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MS3 > Peds 2 > Flashcards

Peds 2 Flashcards

1
Q

Describe the events of bilirubin creation and metabolism starting with hemoglobin breakdown

A

♣ Hemoglobin broken down into heme and globin
♣ Heme then broken down into iron and protoporphyrin
♣ Protoporphyrin converted into unconjugataed bilirubin (water insoluble)
♣ UCB binds to albumin to be brought to the liver
♣ Liver conjugates UCB into CB (water soluble)
• UDP glucuronyl transferase (UGT) is the enzyme in the hepatocytes that conjugates bilirubin
♣ CB dumped into bile canaliculi to be sent to the gallbladder

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2
Q

Causes of elevated unconjugated bilirubin (broad categories)

A
  • Increased bilirubin production
  • Impaired bilirubin uptake and storage
  • Decreased UDP-GT activity
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3
Q

Causes of increased bilirubin production

A
  • Hemolytic anemia
  • Sickle cell disease
  • Hematoma breakdown
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4
Q

Causes of impaired bilirubin uptake and storage

A
  • Viral hepatitis

- Drugs

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5
Q

Causes of decreased UDP-GT activity

A
  • Gilbert syndrome
  • Crigler Najjar syndrome
  • Neonatal physiologic jaundice
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6
Q

Causes of elevated conjugated bilirubin (general categories)

A
  • Impaired transport of bilirubin
  • Biliary epithelial damage
  • Intrahepatic biliary obstruction
  • Extrahepatic biliary obstruction
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7
Q

Causes of impaired transport of bilirubin

A
  • Dubin Johnson syndrome

- Rotor syndrome

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8
Q

Causes of biliary epithelial damage

A
  • Hepatitis
  • Cirrhosis
  • Liver failure
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9
Q

Causes of extrahepatic biliary obstruction

A
  • Pancreatic neoplasms
  • Pancreatitis
  • Cholangiocarcinoma
  • Choledocholithiasis
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10
Q

Describe physiologic jaundice of the newborn

A
  • Newborn livers have low UGT activity (enzyme that conjugates bili), leading to increased UCB
  • Too much UCB can deposit in the brain kernicterus
  • Treatment = Phototherapy – makes UCB water soluble
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11
Q

Describe physiologic jaundice of the newborn

A
  • Newborn livers have low UGT activity (enzyme that conjugates bili), leading to increased UCB
  • Too much UCB can deposit in the brain kernicterus
  • Treatment = Phototherapy – makes UCB water soluble
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12
Q

Most common hemolytic causes of hyperbilirubinemia

A
  • ABO or Rh incompatibility
  • Sepsis
  • Membrane disease
  • Enzyme defects (G6PD or pyruvate kinase deficiency(
  • Hemoglobinopathies (sickle cell, thalassemia)
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13
Q

What is breast milk jaundice

A

Thought to be due to human milk causing increase of intestinal absorption of bilirubin

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14
Q

Describe breastfeeding failure jaundice

A

Decreased intake causes slower bilirubin elimination and increased intrahepatic circulation

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15
Q

Describe why high bilirubin is dangerous

A

UCB can cross the BBB and cause cell death by apoptosis and necrosis

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16
Q

Describe major features of kernicterus

A
  • Choreoathetoid cerebral palsy
  • Significant hearing loss due to auditory neuropathy
  • Gaze abnormalities, especially limitation of upward gaze.
  • Dental enamel dysplasia
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17
Q

What is acute bilirubin encephalopathy (ABE)

A

Usually occurs before kernicterus

3 phases:

  • Sleepy but arousable with possible hypotonia
  • febrile, lethargic, irritable, hypertonia
  • apnea, inability to feed, seizures, coma
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18
Q

How does G6PD deficiency cause hyperbilirubinemia

A

♣ Glutathione neutralizes H2O2 but becomes oxidized in the process
♣ NADPH needed to reduce glutathione

In G6PD, no NADPH created in order to reduce glutathione, which is needed to protect RBCs from oxidative damage

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19
Q

What is haptoglobin

A

Protein that carries Hb to the spleen

Will have decreased serum haptoglobin in hemolysis

20
Q

How does pyruvate kinase deficiency cause hyperbilirubinemia

A

♣ Glycolytic enzyme deficiency = inability to generate ATP

♣ Cannot maintain Na+/K+ ATPase = RBC swelling and lysis

21
Q

Describe neurostorming

A

Following TBI, caused by increased stress response (corticoids and catecholamines)

Symptoms can include alterations in level of consciousness, increased posturing, dystonia, hypertension, hyperthermia, tachycardia, tachypnea, diaphoresis, and agitation

