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PCM II Exam 1 > Abdominal CCP (king-2) > Flashcards

Abdominal CCP (king-2) Flashcards

1
Q

characteristics of visceral pain

A

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)

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2
Q

visceral pain description

A

dull
poorly localized
felt midline

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3
Q

parietal pain characteristics

A

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

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4
Q

parietal pain description

A

sharp
intense
localized
coughing/moving aggravates it

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5
Q

referred pain characteristics

A

like parietal pain but felt in remote area
supplied by same dermatome as affected organ
shares central pathway for afferent neurons from different sites

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6
Q

mesenteric lymphadenitis

A 
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)
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7
Q

mes lymphadenitis epidemiology

A

misdx as appendicitis and pt undergo appy when they have mesenteric adenitis
benign
equal in genders, more yesinia in male
common in children <15

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8
Q

mes lymphadenitis tx

A

supportive care: hydration and pain mgmt
no antibiotics in mild cases
surgery if peritonitis dev, or is appy

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9
Q

direct/conjugated hyperbilirubinemia

A

uncommon

primarily biliary obs and metabolic disorders

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10
Q

indirect/unconjugated hyperbilirubinemia

A

more common (prehepatic like anemia)

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11
Q

neonatal hyperbilirubinemia

A
  1. inc bili load from:
  2. dec bili conjugation
  3. impaired bili excretion
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12
Q

causes of inc bili load

A 
hemolysis
non hemolytic:
extravascular sources
polycythemia
exaggerated enterohepatic circulation
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13
Q

causes of hemolysis

A 
RH incomp
ABO incomp
minor Ags (D type)
RBC cell mem defects
RBC enz defects
Rxa
Hb-opathies
sepsis
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14
Q

RBC cell membrane defects

A

spheroctosis

elliptocytosis

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15
Q

RBC enz defects

A

G6PD

PK

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16
Q

hemoglobinopathies

A

sickle cell anemia

17
Q

causes of extravascular sources

A

cephlohematoma
CNS hemorrhage
swallowed blood
bruising

18
Q

causes of polycythemia

A

fetal-maternal transfusion
delayed cord clamping
twin-twin transfusion

19
Q

causes of exaggerated enterohepatic circulation

A 
CF
ileal atresia
pyloric stenosis
breast milk jaundice
Hirschsprung's disease (megacolon)
20
Q

causes of dec bili conjugation

A 
physiologic jaundice from breast feeding
breast milk
Gilbert's
Criglar-Najar T1&2
hypothyroidism
21
Q

causes of impaired bili excretion

A

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)

22
Q

Coombs test

A

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 (+)

23
Q

newborn bili production

A

6-8 mg/d
2x adult rate
declines in 10-14 d

24
Q

why is hyperbilirubinemia more common in neonates?

A

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

25
Q

Heme deg pathway

A

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

26
Q

jaundice clinically detected at?

A

5 mg/dL

27
Q

inc direct and indirect bili
(-) coombs test
normal retic count

A 
ddx:
hepatitis
metabolic disorder
obs disorder
sepsis
28
Q

inc indirect bili
(-) coombs test
normal retic count

A

ddx:
physiologic
breast milk jaundice
familial non hemolytic jaundice (gilbert, crig-na)

29
Q

inc indirect bili

inc retic count

A

ddx:
hemolysis due to ABO/Rh incomp
RBC defects (cell membrane or enzymatic)

30
Q

physiologic jaundice

A 
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)
31
Q

breast feeding jaundice

A

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

32
Q

breast milk jaundice

A

appears d3-4, peaks d6-14
cause: idio, may be component of milk
dx if serum bili predom unconj

33
Q

pathological jaundice

A 
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
34
Q

bili toxicity

A

unconj bili in brain

XS unconj is unable to bind albumin, crosses BBB, leads to asphyxia, acidosis, hypoxia, hypoperfusion, hyperosm, sepsis

35
Q

toxic level of bili

A

> 25 mg/dl in term neo

36
Q

kernicterus

A

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

37
Q

tx for unconj hyperbili

A
  1. Monitoring: inc feeding, repeat levels frequently
  2. phototherapy: 1-2 d, conj bili into isomers to be excreted
  3. exchange transfusion: reduce bili in blood quickly, has risks

PCM II Exam 1 (7 decks)

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