Gastrointestinal Flashcards

1
Q

intussusception-def, pt pop, location, presentation (3)

A

invagination of a portion of intestine into lumen of the adjacent intestinal wall (like collapsed telescope)
-seen in children younger than 2 yrs
region of ileocecal valve
intermittent, sever, colicky abdominal pain, “currant jelly” stools and sometimes a palpable mass in right lower abdominal quadrant

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2
Q

poison/treatment

  • arsenic
  • lead/mercury
  • cyanide
  • iron
  • methemobloginemia
A
  • Dimercaperol
  • CaNa2EDTA
  • amyl nitrite
  • deferoxamine
  • methylene blue
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3
Q

symptoms of arsenic poison, mech, mech and name of treatment

A
  • stomach pains, vomiting and delirium and garlic odor on breath*
  • inactivates enzymes by binding to sulfhydryl groups
  • treat with chelating agent dimercaprol
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4
Q

which cytokines are responsible for the down regulation of local cytokine production and inflammatory rxn?

A

TGF-beta (inhibits cells) and IL-10 (inhibits cytokines)

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5
Q

which cytokine can produce fever? (pyrexia)

A

Il-1

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6
Q

which cytokines are released by Th2 cells?

A

IL-4, IL-5, IL-10

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7
Q

name some pro-inflammatory cytokines?

A

IL-1, IL-4, IL-5, and IL-12

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8
Q

reperfusion injury leads to damage to what part of the cell?

A

cell membrane?

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9
Q

glutathione peroxidase

A

reduces cellular injury by catalyzing free radical breakdown

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10
Q

murmur in aortic regurg- 2 causes

A

early diastolic if mild and holodiastolic if severe

caused by aortic root dilation or a bicuspid aortic valve

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11
Q

aortic regurg murrmur due to aortic dilation is best heard

A

at right sternal border, vs left sternal board for normal aortic regurg

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12
Q

abnormal rotation and fixation of midgut early in fetal life results in- two main manifestations, location of cecum

A
  • intestinal malrotation
  • intestinal obstruction-due to compression by adhesive bands
  • midgut volvulus-intestinal ischemia due to twisting around the blood vessels
  • right upper quadrant fixed with Ladd’s bands (fibrous bands) to 2nd part of duodenum
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13
Q
MHC class II
MCH class I
B7
CD28
TCR
A
  • expressed on surface of APCS
  • expressed on surface of all nucleated cells except RBCs
  • co-stimulation receptor in APC
  • co-stimulation receptor in T-cell
  • T-cell receptor that binds antigen MHC complex
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14
Q

failure to acidify lysosomes in antigen presenting cells (APCs) would prevent

A

removal of invariant chain on MHC II, decreased formation and expression of antigen-MHC complex, decreased interaction between APCs and Tcells

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15
Q

name 3 antigen presenting cells (APCs)

A

dendritic cells, macrophages, and B-lymphocytes

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16
Q

secretory vs inflammatory vs osmotic diarrhea

A
  • no pus, blood. tea color and odorless (i.e VIPoma)
  • pus and blood
  • improves with dietary modification (i.e lactose intolerance)
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16
Q

VIPomas-hypersecretion of what from where? loss of which ions, inhibits which hormone, treatment?

A

non-beta pancreatic islet cell tumors hypersecrete VIP. VIP increases intestinal chloride loss in stool, leads to loss of water Na+, and K+. inhibits gastric acid secretion. WDHA (watery diarrhea, hypokalemia, and achlorhydria) treat with somatostatin

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17
Q

somatostatin decreases production of which GI hormones

A

aka octreotide. all of them- VIP, cholecystokinin, secretin, gastrin, and glucagon (not motilin or glucose-dependent insulinotropic peptide)

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19
Q

VIPomas vs gastrnoma, vs glucagonoma

A
  • inhibits gastric acid release caused WDHA syndrome
  • increases gastric acid release leading to intractable peptic ulcer disease (Zollinger-Ellison syndrome)
  • can lead to secondary diabetes mellitus and necrolytic migratory erythema of skin (blistering rash lower abdomen, buttocks, perineum, and groin.)
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20
Q

imperforate anus results from? manifests when? most often associated with? can also be associated with what rarer syndrome?

A

abnormal development of anorectal structures.

  • during 1st days of life by inability to pass meconium
  • urogenital tract anomalies (i.e urorectal, urovesical, or urovaginal fistulas)
  • VACTERL syndrome
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21
Q

VACTERL syndrome

A
Vertebral defects
Anal atresia
Cardiac anomalies
Tracheoesophageal fistula
Esophageal atresia
Renal anomalies
Limb anomalies
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22
Q

location of esophagus on CT

A

between trachea and vertebral bodies. typically collapsed with no visible lumen on CT images

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23
Q

migration of neural crest cells in intestinal wall plexi occurs in which direction? name of syndrome

A
  • migrate caudally so rectum is always involved

- Hirschsprung disease

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24
Q

strain of E.coli that doesn’t ferment sorbitol or produce glucuronidase? mech of toxin produced?

