GI Flashcards
1
Q
Hep B
A
• General: most well known virus of the hepadnavirus, its a DNA virus (blues and greens), enveloped virus
◦unique: replicates inside AND outside the nucleus (intranuclear and cytoplasmic); circular genome thats partially dbl stranded (becomes fully dbl
during replication) double stranded (single stranded: parvo)…kumbaya circle
◦Progression of replication: from partially dbl-stranded DNA -> intermediate single-stranded RNA -> dbl progeny DNA
• Transmission (similar to Hep C): through sex, sharing blood products, sharing needles, vertical transmission (mother->child, blood in childbirth; it doesnt
cross placenta, would only get transferred isblood mixes during delivery); healthcare workers at risk via needle sticks (transmission level is low)
• Symptoms: hepatitis (inflammation of the liver), in addition to RUQ pain, jaundice, etc…some acute (go away with time), some chronic (less likely than C;
only 5-10% of adult, younger kids and newborn more likely (90-95% of newborn)
• Extra-hepatic manifestations: prodromal serum-sickness type illness with purpuric rash (non blanching dark macules) and arthralgias, glomerular
nephritis, or polyarthritis nodosa (PAN)-systemic vasculitis of medium/small arteries-small aneurysms that form are said to have a beads on a strong
◦PAN can affect blood vessels leading to the kidney, manifest as: reduced GFR and HTN
◦Other renal dz: membranous glomerulernephritis (thickened glomerular membrane) and membranoproliferative GN (deposits in the mesangium
expanding into the glomerular BM causing a tram-track appearance)
• Liver enzymes and serologies
◦viral hepatitis: elevationin liver enzymes and so does hepatitis form alcohol
◦Alcoholic hepatitis: AST>ALT, viral (acute): ALT>AST…ALT will fall after symptomatic stage is over (may not go back to nml)
◦Serum ALT is nml early in neonatal hepatitis
• Serologies: we’re all one SPECIES
◦red: Hep B surface antigen: HBSAg (marker of active infection [acute or chronic], first one that is clinically measurable)
◦Orange: HBeAg (hep B envelope antigen)-highly correlates with infectivity, if its high, person is usually highly infectious
◦Red S, and orange E are both Ag, havent had enough time to make Ab; timeframe for symptoms
◦Yellow C: Anti-HBc (Hep b core Ab) is positive during the window period-when pt has started to develop anti-Hep B surface Ab so they Ab
have started to bind the Hep B surface Ag and neither of them may be detectable=window pd/false reassurance that person is NOT infected
(BUT: Anti-HBcore Ab will be positive, aka they still have an infection)…recovered ppl will have Anti-HBe or anti-HBcore Ab in addition to Anti-
HBsAb
◦ green E: Anti-HBe=low infectivity
◦Second S, blue: Anti-HBsAb indicates recovery and end of infection (acute and chronic); this is the value checked for anyone who has been
immunized, they will check positive for this)
• Tx: acute cases clear up by themselves, pregnant women and ppl who have progressed to chronic infxn need tx (minimizes dz by preventing
replication…ANTI-virals (LAMIVUDINE) and other nucleoside RTI, interferon alfa
◦Pregnant women prior to delivery if Hep B positive give newborn baby Anti-Hep B immunoglobulin along with Hep B vaccination for both active
and passive immunity
‣ uses reverse transcriptase (like HIV), though NOT technically a retrovirus-doesnt integrate into the host chromosome
susceptible/natural/immunization/acute/chronic/? CHART
2
Q
What are the causes of SBO (small bowel obstruction) <4>
A
- bilious vomiting
- abdominal distention
- air fluid levels
