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IM MOD-B > GASTRO > Flashcards

GASTRO Flashcards

1
Q

test for CHO malabs

A

Xylose Absorption test

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2
Q

fixed dose of xylose

A

25g d-xylose

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3
Q

to visualize the GIT and allow collection of specimen

A

EGD or Esophagogastroduodenoscopy

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4
Q

give Barium to the patient for visualization under xray

A

small bowel series

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5
Q

visualize colon and terminal ileum with the use of barium

A

Barium enema

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6
Q

endoscopic procedure, direct visualization of mucosa, identify lesions, take histological samples

A

Colonoscopy

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7
Q

insert long tube in the small bowel, inflate with methyl-cellulose, take xray pic

A

enteroclysis small bowel enema

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8
Q

patient ingests capsule which contains a camera, transmitter and a battery. it captures images as it passes through the GIT. reduce gap between UEE and Colonoscopy

A

video capsule endoscopy

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9
Q

test for pancreatic insufficiency

A

secretin test (secretin - produced by upper duodenum and stimulates pancreas to release enzymes)

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10
Q

test for B12 abs

A

schilling’s test

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11
Q

test for bacterial overgrowth

A

breath test (lactulose, glucose-hydrogen), culture ((+) if bacterial colonies exceed 10’4)

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12
Q

disorders that need biopsy

A

giardiasis, crohn’s, whipple’s/ celiac sprue

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13
Q

s/s of malabs (common)

A

malnut, wt loss, diarrhea

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14
Q

causes of malabs:

A
  1. Inadequate digestion
  2. Inadequate absorptive surface short bowel syndrome
  3. Bacterial overgrowth of SI
  4. Lymphatic obstruction
  5. Defects in mucosal structure and function
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15
Q

inadeq digestion

A
  1. Liver and biliary tract disorders
    a. liver cirrhosis
    b. biliary tract obstruction
    c. pancreatic insuff
  2. Post Gastrectomy malabs
    a. dec CCK and Secretin
    b. inadeq mixing
    c. stasis
    d. loss of gastric reservoir function
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16
Q

stim release of bile salts and pancreatic secretions

A

CCK and Secretin

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17
Q

inadeq absorptive surface

A
  1. massive resection
  2. anti-obesity operation
  3. jejunal bypass
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18
Q

resection of _____% of SI is well-tolerated

A

<40-50%

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19
Q

bacterial overgrowth of SI

A

a. Bacterial deconjugation of bile salts
b. Bacterial production of toxins vs enterokinases (digestive enz)
c. Destruction of intestinal mucosa by bacterial toxins
d. Bacterial consumption of Vit B12

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20
Q

part of SI that is sterile

A

proximal SI

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21
Q

sterility of Proximal SI is d/t:

A

a. Acid milieu of stomach
Intestinal peristalsis
secretion of Ig in the lumen of SI (coproantibodies)

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22
Q

plays a major role in maintaining the low level of bacteria

A

Peristalsis

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23
Q

bile salts are effective when it is in _______ form

A

conjugated form

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24
Q

conditions that poses risk of bacterial overgrowth in the SI:

A
  1. Chronic intestinal pseudoobstruction
  2. Tropical sprue
  3. Scleroderma
  4. Malabs in AIDS
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25
Q

decreased motility -> Stasis -> Bacterial overgrowth

A

Chronic Intestinal Pseudoobstruction

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26
Q
  • affects visitors or residents of tropical countries
  • chronic diarrhea, anemia, malnut, nutrient def
  • theory: coliform org
A

Tropical sprue

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27
Q
  • impaired intestinal motility, jejunal diverticulosis
  • involve intestinal wall itself
A

Scleroderma

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28
Q

overgrowth of microorg d/t depressed immunity

A

Malabs in AIDS

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29
Q

lymphatic obstruction

A
  1. Whipple’s disease
  2. Intestinal lymphoma
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30
Q
  • rare dse
  • arthralgia, ab pain, diarrhea, wt loss, impaired intestinal abs
A

whipple’s dse

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31
Q

diagnostic tool for whipple’s dse:

A

tissue dx, PCR

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32
Q

causative agent of whipple’s dse
rod shaped microorganism identified by PCR

A

Trophyrema whipplei

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33
Q

DOC for whipple’s = __________________
Alternative for whipple’s = ______________