A

enterohemorrhagic e. coli (EHEC), Siga-like toxin-inactivate ribosomal 60S

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25
Q

toxins produced by

  • EHEC
  • ETEC
A
  • shiga-like toxin- inactivate ribosomal 60S
  • LT (heat liable-activates adenylate cyclase and increass cAMP))/ST (heat stable- activates guanylate cyclase and increase cGMP)
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26
Q

lesser omentum-def, extends from where to where?, divided into which two structures? what structures (5) run in free right margin?

A

double layer of peritoneum.

  • extends from liver to lesser curvature of stomach and beginning of duodenum
  • divided into hepatogastic and hepatoduodenal ligamment
  • right sided free margin contains portal triad (hepatic art, common bile duct, and portal vein) also contains lymphatics and hepatic plexus
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27
Q

define polycistronic mRNA? common in eukaryotes or prokaryotes? give GI related example? number of promoters, operators and regulatory elements involved?

A

one mRNA codes for several proteins

  • more common in prokaryotes
  • E. coli lac operon that codes from proteins needed for lactose metabolism.
  • the transcription and translation of these bac proteins is regulated by a single promoter, operator, and set of regulatory elements
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28
Q

true vs false diverticulum- def and examples

A
  • true contains all three layers (mucosa, submucosa, and muscular layers)=Meckel’s, normal appendix
  • false contains 2 layers (mucosa and submucosa)=Zenker esophageal, common colon “ticks”
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29
Q

Rule of 2 for Meckel’s diverticulum

A

“2% population
2 feet from ileocecal valve, 2 inches in length, 2% symptomatic and males are 2X more likely to be affected, 2 yrs of age

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30
Q

in pancreas divisum which duct drains majority of pancreas?

A

normally major pancreatic duct (of wirsung) doesvia major papilla
-but in divisum the accessory duct of (Santorini) via the minor papilla does

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31
Q

ulcer in this GI location is less likely to develop into cancer.

A

duodenum

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32
Q

when should doctor administer life saving treatment against an adult’s wishes? against a parent’s wishes for their children?

A

adult pt who are competent or have their wishes in a living will have authority to refuse life saving treatment

  • if there is any doubt in a clinician’s mind concerning the wishes of the pt the best thing is to treat.
  • in am emergency physician should always provide potentially life-saving therapy to a minor
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33
Q

diagnose Meckel diverticulum

A

look for lower GI bleeding
-99mmTc-pertechnetate scan can be used to identify ectopic gastric epithelium found in M.D causing ulceration and bleeding.

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34
Q

Meckel’s vs acute appendicitis

A

both can cause acute right lower quad pain.

  • meckel’s look for currant jelly, or intussesception
  • migration of pain from center of umbilicus, acute
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35
Q

abnormal midgut rotation around superior mesenteric art vs abnormal hindgut descent along inferior mesenteric artery

A
  • leads to intestinal malrotation, intestine is fixed by fibrous adhesive bands that can cause obstruction
  • can lead to different degrees of anal ageneis of imperforate anus
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36
Q

E. coli strain associated with “stacked-brick” intestinal adhesion

A

EAEC enteroaggregatve e. coli. they adhere to jejunal, ileal and colonic mucosa in this pattern and do not invade.
-causes diarreha in children in developing coutries

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37
Q

periodic, non-peristaltic contractions of esophagus-disease, mech, presentation, appearance on barium esophagogram, mimics what serious disease that should be ruled out?

A

diffuse esophageal spasm- uncoordinated contractions of esophagus

  • dsyphagia and chest pain
  • “corkscrew” esophagus
  • can mimic unstable angina
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38
Q

diffuse esophageal spasm (DES) vs GERD

A
  • crampy pain

- burning pain

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39
Q

explain the process of base excision repair

A

is used to correct defects in single bases caused by spontaneous/toxic deamination.
1-glycoslyase recognizes altered base and creates AP site (apurinic/apyrimidinc)
2-endonuclease cleaves 5’ while lyase cleaves 3’ sugar phosphate
3-DNA polymerase-beta fills gap
4-ligase seals gap

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40
Q

base excision repair vs nucleotide excision repair

A

both utilize endonucleases, DNA polymerase, and ligase

  • BER is used to correct defects in single bases, creates AP sites
  • NER is used to repair bulky helix distorting lesions (endonuclease releases oligonucleotide-containing damaged bases)
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41
Q

deamination result of
cytosine
adenine
guanine

A

uracil
xanthine
hypoxanthine

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42
Q

two common bacteria in intra abdominal infections

A

e. coli

baxteroides fragilis

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43
Q

how to control for confounding vs how to control for selection bias?