- small bowel dilatation
3
Q
Vitamin Deficiencies
- Thiamine
- Retinoic acid
- Riboflavin
- Pyridoxine
- Niacin
- Abscorbic acid
- Cobalamin
A
1.Thiamine (Vitamin B1) deficiency (this one is mine)
>associated with infantile and adult beriberi and Wernicke-Korsakoff syndrome in alcoholics
>infantile beriberi: age 2-3 mo, include fulminant cardiac syndrome with cardiomegaly, tachycardia, cyanosis, dyspnea, and vomiting
>>Adult:
dry: symmetrical peripheral neuropathy accompanied by sensory and motor impairments, especially distal extremities
wet: dry neuropathy and cardiac involvement (cardiomegaly, cardiomyopathy, CHF, peripheral edema, tachycardia)
>>CP: high output congestive HF and neuro symptoms
- Retinoic acid/Vit A deficiency: (Ret is an A student)
>>CP: night blindness, xerophthalmia, and vulnerability to infection (especially measles)
3. Vit B2 (Riboflavin) deficiency: (flava, peace out)
>>CP: cheilosis, stomatitis, glossitis, dermatitis, corneal vascularization, and ariboflavinosis
- Pyridoxine (Vit B6) deficiency: (pyramid at 6)
>>CP: cheilosis, glossitis, dermatitis, peripheral neuropathy
- Niacin (Vit B3) deficiency: (n-i-i-i-ce)
>>CP: pellagra (dementia, dermatitis, and diarrhea)
- Absorbic acid (Vit C): (A-B-C)
>>CP: scurvy (hemorrahge, bleeding into joint spaces, gingival swelling, impaired wound healing, weakened immune response to local infections)
- Cobalamin (Vit B12) deficiency:
>>frequently associated with pernicious anemia
>>CP (of pernicious anemia): older, mentally slow woman of N. European descent who is “lemon colored” (anemic and icteric), has a smooth, shiny tongue indicative of atrophic glossitis, and demonstrates a shuffling broad-based gait
4
Q
Hemochromatosis
A
- mutation: HFE prot most common
- HFE inactivation= decrease in hepcidin synthesis by hepatocytes and increase in DMT1 expression by enterocytes =iron overload
- at increased risk for liver cirrhosis and HCC (hepatocellular carcinoma)
- in women progression is slowed by physiologic iron loss through menstruation and pregnancy
- late stage: bronze diabetes
- Triad: skin hyperpigmentation, DM, pigment cirrhosis with hepatomegaly
5
Q
Carcinoid tumors
A
- confined to the intestine
- dont cause carcinoid syndrome because secretory products are metabolized by liver before entering systemic circulation
- VERSUS
- intestinal carcinoids: metabolize to the liver and extraintestinal (bronchial)
- carcinoids release vasoactive substances that AVOID first-pass metabolism
- avoidance of first pass leads to carcinoid syndrome
- composed of islands/sheets of uniform cells with eosinophilic cytoplasm and oval-to-round stippled nuclei
- derived from neuroendocrine cells inthe GI tract
- most appendiceal carcinoids are enign
- may cause appendicitis
- rarely: carcinoid syndrome with liver metastasis
- CP: flushing, diarrhea, bronchospasm
6
Q
Schilling Test
A
- help differentiate between dietary deficiencyof vit B12, pernicious anemia, and malabsorption syndromes
- low absorption of cobalamin not correctableby IF=malabsorption due to
- ileal disease
- pancreatic insufficiency
- bacterial overgrowth
7
Q
Hepatic angiosarcoma
A
- associated with exposure to carcinogens:
- arsenic
- polyvinyl chloride
- thorotrast
- tumor cells express CD31, an endothelial cell marker
8
Q
What is one of the most common causes of folate deficiency anemia?
A
- Alcoholism!
- can develop in weeks
- peripheral smear: macrocytosis, ovalocytosis, neutrophils with hypersegmented nuclei
9
Q
Colorectal adenocarcinoma
A
- prognosis directly related to STAGE of tumor (NOT to the grade!!)
