrush is candida usually albicans in immunosuppressed or those with altered immune flora (antibiotics)
pseudomembranous means it can be scraped off. |
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What is the derivation and location of a thyroglossal tract cyst?
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remnant of dvlptal tract of thyroid gland migration from foramen cecum.
midlien neck base of tongue, epithlium lined cyst up to 4 cm. |
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What is the derivation and clinical behavior of carotid body tumor?
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arises at bifurcation of carotid body;
numor of neuroendocrine cells in older adults. kills people from local invasion |
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Review causes of sialadenitis. What are the consequences of autoimmune sialadenitis? How is it diagnosed? What are some other causes of xerostomia?
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inflammation of the salivary glands;
viral: mumps, HIV bacteiral oral flora autoimmune: sjorgen's syndrome w/w/o RA--> xerostoma, keratoconjunctivitis. lip biopsy xerostomia: radiation therapy or drugs |
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What are mucoceles? What is the cause? Where are the most common locations?
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blockage or rupture of salivary gland duct: fluid filled cyst lined by inflammatory/granulation tissue; fills upon anticipation of food
ranula is under the tongue |
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Define sialolithiasis; sialadenitis. How are they related?
|
sialolithiasis: stones in the salivary ducts; causes sialadenitis: grwoth of S aureus or S viridians.
enlargement of salivary gland with suppruative infection. |
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List salivary gland tumors from text. Which are Malignant?
|
Pelomorphic adenoma: usually benign
warthin's tumor: benign mucoepidermoid carcinoma acinic cell carcinoma adenoid cystic carcinoma 30 others |
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|
What are synonym, frequency and clinical behavior of pleomorphic adenoma of the salivary gland?
|
synonym: mixed tumor
most common salivary gland tumor usually salivary painless slow growing mass tend to recurr after surgery unlikely but may progress to highly aggressive carcinoma ex pleomorphic adenoma mixture of epithelium forming glands and matrix: myxoid, chondroid and osseus tissue derived from ductal reserve cells or myoepithlial cells. |
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What are the morphologic features, associations and behavior of Warthin tumor?
|
smokers over 40
multifocal parotid gland tumor benign, do not reccur. double layer of oncocytic cells lining spaces oncocytes: pink cytoplasm from abundant mitochodria dense stroma of infiltrate cells |
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What is the most common malignant tumor of salivary gland? Describe association and morphologic features.
|
mucoepidermoid carcinoma; mostly parotid glands. radiation induced;
mucin producing malignant glands and sheet of squamous epidermoid cells. |
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What are the associations of follicular hyperplasia of the thymus?
|
icnrease in B cells: myasthenia gravis, other autoimmune disease
|
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|
List tumors of the thymus.
|
NOT FOLLICULAR HYPERPLASIA
lymphomas: T lymphoblastic, B cell, hodgkins germ cell tumors thymoma: thymic epithelial cell tumors |
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How is clinically benign thymoma distinguished from malignant thymoma?
|
cytology:
non-invasive: benign spindle cells malignant: invasion or metastases, spindle cell proliferaction thymic carcinoma: squamous cell carcinoma assoc with EBV. |
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|
what conditions are associated with thymoma?
|
Myasthenia gravis
pure red cell aplasia curshing syndrome, grave's disease pernicious anemia dermatomyositis polymyositis |
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Secretory Diarrhea
volume of stool, relationship to meals, characteristic labs and causes. |
Volume >500ml/day
Meals: persists during fasting Labs: isotonic fluid, osmotic gap approaches that of plasma <50mOsm Causes: toxigenic E coli, cholera, C diff & other infxn tumor elaborated peptides: VIP, serotonin laxative use |
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Osmotic Diarrhea
volume of stool, relationship to meals, characteristic labs and causes. |
Volume >500ml/day
Meals: abates with fasting Labs: [elyte] >50mOsm Causes: lactase/disaccharidase deficiency; theraputic lactulos, mgSO4, excess sorbitol sweetener, sequelae of viral diarrhea, rotovirus adenovirus, componenet of malabsorbtion syndromes |
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Exudative Diarrhea
volume of stool, relationship to meals, characteristic labs and causes. |
Volume: low volume
Meals: persists during fasting Labs: purulent bloody stools Causes: Inflammatory disease: enteroinvasive bacteria, cytotoxic bacteria, entameoba histolytica, ideiopathic IBD, ischemic colitis |
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What are the consequences, both nutritional and alimentary tract of malabsorption?