A
  • multiple repeated studies, crossover (subjects act as their own control) or matching (pts with similar race, age etc act are in control and treatment group)
  • randomization, ensure choice of right comparison/reference group based on exposure not race, age etc…
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44
Q

describe pathogenesis of hepatic encephalopathy?

A

hyperammonemia results in depletion of alpha ketoglutarate, causing inhibition of Kreb’s cycle
-also excess ammonia depleted glutamate (an excitatory neurotransmitter) and causes accumulation of glutamine resulting in astrocyte swelling and dysfunction

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45
Q

name three types of adenomatous polyps

A
  • tubular, villous, and tubulovillous
  • villous are larger sessile and more severely dysplastic than tubular type. aka velvety or cauliflower-like projections
  • tubular are dysplastic colonic mucosal cells that form tubular shaped glands
  • tubulovillous is a combination of both
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46
Q

symptoms of villous adenoma

A

mc asymptomatic

-bleeding, secretory diarrhea, and partial intesting obstruction

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47
Q

colon/biopsy manifestations of

adenocarcinoma vs Kaposi’s sarcoma

A
  • protuberant mass; dysplastic mucosal cells with variable degree of gland formation
  • reddish/violet, flat maculopapular lesions or hemorrhagic nodules; spindle shaped tumor cells with small-vessel proliferation
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48
Q

colon/biopsy manifestations of

  • cytomegalovirus
  • crytosporidium
  • entamoeba histolytica
  • ulcerative colitis
A
  • multiple ulcers and mucosal erosions; cytomegalic cells with inclusion bodies
  • non-ulcerative inflammation; basophilic clusters seen on surface of intestinal mucosal cells
  • numerous discrete, flask shaped ulcerative lesions; trophozoties containing red blood cells
  • contigupuous area or erythematous friable, granular mucosa with possible pseudopolyps; inflammatory infiltrate involving mucosa and submucosa with crypt abscessses
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49
Q

histology of esophageal SCC. risk factors of SCC vs adenocarcinoma

A
  • keratin nests and pearls
  • alcohol use, tobacco smoke, consumption of N-nitroso-contianing foods, esp in Asian countries
  • Barrett’s eso, GERD, obesity, and tobacco use
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50
Q

name three phases of ATN

A

initiation stage: ischemic injury to renal tubules, precipitated by hemorrhage, acute MI, sepsis, surgery

  • maintenance: decreased urine output, fluid overload, increasing Cr/BUN hyperK
  • recovery: increased urine output, electrolyte abnormalities (hypo K, Mg, PO4, and Ca) b/c of slow recovering tubular function
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51
Q
  • factors need to progress from normal colon to adenoma

- genes needed to progress from adenoma to carcinoma

A
  • APC- normal colonic mucosa to hyper proliferative epithelium
  • methylation abnormalities and COX-2 overexpression (pts that take aspirin are protected). from hyperproliferative to small adenoma
  • K-ras-unregulated cell proliferation. small to large adenomatous polyps
  • DCC (“deleted in colon cancer”- large adenomatous polyps to adenocarcinoma)
  • P53 (tumor supressor gene)-adenocarcinoma to carcinoma
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52
Q

MSH2 gene

A

responsible for DNA mismatch repair. leads to Lynch syndrome

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53
Q

how does glucose affect lac operon?

A
  • glucose decreases the activity of adenylyl cyclase and leads to a reduction in intracellular cAMP
  • decreased cAMP causes poor binding of catabolite activator protein (CAP) to the CAP-DNA binding domain leading to decreased expression of the structural genes of the lac operon.
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54
Q

lowering cut off point has what effect on sensitivity? FP, PPV and FN

A

-increase sensitivity, increase FP, and decrease PPV and FN

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55
Q

impetigo is caused by? not strep pneumoniae b/c

A
  • caused by group A strep (strep pyogenes)

- strep p causes MOPS (meningitis, otitis media, pneumonia, and sinusitus)

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56
Q

difference b/t live attenuated vaccine for polio (Sabin) vs killed vaccine (Salk)

A

-live promotes synthesis and secretion of local mucosal IgA than does killed vaccine b/c oropharyngeal and intestinal are sites of entry

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57
Q

MTX mech of action, causes buildup of

A
  • antimetabolite similar to folic acid
  • inhibits dihydrofolate reductase synthesis of tetrahydrofolate
  • causes buildup of dihydrofolic acid polyglutamate
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58
Q

two rxn mediated by dihydrofolate reductase. what does end product help create (3)

A
  • folic acid to DHF and DHF to THF

- THF donates 1 Carbon group to produce amino acid, -purines, and thymidylic acid

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59
Q
  • presentation of neonatal tetanus
  • how to prevent?
  • pt pop
A
  • rigidity and spasms
  • immunize mothers. IgG crosses placenta to protect baby
  • developing countries b/c of no vaccines
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60
Q

mech of ribavarin

A
  • lethal hypermutation
  • inhibiting DNA polymerase
  • inosine monophosphate dehygrodenase (depelted GTP), causing 5’cap on viral RNA transcipts
  • modulating a more effective immune response (enhances Th1 which inhibiting Th2)
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61
Q

giardia on gram stain

A

-negative, pear-shaped bilaterally symmetric orangism with four pairs of flagella and two nuclei

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62
Q

gastroenteritis acquired from domestic animals. associated with what neurological disorder?

