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HD4 > GI > Flashcards

GI Flashcards

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

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

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

A

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

22
Q

Rome 3 Criteria

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

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
Q

Rotavirus

A

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
Q

Salmonella Typhi

A

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
Q

Unique characteristics of Rotavirus organism

A

Hardy! non-enveloped, has complex replication process –> evades natural human defenses!

27
Q

major functions of the Liver

A
  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
Q

Use of serum albumin as liver function test

A

NON-specific indication of hepatic function,
~long half-life
Affected by: synthesis, distribution, and catabolism

29
Q

Liver Function tests

A
  1. Serum albumin
  2. INR
  3. Bililrubin
30
Q

Liver enzyme tests

A
  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
Q

Common locations for varices

A
  • Esophageal (v. to azygous v.)
  • Umbilical v.
  • Inferior mesenteric & Superior hemorrhoidal v. (to IVC)
  • Retroperitoneal v. (to IVC)
32
Q

Zenker’s Diverticulum

A

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
Q

Midthoracic Diverticula

A

true diverticulum of middle esophagus,

due to mediastinal inflammation/infection (fungal, TB), or dysmotility (achalasia, diffuse esophageal spasm)

34
Q

Epiphrenic diverticula

A

true diverticulum of distal esophagus due to motility disorders (achalasia, diffuse esophageal spasm)

35
Q

primary vs. secondary peristalsis (of esophagus)

A

Primary peristalis: controlled by central NS, triggered by swallowing

Secondary peristalsis: controlled by central & peripheral NS, triggered by distention of esophageal wall.

36
Q

Deglutative inhibition

A

inhibition of skeletal muscle of esophagus OR relaxation of the LES during rapid consecutive swallows (chugging)

37
Q

2 possible etiologies for esophageal reflux

A
  1. decreased LES tone (LES = Lower Esophageal Sphincter)
    * promoted by gastric distention
  2. hernia (not enough pinching of LES by diaphragm)
38
Q

Achalasia vs. Scleroderma vs. Diffuse Esophageal Spasm

A

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
Q

Nutcracker Esophagus

A

aka: hypertensive peristalsis.
condition of HIGH force contractions when peristalsis occurs
=> increased amplitude &/or duration of contractions.

40
Q

NERD

A

“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
Q

3 phases of Fasting Motor Complex

A

= 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
Q

GI emptying/motility rates

A

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
Q

gastroparesis (Defn, Dx, Tx)

A

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
Q

Causes of gastroparesis

A

Diabetes, post-surgical, meds, idiopathic, etc.

45
Q

Factors affecting colonic transit time:

A
  1. outlet obstruction (ie: incomplete relaxation of puborectalis m.)
  2. pelvic floor weakness
  3. voluntary suppression
46
Q

Charcot’s Triad

A

RUQ pain, fever, & jaundice

=> in 60% of Ascending Cholangitis cases (inflamed common bile duct)

47
Q

Reynold’s Pentad

A

Charcot’s triad (RUQ pain, fever, jaundice) AND hypotension, confusion
= sign of sepsis from ascending cholangitis

HD4 (6 decks)

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