CCP of Abdomen Flashcards

1
Q

visceral pain

A

dull, poorly localized, usually felt in midline
transmitted via unmyelinated fibers
- stimuli resulting in tension, stretching and ischemia
- tissue congestion and inflammation lower threshold for stimuli
- transmitted via unmyelinated fibers

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2
Q

parietal pain

A
  • noxious stimuli to parietal peritoneum, transmitted - via myelinated afferent fibers to specific dorsal root ganglia
  • described as sharp, intense, localized
  • occurs on same side and same dermatomal level as original pain
  • could be due to ischemia, inflammation or stretching.
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3
Q

referred pain

A

similar to parietal pain, but felt in a remote area.

- due to shared central pathway for afferent neurons from different sites

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4
Q

hx: patient presents with periumbilical, poorly localized pain. Some diarrhea. tiny lymph nodes palpated cervically. Diffuse pain palpated in RLQ, no rebound and no HSM. 101F fever.

A
  • acute appendicitis
  • could also be pregnancy, gastroenteritis (Viral GI bug = “stomach flu”), pharyngitis (maybe didn’t fully take Ab for strep throat)

but. with CT see lymph nodes! it is Mesenteric Lymphadenitis

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5
Q

Mesenteric Lymphadenitis

A
  • inflammation of mesenteric lymph nodes - easily missed and often mistaken for appendicitis.
  • generally benign
  • usually occurs to age <15 years old
  • caused by viral/bacterial agents
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6
Q

hx: 4 day old, normal baby, milk came in today, stooling 2-3 x/day, still meconium stools, everything is noted to be normal except for mild jaundice of facial skin.

A

ddx: indirect (unconjugated) hyperbilirubinemia

physiologic jaundice due to breast-feeding

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7
Q

hyperbilirubinemia

A
  1. increased bilirubin load (hemolysis, nonhemolytic causes such as bruising polycythemia, exaggerated enterohepatic circulation)
  2. decreased bilirubin conjugation
  3. impaired bilirubin excretion
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8
Q

reasons for hemolysis

A

Rh incompatibility
ABO incompatibility
Minor antigens (D type…)
RBC cell membrane defects, enzyme defects
mediationcs
hemoglobinopathies (i.e. sickle cell disease)
Sepsis

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9
Q

nonhemolytic causes of increased bilirubin load

A
  1. Extravascular sources (Cephlohematoma, CNS hemorrhage, swallowed blood, bruising)
  2. Polycythemia (fetal-maternal transfusion, delayed cord clamping, twin-twin transfusion)
  3. exaggerated enterohepatic circulation (exaggerating the process of bilirubin being conjugated in liver, it is being unconjugated and is going back into the liver)
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10
Q

decreased bilirubin conjugation

A
phys. jaundice
Gilbert's
Crigler-Najjar
Hypothyroidism
Breast milk
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11
Q

tests for the baby?

A

fractionated bilirubin level
CBC
Retic count
Peripheral smear

  • If it is less than 24 hours with jaundice presenting, then need a greater amount of tests taken to look out for Sepsis.
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12
Q

Jaundice

A

usually begins on the face and progresses caudally, more intense color suggests a higher bilirubin
- seen at about 5 mg/dL

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13
Q

regular physiologic jaundice hyperbilirubinemia in a neonate

A

bilirubin levels of 12 mg/dL by 3 days of life

  • indicates physiologic immaturity, peaks at day 4-5, disappears at 2 weeks.
  • predominantly unconjugated
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14
Q

two types of physiologic jaundice?

A
  • breastfeeding jaundice: related to fact mom’s milk isn’t coming in right away, causing dehydration - low blood volume, results in higher concentration of bilirubin. This peaks a little bit later than typical physiologic.
  • breast milk jaundice: appears by day 3-4,
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15
Q

pathologic jaundice

A
appearance of jaundice within 24 hours
increased bilirubin beyond 5 mg/dL/day
high peak levels
jaundice beyond 2 weeks
elevated conjugated bilirubin
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16
Q

HPI: 11.5 y/o girl, abdominal pain, vomiting, fever, 2 days history of abdominal pain. no blood in vomit. pain is periumbilical and hard to localize and rating 8/10. described as crampy and constant, feels better when lying in fetal position, pain in RLQ
negative obturator, psoas and rovsings
PMH: had strep 1 week prior
ROS: fatigue, appetite was poor, headache, fever, diarrhea since symptoms started, menstrual period 2 weeks ago.