A
  • campylobacter

- Guillain-Barre syndrome

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63
Q

leptin-produced where? mech? mutation causes?

A
  • produced in adipocytes in proportion to quantity of fat stored
  • acts on arcuate nucleus of hypothlaamus to inhibit produciton of neuropeptide U (decreasing appetitie) and stimulate productions of alpha MSH (increasing satiety)
  • mutations cause hyperphagia and profound obesity
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64
Q

why are s. aureus and b. cereus able to cause rapid onset food poisioning?

A
  • highly heat stable exotoxin is preformed prior to consumption
  • s. aureus is found on mayonanaise containing products
  • b. cereus is found in reheated fried rice
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65
Q

vitamin deficiencies

  • decreased exposure to sunlight
  • strict vegetarian diet
  • biiliary obstruction
A
  • vit D
  • colbalamin
  • fat soluble vitamins ADEK
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66
Q

dd for acquired nyctalopia

A
  • although most common cause of night blindness id hereditary retinitis pigmentosa other causes of acquired night blindness are
  • toxic retinopathy (phenothiazines or chloroquine)
  • vit A def
  • congenital rebella, syphillus, or other infections
  • diabetic retinopathy
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67
Q

what are branches of splenic artery (3) name distribution. where does splenic art originate from? which branch is most susceptible to injury following splenic art blockage?

A

pancreatic branches (run posterior to upper border of pancreas supply body and tail)

  • left gastroepiploic artery (supply middle part of greater curvature of stomach)
  • short gastric (supplies upper part of greater curvature of stomach)
  • celiac artery
  • short gastric b/c of poor anastomoses
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68
Q

three risk factors for gallbladder disease

A

forty, faty, and female

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69
Q

secretin-produced from? action?

A

pancreas

promotes bicarbonate secretion

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70
Q

VIP-producede from? action?

A

pancreas

stimulates intestinal water secretion, counteract gastrin in stomach, and promote bicarb secretion

71
Q

motilin-produced from? action

A

from small intestine, promotes intestinal motility

72
Q

somatostatin-producted from? actitons? what inhibits it’s release?

A

numerous tissues (hypothalamus, stomach, intestine, and pancreas) in response to low pH

  • inhibits release of GH and TSH and suppresses release of gastrin, CCK VIP, secretin, insulin, and glucagon
  • vagal stimulation inhibits somatostatin release?
73
Q

CCCK-produced where? action?

A

duodenum and jejunum in response to fatty acids and amino acids
gallbladder contraction

74
Q

hereditary pancreatis

A

rare disorder that results from mutation involving trysingogen or SPINK1 genes
-trypsin is active and causes reoccurring attacks of acute pancreatitis

75
Q

ways to inhibit trypsin

A
  • self inhibition (trypsin cleaves itself into and inactive form)
  • SPINK1 secreted by acinar cells to block trypsin that is prematurely activated
76
Q

describe adenoma to carcinoma sequence in colon cancer. not over expression of cyclin D b/c?

A

APC mutation causes normal mucosa to small polyp

  • k-ras mutation causes increase in size of polyp
  • p53 and DCC mutations cause malignant transformation
  • cyclin D over expression causes breast, lung, and esophageal cancers, and certain types of lymphomas
77
Q

pathophysiology and presentation of drug induced biliary colic. drugs that can cause this?

A
  • contraction of smooth muscles in spinchter of Oddi increased bile duct pressure and gallbladder leading to RUQ pain, cramping, jaundice in skin and eyes
  • all mu agonists.
78
Q

since all mu agonist cause biliary colic of them what is drug of choice in pts with bilary and pancreatic pain? what other drugs can be used?

A

meperidine (little evidence to support this but ppl use it), or NSAIDs (diclofenac, ketorolac)

79
Q

gross, x-ray, histo of Crohn’s vs Ulcerative colitis

A

crohns: cobblestone, string sign, transmural inflammation and noncaseating granulomas
- UC: pseudopolyps, lead pipe, no granuolmas mucosal and submucosal inflammation only

80
Q

which genes are involved in mismatch repair?

A

MSH2 and MLH1 which code for MutS and MutL homologs

81
Q

which drugs can cause pill induced esophagitis?

A

tetracycline antibiotics and potassium chloride and bisphosphates

82
Q

name two forms of IgA

A
  • secretory form (dimer) has J chain and secretory component, in colostrum, tears, saliva, and mucus
  • monomer form in serum
83
Q

erosion vs ulcer

A
  • do not fully penetrate muscular mucosa

- extend into submucosal layer and musclaris propria (inner circumferential and outer longitudinal smooth muscle layers)

84
Q

using curves how do you define bioavailability? why not just area under curve?

