GI Cases (Dr. King's CCP)

Question 1

Why is the female in case one unable to localized her pain?

Answer 1

•Visceral pain
–Stimuli resulting in tension, stretching and ischemia
–Tissue congestion and inflammation lower threshold for stimuli
–Bilateral pain fibers
–Unmyelinated fibers
–Enter spinal cord at multiple levels•Described as dull, poorly localized and usually felt midline

Question 2

What can sensitize nerve endings in the abdomen?

Answer 2

Tissue congestion and inflammation… lower threshold for stimuli

Question 3

Define and describe parietal pain

Answer 3

–Noxious stimuli to parietal peritoneum
•Ischemia, inflammation, or stretching
–Transmitted via myelinated afferent fibers to specific doral root ganglia
•Occurs on same side and same dermatomal level as original pain

•Described as:
–Sharp, intense, localized
–Coughing or moving can aggravate it

Question 4

Referred pain?

Answer 4

–Characteristics similar to parietal pain but felt in remote area
•Usually supplied by same dermatome as affected organ
•Shared central pathway for afferent neurons from different sites

Question 5

Be familar with this chart:

Answer 5

Question 6

Acute abdominal pain with high white count?

Answer 6

Either appendicitis or mesenteric lymphadenopathy (could be a hundred other dx’s but these two were discussed)

Question 7

Mesenteric Lymphadenitis

Answer 7

Mesenteric lymphadenopathy in a 28-year-old man who presented with acute abdominal pain. CT images show innumerable lymph nodes in the mesentery of the right lower quadrant (arrows in a) and at the mesenteric root (arrows in b). The CT findings were otherwise unremarkable. This appearance represents mesenteric adenitis.

Question 8

Mesenteric Lymphadenitis definition and causes…

Answer 8

•Inflammation of mesenteric lymph nodes
•Clinical presentation often difficult to differentiate from acute appendicitis
•Causative agents
–Beta hemolytic streptococcus
–Staphlococcus species
–E. coli
–Streptococcal viridans
–Yersinia species (most cases currently)
–Mycobacterium tuberculosis
–Viruses

Question 9

Epidemiology of ML

Answer 9

•Generally thought to be common
–Often easily missed or mistaken for another dx
–Up to 20% of pts undergoing appendectomy have been found to have mesenteric adenitis
•Morbidity/mortality
–Generally benign
•Male = Female
–Yesinia more common in males
•Age
–Can occur in adults but more likely in children <15 years

Question 10

Tx of ML

Answer 10

•General supportive care
–Hydration
–Pain medication

•No antibiotics in mild uncomplicated cases

Question 11

When to do surgery?

Answer 11

•Surgery if signs of peritonitis or cannot differentiate from acute appendicitis

Question 12

Case 2: DDX of neonatal hyperbilirubinemia

Answer 12

•Direct (conjugated) hyperbilirubinemia
–Relatively uncommon
–Primarily biliary obstruction and metabolic disorders

•Indirect (unconjugated) hyperbilirubinemia
–More common

Question 13

Classification of neonatal hyperbilirubinemia

Answer 13

1. Increased Bilirubin load

• Hemolysis
• Nonhemolytic causes
• Extravascular sources
• Polycythemia
• Exaggerated enterohepatic circulation

2. Decreased bilirubin conjugation
3. Impaired bilirubin excretion

Question 14

List some diseases of RBC’s

Answer 14

Rbc defects include spheroctosis, elliptocytosis…; rbc cell enzyme defects include G6PD, pyruvatekinase def…; hemoglobinopathies include sickle cell

Question 15

Hemolytic causes of increased bilirubin load

Answer 15

–Hemolysis
•Rh incompatibility
•ABO incompatibility
•Minor antigens (D type…)
•RBC cell membrane defects
•RBC enzyme defects
•Medications
•Hemoglobinopathies
•Sepsis

Question 16

Nonhemolytic causes of increased bilirubin:

Answer 16

•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

Question 17

Causes of decreased bilirubin conjugation (just be familiar with these… Dr. King didn’t even finish this lecture)

