Small Bowel/ Colon Flashcards

1
Q
  • Tumors of the appendix common? 2 types? Can lead to?
    Small Intestine:
  • Malabsorption leads to 4? Deficient in? (8)
    1.) Pan Insuf: How much must be lost? What malabs. first? Causes? (2)
    2.) Bacterial overgrowth: Due to? (4) B12? Folate? Treatment?
    3.) Celiac: Incidence increases with? Inflammatory? Atypical signs? (4) HLA’s? (2) APC type? Antibody? Treatment?
    4.) Tropical spure: Due to? Leads to?
    5.) Whipple’s Disease: Type bacteria? SI and what?
    6.) Mesenteric Ischemia: 2 types?
A
  • Rare; Carcinoid, Epithelial
  • Weightloss, diarrhea, steatorrhea, Panc. Insuffic.; DEAK, B12, Fe, Ca, D
    1. ) >90%; Fats; Chronic pancreatitis/ CF
    2. ) Anatomic, hypomobility (scleroderma/DM), lower acid, obstruction; low (bacteria eat it); high; Ciproflaxin
    3. ) Age; Yes; Iron def. anemia, derm. hep., osteoporosis, ataxia; DQ2/8; MHC2; tTG; diet change
    4. ) aerobic toxins; Megaloblastic anemia (B12/Folate)
    5. ) Gram +; neuro
    6. ) Chronic (CVD) and acute (thrombus)
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2
Q
  • SI tumors common? 2 types?
  • 2 causes of diarrhea? 4 types?
  • 1a.) Watery Osmotic: Due to?
  • 1b.) Watery Secretory: 3 ex? Calculation?
    2. ) Fatty diarrhea: Due to? Ex? (4)
    3. ) Inflammatory: Ex? (4)
  • No organic cause?
A
  • No; Adeno from crohn’s, carcinoid
  • Decrease absorption, increased secretion; fatty, watery, exudative, functional
    1a. ) Carb malabs; laxative
    1b. ) Cholera, IBS, DM; 290- 2(Na + K); >50 = osmotic
    2. ) Malabs.; Celiac, Whipples, Bac overgrowth, PI
    3. ) Infection, Crohns, UC, Ischemia
  • IBS
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3
Q

Colon:

  1. ) IBD: Diagnosed how?
  2. ) Microscopic Colitis: Typically in who? Prognosis? Autoimmune? Type of diarrhea? 2 types?
  3. ) Ischemic Colitis: Usually where? Diarrhea? Recovery?
  4. ) Infectious: Diarrhea? Bloody?
  5. ) Drug induced?
  6. ) Radiation: Proctotis when?
  7. ) Diverdiculosis: Mostly in? Due to? (2) Hemorrhage due to? Painful?
  8. ) Diverticulitis: What happens? Dx with? Not?
A
  1. ) Direct visual and biopsy
  2. ) Older women; good; yes; secretory; collagenous/lympho
  3. ) Watershed regions; MILD!, 1-2 weeks
  4. ) Yes; sometimes
  5. ) NSAID
  6. ) Years after radiation
  7. ) Elderly; low fiber/increased colonic pressure; vasa recta bleed; no but heavy
  8. ) Food gets lodged and infection occurs; CT/MRI; SCOPE!
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4
Q

Dz of GI:

  1. ) 4 ways to obstruct?
  2. ) Celiac: What complexes with tTG? Type of lymphos? Related to what lymphoma?
  3. ) Whipples: Villi swollen with?
  4. ) Infectious: Common in US with contam. food? Worldwide problem with high infectivity and cause pseudo? Typhoid with this? 4 types? implicated by 3rd gen ceph?
A
  1. ) Herniation, volvulus, adhesion, intussusception
  2. ) a-glaidin peptide; T cell; EAT
  3. ) Macs
  4. ) Campylobacter; shigella, salmonella, e.coli, c diff
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5
Q
  • infectious Disease:
  • Who does diarrhea effect? Leading reason for death? Treatment?
  • Watery (non-inflamm) occurs where? Inflammatory where?
  • Non-inflammatory:
    1. ) Cholera: cAMP? Histology? 3 other symptoms? Treat?
    2. ) Rota: How long? Effects? Vaccine? Route?
    3. ) Noravirus: Virulence? Length? Transmission? Commun?
    4. ) Giardia: Type of organism? Common in what?
A
  • Old/young; Dehydration; Rehydration
  • SI; Colon
    1. ) Increase; Fine; Met Acid (lose bicarb), hypoglycemia, hypokalemia; NaCl and glucose
    2. ) Prolonged; Develping world; Live Atten., F-O
    3. ) High; short; F-O; Yes
    4. ) Protozoa; water
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6
Q