A
  • F=(area under the oral curve*IV dose)/ (area under the IV curve * oral dose)
  • bioavailability is a fraction of the drug that reaches systemic system in unchanged form
  • area under the curve is just total amt of drug absorbed and made available in systemic system before it was eliminated
85
Q

name retroperitoneal structures

A

major vessels-abdoinal aorta, inferior vena cava, and branches
solid organs-pancreas (except tail), kidneys, and adrenal gland
hollow organs-parts 2, 3 and a part of 4 of the duodenum, ascending and descending colon (secondarily retroperitoneal), rectum, ureters, and bladder
vertebral column and muscles

86
Q
  • stool with mucus and some epithelial cells
  • many leukocytes and neutrophils
  • many erythrocytes and some leukocytes
A
  • a bacteria that doesn’t invade just purely toxins that don’t cause cell death (v. cholera and ETEC
  • a bac that invades (salmonella, EIEC), no hemorrhage needed
  • a bac whose toxin causes cell death causing mucosal hemorrhage and necrosis, (EHEC) doesn’t have to invade
87
Q

life cycle of strongyloides infection, diagnose how, live threatening complication, treatment?

A
  • skin penetration, lungs, swallowed into GI tract
  • diagnose by finding rhabitiform (non infectious) larvae in stool
  • hyperinfection syndrome (maturation of rhadtiform in GI tract causing autoinfection)-multiorgan failure and shock
  • ivermectin
88
Q
  • rhabditiform larve in stool
  • parasite eggs in stool
  • perianal egg deposition
  • proglottids in stool
  • trophozoites and cysts in stool
A
  • stronglyoides stercoralis
  • schistosomiasis
  • enterobious vermicularis (pinworms)
  • intestinal tapeworms (taenia solium, t saginata, diphyllobothrium latum)
  • protozoal infections (giardia lamblia)
89
Q

which bac have small inoculation threshold? (4)

A
shigella (10 cells)
campylobacter jejuni (500)
clostridium perfringens (500)
entamoeba histolytica (1)
giardia lamblia (1)
90
Q

left side colon cancer vs right sided colon cancer

A
  • left: partial intestinal obstruction (abdominal pain, distention, and nausea)
  • right (large calliber so no obstruction): iron deficiency anemia and systemic symptoms
91
Q

which disorders are benign

  • essential fructosuria vs hereditary fructose intolerance
  • galactokinase def vs classic galactosemia
A
  • esstential fructosuria (missing fructokinase)

- galatokinase deficiency

92
Q

risk factor of esophageal SCC vs adenocarcinoma

A
  • smoking, alcohol, achalasia, plummer-vinson, nitrosamine containing foods
  • barrett’s eso
93
Q

energy in 1g of protein
1g of fat
1g of carbs
1g ethanol

A
  • 4cal
  • 9cal
  • 4cal
  • 7cal
94
Q

diagnosis of toxic megacolon not abdominal ultrasounds b/c? not barium contrast or colonoscopy studies b/c?

A
  • flat plain X ray
  • US is not useful in this case
  • these can cause perforation
95
Q

diphenoxylate vs octreotide in treatment of diarrhea

A
  • targets MOTILITY: opiate anti-diarrheal structurally related to meperidine. slows motility, use low dose and combine with atropine to prevent dependence and abuse
  • targets OVERSECRECTION helpful for secretory diarrhea (so do bismuth subsalicylate, and probiotics)
96
Q

are there any drugs used for diarrhea that increase absorption of water or electrolytes?

A

no

97
Q

pancreatic juice ion concentration compared to plasma
-Na
-K
-Cl-
-HCO3-
what happens to concentrations in response to secretin?

A
  • Na and K+ are isotonic
  • HCO3 concentration is higher in pancreatic juice
  • Cl- is lower in pancreatic juice
  • secretin is released in response to high H+ and causes chloride content to decrease in proportion to increase in bicarb concentration (b/c chloride and bicarb are exchanged for each other at apical surface of ductal cells)
98
Q

main source of fatty lipid digestion? absorption? effect of chlectystectomy

A
  • duodenum
  • jejunum
  • it typically have little effect on lipid digestin and absorption though pt may find it difficult to eat a large fatty meal b/c bile acids are needed to absorb fatty acids
99
Q

mech of polyethlyene glygol in constipation?

A

osmotic LAXATIVE

like magnesium hyroxide, magnesium citrate and other magnesium containing drugs

100
Q

name three things that can increase gastric pH

A

achlorhydria, food ingestion and antacid ingestion

101
Q

how to detect C. difflcile toxin

A

-look for genes in stool with PCR

102
Q

causes of infectious diarrhea

  • undercooked fish
  • not taking vaccine before travel
  • travel to mexico
  • antibiotics
A
  • v.cholera
  • HAV and typhoid fever
  • ETEC, campylobacter, salmonella and shigella or parasites (entamoeba and giardia)
  • c. difficile
103
Q

how to differentiate between no lactose fermenting oxidase negative bacteria?