|
Osmotic diarrhea
flatus, borborygmi abdominal pain and distention anorexia w/ weight loss mucosal inflamation from vitamin deficiencies steatorrhea iron, folate, B12 and B6 deficieny anemias bleeding from vitamin K deficiency osteopenia, 2ndry hyperparathyroidism and tetany from calcium deficiency scurvy et all epidermal manifestations neuropathies from Vitamin A, B12 deficiency amenorrhea, infertility, delayed puberty |
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What are the clinical features and pathogenesis of malabsorption in cystic fibrosis?
|
defective luminal hydration leads to intraductal obstrx--> trypsinogen pancreatic auto-digestion -->absense of pancreatic enzymes
|
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|
) Describe the pathogenesis of celiac disease
|
immune mediated injury to small intestinal mucosa 2ndry to gliadin (ETOH soluble water insoluble nondigestible gluten particle in wheat, barley, rye) exposure. HLA class II susceptibility gene among whites, esp w/ infx by adenovirus. CD8 lymph activation.
gliadin crosses epithlium, deamidated by tissue transglutaminase, then interacts with HLADQ2 or HLA DQ8. CD4's produce IL15, CD8's activated. |
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Recognize microscopic morphology of celiac Disease.
|
diffuse enteritis (inflammation of the SI), bluted/totally lost villi. increased intraepithelial T lymphs, crypt hyperplasia. not specific for celiac disease; B's produce ab, not the source of the damage, helpful in dx.
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diffuse enteritis (inflammation of the SI), bluted/totally lost villi. increased intraepithelial T lymphs, crypt hyperplasia.
|
morphology of celiac disease
|
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|
What are the clinical features of celiac disease?
|
Silent: positive serology with villous atrophy, no sx
latent: positive serology w/o villous atrophy, no sx Classic: sx onset w/ weening: failure to thrive, abdominal distention, chronic diarrhea. general sx of malabsorption dermatitis herpetiformis: vesicular skin rash with deposits of IgA attacking the protein which anchors the dermal papillae to the epithelium |
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How is celiac disease diagnosed and treated?
What are the complications? |
anti-gliadin, anti-tissue transglutaminase IgA, anti-endomysial antibodies all suggestive.
definitive diagnosis vis 1. clinically observed malabsorption, 2 intestional biopsy, 3 improvement of sx/histology via gluten free diet complications: lymphocytic gastritis, colitis refractory disease no longer responsive to gluten free diet increased risk for t cell lymphoma of SI, increased risk for other alimentary malignancies incl. small intestine adenocarcinoma |
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Describe the clinical features of tropical sprue including predisposing factors, morphology.
|
folate defficiency followinging days of acute diarrhea. toxigenic e coli, responds to antibiotic tx. tropics but not jamaca.
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What are the cause, mechanism (see table 17-6) morphology and clinical features of Whipple Disease?
|
trophyeryma whippelii gram positive actinomyete. T cell failure --> no activated macrophage--> impaired lymphatic transport. diarrhea, malabsprtion, weight loss. multisystem complaints- arthritis fever anemia, endocarditis, CNS, etc.
Micro: PAS positive macrophages in lamina propria of SI, lysosomes filled with bacteria. |
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What are the features of IPEX syndrome?
|
X linked
Severe persistent diarrhea, starting in childhood due to autoantibodies to gut epithlium. Immunodysregulation, polyendocrinopathy, enteropathy, foxp3 mutation. Tx: immunosuppression |
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What are the mechanism, clinical and lab features of lactase deficiency. Which groups are more prone to this deficiency?
|
lactase not on brush border. ethicity or giarrdia. osmotoc diarrhea.
labs: exhaled hydrogen from bacterial production, enzyme activity on biopsy, lactose blood surgar "tolerance" test ethnicity: afroamericans, native americans, chinese clincal congenital (rare) explosive watery frothy stools adults: cramps & gas with milk ingestion, corrected w/ abstinence form milk |
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What are the cause, mechanism, and clinical features of abetalipoproteinemia?
|
microsomal triglyceride transfer protein mutated, unable to syntehsize export lipoproteins. unable to export lipids from SI.
RBC's = acantrhocytes "burr cells" from membrane defects, hemolytic anemia failure to thrive, steatorrhea |
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Review and list assorted additional causes of malabsorption syndromes
|
Decreased surface area
surgical resection "short bowel" Crohn's disease Bacteiral overgrowth diabetic neuropathy scleraderma of amyloidosis blind loop syndrome congeintial intestinal transport diseases congential acnd acquired lymphangiectasia |
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|
List diverse lab studies used to detect malabsorption
|
D-xylose absorption test: blood and urine levels, measure intestinal phase of absorption
14CO2-cholyl-glyceine breath test: radioactive exhaled CO2 measured. dx of blind loop, stagnant loop and ileal absportive fnx Schilling test: B12 deficiency due to defects in ileal absorption, pancreative fnx, overgrwoth |
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|
) What are the two types of gastric ulcers?
|
Acute or "stress"
Chronic or peptic |
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What are the morphologic features of acute ulcers? (Recognize photographs)
|
variable depth, often multipe, <1cm, stained by acid digested blood. margins/base demonstrate no fibrosis, scarring or vascular thickening. complete healing may occur.