A

Trimethoprim sulfamethoxazole for 1 yr
Chloramphenicol

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34
Q
  • increased lymphomatous cells
  • resemble celiac sprue but w/ incomplete response to gluten free diet
  • biopsy: total absence of vili, lesser degree of blunting, and shortening, infiltrated lamina propria
A

intestinal lymphoma

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35
Q

defects in mucosal structure and function

A
  1. Inflammatory bowel disease
    a. Crohn’s
    b. Regional enteritis
  2. Biochemical and genetic abnormalities
    a. Celiac sprue
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36
Q

mechanisms of IBD

A

a. Interruption of enterohepatic circulation
b. Deconjugation of bile salts
c. Impaired mucosal cell function
d. Inadeq absorptive cell function
e. Severe protein depletion

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37
Q
  • destruction of ileum d/t resection, fistulas, impairing reabs of bile salts
  • diffuse ulceration of SI
  • short bowel syndrome
A

crohn’s disease

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38
Q
  • malabs, abnormal small bowel structure
  • lack enz againts gluten/ intolerance to gluten
A

celiac sprue

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39
Q

gluten contains ______ w/c is toxic to intestinal cells

A

gliadin

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40
Q

pathogenetic theories of celiac sprue

A

a. Deficiency in specific mucosal peptidase (break down gluten to smaller products)
b. gluten may initiate immune reaction vs intestinal mucosa
c. viral etiology

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41
Q

diagnostic tools in celiac sprue

A

Jejunal biopsy
- in celiac, the vili are short and atrophied

Serology
- IgA anti gliadin ab

-IgA anti endomysial ab

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42
Q

water content of stool exceeds 200 ml per day

A

diarrhea

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43
Q

at the end of the day, the stool water content should not exceed ________

_______ is being rebsorbed

A

200 mL per day

8.8 L

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44
Q

driving force of water reabs from the lumen of intestine to the cells of intestine

A

Sodium

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45
Q

driving force for water secretion from cells of the intestine to the lumen

A

Chloride

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46
Q
  • cAMP is generated from the cells via adenylate cyclase system
  • conditions that stimulate adenylate cyclase system -> release chloride followed by water
A

cAMP Regulating Chloride Channel

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47
Q

vibrio ingested -> secrete toxin -> bind to specific receptor in the intestines -> trigger adenylate cyclase system -> ATP to cAMP -> opening of chloride gate -> chloride will be secreted followed by water

profuse rice watery stool
can loose approx 10L or water

A

cholera diarrhea
(Exogenous factor)

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48
Q
  • endogenous opioid peptide
  • decreases cAMP production -> close chloride gates -> inhibit secretion of chloride and water
A

enkephalins
(Endogenous factor affecting cAMP levels)
help decrease levels of cAMP

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49
Q
  • feedback mechanism
  • neutralizes the effects of enkephalins
A

enkephalinase / enkephalin inhibitors

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50
Q
  • inhibit enkephalinase -> inhibit neutralization of enkephalins -> decrease cAMP -> inhib sec of chloride and water
A

enkephalinase inhibitor
can be considered as anti-diarrheal or anti-secretory
brand: Hidrasec, Acetorphan, Racecadotril

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51
Q
  • inc daily stool wt >200g (most objective definition in research)
  • inc stool frequency
  • inc stool fluidity
A

Diarrhea

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52
Q
  • inc defecation w/o inc in daily stool wt
    e.g., IBS, hyperthyroidism
A

Pseudodiarrhea/Hyperdefecation

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53
Q
  • invol release of rectal contents
  • seen in px w/ spinal cord prob, elderly
A

Decal incontinence

54
Q

classif of diarrhea

A

Acute = <7-14 days
Chronic = >4 weeks
Persistent = 2-3 weeks

55
Q

most common cause of acute diarrhea ________
other causes _________

A

infectious agents

mg containing drugs, toxins, chemo

56
Q

most common mode of trans of diarrhea

A

fecal oral route

57
Q

pathophysio mech of Diarrhea

A
  1. toxin prod
  2. enteroadherance
  3. mucosal invasion
  4. systemic infection
58
Q

toxin prod

A

a. preformed toxin
b. enterotoxin
c. cytotoxin

59
Q

preformed toxin

A
  • bacillus cereus, clostridum perfringens, staph au
  • in cases of food poisoning
  • IP: 6 hrs
60
Q