A

these are salmonella proteus shigella and yersinia

  • TSI agar
  • no H2S production (Shigella)
  • H2S production turn black (salmonella and proteus)
104
Q

most significant viral factor for shigella? how does it enter host?

A
  • mucosal invasion

- enters M cells in Peyer’s patches

105
Q

name bac that can survive in blood

A
e. coli (sepsis)
salmonella typhi (sepsis, typhoid fever)
pseudomonas aeruginosa (sepsis, endocarditis and osteomyelitis)
klebsiella (sepsis)
proteus (sepsis)
106
Q

which bac proliferate in lymph nodes

A

salmonella and yersinia entercolitica (reason why Y. enter can lead to lower right quad pain confused with appendicitis)

107
Q

schilling test

A
  • give intrinsic factor and see if vit B12 is absorbed
  • determines cause of abnormal vit B12 absorption
  • diagnose pernicious anemia
108
Q

blunting of villi along a chonic inflammatory infiltrate in small intestine

A

celiac disease

109
Q

mc location of tumor in zollinger-ellison syndrome

A

pancreas

110
Q

chronic gastritis with antral sparing vs antral predominate gastritis

A
  • autoimmune gastritis

- H.pylori

111
Q

distal duodeunal ulcer vs proximal

A

distal-Zollinger Ellison

proximal-peptic ulcer disease

112
Q

type A vs type B gastritis (causes, location, assocaitions)

A

type A- autoimmune, body of stomach, megaloblastic anemia (vit B 12 malabsorption)
type B-h. pylori, antrum, gastric adenocarcinoma and MALT lymphoma

113
Q

granulomatous gastritis

A

idiopathic, intramucosal epithelioid granulomas that cause narrowing of antrum secondary to transmural inflammation

114
Q

two types of gastric adenocarcinoma and ways to tell them apart?

A

intestinal type-looks like colonic adenocarcinoma

-diffuse type-signet ring cells

115
Q

2 types of ulcers due severe trauma or burns? (location)

A
  • Curling ulcers (proximal duodenum)

- Cushing ulcers due to high intracranial pressure (esophagus, stomach, duodenum, prone to perforation)

116
Q

paneth cells-location, function (2)

A
  • occur in small groups in base of intestinal cells
  • phagocytic and secretory properties
  • secrete lysozyme and defensins (polypeptide) both of these have antmicrobial and antiparasitic properties
117
Q

M cells-location, func

A
  • base of mucosal villi in Peyer’s patch

- sample contents of gut lumen and transfer antigens to basal lamina

118
Q

mc location of anal fissure? why?

A

posterior midline distal fo dentate line

-b/c it’s poorly perfused

119
Q

systemic mastocytosis define and effect on GI system

A
  • abnormal proliferation of mast cells and increased histamine secretion
  • increases production of gastric acid by parietal cells
120
Q

tertodotoxin

A

puffer fish toxin

inhibits voltage gated Na+ channels

121
Q

what keeps clostridium from causing infection? not gastric acid b/c?

A
  • microbial flora

- c. difficile can form spores and survive gastric juices

122
Q

presentation of circopharyngeal muscle dysfunction

A
  • diminished relaxation of pharyngeal muscles during swallowing
  • oropharyngeal dysphagia, couching, choking, and recurrent aspiration (recurrent pneumonia)
123
Q

diverticulum in upper esophagus vs middle esophagus

A
  • upper is usually due to circopharyngeal muscle dysfunction (posterior hypopharynx) leading to Zenker diverticulum
  • lower is usually due to TB or fungal infections that cause scarring and traction leading to true diverticula
124
Q

false vs true diverticulum

A

false has only mucosa

true has all layers of organ wall herniated

125
Q

phases of swallowing aka

A

oral-voluntary
pharyngeal- involuntary pharyngeal muscle contractions to propel food forward
esophageal phase- peristalsis moves food downward until relaxation of LES allows food into stomach

126
Q

amatoxins vs ricin

A
  • found in various poisonous mushrooms (Amanita phalloides) and inhibits RNA polymerase II (halting mRNA synthesis)
  • found in castor oil plant and inhibits rRNA protein synthesis by cleaving 60S
127
Q

name art that supplies proximal lesser curvature vs distal lesser curvature of stomach. these are at risk of?

A
  • proximal (left gastric from celiac)
  • distal (right gastric from proper hepatic from common hepatic from celiac)
  • at higher risk of perforation from ulcers which tend to occur on lesser curvature
128
Q

name art that supplies proximal greater curvature above splenic art vs proximal greater curvature vs distal greater curvature

A
  • prox above splenic (short gastric art from splenic from celiac)
  • proximal (left gastroepiploic from splenic from celiac)
  • distal (right gastroepiploic from gastroduodenal from common hepatic from celiac)
129
Q

D-xylose-def, absorption, use

A
  • monosaccharide
  • doesn’t require pancreatic enzymes to be absorbed
  • used to differentiate between malabsorption of pancreatic insufficiency vs gastrointestinal mucosal etiology
130
Q

where is the antrum vs cardia vs fundus?

A
  • pre-pyloric
  • near esophagus
  • above cardiac notch and body
131
Q

structures near

  • second part of the duodenum
  • third part of duodenum
A
  • peritoneal, courses inferiorly from L1-L3 (closely related to head of pancreas and ampulla of Vater is here*)
  • retroperitoneal, courses horizontally (L1) across abdominal aorta and IVC at level of 3rd vertebra (closely related to SMA*)
132
Q

olive sized mass felt on deep palpation? what causes this?

A
  • congenital pyloric stenosis

- hypertrophy of pyloric muscularis mucosae

133
Q

posterior ulcer in duodenal bulb vs anterior ulcer

A
  • posterior can cause erosion and bleeding of gastroduodenal artery
  • anterior ulcer can cause perforation
134
Q

presentation/intestinal complications of Crohn’s vs UC

A
  • Crohn’s abdominal pain/fistulas, strictures (lead to intestinal obstruction)
  • UC blood diarrhea/toxic megacolon
135
Q

presentation of mesenteric adenitis that allows you to tell it apart from everything else?

A

clinical manifestations are nonspecific

5-14 years old

136
Q

whipple’s disease-def, symptoms, histo, pt pop

A
  • infection with Tropheryma whippellii (gram positive)
  • GI symptoms+ CNS+ ocular+ rheumatolotic (joint problems)
  • intestine mucosa with enlarge foamy macs with both rod shapped bacilli and PAS-positive* diastase-resistance granules*
  • middle age caucasian male
137
Q

T cell vs neutrophil defense against candida

A
  • T-cell defend against superficial infection (HIV pts)

- neutrophils protect against systemic infection (neutropenic pts)

138
Q

cells recruited by C5a vs C3a

A
  • C5a neutrophils, eosinophils all of them basically

- C3a no neutrophils just eosinophils and basophils

139
Q

name 2 mc causes of acute pancreatitis

name the other causes

A
  • alcohol and gallstones
  • GET SMASHED (gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion sting, mumps, hypercalcemia/hypertriglyceridemia, ERCP, Drugs (sulfa))
140
Q

acute pancreatitis + megaloblastic anemia should make you think?

A

it’s due to alcohol b/c alcohols have poor diet and can have folate or cobalamin deficiency
measure AST:ALT >2=alcoholic

141
Q

name 4 common non-neoplastic polyps

name 1 common neoplastic polyp, which shape is more likely to become cancerous?

A

hyperplastic (from glands or crypts), hamartomastous (Peutz-Jeghers or juvenile polyposis), inflammatory (Crohn’s or UC), lymphoid (children)
-adenomatous (villous is more likely than tubular to progress to adenocarcinoma)

142
Q

when does a carcinoid tumor have symptoms?

A

when is metastasizes to liver to in extra-intestinal site (lung) then the liver cannot metabolize the secretory products

143
Q

diarrhea, weight loss, epigastric pain with chronic alcoholism is? what causes calcifications on imaging? not bile salt deconjugation b/c?

A
  • chronic pancreatitis
  • alcohol causes protein precipitiation which calcify
  • bile salt deconjugation occurs when bac have gained access to small intestine. this results in steatorrhea and failure of micelle formation
144
Q
clinical presentation of nutrient deficiencies related to malabsorption
-iron, folate, vit B12
-protein
-vit K
calcium/vit d
-vit A
-gross presentation of stool
-how to screen for malabsorption?
A
  • anemia
  • muscle wasting and edema
  • petechiae and easy bruising
  • bone pain, muscle weakness, tetany
  • hyperkeratosis and night blindness
  • foul-smelly, bulky floating, greasy stool
  • Sudan III stain which identifies fat
145
Q

abetalipoproteinemia-def, histo on intestine and blood smear, gene involved

A
  • inability to synthesize APO B needed for absorption of lipids
  • enterocytes with clear or foamy cytoplasm
  • acanthocytes
  • MTP gene
146
Q

how is lac operon regulated (positive and negative)

A
  • negatively by binding of repressory protein to operator locus
  • positively by cAMP-CAP binding upstream from promoter region
147
Q

which drugs block gastric parietal cell at

  • M3
  • H2
  • H/K ATP pump
  • binds to base of mucosal ulcers?
A
  • atropine
  • cimetidine
  • lansoprazole
  • sucralfate
148
Q

presentation of mets of gastric cancer?