Answer 17

–Physiologic jaundice
•Breast feeding

–Breast milk
–Gilbert’s
–Criglar-Najar
–Hypothyroidism

Question 18

Causes of impaired bilirubin excretion

Answer 18

–Biliary obstruction
–Infection
–Metabolic disorders
–Chromosomal abnormalities
–Drugs

Question 19

Coombs test (aka antiglobulin test, AGT)

Answer 19

AGT refers to two clinical blood tests used in immunohematology and immunology. The two Coombs tests are the direct Coombs test (DCT, also known as direct antiglobulin test or DAT), and the indirect Coombs test (also known as indirect antiglobulin test or IAT).

The more commonly used test, the Direct Coombs test, is used to test for autoimmune hemolytic anemia.

In certain diseases or conditions an individual’s blood may contain IgG antibodies that can specifically bind to antigens on the red blood cell (RBC) surface membrane, and their circulating red blood cells (RBCs) can become coated with IgG alloantibodies and/or IgG autoantibodies. Complement proteins may subsequently bind to the bound antibodies. The direct Coombs test is used to detect these antibodies or complement proteins that are bound to the surface of red blood cells; a blood sample is taken and the RBCs are washed (removing the patient’s own plasma) and then incubated with antihuman globulin (also known as “Coombs reagent”). If this produces agglutination of RBCs, the direct Coombs test is positive, a visual indication that antibodies (and/or complement proteins) are bound to the surface of red blood cells.

Question 20

Bilirubin review…

Answer 20

•Bilirubin is the final product of heme degradation
•It is insoluble in plasma when the pH is normal
•Bound to albumin
•It is conjugated in the liver
•Is excreted in bile
–Becomes the main coloring component of feces
•Newborns produce bili at a 6-8mg/day
–2x the adult rate
–Declines to normal adult levels by 10-14 days after birth

Question 21

Why is hyperbilirubinemia more common in neonates?

Answer 21

–Shortened life span of their red blood cells
–Declining hematocrit
–Immature liver uptake & conjugation of bilirubin
–Increased enterohepatic circulation
•Increased intestinal reabsorption of bilirubin
•Intestinal bacteria can deconjugate bilirubin allowing for reabsorption of bilirubin into the circulation.

Question 22

Heme degradation pathway

Answer 22

• 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
• Uridinediphosphateglucuronyltransferase (UDPGT) conjugates bilirubin into an excretable form.

Question 23

Characteristics of Jaundice

Answer 23

• Usually begins on the face and progresses caudally
• Generally, the farther the jaundice progresses down the body, the higher the total serum bilirubin
• The more intense the color (which can approach a yellow-orange) also suggests a higher total serum bilirubin
• Jaundice may be clinically detected with a total serum bilirubin of 5 mg per dL.

Question 24

Causes of jaundice

Answer 24

Elevated serum indirect bilirubin with normal reticulocyte count and negative Coomb’s test is associated with physiologic, breast milk jaundice, or familial nonhemolyticjaundice. Elevated serum indirect bilirubin with increased reticulocyte count is indicative of increased hemolysis seen with ABO/Rh incompatibility and red blood cell abnormalities.Elevation of both direct and indirect bilirubin with a negative Coomb’s test and normal reticulocyte count is indicative of hepatitis, metabolic or obstructive disorders, or sepsis.

Because of active in uteroerythropoiesis, the reticulocyte count at birth is 3 to 7% in full-term babies and 8 to 10% in premature babies. This declines to 0 to 1% by the first week of age, reflecting diminished erythropoiesis.

Question 25

Which clinical finding is most suggestive of physiologic hyperbilirubinemia in a neonate?

A.Clinical jaundice before 24 hrs of age.
B.Clinical jaundice lasting beyond 14 days.
C.Bilirubin levels of 12 mg/dl by 3 days of life
D.Serum bilirubin level increasing by more than 5 mg/dl/day

E.An elevated conjugated bilirubin >2mg/dL

Question 26

What is physiologic jaundice?