- stage=extent of tumor expansion
- grade=degree of tumor differentiation
- well-differentiated–to–anaplastic
10
Q
Barrett’s esophagus
A
- metaplastic condition; nml squamous epithelium of distal esophagus is replaced by intestinal-type columnar cell
- gross enoscopy: tongues of beefy red mucosa extending above the lower esophageal sphincter into areas of nml pale pink squamous mucosa
- can occur in trachea of chronic smokers
- complication of long-standing GERD
- increased risk of esophageal adenocarcinoma
11
Q
Dubin-Johnson syndrome
A
- benign D/O
- defective excretion of bilirubin gluco across canalicular mebrane=direct HYPERbilirubinemia and jaunduce
- gross: black liver due to impaired excretion of epi metabolites
- histo: dense pigments within lysosomes
12
Q
tenia coli
A
3 seperate smooth muscle ribbons that travel longitudinally on outside of colon, converge at root of vermiform appendix (help find appendix)
13
Q
acute appendicitis
A
- cause: obstruction of lumen of the appendix
- most common obstructors: fecaliths (can also be: hyperplastic lymphoid follicles, foreign bodies, nematodes, carcinoids)
- retained mucus causes appendicular wall to distend which impairs venous outflow
- resulting hypoxia causes ischemia and associated bacterial invasion
- inflamm fluid and bacterial contents can spill into the peritoneal cavity, causing peritonitis
- CP: RLQ abdo pain, N/V/D, fever
14
Q
adenoma to carcinoma sequence
A
- nml colon-APC INactivation
- HYPERproliferative epithelium-methylation abnormalities COX2 OVER-expression
- Adenoma
- K-ras activation
- DCC INactivation
- p53 INactivation
- further accumulation of genetic abnormalities leads to CARCINOMA
15
Q
Pringle manuever
A
- occlusion of portal triad to get source of RUQ bleed
- if hepatic bleeding persists afterocclusion of the portal triad, the IVC or hepatic veins are likely to be injured
16
Q
chronic alchoholic pancreatitis
A
- hx: epigastric calcification and hx of alcohol abuse
- alcohol inducted secretion of protein rich fluid
- protein secretions precipitate within pancreatic dicts and leads to ductal plugs which calcify and obstruct
- leads to exocrine insufficiency
- impedes secretion of -ases and thus get malabsorption (diarrhea/steatorrhea)
- CP: weight loss, bulk frothy stools
17
Q
Nutrient deficiencies associated with malabsorption
A
- anemia-Fe, folate, B12
- muscle wasting and edema-protein
- petechiae and easy bruising-Vit K
- bone pain, muscle weakness, tetany-Vit D, Ca2+
- hyperkeratosis + night blindness-Vit A
18
Q
Polyethylene glycol
A
- osmotic laxative
- diarrhea associated with lactase deficiency
19
Q
Gilbert syndrome
A
- common familial disorder to bilirubin glucuronidation with reduced production of UDP glucuronyl transferases
- pts with no apparent liver dz who have mild unconjugated HYPERbilirubinemia that appears provoked by one of the classic triggers:
- hemolysis, fasting, physical exertion, febrile illness, stress, fatigue
20
Q
hepatic metab of bili
A
- uptake from bloodstream
- storage within hepatocyte
- conjugation with glucoronic acid
- biliary excretion
21
Q
Gallstone ileus
A
- mechanical bowel obstruction caused when a large gallstone erodes into the intestinal lumen through a cholecystoenteric fistula
- pneumobilia (air in the biliary tract) is common finding (abdo x-ray)
- may come to rest in the ileum, which has the smallest lumen of the intestinal tract
22
Q
pernicious anemia
A
- vitamin B12 deficiency
- caused by autoimmune destruction of parietal cells (chronic atrophic gastritis)
- parietal cells secrete HCl and IF and are found primarily in the superficial regions of the gastric glands
23
Q
Cirrhosis
A
- end stage of many chronic liver diseases
- characterized by:
- diffuse hepatic fibrosis with replacement of the nml lobular architecture by fibrous-lined regenerative parenchymal nodules
- most common causes:
- chronic viral hepatitis (Hep B and C)
- alcohol
- hemochromatosis
- non-alcoholic fatty liver dz
- in advanced cirrhosis get portal HTN from increased resistance to hepatic blood flow which can lead to developement of gastroesophageal varices
- untx varices are prone to rupture and can result in a massive GI hemorrhage and possbily death
24
Q
Leptin
A
- protein hormone produced by adipocytes in proportion to the quantity of fat stored
- tells the body: “IM FULL, STOP EATING”
- acts on the arcuate nucleus of the hypothalamus to inhibit production of <pomc> <em>neuropeptide Y</em> (decreasing appetite) and stim production of alpha-MSH (increasing satiety)</pomc>
