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Course 1 > GI > Flashcards

GI Flashcards

1
Q

Characteristics of Crohns

A

Transmural, gum-bum, skip lesions, mostly ileal

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2
Q

How does Crohns present?

A

Pain, diarrhea, abscess/fistula, wt loss

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3
Q

What are the features of UC?

A

Mucosal, extends from rectum, colon only

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4
Q

Symptoms of UC

A

Urgency, tenesmus, bleeds/diarrhea, nocturnal, fever, wt loss

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5
Q

How is ASUC defined?

A

> 6 bloody BM/day, systemic toxicity

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6
Q

Extra-GI manifestations of IBD

A

Oral ulcers, uveitis, erythema nodosum, pyroderma gangrenosum, sweet’s (fever, neutrophilia, red papules), arthropathy, PSC, CRC

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7
Q

What should you not give patients with IBD?

A

NSAIDS

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8
Q

What concurrent infections indicate high risk UC?

A

CMV, C diff

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9
Q

Why is structuring Crohns a surgical emergency?

A

Can cause complete obstruction

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10
Q

What is the nature of UC surgery?

A

Curative

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11
Q

What are indications that surgery is required in UC?

A

Toxic mega colon, fulminant colitis, sepsis, perforation, hemorrhage

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12
Q

What is fulminant colitis?

A

Doesn’t respond to medical therapy

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13
Q

When is dysplasia in UC an indicator for surgery?

A

Lesions cannot be remixed endoscopically, high grade dysplasia confirmed by 2 pathologists, CRC

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14
Q

What does Truelove&Jewell state about patient conditions after medical therapy?

A

Improvement-stay the course
Deteriorate-surgery
Unchanged-biologics/surgery

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15
Q

How can you tell if medical management for UC is unsuccessful?

A

> 8bm/day, CRP>45, blood, formless stool, clinical deterioration, no improvement by day 5

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16
Q

What major risk is associated with extended steroid use?

A

Immune suppression

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17
Q

What disease location of crohns has the highest risk of relapse post-op?

A

Ileocolic

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18
Q

What are endoscopic hallmarks of Crohns?

A

Cobblestoning, creeping fat, transmural inflammation

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19
Q

What is the nature of surgery for Crohns?

A

Non-curative

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20
Q

What should you be mindful of when performing surgery from Crohns?

A

Preserve length to avoid morbidities

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21
Q

What are indications for surgery in Crohns?

A

Obstruction, fistula, perforation, bleeding, stricturing

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22
Q

How does the likelihood of Crohns and UC needing surgery change with age?

A

Increased surgical need if younger when diagnosed

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23
Q

How does smoking affect IBD?

A

Worse for Crohns, better for UC

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24
Q

What extraGI manifestations of Crohns will NOT improve with resection?

A

PSC, cirrhosis

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25
Q

How is perianal Crohns treated?

A

Drain abscess, sew seton in place to fight infection

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26
Q

What are vascular cushions?

A

Blood vessel, connective tissues, smooth muscles along anal canal, protect against hemorrhoids

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27
Q

Causes of hemorrhoids

A

FHx, increase intra-abd pressure, vascular enforcement, stretching of muscular support

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28
Q

How do you treat hemorroid disease?

A

Fiber (Metamucil)

Rubberband ligation (sclerotherapy), hemorrhoidectomy

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29
Q

What is the dentate/pectinate line?

A

Transition zone from rectal mucosa (columnar) to perianal skin (squamous)

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30
Q

Where is the internal hemorrhoidal plexus located?

A

Above dentate line, no pain

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31
Q

What are the features of internal hemorrhoids?

A

Prox dentate line, columnar epithelial, visceral innervation (bleed, prolapse, protrude, no pain)

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32
Q

What is stage IV internal hemorrhoid?

A

Protrusion that cannot be manually pushed back

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33
Q

What are the features of external hemorrhoids?

A

Distal dentate line, squamous epithelium, somatic innervation (localized pain, swelling, thrombose)

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34
Q

What is an anal fissure?

A

Tear in anoderm by hard stool/dry skin, cause irritation and spasm of internal sphincter (ischemia)

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35
Q

How do you treat TEH (thrombosed external hemorrhoids)?

A

Fiber, sitz bath

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36
Q

What are features of chronic anal fissure?

A

Sentinel tag, hypertrophic anal papilla, exposed internal sphincter fibers

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37
Q

Causes of acute anorectal pain

A

Fissure, TEH, abscess (or cancer)

Don’t do DRE

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38
Q

What is pilonidal disease?

A

Chronic infection of skin and subcutaneous tissues of upper natal cleft

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39
Q

Do hyperplastic polyps have dysplasia?

A

No

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40
Q

What are invasive adenocarcinomas?

A

Invasive glands

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41
Q

Are are post-op UTIs treated?

A

Cipro

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42
Q

What is thumb printing an indication of?

A

Bowel inflammation

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43
Q

Overgrowth of what organism causes psrudomembrane colitis? Where does this happen?