A

DDX: appendicitis, pregnancy, pneumonia, gastroenteritis, pharyngitis

Labs:
CBC- elevated neutrophils
enlarged lymph nodes seen in the CT: mesenteric lymphadenitis

17
Q

What could cause hemolysis?

A

increased indirect bilirubin due to hemolysis

Rh incompatibility
ABO incompatibility
Minor antigens (D type…)
RBC cell membrane defects
RBC enzyme defects
Medications 
Hemoglobinopathies
Sepsis
18
Q

What are nonhemolytic causes of increased indirect bilirubin?

A
Extravascular sources:
Cephlohematoma
CNS hemorrhage
Swallowed blood
Bruising

Polycythemia:
Fetal-maternal transfusion
Delayed cord clamping
Twin-twin transfusion

Exaggerated enterohepatic circulation:
CF, ileal atresia, pyloric stenosis, breast milk jaundice, Hirschsprung’s

19
Q

What can caused decreased bilirubin conjugation?

A
Physiologic jaundice
Breast feeding
Breast milk
Gilbert’s
Criglar-Najar
Hypothyroidism
20
Q

what is newborns bil production? why higher?

A

6-8 mg/day

  • due to the shortened life span of RBC’s
  • declining hematocrit
  • immature liver uptake and conjugation of bilirubin
  • increased enterohepatic circulation (increased intestinal reabsorption of bilirubin intestinal bacteria can deconjugate bilirubin allowing for reabsorption of bilirubin into the circulation)
21
Q

What is heme degredation pathway?

A
  • An RBC dies, a macrophage engulfs it and the heme is released
  • Heme is reduced by hemeoxidase into the components iron and biliverdin
  • Biliverdin is reduced by biliverdin reductase into free bilirubin
  • Free (unconjugated) bilirubin is bound to albumin ( in plasma) and passes into he hepatocytes where it is released from the albumin and conjugated
  • (UDPGT) conjugates bilirubin into an excretable form.
22
Q

What can caused decreased bilirubin conjugation?

A
Physiologic jaundice
Breast feeding
Breast milk
Gilbert’s
Criglar-Najar
Hypothyroidism
23
Q

What does high reticulocyte count indicate?

A

increased hemolysis

24
Q

What is heme degredation pathway?

A
  • An RBC dies, a macrophage engulfs it and the heme is released
  • Heme is reduced by hemeoxidase into the components iron and biliverdin
  • Biliverdin is reduced by biliverdin reductase into free bilirubin
  • Free (unconjugated) bilirubin is bound to albumin ( in plasma) and passes into he hepatocytes where it is released from the albumin and conjugated
  • (UDPGT) conjugates bilirubin into an excretable form.
25
Q

What is progression of jaundice?

A
  • spreads from head to toe

- goes away from toe to head

26
Q

What does high reticulocyte count indicate?

A

increased hemolysis

27
Q

Physiologic jaundice? what is the timing like?

A
  • due to physiologic immaturity
  • appears between 24-72 hours of age
  • peaks by 4-5 days in tern and 7th in preterm
  • disappears by 10-14 days of life
  • predominantly unconjugated levels usually not exceeding 12 mg/dl
28
Q

Breastfeeding jaundice? timing?

A
  • jaundice due to late breast milk coming in: results in mild infant dehydration and decrease in blood volume
  • usually appears between 24-72 hours of age
  • peaks by 5-15 days of life and disappears by third week of life
29
Q

Breast milk jaundice? timing?

A
  • caused by enzyme in breast milk inhibiting the UDPGT enzyme.
  • appears by day 3-4: peaks by day 6-14.
  • predominantly unconjugated bilirubin - will usually subside on its own.
  • seen later and peaks later than breastfeeding jaundice
30
Q

What is timing of pathologic jaundice?

A
  • appears within 24 hours
  • increase in serum bilirubin beyond 5 mg/dl/day
  • presence of clinical jaundice beyond 2 weeks
  • elevated conjugated bilirubin
31
Q

What are signs of kernicterus?

A
  • early signs: lethargy, poor feeding, hypotonia 3-4 days after birth
  • late signs: irritability, seizures, apnea, hypertonia, fever a week after birth
  • kernicterus results in chronic encephalopathy, cerebral palsy, hearing loss, mild MR