-
mutations in the leptin gene or receptor result in hyperphagia and profound obesity
- sustained elevation in leptin levels from the enlarged fat stores results in leptin desensitization
25
Q
Intussusception
A
- invagination of a portion of the intestine into the lumen of the adjacent intestinal segment (collapsed telescope)
- CP: intermittent, severe, colicky abdo pain, “currant jelly” stools (contain blood and mucus), sometimes, a palpable mass in the RLQ
- typical location: ileocolic jxn
- most common in kids<2 yo
- in kids >2yo seek out a lead pt:
- Meckel diverticulum
- foreign body
- intestinal tumort
-
barium enema is diagnostic, may be therapeutic
- if doesnt resolve things, sx intervention is mandated
26
Q
Primary biliary (BARBARA is an ALIEN) cirrhosis
A
- chronic liver disease charac. by autoimmune destruction of the intrahepatic bile ducts and cholestasis (jaundice, pale stool, dark urine) by granulomatous inflamm
- epid: middle-aged WOMEN, insidious onset
- first CP: pruritis (severe at night) + fatigue
- physical findings: hepatosplenomegaly and xanthomatous (hypercholesterolemia) lesions in the eyelids or in the skin and tendons
- as dz progresses: jaundice, steatorrhea, portal HTN, and osteopenia
- lab: elevated alk.phos + cholesterol, elevated serum IgM
- Diagnosis confirmation: demo of anti-mitochondrial Ab in serum
- associated conditions (yayyy, ai dz for dayz): Sjögren’s syndrome, Raynaud’s syndrome, scleroderma, a.i. thyroid dz, hypothyroidism, celiac dz
27
Q
Most common intra-abdo infections
A
- usually polymicrobial
- B. fragilis & E coli=most prominent organisms isolated
28
Q
H pylori
A
- found in greatest concentration in the prepyloric area of gastric antrum
- biopsy of prepyloric area will hav egreatest yield of the organism
- noninvasively detected with urease breath test
- pt consumes 13C-labeled urea and breath monitored
- HP produces urease
- false negs from AB or PPI during the 2-4 wks prior to the test
- pt consumes 13C-labeled urea and breath monitored
29
Q
gastric acid secretion
A
- cephalic and gastric phases stim GAS, intestinal influences reduce GAS
30
Q
Metastasis of gastric cancer
A
- Virchow’s node-mets to the L. supraclavicular sentinel node (first clinical manifestation of occult gastric ca)
- (intestinal) Sister Mary Joseph-mets to periumbilical region, get subq mass
-
(diffuse) Krukenburg tumor:
- in women met spread of adenocarcinoma to one or both ovaries in association with primary ca of stomach, breast, pancreas, gallbladder
- mucin-producing, signet-ring neoplastic cells in the ovarian stroma
- one of the most common types of metastatic ovarian ca
31
Q
Malabsorption
A
- syndrome of impaired intestinal digestion and absorption
- fats are typically most severely affected
- test for stool fat: Sudan 3 stain=most sensitive to screen for malabsorptive d/o
- CP for significant malab: diarrhea, steatorrhea (bulky, foul-smelling; visible oil droplets, greasy toilet ring)
- most often: nonspecific s/s: weight loss, fatigue, vague abdo discomfort
- general malsb is common due to defects in:
- pancreatic secreetion (chronic pancreatitis, CF)
- mucosal d/o (celiac dz, inflamm bowel dz)
- bacterial overgrowth (surgical alteration in GI tract anatomy, abnml motility)
- parasitic dz (Giardia)
32
Q
Chronic alcoholic pancreatitis (booze and ca.butt.plugs)
A
- CP: epigastric calcification and hx of alcohol use
- develops in pt due to alcohol-induced secretion of protein-rich fluid
- proteinaceous secretions can precipitate within the pancreatic ducts forming ductal plugs that may calcify and be detectable on abdo imaging
33
Q
CCK (EYE)
A
- hormone responsible for:
- GB contraction
- DEC gastric emptying…slowww downnn
- INC pancreatic enzyme secretion (by acinar cells)
- made by I cells in duodenum + jejunum in response to FA + AA when fat/protein-rich chyme enter the duodenum
- 3 well known RF for gallbladder dz: forty, fat, female
34
Q
Dietary Lipids
A
- TG, phospholipids, cholesterol esters-primarily digested in duodenum via action of pancreatic enzymes (lipase, phospholipase A2, cholesterol esterase)
35
Q
CREST syndrome
A
- calcinosis
- raynaud phenomenon
-
esophageal dysmotility
- result of atrophy and fibrous replacement of the muscularis in the lower esophagus
- esophageal body and LES become atonic and dilated=s/s of gastroesophageal reflux (heartburn, regurgitation, dysphagia)