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|
Name two types of acute ulcers and describe the clinical situations are compared with each
|
Severe burns --> "curling ulcers" in somach
CNS trauma--> "Cushing ulcer" esophagus, stomach & duodenum. high risk for perforations |
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What organism is most associated with peptic ulcers of duodenum; stomach, chronic gastritis and gastric neoplasms? Be able to describe diagnostic labs and correlate with virulence factors.
|
H pylori: urease + (rapid urease test = CLO test), CagA+ stains (the cytotoxin involved in peptic ulcer and CA)
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|
What are the two most common sites of peptic ulcers; which is more common?
|
Duodenum 1st portion most common
2nd lesser curvature near antrum:body interface Where else do ulcers occur; correlate with Causes? Margines of gastrojuejunostomy Deuodenum, stomach and jejunum (multiple) of pts w/ Zollinger Ellison syndrome (gastrin secreting tumor) Heterotopic gastric mucosa in Meckel's diverticulum |
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|
What are the causes of 1) gastric ulcers 2) Duodenal ulcers?
|
100% of duodenal PUD assoc. w/ H pylori
2/3 gastric PUD infx w/ H pylori Hyperacidicity, Any cuase Cigarret smoking, aspirin (gastric>duodenum) NSAIDs, prolonged or high dose corticosteroids COPD alpha1 antitrypsin deficiency Cirrhosis of the liver--> duodenal ulcers Uremia: esophagus--> gastric ulcers Genetic, Psychological factors Hypercalcemia --> stimulates gastrin prodxn |
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What is the morphology of peptic ulcers?
|
Location: duodenum: first portion on anterior or posterior wall
gastric: lesser curvature, antrum-body usually single <4cm diamter punched out with straight walls (vs heaped up margins of malignancy) Surrounded by scarred, thickened wall Mucosa may radiate from crater Microscopically: four classic layers 1. fibrinoid debris in ulcer base, 2. acute nonspecific inflam, 3 granulation tissue, 4. fibrosis chronic gastritis in surrounding mucosa hyperplastic mucosa surrounds crater, involved in healing |
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|
What are the symptoms, clinical course and complications of peptic ulcer disease?
|
Epigastric gnawing, burning or aching pain, radiates to T5-9 on Left
worse at night, 3-4 h after meals, relieved by food or alkali chronic blood loss--> iron deficiency anemia acute gi hemorrhage perofration w/ pancreatitis, peritonitis N/v, bloating, belching weight loss Clinical course: chornic PUD |
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|
Complications:
of PUD |
Bleeding most commonly
Perforation most deadly Gastric outlet obstruction rarely: vomitting, surgical Malignancy is rare |
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|
What are the clinical and morphologic features of Ménétrier’s disease?
|
A hypertrophic gastropathy Giant cerebriform enlargement of rugal folds which resemble cancer on imaging and endoscapy. Menetriers is caused by excessive secretion of TGFa. Males 30-50. hyperplasia of foveolar mucus glands leads to excess mucus production.
sx: bleeding, epigastric distress, diarrhea, weight loss. protein losing enteropathy --> hypoalbuinemia, edema. recurrent puptic ulcers, chronic risks gastric carcinoma. |
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What are the pathogenesis, morphology and clinical features of Zollinger Ellison syndrome
|
gastrin production by carcinoid "gastrinoma" in the pancreas or small intestine, most are solitary, sporadic, malignant, but slow. May be 2ndry to multiple endocrine neoplasia (MEN1)sydrome of tumors in multiple endocrine glands. parietal cell hyperplasia with giant rugal hypertorphy--> multiple acid assoc. puptic ulcerations, usually duodenum, but can be unusual
Ulcers at unusual locations (jejunum) think ZE. |
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|
Compare/contrast inflammatory/hyperplastic vs fundic gland vs gastric adenomatous polyps with regard to risk factors and association with gastric adenocarcinoma. (see table 17-4)
|
have fun with that buddy
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|
What are the pathogenesis of gastric adenocarcinoma, intestinal pattern?