A

C diff, large intestine

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44
Q

How is pseudomembrane colitis treated?

A

Vancomycin

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45
Q

The visceral nervous system is sensitive to which stimuli?

A

Stretch, contraction, inflammation, ischemia

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46
Q

What is the nature of visceral pain?

A

Diffuse, dull, colic, unaffected by movement

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47
Q

What is the nature of somatic pain?

A

Sharp, localized, worse with movement

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48
Q

Peritonitis, appendicitis, diverticulitis are all examples of

A

Somatic pain

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49
Q

What is the most common cause of acute abd pain?

A

Appendicitis

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50
Q

What is the pathophysiology of appendicitis?

A

Obstruction, increased lumen pressure, ischemia, bacterial invasion, irritation, parietal peritoneum involvement, necrosis, perforation with peritonitis and abscess

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51
Q

Causes of appendix obstruction

A

Fecalith, lymphoid hyperplasia, fibrosis, foreign body, neoplasia

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52
Q

Symptoms of appendicitis

A

Anorexia, periumbilical pain—>RLQ, nausea, high WBC (bandemia)

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53
Q

What is the best imaging for appendicitis?

A

CT

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54
Q

What is obstipation?

A

Inability to pass gas

55
Q

Colonic diverticula are true/false diverticula?

A

False diverticula (mucosa and submucosa)

56
Q

What signs on auscultation indicate bowel obstructions?

A

High pitched sounds, lack of sounds

57
Q

What is the most common cause of bowel adhesion?

A

Surgery

58
Q

What imaging should be following after percussion a tympanic abdomen? Dull?

A

CT, US

59
Q

What are some presentations of bowel volvulus?

A

Bloody stool, no sepsis (septic fluid cannot leave twist)

60
Q

What is the most common form of bowel obstruction?

A

Adhesion

61
Q

What is intussusception?

A

Telescoping of two segments of bowels that cause obstruction

62
Q

If strictures are seen in UC, what should we suspect?

A

Cancer (mucosal damage should not cause stricturing)

63
Q

How do symptoms of distal and proximal bowel obstructions differ?

A

Distal: more pain and distension
Proximal: more emesis, less tenderness

64
Q

What is an ileus?

A

Lack of bowel movement

65
Q

What can cause an ileus?

A

Acute peritonitis, intestinal dysmotility, severe constipation

66
Q

What laboratory results point towards a bowel obstruction?

A

Hypokalemia, hypochloremia, metabolic acidosis (Lose ions bc body tried to conserve water)

Increased hematocrit, Hb, WBC

67
Q

How do the causes of SB and LB obstructions differ?

A

SB: adhesion, hernia
LB: cancer, IBD, diverticulitis

68
Q

What type of bowel obstruction is associated with aortic aneurysms?

A

Ischemic colitis

69
Q

What part of the bowel is the earliest to be affected by ischemia?

A

Antimesenteric mucosa

70
Q

What are symptoms of ischemic colitis?

A

Pain out of proportion with physical findings, distension, NV, bloody stool if colonic or rectal, sepsis if transmural

71
Q

Tx for ischemic colitis

A

Thrombolysis, heparin, antibiotics, hydration, resection if full thickness necrosis

72
Q

Where does an arterial embolus cause obstructions?

A

Proximal jejunum to mid transverse colon (obstruct SMA at mid colic artery)

73
Q

What is portal venous gas associated with?

A

Full thickness necrosis

74
Q

What dietary modifications should IBS patients implement?

A

Gluten free, low FODMAPS, probiotics

75
Q

IBSD tx

A

Rifaximin, antispasmodics

76
Q

IBSC tx

A

Linaclotide(Increase fluids secretion and transit, decrease pain)

77
Q

Bloating vs distension

A

Bloating: feeling full/gassy

Distension: increased girth

78
Q

Ascites Tx

A

Low Na diet, diuretics (spironolactone), paracentesis

79
Q

What are the causes of exudate ascites (<11)?

A

Malignancy, pancreatitis, nephrotic, infection

80
Q

what are the two pathways of visceral sensation?

A

vagal and spinal

81
Q

what is the vagal pathway responsible for?

A

secretion, absorption, peristalsis

parasympathetic sensing

82
Q

what is the spinal pathway responsible for?

A

pain sensation

sympathetic sensing

83
Q

what is referred pain?

A

convergence of visceral and somatic afferents at same spinal level

84
Q

what pain stimuli are the guts sensitive to?

A

contraction, stretching, injury, ischemia, inflammation

85
Q

what is hyperalgesia?

A

exaggerated response to noxious stimuli

86
Q

what is allodynia?

A

innocuous stimulus perceived as noxious

87
Q

what nerve plexus is located between the two muscle layers of the esophagus? what is its role?

A

myenteric plexus (auerbach), regulate peristalsis

88
Q

what nerve plexus is located between the circular muscular layer and the submucosa? what is its role?

