Abdominal CCP (king-2) Flashcards
characteristics of visceral pain
stimuli results in tension, stretching, ischemia
tissue congestion and ifm lower threshold for stimuli (sensitive n. ends)
B/L pain fibers
unmyelinated fibers
enter spinal cord at multiple levels (can’t localize)
visceral pain description
dull
poorly localized
felt midline
parietal pain characteristics
noxious stimulit to parietal peritoneum:
ischemia, ifm, stretching
transmitted via myelinated afferents to specific DRG:
on same side and same dermatomal level as original pain
parietal pain description
sharp
intense
localized
coughing/moving aggravates it
referred pain characteristics
like parietal pain but felt in remote area
supplied by same dermatome as affected organ
shares central pathway for afferent neurons from different sites
mesenteric lymphadenitis
inflammation of mesenteric LN (LN in stomach) CCP: difficult to differentiate from acute appendicitis caused by: beta hemolytic strep staph species e. coli strep viridans yersinia species (COMMON) mycobac TB viruses (EBV, rubella)
mes lymphadenitis epidemiology
misdx as appendicitis and pt undergo appy when they have mesenteric adenitis
benign
equal in genders, more yesinia in male
common in children <15
mes lymphadenitis tx
supportive care: hydration and pain mgmt
no antibiotics in mild cases
surgery if peritonitis dev, or is appy
direct/conjugated hyperbilirubinemia
uncommon
primarily biliary obs and metabolic disorders
indirect/unconjugated hyperbilirubinemia
more common (prehepatic like anemia)
neonatal hyperbilirubinemia
- inc bili load from:
- dec bili conjugation
- impaired bili excretion
causes of inc bili load
hemolysis non hemolytic: extravascular sources polycythemia exaggerated enterohepatic circulation
causes of hemolysis
RH incomp ABO incomp minor Ags (D type) RBC cell mem defects RBC enz defects Rxa Hb-opathies sepsis
RBC cell membrane defects
spheroctosis
elliptocytosis
RBC enz defects
G6PD
PK
hemoglobinopathies
sickle cell anemia
causes of extravascular sources
cephlohematoma
CNS hemorrhage
swallowed blood
bruising
causes of polycythemia
fetal-maternal transfusion
delayed cord clamping
twin-twin transfusion
causes of exaggerated enterohepatic circulation
CF ileal atresia pyloric stenosis breast milk jaundice Hirschsprung's disease (megacolon)
causes of dec bili conjugation
physiologic jaundice from breast feeding breast milk Gilbert's Criglar-Najar T1&2 hypothyroidism
causes of impaired bili excretion
biliary obstruction (Rotor’s, Dubin-Johnson, gall stones, biliary atresia, choledochal cyst, cancer, neoplasm, primary scleorsingcholangitis)
infection (sepsis, UTI, toxoplasmosis, syph, TB, rubella, herpes)
metabolic disorders (alpha 1 antitrypsin, CF, galactosemia, glycogen storage diseases, wilson’s)
chromosomal abnormalities (turner’s, trisomy 18 and 21)
drugs (ASA, acetaminophen, sulfa, EtOH, ery, tetracycline, steroids)
Coombs test
aka antiglobulin test (AGT)
tests for hemolytic anemia
pt’s blood sample is taken, plasma is washed away, then antihuman globulin is added, if RBC aggregation occurs, test is (+)
newborn bili production
6-8 mg/d
2x adult rate
declines in 10-14 d
why is hyperbilirubinemia more common in neonates?
RBCs have shorter life spans (80 days)
Hct is declining
immature liver uptake and conj of bili
inc enterohepatic circ increases intestinal reabs of bili and intestinal bac can de-conj bili allowing for reabs of bili into circulation
Heme deg pathway
RBC dies
Mph engulfs it, frees heme
Heme via heme oxidase to Fe and biliverdin
Biliverdin via reducatase to bilirubin
unconj bili bound to albumin into hepatocytes
conjugated with UDPGT into soluble form
jaundice clinically detected at?
5 mg/dL
inc direct and indirect bili
(-) coombs test
normal retic count
ddx: hepatitis metabolic disorder obs disorder sepsis
inc indirect bili
(-) coombs test
normal retic count
ddx:
physiologic
breast milk jaundice
familial non hemolytic jaundice (gilbert, crig-na)
inc indirect bili
inc retic count
ddx:
hemolysis due to ABO/Rh incomp
RBC defects (cell membrane or enzymatic)
physiologic jaundice
immaturity of liver b/w 24-72 hours peaks b/w 4-5 d (7 d in premies) gone by 10-14 days predom indirect levels never >12 mg/dl [those w/ risk factors, may rise to 17)
breast feeding jaundice
b/w 24-72 hrs, peaks 5-15 d of life, gone by week 3
cause: not enough mi;k intake=inadequate excretion of bile in stool
breast milk jaundice
appears d3-4, peaks d6-14
cause: idio, may be component of milk
dx if serum bili predom unconj
pathological jaundice
within 24 hrs inc in serum bili beyond 5 mg/dl/d peak above expected nml jaundice of >5mg/dl/d beyond 2 wks elevated conj bili
bili toxicity
unconj bili in brain
XS unconj is unable to bind albumin, crosses BBB, leads to asphyxia, acidosis, hypoxia, hypoperfusion, hyperosm, sepsis
toxic level of bili
> 25 mg/dl in term neo
kernicterus
irreversible
signs: 3-4d postnatal, lethargy, poor feeding, hypotonia
late signs: week 1, irritable, seizure, apnea, hypertonia, fever
chronic signs: encephalopathy (at age 3), cerebral palsy, high freq hearing loss, mild MR
tx for unconj hyperbili
- Monitoring: inc feeding, repeat levels frequently
- phototherapy: 1-2 d, conj bili into isomers to be excreted
- exchange transfusion: reduce bili in blood quickly, has risks