enterotoxin

A
  • aeromonas sp, ETEC, vibrio cholera
  • open Cl gates -> profuse watery stool
61
Q

cytotoxin

A
  • clostridium deficile, EHC
  • destroy cells of intestine -> bloody stools, ab pain, fever
62
Q

enteroadherence

A
  • crytosporidosis, helminthes, EAC, EPEC, giardia
  • cling to the mucosa
63
Q

mucosal invasion

A

a. minimal
b. variable
c. severe

64
Q

minimal mucosal inv

A
  • norwalk virus, rotavirus
65
Q

variable mucosal inv

A
  • vampylobacter sp, salmonella sp
66
Q

severe mucosal inv

A
  • entamoeba histolytica, EIEC, shigella sp
  • can travel bloodstream and go to liver
67
Q

systemic infection

A

legionella, listeria, measles, viral he, psittacosis, RMSF, TSS

68
Q

diff dx of diarrhea

A
  1. Drug-induced diarrhea (ex. coamox)
  2. Acute diverticulitis
  3. Intestinal ischemia
  4. IBD
  5. Pseudomembranous enterocolitis
69
Q

drugs considered in symptomatic cases:
Shigella
C difficile
Traveler’s diarrhea
EPEC EIEC DAEC
Typhoid
Cholera
Salmonella
Amoebiasis
Giardiasis

A

Ampicillin
Metronidazole
Ciprofloxacin
TMP SMX
Chloramphenicol
Tetracycline
Ampicillin
Metronidazole
Metronidazole

70
Q
  • persistent >4 weeks
  • require evaluation
A

chronic diarrhea

71
Q

pathophysiologic types of Chronic Diarrhea:

A
  1. Inflammatory
  2. Osmotic
  3. Secretory
  4. Dysmotility
  5. Factitious
72
Q
  • fever, ab pain, tenesmus, blood pmns in stool
  • inflammatory lesions in the mucosa
  • inflam -> damage mucosa and submucosa
  • e.g., IBD, radiation enterocolitis
A

inflammatory diarrhea

73
Q
  • unusually large amt of non-digested food
  • inc osmotically active subs attracts water
  • diarrhea improves with fasting
    bulky fouls smelling
  • e.g., lactase def
A

Osmotic diarrhea

74
Q
  • secretion>absorption
  • watery diarrhea
  • watery diarrhea persists w/ fasting
  • e.g., carcinoids
A

Secretory diarrhea

75
Q

endoc tumor in panc -> tumor increases sec of vasoactive intestinal polypeptide -> stim guanylate cyclase -> stim cGMP -> open Cl gate -> diarrhea

A

VIPoma or Vasoactive Intestinal Polypeptide tumor
aka “Pancreatic cholera”

76
Q
  • pseudodiarrhea
  • d/t rapid transit of intestinal content
  • e.g., hyperthyroidism, IBS
A

Dysmotility

77
Q
  • self-induced diarrhea, usual in women
  • watery diarrhea w/ hypokalemia, weakness, and edema
  • e.g, laxative abuse
A

Factitious diarrhea

78
Q
  • Immune med chronic intestinal cond
  • Chronic recurrent inflam
  • 2 types:
A

IBD

Ulcerative colitis
Crohn’s dse

79
Q

smoking may prevent what type of IBD?

A

UC

80
Q

appendectomy may prevent what type of IBD?

A

CD

81
Q
  • CD4+ T cell activation -> sec inflam cytokines
  • macrophage, B cells, inflam leukocytes, mononuclear cells are recruited
  • proinflam > anriinflam
  • normal flora is perceived as pathogen
A

IBD

82
Q
  • (+) immune response vs I2, Ompc and Flagellin
  • improved with fecal diversion
  • may benefit from metronidazole, ciprofloxacin
A

CD

83
Q
  • symmetrical lesions
  • continuous distribution
  • involves mucosa and submucosa
  • rectal involvement
  • backwash ileitis (mild involvement of the ileum)
  • toxic megacolon (dilated large intestines -> prone to perforation)
  • compli: colorectal adenoCA
A

