Abdo pain and diarrhea high yield Flashcards
____ is the principal signal in the ENS
Mechanical stretch
C fibers are ____ and mainly responsible for; A delta fibers are ____ and responsible for
unmyelinated; transmission of visceral sensation;
small and myelinated, parietal pain transmission
Descending fibers modulating pain are
predominantly inhibitory; can project on dorsal horn and modify or control the afferent input from the gut
Referred pain:
visceral afferent neurons and somatic afferent neurons converge on second order neurons in spinal cord (central convergence)
Hyperalgesia and allodynia come about from; hyperalgesia often accompanied by
sensitization of secondary neurons from chronic visceral impulses;
spasm
Kehr’s sign:
subdiaphragmatic irritation-ipsilateral shoulder or supraclavicular pain
Carnett Test:
Ask patient to raise head and tense the abdo musculature; if greater tenderness on repeat palpation, test is positive and suggests abdo wall pathology
Hypoactive/absent bowel sounds are;
Hyperactive is
peritonitis;
enteritis, colitis, early part of obstruction
Peptic ulcer:
- epigastric, can radiate to BACK
- gnawing, burning
- gastric: food can aggravate it
- duodenal: nocturnal, relieved by eating
Pancreatitis:
- epigastric, can radiate to back
- deep boring, severe, longer lasting than peptic ulcer
- meals aggravate
- relived by sitting UPRIGHT
- N/V usually positive
Obstruction of hollow viscera described as
colicky pain (small bowel obstruction either supra or periumbilical; chronic obstruction infraumbilical with lumbar rad)
Intestinal angia:
- post prandial (not enough blood flow to meet mesenteric visceral demands)
- sitophobia (aversion to food)
- tenesmus
- frequent and often painful inclination to evacuate bowels with feeling of incomplete evacuation
Biliary pain:
referred pain in right infrascapular region; (Boa’s sign with hyperesthesia in right infrascapular region) with ongoing inflamm, becomes more localized in RUQ;
acute cholecystitis with pos Murphy’s sign
Hepatic pain can be caused by; splenic pain can be caused by
stretching of Glisson capsule;
stretching of capsule or splenic infarct (sickle cell)
Appendicitis:
symptoms are pain, anorexia, nausea, tenderness (PANT); initially periumbilical and then becomes more localized in RLQ
In young female with acute abdo pain;
with upper abdo pain,
rule out ectopic pregnancy;
keep cardiac and respiratory differentials in mind
Median arcuate ligament syndrome (MALS)/Celiac artery compression syndrome
Here, ligament is anterior, leading to compression and irritation of celiac ganglion;
bruit in epigastric region and can have pain after eating
IBS:
recurrent abdo pain or discomfort greater than 3 days/mo in last 3 mos with 2 or more of improvement with defecation, onset associated with change in frequency/form of stool
Thera approach for abdo pain:
opiates, NSAIDs, topical like lidocaine patch or injections;
TCA’s, anticonvulsants, baclofen
Secretion occurs primarily in; absorption in
crypts;
apical epi cells
Two key components in colon ion transport mechs:
electroneutral NaCl absorption, and electrogenic Na absorption
Short chain fatty acids absorbed in colon by
diffusion or anion exchange; BUTYRATE the preferred energy source for colonocytes
Some NT’s released by enteric neurons:
VIP and ACh (both can stim epi cells to secrete Cl)
Acute diarrhea is; chronic diarrhea is
less than 4 wks; greater than 4 weeks (if chronic, unlikely infectious)
Osmotic diarrhea:
Increased osmotic load, no component of increased secretion; think maldigestion and malabsorption syndromes with no nocturnal episodes
What two numbers can tell you secretory vs. osmotic diarrhea?
Sec: stool osmolar gap less than 50, stool Na over 90; could see nocturnal episodes
Osmotic: over 125, less than 60
Two examples of osmotic diarrhea; also includes:
- Cholestasis
- Pancreatic insufficiency;
celiac disease, lactose intolerance, infections;
lactulose, miralax, acarbose, colchicine, PEG
Intestinal secretory mechs:
Electroneutral: Cl/bicarb exchanger at apical membrane;
electrogenic mech: through CFTR channels;
bicarb secretion most prominent at prox duodenum
Bile salt diarrhea induces
secretory diarrhea, or fat malabsorption and steatorrhea (former with normal serum bile acids and high fecal bile acids; latter with low serum bile acids and low fecal bile acids, with stool having fat)
What can cause secretory diarrhea?
Lubiprostone (activates Cl channel), linaclotide (cGMP mediated activation of CFTR channels)
Inflamm diarrhea:
secretion/reabsorption balance affected (toxin-mediated with cytotoxins with abdo pain and can be watery with occasionally bloody diarrhea, enteroadherent, invasive)
V cholera with
cAMP mediated toxin action (increases Cl channel secretion)
Enterohemorrhagic E coli: what is contraindicated?
Antibiotics
Spurious diarrhea
most common cause of diarrhea in practice
For treatment of diarrhea, think
rehydration as the priority (oral as good as IV);
maybe antimotility agents like loperamide (opiate with high first pass effect);
adsorbents like bismuth that can bind enterotoxins;
antibiotics shouldn’t be used with EHEC