GI Re-Up #4 Flashcards
Neonatal jaundice is yellowish discoloration of the skin, sclera, and conjunctiva due to elevated plasma bilirubin in a newborn. This presents on days ________ of life and bilirubin levels fall in about 50% of neonates during the first week of life.
What is a physiologic cause of this condition (specific enzyme activity)?
What are some symptoms?
-What are the specific bilirubin levels associated with both symptoms?
-Days 3-5 is neonatal jaundice
-Transient decrease in UGT enzyme (this conjugates bilirubin).
-Breast milk jaundice - infant liver is not mature enough to process lipids. Mother should continue to breastfeed.
-Jaundice: Yellowing of skin, sclera, conjunctiva. Bilirubin levels > 5.0
-Kernicterus: cerebral dysfunction and encephalopathy (seizures, lethargy, irritability, hearing loss, developmental delays). Bilirubin levels > 20.
Initial management of choice for neonatal jaundice, even though none is needed for physiologic jaundice.
When is this indicated (specific bilirubin levels at a certain age)
Phototherapy
-24 hours of age > 12
-48 hours of age > 15
-72 hours of age > 18
In severe cases of neonatal jaundice, what is the treatment?
Exchange transfusion
What exactly is bilirubin?
What does UGT do?
A yellowish pigment that is made when RBC’s are broken down. It passes through the liver and is excreted from the body.
UGT conjugates bilirubin so it can be excreted from the body. The bilirubin is unconjugated (indirect) if there is decreased UGT activity.
What is Dubin-Johnson Syndrome?
-Hereditary conjugated (direct) hyperbilirubinemia due to decreased hepatocyte excretion of conjugated bilirubin (gene mutation MRP2)
What lab would be shown for Dubin-Johnson Syndrome?
What is seen on liver biopsy?
Treatment?
-Isolated conjugated (direct) hyperbilirubinemia (between 2-5 mg/dL) but can increase with illness, pregnancy, OCPs
-Biopsy: grossly black liver
-No treatment needed
On the other hand, Crigler-Najjar Syndrome is?
What is the pathophysiology of this?
Symptoms, as it occurs in neonates.
-Hereditary unconjugated (indirect) hyperbilirubinemia
-No UGT activity
-Neonatal jaundice with sever progression in the second week, leading to kernicterus (hypotonia, oculomotor palsy, lethargy, deafness)
What is one way to remember the facts about Dubin-Johnson Syndrome?
D’s
-Dubin
-Direct Hyperbilirubinemia
-Dark, Black Liver
Labs for Crigler-Najjar Syndrome
What is the mainstay of treatment?
Isolated indirect (unconjugated) hyperbilirubinemia + otherwise normal liver function tests
(between 20-50 mg/dL)
Phototherapy
On that same note, Gilbert’s Syndrome is?
The pathophysiology of this, like Crigler-Najjar Syndrome is…
What are unique symptoms of this?
-Hereditary unconjugated (indirect) hyperbilirubinemia
-Reduced UGT activity and decreased bilirubin uptake
-Transient episodes of jaundice during periods of stress, fasting, alcohol, or illness.
Much like Crigler-Najjar Syndrome, what do labs for Gilbert’s Syndrome show?
What is the treatment?
-Isolated indirect bilirubin level with otherwise normal liver function tests
-No treatment needed for this mild, benign disease
Anorectal Abscess and Fistulas MC occur at what site?
What is the MCC?
What are some symptoms of an anorectal abscess?
Posterior rectal wall
Staph Aureus
Anorectal swelling, rectal pain worse with defecation/sitting/coughing, focal edema, induration, fluctuant.
What is the mainstay of treatment for an anorectal abscess or fistula?
-Incision and drainage then WASH
–Warm water cleansing, analgesics, sitz baths, high fiber diet
On the other hand, an anal fissure is a painful linear crack/tear in the distal anal canal. What are some symptoms of this?
Explain what this looks like on exam findings.
-Severe painful rectal pain and bowel movements causing patient to refrain from defecating, bright red blood per rectum.
-Longitudinal tear in anoderm that extends no more proximally than dentate line. MC at posterior midline. Skin tags seen in chronic.
Treatment for an anal fissure
> 80% resolve spontaneously
Supportive measures: sitz baths, analgesics, high fiber diet, increased water intake, stool softeners, laxatives, mineral oil.
-Topical vasodilators (Nitroglycerin)
-Botox injections
-Lateral internal sphincterotomy reserved for refractory cases
Ischemic colitis, much like mesenteric ischemia, is decreased colonic perfusion, leading to inflammation. What’s the MCC of this and where does it MC occur?
What are some risk factors for this?
-Due to transient systemic hypotension or atherosclerosis involving super and inferior mesenteric arteries.
-MC occur at splenic flexure and rectosigmoid junction
-RF: Elderly, DM, cardiac catheterization, MI, constipation inducing medications
Symptoms of Ischemic Colitis
What is the first imaging study you would do and what is seen?
-left sided (LLQ) crampy, abdominal pain with tenderness, bloody diarrhea, or hematochezia
CT abdomen: thumb printing: segmented bowel wall thickening
Treatment for ischemic colitis
-Supportive care: restore perfusion, bowel rest, IVF and observe for signs of perforation
Regarding colon polyps, pseudopolyps/inflammatory polyps are due to _____________. These are not considered cancerous.
On the other hand, the MC non-neoplastic polyp type is…
IBD (UC or Crohn’s)
Hyperplastic is the MC non-neoplastic type.
The MC neoplastic colon polyp type
There is a type of this kind that has the least risk (and is the MC) and then the kind that has the highest risk of becoming cancerous.
Adenomatous Polyps
-Tubular Adenoma: MC type and lowest risk
-Villous Adenoma: highest risk of becoming cancerous