Inflammatory:
1.) Campylobacter Jejuni: Common?
2.) EHEC: Effects who? Can lead to? (2) Verotoxin binds what?
3.) C. Diff: Almost always? Type of organism? Toxin?
Enteric Fever:
1.) Salmonella Typhi: Type of bacteria? Passed how?

A
  1. ) MOST COMMON for all ages
  2. ) HUS and Thromb. throbocytopenic purpura; renal endothelial cells
  3. ) Nosocomial; Gram + rod; A/B
  4. ) GNR; F-O via food/water
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7
Q
  • Colonic Polyps:
    a. ) Hyperplastic: Common? Shape? Benign? Location?
    b. ) Adenomatous: Prolif of? Side? 3 steps?
  • 3 risk factors?
    1. ) FAP: AD of what gene? Must remove? + Fibromatosis/osteomas? + CNS tumor?
    2. ) HNPCC: Microsattelite? Mutation to what? Side? Leading to?
    3. ) Increased risk of Strep Bovis with?
A

a. ) Yes; Serrated; Yes; Left colon
b. ) Glands; Right; APC mutation (Chrom 5) –> KRAS forms polyp –> CA = p53 mutation/ Increased COX expression
- Size > 2 cm; sessile; villous
1. ) APC on Chrom 5; Colon/rectum; Gardner; Turcot
2. ) Instability; Mismatch repair; left; Iron defic. anemia
3. ) Carcinomas

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8
Q
  • Pediatric GI Disease:
  • common in both adults and kids? (3)
    1. ) TE fistula: Often related to? (2) H-Type (4%) leads to?
    2. ) Infantile Hyper. Pyloric Stenosis: Presents when? More common in? Vomit type?
    3. ) Meckel Diverticulum: Most common: 2’s? Abnormal remnant of? Histology? Diagnose via?
    4. ) Omphalocele: Due to? Assoc with? (2) Intestines do what? Covering?
    5. ) Gastrothises: Due to? Covering? Assoc with?
    6. ) Intestinal Malrotation: Vomit? Midgut what?
A
  • Celiac, IBD, H. Pylori
    1. ) Cardiac defect/eso achlasia; resp. issues
    2. ) 3 wks; males; non-bilious
    3. ) Yes (2%/ 2 cm/ 2yo); vitalline duct; gastic/panc. tissue; Technetium-99 scan
    4. ) Increased liver size; other mals/incr. maternal age; herniate; peritoneal and amniotic covering
    5. ) Rectus ab wall defect; no amniotic; nothing
    6. ) Billious; volvulus
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9
Q
  • Pediatric GI Disease:
    7. ) GI Duplication: Cystic or?
    8. ) Intestinal Atresia: Duo common with? Etiology? Poly? Vomit?
    9. ) Imperforate Agenesis: Assoc. with? Seen with?
    10. ) Hirschprungs: Defect in? Can lead to? Treatment? Mutations in?
    11. ) Neonate nectrotizing enterocolitis: Often in?
    12. ) 2 types of esophagitis? Treatments?
A

7.) Tubular
8.) Downs; ischemic; polyhydraminos; bilious
9.) Fistulas; Physical Exam
10.) ENS ganglion cells; megacolon; resection; RET gene
11.) Premi’s
12.) Reflux = Incomepetent GI sphincter or haital herniation; acid blockade
Allergic= Immine rx; eisino’s; steroids/diet