|
Helicobacter Pylory
Diety: N-nitroso compounds and benzo[a]pyrenes from smokes, salted meat, pickled vegetables, lack of fresh fruit and veges, Cigarettes, Low SE, Hyperchlorhydria/acholrhydria, Obesity Intestinal Type genetics: Genetics: APC gene (FAP) microsatellite instabliity (familial HNPCC) TGF-Beta mutation genetic variants of pro-inflam and immune responsiveness to H pylori |
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|
What are the most important prognostic factors associated with gastric adenocarcinoma?
|
depth of invasion and extent of nodal & distant metastasis
early: lesion confined to mucosa/submucosa which does not invade musclaris, 90% 5 year survival advanced: invasion through submucosa into muscle <10% 5 year survival |
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|
Characterize the macroscopic morphologies of gastric adenocarcinoma, especially as regards prognosis.
|
prominent mucosal fold or ulcer
litnis plastica "rigid leather bottle" is advanced carcinoma see pictures for staging |
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Compare/contrast intestinal pattern gastric adenocarcinoma with signet ring adenocarcinoma describing microscopic morphology and epidemiology
|
intestinal type form glands, mucin will be in lumens of malignant glands. 55yo males, most arises from chronic gastritis of h pylori
signet ring cells: infiltrating individual cells which do not form glands. mucin will be in the cytoplasm. <50 yo m=f. arises de novo. decreased E cadherin. spreading means advanced, high mortality. |
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How does gastric carcinoma spread and what are sites of distant metastases (define each)? What is the overall prognosis?
|
arises in mucosa, invasion into serosa. mets to LN's more likely w/ increasing depth. extension to duodenum, pancreas, retroperitoneum; cardia extend to esophagus. widespread peritoneal seeding and mets to liver, lungs.
Virchow's node: metastatic cancer to supraclavicular node, may be gastric cancer Sister Mary Joseph nodule: met to periumbilical region Krukenberg Tumor: met signet ring to ovaries, usually from a gastric primary |
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hat are the 1) immunophenotype, 2) gross and microcopic morphology, 3) association(s) and behavior of gastric MALT lymphoma?
|
CD19+ CD20 +, CD5 & 10 negative monoclonal light chains present
one of 3 Mutated Malt lymphoma translocationes "MLT"s strongly associated with H pylori and chornic inflam unresponsive to antibiotics, may progres to large B cell lymphoma Dense lymphocyte infiltrate in lamnia propria lymphoepithelial lesion: lymphs w/in glands, lymph follicles and plasma cells present |
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|
) What are the causes of gastric perforation?
|
newborns during labor
severe vomiting resuscitation carbonated beverages ruptured dilation 2ndry to outlet obstrx or paralytic ileus |
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|
What is a bezoar?
|
luminal concretions of undigestable material: hair, plant fiber,e tc. require surgical removal.
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|
gastroschisis:
|
failure of formation of abdominal wall
|
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|
omphalocele:
|
failure of formation of abdominal muscle w/ herniation into membranous sac
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|
heterotopias, give common examples:
|
normal pancreas, gastric mucosa commonly occur anywhere along GI tract; 50% of meckel's diverticuli have pancreatic or gastric.
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|
atresia
|
complete obstrx, most commonly duodenum
|
|
|
congenital pyloric stenosis
|
palpable "olive" nodule
|
|
|
imperforate anus:
|
failure of cloacal diaphragm to rupture
|
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|
What are the embryology, morphology and complications of Meckel Diverticulum?
|
failure of vitelline duct to involute.
2/in 2 feet of ilieocecal valve true diverticulum w/ all layers of bowe heterotopias present in 50% gastric: risk peptic ulceration/ bleeding pancreatic: location for islet cell tumors other complications: diverticulitis (like appendixicits on the left), intussusception, volvulus, fistula to umbilicus |
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|
Describe the clinical and morphologic features of aganglionic megacolon. What
are associations? Recognize gross/radiographic morphology |
males, esp w/ down syndrome
morphology: absent ganglion cells: aurbach's and meissners submucsoal plexi. affected segment is the narrow segment. megacolon dilated proximal is normal. short egments common, ususally rectum or sigmoid; may involve whole colon, more severe failure to pass meconium; constipation w/ abdominal distention --> diarrhea complciations: toxic megacolon "entercolitis" fluid elyte disturbances, perforation of colon, appendix. stercoral ulcers: mechanically eroded mucosa |
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|
) What are the causes of acquired megacolon?
|
chagas disease: tryapanososmes target enteric plexus
mechnical obstrx from neoplasm/strix narcotics toxic megacolon from inflmmation or infxn of colonic wall |
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Define ileus
|
obstrxn of bowel
|
|
|
What are the consequences of mechanical ileus?