Answer 26

•Physiological immaturity of liver
•Appears between 24-72 hours of age
–Peaks by 4-5 days in term and 7th day in preterm neonates
–Disappears by 10-14 days of life
•It is predominantly unconjugated and levels usually do not exceed 12 mg/dl in those without multiple risk factors (in those may rise as high as 17 mg/dL)

Question 27

Breast milk jaundice?

Answer 27

–Appears by day 3-4; Peaks by day 6-14
–Cause is not known however component of breast milk may interfere with bilirubin conjugation
–Approximately 2-4% of exclusively breast-fed term babies them have bilirubin in excess of 10 mg/dl in the third week of life
–A diagnosis of breast milk jaundice should be considered if the serum bilirubin is predominantly unconjugated, other causes of prolonged jaundice have been excluded and the infant is in good health, vigorous and feeding well and gaining weight adequately.

Question 28

Breastfeeding jaundice?

Answer 28

– in breast-fed babies usually appears between 24-72 hours of age, peaks by 5-15 days of life and disappears by the third week of life.
–Probably caused by not enough milk intake→Inadequate bowel movements→Inadequate excretion of bilirubin

Question 29

Pathological jaundice?

Answer 29

• Appearance of jaundice within 24 hours
• Increase in serum bilirubin beyond 5 mg/dl/day
• Peak levels above the expected normal range
• Presence of clinical jaundice beyond 2 weeks
• Elevated conjugated bilirubin

Question 30

Bilirubin toxicity

Answer 30

•Deposition of unconjugated bilirubin in brain tissue
•Unconjugated form exceeds binding capacity of albumin
–Unbound lipid soluble bilirubin crosses the blood-brain barrier
•If blood-brain barrier damaged albumin-bound bilirubin may cross
•Toxicity levels vary among ethnic groups, maturity level of neonate and presence of hemolytic disease
–>25 mg/dL in healthy term neonate

Question 31

What can cause damage to the blood brain barrier (BBB)?

Answer 31

Include:

asphyxia, acidosis, hypoxia, hypoperfusion, hyperosmolality, or sepsis

Question 32

Kernicterus

Answer 32

•Effects are often irreversible
•Early signs
–Subtle
–3-4 days after birth
–Lethargy, poor feeding, hypotonia
•Late signs
–Occur after first week of life
–Irritability, seizures, apnea, hypertonia, fever, etc.
•Chronic signs
–If neonate survives, chronic encephalopathy is seen
•Evident by 3 years of age
–Cerebral palsy, high frequency hearing loss, mild MR

Question 33

Treatment for Unconjugated Hyperbilirubinemia

Answer 33

•Continued monitoring
–Increase feeding
–Repeat levels frequently

•Phototherapy
–Usually 1-2 days
–Certain wavelength of light transform unconjugated bilirubin into isomers that can be excreted.

•Exchange Transfusion
–Rapidly reduce bilirubin in blood but is not without risks

Question 34

Case 2 Tx?

Answer 34

•Her jaundice is physiological
–Breastfeeding
–Cephalohematoma
–Weight loss (weight loss of 6%)
•No photo therapy needed
•Advise about increase feeding frequent to Q2 hrs and well as not letting infant sleep more than a 4 hour stretch before feeding
•Monitor wet diapers and stools
•Place in indirect sunlight
•Follow up in 2 days to recheck physical examination (check skin) and weight gain

Question 35

Objectives for case 2:

• Describe the risk factors for neonatal hyperbilirubinemia.
• List the effects of bilirubin toxicity.
• Compare and contrast physiologic and pathologic jaundice.
• Describe the differences between breast feeding jaundice and breast milk jaundice.
• Describe the progression of dermal icterus with increasing total serum bilirubin levels.
• Describe phototherapy including how it helps decrease unconjugated serum bilirubin, when to initiate therapy and contraindications.
• Describe what exchange transfusion is and indications to begin this therapy in a neonate.

Answer 35

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