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10
Q
  • What causes SM contraction in GI? (2)
  • BER? Stomach? Duo? Ileum?
  • 3 phases of swallowing? Autonomic after what?
  • Stomach storage increases? Not? Motility in stomach?
  • Effect of fat in duo? Acid? Hyper/hypotonic?
  • Role of gatrin from antrum? (3) Inhibited by? GIP?
  • 2 parts of intestinal motility?
  • 2 parts of colonic motility?
A
  • ACH/pns
  • Basal rate; 3/min; 12/min; 9/min
  • Voluntary; pharyngeal; esophageal; past oropharynx
  • Volume not pressure; starts slow in body and increases
  • CCK to stim panc release and decrease gastric motility; secretin release = bicarb release and decreased molitiliy; slow gastric emptying
  • Increase H+, motility and mucosa; somatostatin (SLOW); Insulin release
  • Segmentation = BER; MMC b/n meals
  • Mass movement (intense/long) and segmentation BER
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11
Q
  • Reflexive defecation? Occurs when? By what? Gastroileal? Gastrocolic?
  • Stomach: Pumps on Lumen side? (3) BL sides? (3) Inside? PPI’s target what?
  • 3 seretalogues? H released from? A/G direct effect? Indirect? What do somato/ PG’s do?
  • Gastric acid follows what rhythm? Day? Night?
    1. ) Cephalic phase: Caused by? 3 effects?
    2. ) Gastric phase: Caused by effect?
    3. ) Intestinal phase: Caused by? Effect?
  • 3 protective mechanisms?
  • 3 roles of HCl?
  • Swallowing: Supstream? (2) Downstream? (2)
A
  • Relax IS and contract ES; After meal colonic activity; pelvic reflex; stomach activity stim chyme through ileocecal; food in stomach causes mass movement
  • From diagram
  • Histamine, ACH, gastrin; ECL cells; stim parietal cells; stim Histamine release; inhibit cAMP to shut off parietal
  • Circadian; low acid; high
    1. ) High ACH/gastrin/inhibit somatostatin
    2. ) Vasovagal reflex to distend stomach; stim gastrin release
    3. ) AA’s/partially digested peptides; more gastrin
  • Goblet cells, mucus, bicarb
  • Denature protein, kill bacteria, pepsinogen to pepsin
  • ACH/sub p contract; NO/ATP to relax
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12
Q
  • 3 absorbed sugars? Lactose into? Sucrose? Starches? Enzyme location?
  • 3 luminal transports? 2 Blood transports?
  • Increased carb consumption =? (2)
  • Chief cells secrete? Active at? Cleaves where?
  • Endopeptidases?
  • Exopeptidases?
  • Proteases activated by? This is activated by?
  • Proteins absorbed as? (3) FAA cotrans with? D/T with? Which is faster?
A
  • gla, glu, fru; glu/gal; glu/fru; glu/glu; brush borders
  • Diagram
  • More transporters and more absorption
  • Pepsinogen; ph1-3; proteins at aromatic AA’s
  • Hyrdolyze AA’s peptide bonds
  • Hydrolyze one AA at a time
  • Trypsin; enterokinase
  • FAA; Di/Tri; Na; H+; Di/Tri
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13
Q
  • Lipid digestion: Mouth? Stomach? SI? Pancreas?
  • Miscelles?
  • Chylomicrons?
  • Exoctytosed as? Into?
  • Jejunum: 2 Lumen transports? 3 Blood?
  • Colon: 2 Lumen? 2 Blood?
  • Vit D: Intestine as? Liver as? Kidney as?
A
  • Lingual ligase; gastric lipase/CCK to decrease emptying; fat droplet emulsified by bile salts; colipase/lipase
  • Transport products of fats
  • Resyntehsized in cell
  • LDL/HDL; lacteals
  • See diagram
  • See diagram
  • VD3, 25-OH-D3; 1,25-OH-D3
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