pom from jennifer-Abdominal Pain Flashcards
o Nociceptors – free nerve endings present throuought the entire thickness of the bowel. However, there are fewer number of receptor nerve endings in the viscera than say, on the skin (somatic receptors).
• Cell bodies of these free nerve endings are in the DRG
o The principle signal is mechanical stretch; these receptors are found primarily between the circular and longitudinal muscle layers in the myenteric plexus
o Chemical nociceptos predominate in mucosa/submucosa
• Affernent pathways:
o Unmyelinated C fibers – mainly responsible for transmission of visceral sensation
o Myelinated Aδ fibers – small, primarily mediate parietal pain
o The fibers run with regional splanchnic nerves through the sympathetic chain, and terminate in dorsal horn
o Afferent fibers synapse above and below level of entry (Somatic afferents synapse mainly at one level). This results in an incoming signal that is poorly localized. From here, sensation is carried cranially via the spinothalamic, spinoreticular and dorsal column tracts. It’s then relayed to the thalamus and projected to the cerebrum where the “mapping” is done by somatosensory cortex.
• Spinoreticular pathways make multiple synapses in the RAS→ modulates pain related arousal
• Remember: spinothalamic tracts cross immediately, while the dorsal column tracts ascend ipselaterally
• Efferent pathways:
o Descending modulation of pain; primarily inhibitory in nature [enkephalins – endogenous opioids]
o The inhibitory pathways project onto the dorsal horn and modify the afferent input from the gut, and descend down the cord through spinal nerves thru both sympathetic and parasympathetic means.
• Ex: if there was an obstruction, parasympathetic efferents would stimulate peristalsis.
• Ex: if there was a noxious stimulus, parasympathetics would elicit secretions.
• Referred pain – pain that is felt at a remote site away from the diseased organ.
o Results when visceral and somatic afferent neurons from a different anatomic region converge on second order neurons in the spinal cord at the same spinal segment (central convergence).
o All spinal neurons that receive afferent input from the viscera also receive input from the skin.
o The brain attributes pain from a convergent pathway to the corresponding somatic site.
• Ie., it reads the visceral pain as coming from the skin dermatone.
• Chronic visceral pain:
o There is sensitization of the secondary neuron from the constant visceral impulses; this is translated into exaggerated reponse to inccocuous somatic stimuli →hyperalgesia and allodynia
• Allodynia= a pain due to a stimulus which does not normally provoke pain (ie: light touch).
• Hyperalgesia of muscle is often accompanied by spasm (ex: gaurding/rigidity).
o Kehr’s sign – Ipsilateral subdiaphragmatic irritation causing pain in the shoulder or supraclavicular areas.
A. Self limiting, resolved in a short period (i.e. gastroenteritis)
o B: Colicky pain, happens with obstruction and peristaltic activation.
C: Progressively worsening pain (i.e. appendicitis)
o D: Catastrophic onset, sudden onset of very severe pain (i.e. ruptured aortic aneurysum or perforation).
• Qualifying characteristics in the history: (oldcarts) Site/radiation; origin, duration, progression; Nature (burning, crampy, boring); aggravating and alleviating factors; association with other symptoms.
• Inspection: Look for signs of Peritonitis (quiet abdomen), Cullen’s sign (bruised belly button), Frank Turner’s sign (retroperitoneal hemorrhage), distension/mass. Hernia, diastasis recti [separation of the rectus abdominis muscle into right and left halves].
• Palpation/Percussion : Guarding, rigidity, rebound tenderness, Murphy’s sign (gallbladder), Rovsing’s sign (appendix – push on left and the right side hurts).
o Carnett test – to determine if abdominal pain is arising from the abdominal wall or has intraabdominal origin. Patient asked to raise head (like doing a crunch) so abdominal musculature is tensed. If greater tenderness on repeat palpation, the test is positive and suggests abdominal wall pathology.
• Positive in Chronic Abdominal wall syndrome (depressed, obese women usually
• Auscultation:
o Hypoactive or absent sounds – think peritonitis. More ominous
o Hyperactive – think enteritis, colitis, or early obstruction.
epigastric pain, may radiate to back. gnawing/burning pain lasting for 1-3 hours. Food aggravates a gastric ulcer. Duodenal ulcer is more likely nocturnal, and relieved by eating.
PEPTIC ULCER
epigastric pain radiates to the back, severe pain relieved by sitting upright/leaning forward – separating pancreas from the rest of the abdominal cavity), often nausea and vomiting and associated ileus.
o Meals typically aggravate symptoms.
• Intestinal angina (or mesenteric ischemia
• Acute pancreatitis
– post prandial pain (after eating), occurs in individuals with insufficient blood flow to meet mesenteric visceral demands; + weight loss/ often have aversion to food. Frequently want to evacuate bowels, but often feel incomplete evacuation [Tenesmus]. Sign of colitis.
• Intestinal angina (or mesenteric ischemia)
dull in epigastric, often radiates to RUQ and right shoulder/infrascapular area, (+) Murphy’s sign.
o Obstruction of cystic duct or bile duct→ ↑ intraluminal pressure→ repetitive biliary contractions
o Chronic cholecystitis Boa’s sign: hyperesthesia in right infrascapular region→ phrenic nerve irritation, irritation of cutaneous nerves in referred dermatome
• Biliary pain
PANT (Pain, anorexia, nausea, and tenderness). Initially pain is periumbilical, then becomes more localized in the RLQ at McBurney’s point (2/3 of the way from umbilicus to ASIS).
• Appendicitis
Deep lesions in the liver parenchyma are typically painless, Hepatic pain is produced by stretching of the Glisson capsule (inflammation, vascular engorgement, rapidly expanding lesions underneath surface
• Hepatic pain
LUQ; occurs when splenic enlargement causes stretching of capsule, splenic infarct (sickle cell)
• Splenic pain:
