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GI Flashcards

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0
Q

Osmotic vs. Secretory Diarrhea

A

Osmotic: >125 stool osmolar gap, ingestion of a poorly absorbed cmpd (or loss of nutrient absorption, ie: lactose intolerance)

Secretory: <60 stool osmolar gap, wider range of causes (esp. internal disorders)

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1
Q

pathophysiologic mechanisms of digestion => maldigestion

A
  1. Liberation (chewing and salivary enzymes)
  2. Digestion (breakdown on food particles)
  3. Solubilization (bile effect on fat)
  4. Chemical Change (specific pH for absorption)
  5. Mucosal Absorption (enough SA & contact time)
  6. Sensory/Motor function (contact time & mixing)
  7. Transport (via lymphatics)
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2
Q

Visceral abdominal pain

A

poorly localized territory of pain, usually dull/gnawing,
- gradual onset & long duration
- along midline
+/- ANS Sxs (nausea/vomiting, sweating, pallor, shaking)
* transmitted by C fibers

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3
Q

Somatic parietal abdominal pain

A

More specific pain from skin, muscle & parietal peritoneum

  • acute/sudden,
  • sharp
  • Well-localized, often lateralized
  • via a-delta fibers (travel along spinal somatic nerves)
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4
Q

Alarm symptoms w/ abdominal pain

A
  1. fevers
  2. weight loss
  3. jaundice
  4. overt gastrointestinal bleeding (hematemesis, hematchezia, melena)
  5. anemia (acute hemorrhage or chronic severe nutritional def.)
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5
Q

hematochezia

A

= stools with bright red blood in them

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6
Q

main etiologies of pancreatitis

A
  1. Alchoholism
  2. Biliary cholecystitis/bile duct & pancreatic duct obstruction
  3. autoimmune
  4. hypertriglyceridemia
  5. congenital variants of pancreatic drainage structures (divisum, may need additional predisposing factor)
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7
Q

Right Upper Quadrant abdominal pain = from…?

A
  1. Liver
  2. Gallbladder –>cholecystitis
  3. kidney –> pyelonephritis
  4. Diapragm –> pneumonia
    Also: colon (hepatic flexure & transverse), duodenum, pancreas (head), stomach pylorus
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8
Q

Left Upper Quadrant abdominal pain = from…?

A
  1. stomach
  2. spleen –> splenic infarct
  3. pancreas –> pancreatitis
  4. aorta
  5. kidney –> pyelonephritis
  6. diaphragm –> pneumonia
  7. colon (transverse, splenic flexure)
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9
Q

Right Lower Quadrant abdominal pain = from…?

A
  1. Appendix –> appendicitis
  2. terminal ileum –> IBD
  3. ovary *hernia
  4. kidney
  5. colon (cecum)
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10
Q

Left Lower Quadrant abdominal pain = from…?

A
  1. Colon (descending/sigmoid) –> diverticulitis (#1)
  2. ovary
  3. kidney –> pyelonephritis
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11
Q

structures associated with epigastric pain:

A
  1. heart –> MI, aneurysm
  2. esophagus –> esophagitis
  3. stomach
  4. pancreas –> pancreatitis
  5. small bowel, transverse colon
  6. gallbladder –> cholecystitis
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12
Q

structures (& disease) associated with periumbilical pain:

A
  1. small bowel –> obstruction
  2. colon
  3. appendix –> early appendicitis
  4. aorta –> aneurysm,
    * mesenteric ischemia
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13
Q

structures associated with suprapubic pain

A
  1. ovaries, uterus
  2. bladder –> UTI
  3. small bowel –> IBD
  4. colon –> diverticulitis
  5. kidneys
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14
Q

DDx for diarrhea

A

NOT bloody: Celiac, pancreatic insuff, IBS, infection, tumors (endocrine, colon)
Bloody: infection/STD, NSAIDs, colorectal cancer, ischemic bowel, acute GI bleed

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15
Q

Use of Aminosalycilates for IBD

A

(ie: sulfathalazine)
#1 to achieve & maintain remittance
bc anti-inflammatory via multiple mechs

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16
Q

Use of Immunomodulators for IBD

A

1 = Azathioprine/6MP (also methotrexate, tacrolimus, cyclosporine)

effective -> maintain remittance & preventing complications,
* esp. post-surgery.
=> Tx of choice for moderate Ulcerative colitis OR Crohns

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17
Q

anti-integrin therapy for IBD

A

= humanized IgG4 monoclonal Ab -> blocks leukocyte adhesion & migration.
BUT $$$$, need to use long-term for benefit.
=> only use if moderate/severe IBD, refractory to other Txs

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18
Q

link between EtOH and acute pancreatitis

A

EtOH causes increased inflammation by:
1. increase sensitivity to inflamm. markers (NF-kB)
2. decrease caspase expression (less apoptosis)
3. increase trypsin activation (via cathepsin B)
4. decrease microperfusion
5. synth of FA ethyl esters
(-> high intracel. Ca -> mito injury -> less ATP => necrosis)

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19
Q

relationship between hypertriglyceridemia and acute pancreatitis

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A

=> pancreatic injury -> inflamm –> pancreatitis

  1. Lots of free FAs -> acinar injury
  2. excess chylomicrons -> capillary plugging -> ischemia
  3. excess trypsinogen activation -> autodigestion
20
Q

rating severity of acute pancreatitis

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A

Mild: no organ failure, no complications
Moderate: a) transient organ failure OR b) local/systemic complications but no organ failure
Severe: persistent organ failure, may be multi-organ.

21
Q

types of complications from acute pancreatitis

Study These Flashcards
A

Early (4 wks): pseudocyst, walled-off necrosis

22
Q

Rome 3 Criteria

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A

criteria for diagnosis of IBS:

  1. recurrent abdominal pain/discomfort at least 3 days/wk for 3+ months
  2. relieved with bowel mvmts
  3. onset associated with change in frequency OR consistency of stools
23
Q

Norovirus

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A

1 cause of diarrhea (explosive!)
* Fecal-oral spread, 24-48 hr incubation period
Dx: clinical signs
Tx: supportive (self-limited) *Hx of infection => partial immunity

24
Rotavirus
HIGHly widespread cause of dehydrating diarrhea, esp. in young kids. *peak: 6-24 months old. Spread: person - person. Dx: clinical (likely present w/ significant dehydration) Tx: supportive therapy, #1 = fluids (oral if mild/mod; IV if severe) * vaccines available but some risk of intestinal intussiception
25
Salmonella Typhi
Cause of systemic infection w/ fever (#1) and abdominal pain, +/- diarrhea OR constipation. + coated tongue & splenomegaly. Spread: fecal contamination (food or water-borne) Dx: culture blood, bone marrow, or stool/duodenal secretions Tx: antibiotics (quinolones, 3rd gen. cephalosporins) *increased risk severe illness if immuno-compromised or co-infection
26
Unique characteristics of Rotavirus organism
Hardy! non-enveloped, has complex replication process --> evades natural human defenses!
27
major functions of the Liver
1. Synthesis (albumin & coag factors) 2. Metabolism 3. Biotransformation (bilirubin conjugated for excretion) 4. Bile salt synthesis 5. reticulo-endothelial f(x) (clear drugs, etc.) 6. Storage (glycogen, copper)
28
Use of serum albumin as liver function test
NON-specific indication of hepatic function, ~long half-life Affected by: synthesis, distribution, and catabolism
29
Liver Function tests
1. Serum albumin 2. INR 3. Bililrubin
30
Liver enzyme tests
1. ALT (more specific to liver) 2. AST (less specific, more affected by mitochondrial diseases) * may be increased after injury/disease in cardiac or skeletal muscle
31
Common locations for varices
- Esophageal (v. to azygous v.) - Umbilical v. - Inferior mesenteric & Superior hemorrhoidal v. (to IVC) - Retroperitoneal v. (to IVC)
32
Zenker's Diverticulum
True diverticulum (all 3 layers) of proximal esophagus, bc poor relaxation of UES => herniation through posterior pharyngeal wall (Killian's triangle) *MOST common. Complications: aspiration pneumonia, bleeding, rupture
33
Midthoracic Diverticula
true diverticulum of middle esophagus, | due to mediastinal inflammation/infection (fungal, TB), or dysmotility (achalasia, diffuse esophageal spasm)
34
Epiphrenic diverticula
true diverticulum of distal esophagus due to motility disorders (achalasia, diffuse esophageal spasm)
35
primary vs. secondary peristalsis (of esophagus)
Primary peristalis: controlled by central NS, triggered by swallowing Secondary peristalsis: controlled by central & peripheral NS, triggered by distention of esophageal wall.
36
Deglutative inhibition
inhibition of skeletal muscle of esophagus OR relaxation of the LES during rapid consecutive swallows (chugging)
37
2 possible etiologies for esophageal reflux
1. decreased LES tone (LES = Lower Esophageal Sphincter) * promoted by gastric distention 2. hernia (not enough pinching of LES by diaphragm)
38
Achalasia vs. Scleroderma vs. Diffuse Esophageal Spasm
Achalasia: increased basal LES tone & incomplete relaxation, & uncoordinated peristalsis Scleroderma: normal LES & prox. peristalsis, but weak/no distal peristalsis Diffuse Esophageal Spasm: simultaneous contraction of >10% esophagus. +/- LES abnormalities
39
Nutcracker Esophagus
aka: hypertensive peristalsis. condition of HIGH force contractions when peristalsis occurs => increased amplitude &/or duration of contractions.
40
NERD
"Non-Erosive/Negative Endoscopy Reflux Disease" = GERD Sxs, BUT no evidence of mucosal damage/erosion. * most common presentation of GERD (vs. erosive esophagitis or Barrett's esophagus) * may have visceral hypersensitivity
41
3 phases of Fasting Motor Complex
= to clear secretions from GI tract. Cyclic, every 60-90 min. 1. quiescence 2. intermittent pressure activity 3. active front (high freq. contractions in stomach & intestines)
42
GI emptying/motility rates
Stomach: liquids faster than solids, 3-4 hrs for solids Small Intestine: liquids & solids = same rate, rate proportional to # calories from meal (1 hr/200 calories ingested) Colon: high amplitude contractions 5-6 times/day (36 hr transit time)
43
gastroparesis (Defn, Dx, Tx)
chronic delayed gastric emptying w/ no mechanical obstruction Dx: 1. rule out obstruction, 2. scintography, 3. try Tx(s) Tx: diet/lifestyle changes #1, pro-kinetic meds, gastric pacing or surgery if severe & persistent
44
Causes of gastroparesis
Diabetes, post-surgical, meds, idiopathic, etc.
45
Factors affecting colonic transit time:
1. outlet obstruction (ie: incomplete relaxation of puborectalis m.) 2. pelvic floor weakness 3. voluntary suppression
46
Charcot's Triad
RUQ pain, fever, & jaundice | => in 60% of Ascending Cholangitis cases (inflamed common bile duct)
47
Reynold's Pentad
Charcot's triad (RUQ pain, fever, jaundice) AND hypotension, confusion = sign of sepsis from ascending cholangitis

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