|
ischemic perforation--> peritonitis, septicemia, septic shock, death
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|
Know causes of Mechanical ileus.
|
adhesions, hernias, volvulus, intussception, tumors, gallstones/fecoliths/foreign bodies, congenital lesions, mucoviscoidosis (mecoium ileus)
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|
Define abdominal hernia. Know common locations. What are the complications?
|
protrusion of peritoneum lined hernia sac trhough weakness/defect in abd wall
lcoations: inguinal femoral, umbilical, surgical scars, retropertoneal under ligament of trietz (rare) Complciations: incarceration of contents, strangulation of vessels, intestinal infarction |
|
|
What are the causes and complications of adhesions?
|
Causes: abdominal surgery, peritoniti-perforated viscus, endometriosis
consequences: internal herniation, obstrx, and strangulation |
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|
Define intussuception. What are the clinical features and complications? How might this be treated? Recognize radiographs
|
telescoping of segment into adjacent segment
children spontaneous adults: ileocecal lipoma or adenocarcinoma clincial features: "currant jelly stool" , may reduce with BE produces obstrx and infarction |
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24) Define volvulus. What are usual sites and complications?
|
complete twisting loop of bowel at its mesenteric base
consequences: obstx, infarction common loation: sigmoid colon, cecum, small bowel |
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25) Summarize all cause of intestinal perforation. What are the consequences?
|
foreign bodies, inserted anally or ingested (chicken bones, tooth picks)
ulcers and inflammatoin: peptic upcers, appendicits, diverticulitis, typhilitis ischemic injurry: infarction, volvulus, strangulated hernia tumors and megacolon trauma, surgery consequences? peritonitis |
|
|
What is the most common congenital tracheosophageal fistula?
|
Blind upper segment with fistula between trachea and lower segment
What are the symptoms? Aspiriation, suffocation, pneumonia |
|
|
What is the location and name for the three esophageal diverticulum?
|
actually pseudodiverticula of mucosa & submucosa, caused by increase in wall stress from motor disorders of the esophagus
Zenker diverticulum immediately above UES Traction Diverticulum near midpoint Epiphrenic diverticulum immediately above LES |
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|
Describe the Zenker diverticulum clinically
|
immeidately above the UES
several cm's in size, accumulates significant amts of food. eck mass, food regurgitation w/o dysphagia, aspiration pneumonia risk |
|
|
What is achalasia?
What are the three major abnormalities associated with achalasia? |
esophageal dysmotility disorder
incomplete LES relax'n, increased LES tone, aperistalsis of the esophagus |
|
|
Describe the morphology, symptoms and complications for a hiatal hernia
|
separation of the diaphragmatic crura w/ protrusion of the stomach through the gap
Sx: heartburn, regurgitation worse when bending forward, supine complications: ulceration with bleeding, perfusion |
|
|
Describe the morphology and clinical features of the Mallory Weiss syndrome
|
longitudinal tears in the esophagus at esophagastric jnx
linear, irregular lacerations oriented in axis of elumen usually astrid jnx or in proximal gastric mucosa. may eitehr involve musoca or peentrate wall 8% of upper GI bleeds, often self limited: tx vasoconstrictors, baloon tamponade. |
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|
Boerhaave syndrome
|
catastrophic spontaneous esophageal rupture w/ tears
|
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|
Define varicesWhat are the underlying causes, morphology, clinical features, complciations
|
collateral channels between protal and caval systems
portal hypertension: alcoholic cirrhosis or hepatic schistosomiasis tortuous dilated vessels w/in submucosa of distal esophagus and proximal stomach. irreulgar protrousion of overlying mucosa from dilated venous channels. mucosa may inflam/erode. rupture produces massive hemororhage. aSx until rupture, massive hematemesis. 1/2 deaths of cirrhosis from ruptured varix What are the complications |
|
|
What are the steps in the final common pathway for esophagitis?
|
Severe acute inflammation --> superficial necrosis and ulceration --> formation of granulation tissue--> fibrosis
|
|
|
Define GERD
List factors that decrease LES tone or increase abdominal pressure related to GERD What are the three morphologic features What are the symptoms and complications |
reflux of gastric contents into lower esophagus
EtOH, Obesity, Tob, CNS depressants, pregnancy, hiatal hernia Inflammatory cells- eosinophils early, PMN's if severe Basal zone hperplasia which exceeds 20% of epithlial thickness Elongation of lamina propria papillae w/ congestion Dysphagia, heartburn, sometimes regurgitation Complication: bleeding, stricture, barret esophagus |
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|
Barret's esophagitis: morpholgoy gross and micro, risk from?