- increased risk of barrett’s esophagus and fibrous stricture formation
- sclerodactyly
- telangiectasia
- [limited variant of systemic sclerosis with skin dz that primarily affects the face, forearms, fingers]
36
Q
Statins
A
- first line for pts with hypercholesterolemia
- competitively inhibit HMG CoA reductase (enzyme responsible for conversion of HMG CoA to mevalonate)–rate-limiting step in hepatic cholesterol synthesisi
- inhibition decrease hepatic cholesterol synthess
- resulting upregulation of LDL receptors causes increased uptake of LDL from circulation
37
Q
Bile acid-binding resins
A
- work by binding bile aceids in the GI tract and thus interfere with the enterohepatic circulation of bile acids and causing increased bile acid excretion
- result: hepatic synthesis of new bile acids-consumes liver cholesterol stores
- combo therapy with statins=increased hepatic cholesterol and bile acid synthesis
38
Q
Hepatic Abscess
A
- CP: fluid-filled cavity inthe liver in conjunction with fevers, chills, and RU abdo pain
- in LSEC high incidence, usually caused by parasitic infections
- in HSEC uncommon, caused by bacterial infection (80% of cases)
- pyogenic bacteria gain access to liver through:
- biliary tract infection (ascending cholangitis)
- portal vein pyemia (bowel or peritoneal sources)
- hepatic artery (ystemic hematogenous seeding)
- direct invasion from adjacent source (peritonitis, cholecystitis)
- penetrating trauma or injury
39
Q
Hep B infection
A
- one of the most common causes of hepatic injury in the US, frequently sexually transmitted or via percutaneous inoculation (IVDU)
- accumulation of hep B surface Ag within infected hepatocytes
- histo: finely granular, homogeneous, dull eosinophilic inclusions that fill the cytoplasm (ground glass hepatocytes)
- other nonspecific morphologic changes: hepatocyte necrosis (ballooning degeneration) and apoptosis, steatosis, portal inflamm with mononuclear inclusions (lymphocytes, macrophages)
40
Q
Traveler’s diarrhea
A
- most frequently related to enterotoxigenic E. coli (gram neg motile enteric rods) that produces heat labile and heat stable enterotoxins
- LT enterotoxin (similar to cholera toxin) activated adenylate cyclase leading to increased intracellular cAMP
- ST enterotoxin (heat stable) activates guanylate cyclase leading to increased intracellular cGMP
- both cause water and electrolyte loss and watery diarrhea
41
Q
Crigler-Najjar syndrome
A
- AR d/o of bilirubin metabolism caused by genetic lack of UGT enzyme needed to catalyze bile glucuronidation
- unconjugated hyperbilirubinemia develops in these infants, causing kernicterus and often death
42
Q
Inhaled anesthetics-Halothane
A
- can be associated with a highly lethal fulminant hepatitis that cannot be distinguised histoogically from acute viral hepatitis
- CP: fever, anorexia, nausea, myalgias, arthralgias, rash
- PE: tender hepatomegaly (reflecting widespread liver inflamm) and jaundice
- pts have significantly elevated aminotransferease levels due to massive hepatocellular injury and prolonged prothrombin time due to failure of hepatic synthetic function
- deficiency of factor 7 (shortest t1/2 of all the procoagulant factors)
43
Q
Acute Hep A infection
A
- liver biopsy findings and recent travel to an endemic region
- histo: spotty necrosis with ballooning degeneration (hepatocyte swelling with wispy/clear cytoplasm), councilman bodies (eosinophilic apoptotic hepatocytes) and mononuclear cel infiltrates
- CP: acute: prodrome of fever, malaise, anorexia, N/V, RUQ abdo pain
- several days (approx 1 wk): less prodromal; signs of cholestasis–jaundice, pruritus, dark-colored urine (due to increased conjugated bilirubin levels) and alcoholic stool (lacks bilirubin pigment)
- prog: self-limited, does NOT progress to chronic hep, cirrhosis, or hepatocellular carcinoma
44
Q
Trypsin and hereditary pancreatitis
A
- trypsin can activate all the proteolytic pancreatic enxymes, including its own zymogenic form
- premature activatio of trypsinogen before it reaches the duodenal lumen can result in auto-digestion of the pancreatic tissues
- multiple inhibitory mechanisms exist to reduce the premature activation including cleavage inactivation of trypsin by trypsin itself
- gene muts that render trypsin insensitive to cleavage INactivation cause hereitary pancreatitis
- mut involving the trypsinogen or SPINK1 gene
45
Q
Crohn’s dz
A
- PP:
- assoc with mut in NOD2 resulting in decreased activity of the NFKB protein with reduced cytokine production=impaired innate barrier fxn of intestinal mucosa-allows intestinal microbes to induce exaggerated response by adaptive immune system=chornic GI inflamm
- increased activity of TH1 helper cells increases production of IL-2, interferon-gamma, and TNF, causing subsequent intestinal injury
- noncaseating granulomas seen on light microscopy of the intestine–resemble sarcoid granulomas
- causes transmural inflammation of any area of the GI tract
- most common complication: strictures and fistula formation
- granulomas NOT seen in UC
- other classic crohns findings:
- linear or serpingenous ulcerations
- cobblestone appearance of the mucosa
- transmural inflamm infiltrate (ENTIRE thickness)
- associated with oxalate kidney stones
- impaired bile acid absorption in the terminal ileus leads to loss of bile acids in feces with subsequent fat malabsorption
- lipids then bind calcium ions, resulting soap complex is excreted
- free oxalate (nmly bound by calcium to form an unabsorbable complex) is absorbed and forms urinary calculi (enteric oxaluria)
- perianal dz (skin tags, fissures) are also common
46
Q
ulcers and gastroduodenal artery
A
- gastroduodenal artery lies slong posterior wall of the duodenal bulb and is likely ot be eroded by posterior duodenal ulcers
- uleration into the gastroduodenal artery can be a source of life-threatening hemorrhage
47
Q
extrahepatic biliary atresia
A
- occurs due to complete obstruction of extrahepatic bile ducts
- pts develop persistent jaundice around 3rd or 4th wk of life accompanied by: dark urine, alcoholic stools and a conjugated hyperbilrubinemia
- liver biopsy: marked intrahepatic bile ductular proliferation portal tract edema and fibrosis, and parenchymal cholestasis
48
Q
C diff tx
A
- Tx:
- oral metronidazole for mild to moderate cases
- vancomycin for severe cases
- also: fidaxomicin-macrolytic AB (related to macrolides) inhibits sigma subunit of RNA polymerase=inhibition of protein synthesis and cel death
- bacterocidal, minimal systemic absorption, narrow spectrum
- also: fidaxomicin-macrolytic AB (related to macrolides) inhibits sigma subunit of RNA polymerase=inhibition of protein synthesis and cel death
- in the absence of nml intestinal microbial flora (ex: after a course of AB), C diff can overgrow and produce enterotoxin (toxin A) and cytotoxin (toxin B)
- Clinical dz from c diff: transient diarrheas to severe pseudomembranous colitis
- white/ylw membrane-like plaques on colonoscopy=pathognomonic
49
Q
chronic non-atrophic gastritis
A
- most often due to H pylori infection whic primarily affects the antrum and in time spreads to gastric body
- acute phase: inflamm infiltrate has neutrophils; chronic: lymphocytes, lymphoid follicles, and plasma cells
- involvement of the gastric body in longstanding infection is associated with n increased risk of gastric adenocarcinom and mucosa-associated lymphoid tissue (MALT) lymphoma
50
Q
Cholestatic liver disease
A
- can cause malabsorption and nutritional deficiencies of fat-soluble vitamins
- intrahepatic auses of cholestasis:
- drug induced (erythromycin, contraceptives)
- primary biliary cholangitis
- cholestasis of pregnancy
- primary sclerosing cholangitis
- extraheptaic:
- cholendocholithiasis
- malignancy (eg pancreatic, gallbladder)
- end up with deposition of bile pigment within the hepatic parenchyma, with green-brown plugs in the dilated bile canaliculi
- when prolonged, reduction in bile flow causes intestinal malabsorption of fats and fat-soluble vitamins (ADEK) which require bile salts for digestion
51
Q
Celiac dz
A
- IgA anti-tissue transglutaminase and IgA endomysial Ab are very sn and sp for diag of celiac
- small intestinal biopsy is confirmatory
- strophy of villi, flattening of mucosa, chronic inflam of lamina propria
- histo: severe atrophy and blunting of the villi along with a chronic inflammatory infiltrate of the lamina propria
- CP: diarrhea, steatorrhea, nutritional deficiencies
- tx: gluten-free diet
52
Q
Niacin
A
- decreases hepatic synthesis of triglycerides and VLDL and reduces clearance of HDL
- Niacin can decrease renal excretion of uric acid, precipitating acute gouty arthritis
53
Q
colonic diverticular
A
- often involve the sigmoid and develop due to increased intraluminal pressure (PULSION) created during strained bowel movements (due to chronic constipation) causing outpouching of the mucosa and submucosa through the muscularis (false diverticula)