A

submucosal plexus (meissner’s), digestion control

89
Q

what role does the interstitial cells of cajal play?

A

perpetuate nerve signals

90
Q

5HT serotonin is release by what cell?

A

ECM cells

91
Q

what is gastroparesis?

A

impaired gastric emptying

92
Q

what red flag must we look for when dealing with motility disorders?

A

GIB, nighttime stooling, B symptoms

93
Q

what is the major difference between IBS and motility disorders in regards to pain?

A

IBS is defined by pain, motility problems do not include pain

94
Q

what are osmotic laxatives?

A

not absrobed in SB, cause water/electrolyte secretion, increase stool mass

include PEG, lactulose, milk of magnesia

95
Q

what are stimulant laxatives?

A

cause direct irritation of smooth muscle, lead to water/electrolyte secretion

diphenylmethane derivatives and anthrquinones

96
Q

how does linactotide work?

A

pro-secretory drug, activate CAMP and cause Cl- excretion (like cholera)

decrease abd pain (CAMP interact with nerves)

97
Q

how do bile acid sequestrants help with IBSD?

A

resorption of bile acids

98
Q

what drug class do opioids fall under?

A

Mu receptor agonists

99
Q

how do Mu receptors work on IBSD?

A

decrease Ach, increase NO (decrease paristalsis and slows motility, thus preventing stretch related pain)

100
Q

what drug classes help with nausea?

A

anti-histamine, ondansetron, prokinetics, D2RA, erythromycin

101
Q

what area of the brain is targeted by anti-nausea drugs?

A

CTZ

102
Q

what are the symptoms of gastroparesis?

A

early satiety, NV, bloating, upper bad pain, burning

103
Q

which form of nutrient is the preferred energy source?

A

carbs

104
Q

what is the most energy dense macronutrient?

A

lipids

105
Q

what is recommended daily intake of proteins?

A

10-35% of diet (0.6-0.8g)

106
Q

how many essential amino acids are there?

A

9

107
Q

what is the difference between soluble and insoluble fibre?

A

soluble: dissolves, slows gastric emptying/digestion, increase stool volume
insoluble: passes through bowels unchanged, speeds transit, increase stool wt

108
Q

what is the normal BMI range?

A

18.5-25

109
Q

which fatty acid is required to prevent EFAD?

A

linoleic acid

110
Q

when considering enteral feeding, when should bolus feeding never be used?

A

if feeding to jejunum

111
Q

which micronutrients will not be found in parenteral feeding?

A

Vit ADK, Fe

112
Q

what is the refeeding symdrome and what are its implications?

A

sudden increase in kcal in chronically malnourished patient

electrolyte abnormalities, volume overload, insuline resistance, cardiac arrhythmia

prevent by starting at 50% kcal needs

113
Q

where is ghrelin secreted from and what does it do?

A

stomach, increase appetite and lead to fat storage

114
Q

where is CCK released and what does it do?

A

SB, reduce intake

115
Q

where is PYY produced?

A

L cells throughout gut

116
Q

what is the result of leptin deficiency?

A

increased appetite and obesity

117
Q

which cytokine leads to decreased adiponectin secretion?

A

IL6

118
Q

what is the pathophysiology of cholera?

A

vibrio cholerae toxin activates CAMP, lead to Cl- efflux, draw water out of stool (secretory diarrhea)

119
Q

what combo is usually given to rehydrate patients?

A

water, glucose, sodium

120
Q

what components of digestion happen in the stomach?

A

pepsin (protein)
iron conversion to ferrous
IF production

121
Q

where is most fat absorbed in the body?

A

jejunum

122
Q

what transporter is responsible for the absorption of fluids?

A

Na+/glucose

123
Q

how does the laboratory testing for acute and chronic pancreatitis differ?

A

acute: elevated lipase
chronic: decreased lipase, elastase in stool

124
Q

where are bile salts resorbed?

A

ileum

125
Q

where do carb, protein, and lipid digestion start?

A

carb-mouth (amylase)
protein-stomach
lipids-SB

126
Q

how do function and organic abd diseases differ?

A

functional: disease of gut-brain interaction, no structural/metabolic abnormalities
organic: related to gut structure, disease based

127
Q

how is failure to thrive in children identified?

A

wt fall, ht fall, head circumference low

128
Q

should acid blockers be given to infants with GERD?

A

no

129
Q

how is EoE treated in kids?

A

steroids, dilatation

130
Q

what are the PE findings for celiac disease in kids?

A

FTT, distended stomach, Fe deficiency signs, diarrhea

131
Q

what increases the risk of celiac disease in kids?

A

trisomy 21, type 1 DM

132
Q

how does the presentation of peds IBD differ from adult IBD?

A

peds-more extensive disease

adults-more localized

133
Q

how are peds functional disorders treated?

A

clean out with PEG 3350 (osmotic laxative), include fiber in diet, dietary and behavioral changes

134
Q

what is the most common form of toddler’s diarrhea?

A

osmotic (surgar)

Course 1 (6 decks)

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