|
a complication of? longstanding reflux
grossly- red, velvety mucosa smooth between pale squamous mucosa of esaphagus and lush, light brown-pink gastric mucosa, either as patches/tongues or broad band micro- metaplastic columnar epithlium w/ mucosal glands above the GE jnx, incl intestinal goblet cells dysplasia- cytologic and architectural abnormalities extending to luminal surface Describe the clinical features- male ~40-6 w/ reflux sx, local ulceration w/ bleeding and strix. dx via endoscopy & biopsy. increases isk forsophageal adenocarcinoma |
|
|
What are the two main malignant tumors of the esophagus
|
Squamous cell, more common
Adenocarcinoma |
|
|
Squamous cell carcinoma of the esophagus describe the risk factors, age and sex, morphology and clinical features
|
Risk factors: EtOH & Tob, nutrititional deficiencies (listed), less of p53
Male over 45 benign as in situ, early leasions small, gray white, plaque like thickenings, eventually may circle lumen, 1/2 found in middle 1/3 of esophagus thee patterns protruded = polypoid exophytic lesion (majoirty) some flat- tends to narrow lumen excavated (1/4) necortic ulceration, may erode into respiratory tree or arorta causing pneumonia, or exsanguination moderately well differentated, most large and invasive at Dx. Clinical: insidious onset: produces dysphagia and obstrxn late. diet from solid to liquid, debilitation and extreme weight loss, may aspirate thru fistula. 5 year survival 5% |
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|
Adenocarcinoma of teh esophagus
describe the risk factors, age and sex, morphology and clinical features |
Risk Factor: barret mucosa, point mutation in p53
Morphology: distal esophagus, flat raised initially become nodular masses, deeply infiltrative or ulcerated mucin producing glandular tumors with intestinal type features white men over 40 hx barrets: dysphagia, weight loss, bleeding, chest pain, vomiting. 5 year survival 30% |
|
|
Describe all the features of congenital hypertrophic pyloric stenosis (slide 98)
|
infant boys, multifactorial inheritance
regurgitation, persistent projectile vomitting 2nd & 3rd wks of life visible peristalsis, firm ovoid palpable mass: musclaris propria. surgical msucle splitting curative. |
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|
Describe the risk factors, morphology and clinical features of acute gastritis
|
Risk factors: page 100
Morphology: PMN's above basement membrane mild: lamina propria w/ edema and vascular congestion, scattered PMN's severe: erosion and hemorrhage, loss of superficial epithlium, defect which does not corss muscularis mucosa, fibrin containing purulent excudate extrdued into lumen. hemorrhage may occur. clinical features: aSx: maybe epigastric pain w/ n/v. hemorrhage, mssive hematemesis, potentially fatal blood loss. common among EtOHlics, and dairly aspirin takers (RA) |
|
|
Define chronic gastritis
What is the most important assocaiteion |
chornic mucosal inflam changes --> mucosal atrophy and epithelial metaplasia w/o erosions. epithlial changes may become dysplastic and lay background for dvlpt of carcinoma
H pylori |
|
|
Describe H. pylori with respect to risk factors, morphology and associated diseases
|
Risk factors: poverty, crowding, uneducated, rural-dwelling immigrants from Mexico or Africa
Morphology: gram negative rod w/ flagellar motility, ureas, adhesins and toxins Assoc diseases: Gastric adenocarcinoma Gastric MALToma treatable via eradication, better prognosis squamous cell esophageal cancer thrombocytopenic purpura due to anti-CagA abs cross react w/ platelet antigens HP eradication may cause peptic esophagitis due to protective action of bacteria on cardia area. |
|
|
What are the clinical features of autoimmune gastritis
|
Antibodies to parietal cells and intrinsic factor early, 20+ year progression to gastritis. Dx ~60 yo, assoc. w/ other autoimmunities. may be cause of pernicious anemia.
|
|
|
Describe eosinophilic gastritis
|
tissue damaging eosinophilic infiltrates usually reacting to soy and cow milk, else drugs. may occur with systemic collagen vascular diseases and assocaited w/ peripheral eosinophelia and increased serum [IgE]
|
|
|
Use table 17-3 to compare and constrast H pylori vs. autoimmune gastritis
|
have fun buddy
|
|
|
With regard to infectious enterocolitis, know Table 17-7. Know what organisms cause dysentery. What are the general and specific morphologic features of these infections. What is the differential diagnosis of noninfectious causes of dysentery? What systemic manifestations are associated with each cause of dysentery?
|
As far as the chart goes: she will always provide us the site of the infx.
then know the ones will blood in them. what do you clinically: lymphoctyes and occult blood |
|
|
non-infectious causes of dysentery:
|
ideeopathic inflammatory bowel disease: ulcerative colitis, crohn's colitis, ischemic colitis
|
|
|
Shiga toxin producing E coli may precipitate HUS
Campylobacter jejuni may produce ascending Gullian Barre non typhoidal salmonella: hematogenous disseminiation to bone, joints, esp risk for osteomyelitis in sicke clellpts yersinia causes mesenteric lymphadenitis w/ necrotizing granulomas; also granulaoms in ileum, appendix. thalassemia pts at great risk . protrated, ptoentailly fatal. |
important I gues
|
|
|
What are the clinical scenarios in which spontaneous bacterial peritonitis occurs?
|
children with nephrotic syndrome
cirrhosis of the liver bacteira extend through intact wall of intestine or are bloodborne in pt with ascites |
|
|
Review case study and answer questions. What are the various mechanisms of peritoneal infection? Review causes of infectious peritonitis.
|
mechanisms:
extension of bacteria through wall of viscus perforation of viscus ascending to pelvis via female gential tract |
|
|
List cause of sterile peritonitis.
|
perforation of biliary tract
actue hemorrhagic pancreatitis endometriosis rupured dermoid cyst |
|
|
Describe the pathogenesis, morphology (recognize gross appearance) and clinical features of acute appendicitis, including complications.
|
osbstructed lumen --> accumulated secretions --> intraluminal presure--> vascular compromise --> ischemic injury--> bacterial proliferation, edema, exudation
Morphology: PMNs in muscularis prorpia early acute: dull, granular serosa w/ dilated vessels; fibrinopurulent exudate covers serosa, ulcerations and necrosis of mucosa. acute gangrenous: hemoorhage w/ necrosis prone to perforation leukocytosis complications: perforation, peritonitis and abscess, pyelophlebitis (inflamed portal vein) with risk of thrombosis, hepatic abscess, bacteremia |
|
|
complications of hemorrhoids:
|
thrombosis
prolapse of internal hemorrhoids with strangulation and infarction superficial ulceration, fissures bleeding |
|
|
Define hemorrhoids. What are the predisposing factors? Compare/contrast morphology of internal and external hemorrhoids.
|
Variceal dilation of anal and perianal venous plexuses
predisposing factors: constipation & straining, venous stasis of pregnancy/obseisty; protal hypertension Extenral hemoorhoids: dvlp in inferior hemorrhoid plexus, covered by squamous epithlium: painfuil and itchy internal hemorrohoids: devlp in superior hemorrhoidal plexus, covered by colonic mucosa commonly co-occur |
|
|
What is angiodysplasia of the GI tract? Where does it commonly occur? What are the clinical features?
|
NON PRECANCER
tortuous dilations of submucosal and mucosal capillaries, veins occurs in elderly in CECUM AND RIGHT COLON painless episodic intestinal hemorrhage |
|
|
What are causes of bowel ischemia secondary to other conditions? What are the features of each, including predisposing factors and (for CMV), what is the microscopic morphology (fig. 8-15 and similar).
|
Cytomegalovirus- immunosuppression, AIDS; tropic for endothelium
radiation entercolitis: acutely apoptosis of epithelium, chronically non-healing ulcers, strictures |
|
|
transmural infarction
|
full thickness
progressive mural infarction acute and complete compromise of major mesenteric blood vessel: most commonly arterial morphology: arterial occulsion sharp demarcation, venous indistinct demarcation. red hemorrhagic infartion with dusky-red/purple congestion. bacteiral gangrene occurs w/in 4 days--> purulent serositis, septic shock reperfusion more damaging than hypoxia: free radicals from PMN's |
|
|
Mural infarction involving mucosa and submucoa
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causes: hypoperfusion
acute: heart failure, dehydration, shock, vasoconstrx Rx, marathon runners chronic: arterial compromise most commonly at watershed areas: splenic flexure, rectum esp with atherosclorisis morphology: hemorrhagic, ulcerating mucosa mimics pseudomembranous colitics. Surface sloughing atrophy. chronically results in stricture fibrosis Clincially: mimics IBD: crampy diarrhea, GI bleed/fecal occult, fecal leukocytes; stricture may be presenting problem. |
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What are the clinical features and complications of diverticular disease? Answer questions related to cases study.
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focal weaknesses in colonic wall and increased intraluminal pressure related to lack of fiber bulk in feces
complications: divertiulitis perf pericolic abscess peritonitis fistula (rectal vesical, rectal vaginal) stricture w/ obstrx hemorrhage |
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What are the pathogenesis, morphology, including common locations, gross and microscopic appearance and description of colonic diverticular disease?