- cp: >60yo, may be asymptomatic or present with hematochezia or diverticulitis
54
Q
Diphenoxylate
A
- opioid anti-diarrheal drug
- binds mu opiate receptors in the gut to slow motility
- overuse can lead to euphoria and physical dependence
- to discourage abuse, is combined with atropine which induces adverse effects if taken in high doses
55
Q
Stress-related mucosal dz
A
- usually caused by local ischemia in the setting of severe physiologic stress (shock, extensive burns, sepsis, severe trauma)
- ulcers arising in the setting of severe trauma/burns =Curling’s ulcers (curling iron)
- ulcers from intracranial ulcers caused by direct vagal stimulation=Cushing’s ulcers (brain cushioning)
56
Q
Zenker “false” diverticulum
A
- CP: elderly pts with oropharyngeal dysphagia, halitosis, regurgitation, and recurrent aspiration
- PP:
- diminished relaxation of cicopharyngeal muscles during swallowing results in increased intraluminal pressure in the oropharynx
- may eventually cause the mucosa to herniate through a zone of muscle weakness in the posterior hypopharynx forming a Z-d
57
Q
SMA syndrome
A
- when the transverse portion of the duodenum is entrapped between the SMA and aorta
- CP: s/s of partial intestina obstruction
- PP: when the aortomesenteric angle critically decreases, secondary to diminished mesenteric fat, pronounced lordosis, or surgical correction of scoliosis (lengthens the spine)
- also occurs with low body weight, recent weight loss, severe burns or other inducers of catabolism, and prolonged be drest
58
Q
External hemorrhoids
A
- originate below the dentate line
- covered by modified squamous epithelium and have cutaneous (somatic) nervous innervation from the inferior rectal nerve (branch of the pudendal nerve)
- branches of pudendal supply the perineum and external genitalia in males and females and are very sensitive to touch, temperature, and pain
- CP: generally asymptomatic, can become painful if they thrombose
59
Q
Internal hemorrhoids
A
- originate above the dentate line
- covered by columnar epithelium
- autonomic innervation from th einferior hypogastric plexus-which is only sensitive to stretch and not pain, temp, or touch
60
Q
D-xylose
A
- monosaccharide whose absorption is not affected by exocrine pancreatic insufficiency, can be used to differentiate between pancreatic vs. mucosal causes of malabsorption
61
Q
organisms that can cause diarrhea with only a small inoculum
A
- Campylobacter jejuni (500 cells)
- E. histolytica (1-10 organisms)
- G. lamblia (1-10 organisms)
- Shigella (10-500 cells)
62
Q
Shigellosis
A
- infectious dz that can be causes by variety of Shigella species
- in industrialized, S. sonnei is most commont causes
- shigella incades the GI mucosa by gaining access to microfold cells in ileal Peyer pathches through endocytosis
- Shig then lyses the endosome and spreads laterally into other epithelial cells, causing cell death and ulceration with hemorrhage and diarrhea
63
Q
CV dysphagia
A
- can result from pressure on the esophagus by a dilated LA
- LA commonly enlarged in pts with mitral stenosis and LV failure
64
Q
Diffuse esophageal spasm
A
- CP: periodic, simultaneous and non-peristaltic contractions of the esophagus due to impaired inhibitory innervation within the esophageal myenteric plexus
- Cp: liquid/solid dysphagia and CP due to inefficient propulsion of food into the stomach, heartburn, and food regurg
65
Q
Gastric varices
A
- dilated submucosal veins that can cause life-threatening bleeding in the upper GI tract
- PP: portal HTN (which can be a complication of cirrhosis)
- also seen with: splenic vein thrombosis due to: chronic pancreatitis, pancreatic ca, and abdominal tumors
- splenic vein runs along the posterior surface of the pancreas and can develop a blood clot from pancreatic inflammation
- also seen with: splenic vein thrombosis due to: chronic pancreatitis, pancreatic ca, and abdominal tumors
- short gastric veins drain the fundus of the stomach into the splenic vein
- splenic vein thrombosis can increase pressure in the short gastric vein and cause gastric varices only in the fundus
- rest of the stomach and esophagus are usually unaffected
- splenic vein thrombosis can increase pressure in the short gastric vein and cause gastric varices only in the fundus
66
Q
Acute interstitial pancreatitis
A
- pancreas is grossly edematous
- light microscopy: focal areas of fat necrosis, calciu deposition, interstitial edema