UC

84
Q
  • asymmetrical
  • segmental distribution
    (1. ileocolic, 2. small colonic, 3. isolated colonic distribution)
  • skip lesions
  • transmural involvement (more layers are involved) -> deeper inflam -> heal -> scarring -> stricture -> obstruction
  • rectal sparing
  • small bowel involvement
  • recurrence after surgery
  • see granulomas (non-caseating), fissure, fistula (can form communication with other GI organs since this condition involves transmural)
  • intestines may become palpable in emancipated px
A

CD

85
Q

diagnostic tools in IBD

A
  1. Biochemical
    - elev acute phase reactants
    - dec albumin
    - dec hemoglobin
    - in WBC
  2. Imaging
    - can ident CD
    - not helpful in UC
  3. Serologic markers
    - pANCA -> UC
    - ASCA -> CD
86
Q

treatment in IBD

A
  1. 5-ASA
  2. Glucocorticoids
  3. Antibiotics
  4. Azathioprine/ 6 mercaptopurine
  5. Methotrexate
  6. Cyclosporine
  7. Tacrolimus
  8. Anti-TNF
87
Q
  • mainstay for mild-mod UC
  • regulates NFKB (inflam med)
  • induction and maintenance in both UC CD
  • sulfasalazine, mesalamine, olsalazine
A

5-ASA

88
Q
  • induction
  • for mod-severe UC CD
    prednisone = 40-60 mg/d
    budesonide = more localized, better
  • prob: adrenal insuf, electrolyte imbal
A

Glucocorticoids

89
Q
  • for CD, no role in UC
  • prevent recurrence
  • metronidazole, cirpofloxacin
A

Antibiotics

90
Q
  • inhib immune response
  • maintenance in both UC CD
A

Azathioprine/ 6 mercaptopurine

91
Q
  • anti-inflam
  • dec Il1
    induction and maintenance in CD
  • also used in rheumatoid a
A

Methotraxate

92
Q
  • inhib cellular and humoral immune system
  • block prod of Il2
  • inhib B cell fxn
  • for those refractry to iv steroids
  • for induction
  • no effect in maintenance if w/co azathioprine
A

Cyclosporine

93
Q
  • macrolide abx
  • for refractory IBD and those w/ extensive small bowel involvement
A

Tacrolimus

94
Q
  • block TNF
  • lyses TNF producing macrophage and T cells
  • for induction and maintenance
A

anti tnf
infliximab, adalimumab, certolizumab, golimumab (antiTNF)
thalidomide (inhib tnf)

95
Q

RF of colorectal CA

A

Diet
Insulin resistance
Dietary fiber
Hereditary factors and syndromes
IBD
Male
Obesity
Smoking
Physical activity
Polyps

96
Q

insulin resistance as RF of colorectal CA

A

T2DM -> insulin resistance -> inc IGF -> stim prolif of intestinal cells

97
Q

mech on how dietary fiber dec incidence of colon neoplasia

A

a. dilute/bind carcinogens and toxins
b. enhance elim
c. dec conc of fecal 20 bile acids and mutagens
d. dec bacterial metabolic enz-b glucoronidase
e. fermented by fecal flora to SCFA -> dec colonic pH -> less favorable for colon formation

98
Q

Hereditary factors and syndromes
- 25% of px have (+) fam hx
- hereditary (autosomal dominant) GI Polyposis Syndromes (100k polyps)
- if px has syndrome = px has lot of polyps

A

Familial Adenomatous Polyposis
Gardner’s syndrome
Turcot’s syndrome
Non-polyposis coli syndrome
Peutz-Jegher’s syndrome
Juvenile polyposis

99
Q

histologic type w/ higher risk of malignant potential
most dev sympt at adolescence
then dev colon CA at 35
may die untreated at 40

A

Adenoma

100
Q

IBD and colon CA

A

longer yr w/ IBD = higher risk of CA
px w/ pancolitis = higher risk

101
Q

non-malignant polyp

A

Hamartomatous (Juvenile)
Hyperplastic Mucosal Proliferation Polyp

102
Q

potentially malignant polyp

A

adenomatous polyp

103
Q

histologic type w/ higher risk

A

villous 3x higher than tubular

104
Q

polyp size

A

<1.0 cm : negligible(<2%)
1.5-2.5 cm : intermediate(2-10%)
>2.5 cm : substantial(>10%)