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left side of colon, occurs beside taeniae coli. compressible sac-like coutpouchings up to 1 cm. thickened musclaris in affected segment. micro: mucosa, musclaris mucosa and serosa protrude/herniate through muscularis.
over 1/2 pop >60 in western world. mostly sigmoid colon. 20% symptomatic: nonspecific. risk chronic or massive hemorrhage. |
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Diversion colitis
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pouch of anus, low rectum ends blindly when an ostomy is created to bypass rectum. microbiotia present, no fecal nutrients
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Collagenous & Lymphoctyic colitis
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chornic watery diarrhea w/o weigh tloss, cramping abdoiman pain w/ stools, no predisposition to chancer. Collagenous: adult women. Lymphoctyic assoc w/ celiac & autoimmune diseases.
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Graft vs host intestinal disease:
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: T cells target GI epithlium: watery diarrhea- crypt cell necrosis w/o inflammatory cell response. fluid, elyte loss, septicemia.
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Compare/contrast Crohn disease with ulcerative colitis (figure 17-32 and table 17-8 strongly recommended). Comparison should include gross and microscopic morphology, clinical features and associated diseases and complications.
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high yeild slides 85 and 86.
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Summarize and describe the pathogenesis of inflammatory bowel disease. Take note of genes related to Crohn disease.
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Inappropriate mucosal immun eactivation; multigenetic pedisposition + commensual microbes = abnormal T cell responses
includes crohn's and ulcerative colitis Crohn's gnees: NOD2 and autophagy genes |
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What are the clinical features, pathogenesis and morphology changes of irritable bowel syndrome?
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Clinical features: abomdinal pain around umbilicus; 3+ days/mo for 3 mo, plus 2_ of
--releived by defication --change in freq of defication --change in consistency of defication female adults; alterations in bowel motility, visceral hypersneitivity, psychosocial factors; no morphologic changes |
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Describe the clinical features of cholera? What is the pathogenesis and how does it explain the symptoms? What is the most common Vibrio infection in the US and how is it acquired?
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noninvasive: preformed enterotoxin causes water secretory diarrhea
motile gram negative vibrio Vibrio parahemolytics most common seafood related enteritis in US B subunits bind GM1 ganglioside of enterocyte membrane; peptide released into cytosol stimulates adenyl cyclase to increase cAMP which opens CFTR and causes osmotic shift inot lumen; causes massive watery diarrhea. Liters of "Rice water" dehdyration leads to hypovolemic shock w/o therapy |
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What are the causes of diarrhea without PMNs or blood in the stool? Who are the risk groups or each, where given?
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Viruses, Norovirus, Rotavirus under age 2, Adenovirus immunosuppressed & infants
Vibrio cholera, C dif, ETEC, Bacillus Cereus, Clostridium perfringens, cryptosporidiosis- AIDS |
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What is bacterial overgrowth syndrome?
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produces malabsorption; bacterial growth in a blind loop created by bariatric surgery. dx: culture the loop or breath test.
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make a chart of slide 14, "Intestines IIA"
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do it
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What are the pathogenesis, clinical and morphologic features of antibiotic-associated colitis? What are some other causes of pseudomembranes?
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watery diarrhea following antibitiocs
exotoxins of clostridium difficile--> cytokine mediated destrx morphology: denuded surface, laminia propria w/ PMN's fibrin thrombi in capillaries. plaque like purulent necortic debries = pseudomembranes "Volcanic eruption/mushroom cloud" of mucopurulent exudate from superficially damaged crypts. non Cdif causes of pseudomembranes: ischemic colitis, volvus necortizing infx w/ staphylococci, shigella, enterohemorrhagic E coli, candida |
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What are the clinical and morphologic features of typhoid fever? What are the complications?
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traveller
intestine: linear enalrgment of peyer's patches ulceration over patches in ileum, risk perforation mesenteric lymphadenopathy splenomagaly typhoid nodules: aggreagtes of macrophages surrounding necrosis in liver clinical: dysentary short resolution, sepsis, bradycardia, maculopaular rose spots anterior trunk; 3rd week peyers ulcerate: GI bleed/shock. Systemic complications: osteomyelitic in sickle cell, gallstones/colonization of gallbadder--> chornic carrier state |
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Systemic assocaitions of bacterial enteritis
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all invasive bacteiral may be followed by reactive arthritis in HLA-B27 population. Reiter syndrome following yersinia, shigella, erythrema nodosum, erythema molitofrme rash
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Infectious entercolitis chart and review it
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do it.
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