- in necrotizing (hemorrhagic) pancreatitis, chalky-white areas of fat necrosis interspersed with hemorrhage are seen on macroscopic examination
67
Q
gallstone formation
A
- elevated cholesterol concentrations increase the likelihood of cholesterol precipitation and gallstone formation
- decreased cholecystokinin release due to lack of enteral stimulation (in pts receiving total parenteral utrition) contribs to development of gallstones
- resection of ileum can also contrib, due to disruption of nml enterohepatic circulation of bile acids
- high levels of bile salts and phosphatidylcholine increase cholesterol solubility and decrease the risk of gallstones
68
Q
Primary lactase deficiency
A
- congenital or acquired
- congenital: rare AR
- acquired: more common, typically arises from decreased or ceased production of lactase by mid childhood (lactase nonpersistence) or inflamm d/o affecting the intestinal brush border
- common in pts of Asian or African acnestry (and hispanic and Native Americans)
- small bowel mucosa is nml on histo
- pp: undigested lactose causes osmotic diarrhea and acidification of the stool
69
Q
Esophageal SCC
A
- histopath: solid nests of neoplastic squamous cells with abundant eosinophilic cytoplasm and distinct borders
- also: aread of keratinization and presence of intercellular bridges
- CP: progressive solid and eventually liquid dysphagia and weight loss; retrosternal discomfort/burning and significant weight loss
70
Q
Hep C
A
- CP: fever, jaundice, anorexia in an IVDU
- acute viral hepatitis causes hepatocyte apoptosis and necrosis
- apoptotic hepatocytes shrink, undergo nuclear fragmentation and become intensely eosinophilic
- may be referred to as acidophilic bodies, councilman bodies, and apoptotic bodies
71
Q
Abetalipoproteinemia
A
- inherited inability to synthesize apolipoprotein B (important component of chylomicrons and VLDL)
- lipids absorbed by the small intestine cannot be transported into the blood and accumulate in the intestinal epithelium, resulting in enterocytes with clear or foamy cytoplasm
- AR loss of function mutation in the MTP gene
- CP: in first yr of life-s/s/ malabsorption (abdo distention, foul-smelling stool)
- lab studies: very low TG and cholesterol; chylomicrons, VLDL, apoB absent
- causes RBC with abnml membranes and thorny projections=acanthocytes and multiple neuro abnormalities
72
Q
Right-sided Colon CA
A
- usually grow as exophytic masses
- grow as large bulky masses that protrude into colonic lumen due to the relatively large caliber of ascending colon
- CP: occult bleeding and symptoms of iron deficiency anemia (fatigue, pallor)
- non-specific s/s: anorexia, malaise, unintentional weight loss
- PP: infiltrate intestinal wall, encircle lumen, cause constipation and symptoms of intestinal obstruction
- rectosigmoid involvement often causes hematochezia
- **ascending colon
- livers and lung=common site of metast
- [left sided tumors (rectosigmoid colon) tend to be smaller]
73
Q
Pancreatic ca RF
A
- age-highest 65-75yo
- smoking=most important environmental RF, DOUBLES the risk
- DM: higher pan ca risk with duration of DM
- chronic pancreatitis-risk is highest after 20yr of chronic pan
- genetic predisposition: hereditary pancreatitis, MEN syndromes, hereditary nonpolyposis colon ca, familial adenomatous polyposis sundromes
- adenocarcinoma at the head of the pan compression common bile duct
- CP: palpable, but nontender GB (Courvoisier sign), weight loss, obstructive jaundice (assoc with pruritus, sark urine, pale stools)
- ca of body and tail dont obstruct CBD, no s/s till they invade the splanchnic plexus and cause midepigastric abdo pain
74
Q
Anal fissures
A
- longitudinal tears in the mucosa
- usually due to the passage of hard stool in pts with chronic constiation
- most occur at the posterior idline, likely due to decreased blood flow in this area
75
Q
GB hypomotility
A
- GB fxn: actively absorb water from bile
- GB hypOmotility (biliary stasis) causes bile concentration which promotes bile precipitation and accumulation of viscous biliary sludge that predisposed to gallstone formation (espec cholesterol stones) and bile duct obstruction
76
Q
Primary biliary cholangitis
A
- chronic autoimmune liver dz
- Charac: lymphocytic infiltrates and destruction of small and mid-sized intrahepatic bile ducts
- similar findings in GvHdz
- donor T cells migrate to host tissue, recog host MHC Ag as foreign
- slin, liver, GI tract-most commonly affected areas
131
Q
Personality D/O
A
132
Q
Key Defense Mechanisms
A