105
Q

polyp gross w/ higher risk

A

sessile > pedunculated

106
Q

AdenoCA sequence

A

normal colon -> daily mutagen or carcinogens -> chromosomal abnorm -> build up -> hyperprolif of colonic ell -> adenoma -> dysplasia -> adenoCA

107
Q

majority of colon CA arise in ________

A

left side (60%)
descending colon, rectum

108
Q

s/s of colon CA in the cecum and ascending colon

A

anemia
palpitation
weakness
possible occult blood

109
Q

s/s of colon CA in the transverse and descending colon

A

obstruction (distention, ab pain) “apple core deformity”
perforation

110
Q

s/s of colon CA in the recto sigmoid

A

tenesmus (painful straining)
narrowing stool caliber
hematochezia

111
Q

mets of colon CA

A

regional LN
liver
lungs or supraclavicular LN via paravetebral veins

112
Q

how many # of positive tumor cells = marker of microscopic spread

A

> 5

113
Q

rectal bleed

A

red -> loc: small bowel, colon
black -> loc: upper GI

114
Q

hard large stool followed by dripping of blood _______

stool is watery and bloody ______

A

anorectal area

lesion might be higher

115
Q

ab pain
pain in the lower ab are often relieved by passage of stool or flatus

pain deep in the pelvis
pain in perineum

A

rectal pain
anal canal pain

116
Q

herniations or sac-like protrusions of mucosa
incidental finding during colonoscopy
males at younger age
50% of affected px > or = 60 yrs
non-existent in the rectum bec of smooth m

A

diverticula of colon

117
Q

most common loc of colon diverticula

A

left side -> sigmoid colon
in the taenia (weak part)

118
Q

pathophy of colonic diverticula

A

colonic circ is supplied by nutrient artery -> nutrient artery penetrates muscularis -> becomes a weak point -> colonic pressure inc -> force the mucosa to herniate out -> diverticula

119
Q
  • mechanical retention of food residue and bacteria in the diverticulum
  • left (3x) > right
  • obstipation, tender on LLQ, fever
A

diverticulitis

120
Q

colonoscopy in diverticulitis is not advised

A

pushing the scope inside -> may ppt perforation

121
Q
  • recurrent LLQ colicky pain w/o signs of diverticulitis
  • relieved by defecation or passage of flatus
  • alternate constip diarrhea
A

painful diverticular disease w/o signs of diverticulitis

122
Q
  • most common cause of painless bleed in px > 60 yo
  • 20% of px w/ diverticula
  • common in right colon
A

bleeding diverticulitis

123
Q
  • diagnostic and therapeutic for bleeding diverticula
  • plug vessel to stop bleeding
A

angiographic treatment
embolization

124
Q
  • ab pain or discomfort w/ disturbed defecation
  • absence of structural abnorm
  • usual loc: lower GIT
  • female, onset of sympt <45 yo, whites, blacks, nonhispanic whites>hispanic whites
A

IBS

125
Q
  • dx for IBS
  • recurrent ab pain, at least 1 day/week
A

Rome IV criteria (2016)

126
Q

IBS commonly presenting Type 1 and 2 bristol stool
IBS commonly presenting Type 6 and 7 bristol stool
IBS commonly presenting Type 1 and 6 bristol stool

A

IBS-C
IBS-D
IBS-M

127
Q

pathophysio of IBS

A
  • altered colonic and small intestine motility

for IBS-D (VS IBS-C)
- inc high amplitude propagated contractions (HAPC’s)
- enhanced gastro-colic response
- rectal hypersensitivity
- Li and Si transit acceleration

128
Q
  • rectal distension causes more pain
  • 60% of IBS px
  • abnormal sensitization within dorsal horn of spinal cord or higher CNS
A

visceral hypersensitivity

129
Q

fermentable oligo, di, monosac, and polyols

A

fodmap

*if px is dx w/ IBS = avoid high fodmap diet

130
Q
  • slow or non-digested substances osmotically active
  • fermented in the colon - abdominal bloatedness
A

high fodmap

131
Q

drug/s for IBS-D

A

anti-diarrhea
TCA e.g., desipramine
alonsetron-5-ht3 antagonist

132
Q

drug/s for IBS-C

A

SSRI e.g., paroxetine
serotonin type 4 receptor antagonist e.g., tegaserod

IM MOD-B (5 decks)

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