22
Q

What is refeeding syndrome

A

he refeeding syndrome is defined as the clinical complications that can occur as a result of fluid and electrolyte shifts during aggressive nutritional rehabilitation of malnourished patients

23
Q

Clinical features of refeeding syndrome

A

●Hypophosphatemia (*hallmark) - lack of phosphate (ATP) leads to tissue hypoxia, causing myocardial dysfunction and respiratory distress

●Hypokalemia

●Vitamin (eg, thiamine) deficiencies

●Congestive heart failure

●Peripheral edema

●Rhabdomyolysis

●Seizures

●Hemolysis

24
Q

Describe difference between acetylcholinesterase inhibitor toxicity and direct cholinomimetic toxicity

A

Unlike direct acting cholinomimetics, acetylcholinesterase inhibitors effect nicotinic receptors in addition to muscarinic receptors

Clinically = flaccid paralysis + DUMBBELS

25
Q

Describe DUMBBELS sx of ACh inhibitor toxicity

A 
D = diarrhea
U = urination
M = miosis
B = bronchospasm
B = bradycardia
L = lacrimation
S = salivation
26
Q

MOA of Pralidoxime

A

Used to treat PERIPHERAL effects of ACh inhibitor toxicity

Regenerates ACh esterase at muscarinic and nicotinic receptors (reverses paralysis as well)

27
Q

MOA of Atropine

A

Treats both PERIPHERAL and CENTRAL effects of AChI toxicity on MUSCARINIC receptors

But does not reverse nicotinic effects, so does not fix paralysis

28
Q

What are the 5 components of apgar score

A

HR, RR, muscle tone, reflex irritability, color

29
Q

What do you do if meconium is present in a vigorous newborn

A

Bulb syringe or large-bore suction to clear airway

30
Q

What do you do if meconium is present in a nonvigorous newborn

A

Intubate and direct suction of trachea before many breaths occur to reduce change of meconium aspiration

31
Q

Diagnose: newborn born with scaphoid abdomen, cyanosis, and respiratory distress

A

diaphragmatic hernia

32
Q

Tx of newborn with respiratory distress in setting of diaphragmatic hernia

A

Endotracheal intubation

Bag-mask ventilation will also push gas into bowel, which is in the chest cavity, causing further respiratory compromise

33
Q

Next step in neonatal rescusitation if HR remains < 60 beats/min despite positive pressure ventilation

A

Chest compressions

34
Q

Next step if chest compressions fail

A

Drug therapy (usually epinephrine)

35
Q

What is choanal atresia and its presentation

A

Obliteration or blocking of posterior nasal aperture (aka nose is not connected to oropharynx)

Presents as baby who can breathe when crying but has respiratory distress when stops. Infants are obligate nose breathers but can breathe through their mouths when crying

36
Q

Tx of choanal atresia

A

Intubation to bypass obstruction until surgical repair can be completed

37
Q

Describe pathogenesis of infant of a diabetic mother

A

♣ In response to maternal hyperglycemia, fetal hyperinsulinism begins
♣ Fetal insulin production causes increased glycogen production which is deposited in fetal liver, heart, kidneys, and skeletal muscle
♣ After delivery and removal from high-sugar in utero environment, the infant’s hyperinsulinism can cause hypoglycemia

38
Q

Clinical features of infant of a diabetic mother

A

♣ Hypoglycemia – seizures, jittery, apnea
♣ Spinal bifida / neural tube defect
♣ Shoulder dystocia, brachial plexus injury (due to large infant being squeezed during delivery)
♣ Hypertrophic cardiomyopathy (due to glycogen deposition)
♣ Hyaline membrane disease, respiratory distress syndrome
♣ Polycythemia
♣ Hyperbilirubinemia, hypocalcemia, hypomagenesia
♣ Renal vein thrombosis
♣ Caudal regression syndrome

39
Q

What causes Respiratory distress syndrome in infant of DM mother

A

♣ insulin interferes with cortisol’s ability to induce surfactant production

40
Q

What causes hypertrophic cardiomyopathy in infant of DM mother

A

♣ Fetal insulin production causes increased glycogen production which is deposited in fetal heart

41
Q

What causes polycythemia in infant of DM mother

A

Due to increased fetal oxygen requirement because of enlarged fetus

42
Q

What causes hyperbilirubinemia in infant of DM mother

A

due to polycythemia

43
Q

What causes renal vein thormbosis in infant of DM mother

A

due to polycythemia

44
Q

Tx of newborn of DM mother with glucose < 40 and NO sx of hypoglycemia

A

♣ If no sx of hypoglycemia, the infant is refed and glucose re-measured 30 min after feeding

45
Q

Tx of newborn of DM mother with glucose < 40 and + sx of hypoglycemia

A

Requires IV glucose

MS3 (88 decks)

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