A

Virchow’s triad (left supraclavicular sentinel node), Sister Mary Joseph nodule (periumbilical subcutaneous mass), Krukenberg (tumor in ovary)

149
Q

clinical symps of lead vs iron posioning

A
  • abdominal pain, constipation, HA, lead line, peripheral neuropathy, microcytic hypochromic anemia and basophillic stippling
  • nausea, diarrhea, abdoinal pain, hemorrhage, hypovolemia, shock. stage 2 pt feels better. stage 3 metabolic acidosis, liver faliure, and hypoglycemia, stage 4 scaring of GI tract
150
Q

watershed areas of Gi tract

A

splenic flexure and distal sigmoid colon

151
Q

NF-kB protein is overexpressed in what GI disease? what is func ?

A

Crohn’s disease

-cytokine production

152
Q

what layer are parietal cells found in? chief cells?

A
  • superficial region of gastric glands

- secrete and synthesize pepsinogen and primary found in deeper region of gastric glands

153
Q

acetyl-CoA carboxylase vs Acyl-CoA dehydrogenase

A
  • fatty acid synthesis (1st rxn and rate limiting step)

- fatty acid breakdown (1st rxn)

154
Q

acyl-CoA synthetase deficiency vs Acyl-CoA dehydrogenase deficicency

A

both involved in fatty acid breakdown and have hypoketonemia

  • synthetase has carnitine deficiency
  • dehydrogenase has normal carnitine levels
155
Q

what is pantothenic acid? which rxn it is important for?

A
  • non active form of coenzyme A
  • binds with oxaloacetate in first step of TCA to form citrate
  • also needed for synthesis of vit A, D, cholesterol, steroid, heme A, fatty acids, amino acids, and proteins
156
Q

which biochemical processes occur in mito

A
  • beta-oxidation of fatty acids
  • TCA
  • ketogenesis
  • urea cycle (1st part)
157
Q

location of fatty acid synthesis vs fatty acid oxidation?

A
  • cytosol

- mito

158
Q

which organ can use glycerol from TG breakdown (fatty acid+glycerol) for energy? enzyme needed?

A

-liver; glycerol kinase

159
Q

earliest manifestation of systemic sclerosis aka?

A
CREST
-esophageal hypomotiity
-C-calcinosis
R-aynaud syndrome
Esophageal dsymotility
Sclerdactyly
Telangiectasia
160
Q

mc location of colon adenocarcinoma?

A

rectosigmoid colon

161
Q

colon adenocarinoma in multiple places vs ascending vs rectosigmoid colon

A
  • Lynch syndrome
  • large bulky, bleeding is major complication
  • obstruction symptoms not bleeding b/c smaller caliber
162
Q

gallbladder can lead to? not phospholipid stones b/c? not brown stones b/c? or black?

A
  • biliary sludge (bile precipitation with cholesterol monohydrate crystals, calcium bilirubinate and mucus)
  • phospholipids aren’t found in stones
  • brown is seen in biliary tract infection
  • black is seen in intravascular hemolysis
163
Q

inhaled anesthetics such as halothane can be associated with what organ failure?

A
  • acute liver injury (can’t distinguish from acute viral hepatitis)
  • elevated aminotransferase levels
  • look for prolonged PTT, eosinophilia, elevated aminotransferase
164
Q

diffuse gallbladder calcification, aka. indicates?

A
  • porcelain galbladder
  • chronic cholecystitis
  • remove b/c of risk of galbladder cancer
165
Q

which comes first anti IgG or IgM?

A

-IgM

166
Q

infectivity of hep B high vs low?

A
  • high=HBeAg

- low=anti-HBe Ag

167
Q

loops of small bowel at level of kidney is

A

jejunum

168
Q

pancreas on abdominal CT

A
  • head is closely associated with 2ns part of duodenum
  • it’s body overlies left kidney, aorta, IVC and superior messenteric vessels
  • tail is in splenorenal ligament
169
Q

where is iron absorbed?

A

duodenum and proximal jejunum

170
Q

7 alpha hydroxlyase

A

converts cholesterol into bile acids

171
Q

risk factors for formation of cholesterol galstones

A
  • caucasian race
  • glucose intolerance
  • female sex hormones
  • malabsorption of bile acids
  • obesity of rapid weight loss
  • glucose intolerance
  • pharmacotherapy with fibrates (inhbits 7 alpha hydroxylase)
  • hypomotility of gall bladder ()
172
Q

acute acalous cholecystitis vs acute calulous cholecystitis

A
  • no gallstones, seen in hospitalized pts

- non obstructing pigment gallstones

173
Q

DD for polyhydramnios in utero

A
  • Gastrointestinal disorders, such as duodenal atresia, esophageal atresia, gastroschisis, and diaphragmatic hernia
  • Brain and nervous system problems, such as anencephaly and myotonic dystrophy
  • Achondroplasia
  • Beckwith-Wiedemann syndrome
174
Q

describe carcinoid tumor histology? where does it arise from?

A
  • nest or sheets of uniform cells with eosinophilic cytoplasm and oval to round stippled nuclei
  • derived from enterochromaffin cells