Gastrointestinal

Question 1

FLUID THERAPY

Answer 1

• %Water (balances @ approx 1y)
  
  • Preemies ~90%
  • NB ~70-80%
  • Adult ~60%
• ECF>ICF before 6 months
• ICF>ECF after 6 months
• ICF– 30-40%, fluid within cells, K+, Phos-
• ECF– 20-25%, fluid surrounding cells (extravascular, intravascular), Na+, Bicarb

Question 2

Maintenance fluid

Answer 2

Wt mL/day Est mL/hr

<10kg – 100mL/kg – 4mL/kg

10-20 – 1000mL + 50mL/kg over 10kg

>20 – 1500mL + 20mL/kg over 20kg

Question 3

Maintenance Fluids Constituents

Answer 3

Water & Glucose (D5W to D20W)

• Provides 20% of normal caloric needs
• Dextrose adds osmoles to fluid
• Infants have a higher glucose need
  
  • Higher BMR (100calories/kg baseline)
  • Calories needed for growth & basal metabolism
  • Low glycogen stores
  • With stress, hypoglycemia results quickly
• Electrolytes – amount based on needs
  
  • Na+ - required in nearly all fluids
  • K, etc. - based on needs
    
    • Always verify adequate UOP before adding K

Question 4

Maintenance Fluids Tonicity: Isotonic

Answer 4

Isotonic Fluids

• Osmolality of fluids equal to plasma osmolality
  
  • 275-295 mOsm/L
• Ideal to keep electrolytes & fluid balanced
  
  • Ex: NS, LR, D5¹/₄NS, D5¹/₂NS, D5¹/₂NS + 20K
  • Resus: NS, LR

Question 5

Hypotonic Fluids

Answer 5

• Infusing fluids with more water (relative to solute) than present in vessel & inside the cells
• Water shifts out of blood vessels into cells>cells swell & burst
  
  • CV collapse from intravascular fluid depletion
  • Increased ICP from fluid shift into the brain cells
  • Red blood cells fill with fluid & rupture = hemolysis
  • Inflammation, phlebitis, and infiltration at IV site
    
    • Assess for signs of infiltration
• Ex: ¹/₂NS, ¹/4NS, D5W

Question 6

Hypertonic Fluids

Answer 6

• 3% NaCl
• Indications:
  
  • Severe hyponatremia with risk of seizures (120-125, 50% sz risk)
  • Increased ICP
• CVL required

Question 7

Sodium

Answer 7

• Most abundant electrolyte in ECF
• Promotes neuromuscular function
• Maintains acid-base balance
• Influence kidney’s regulation of body water & electrolyte status (K+ & Cl- levels)
  
  • When Na+ falls, kidneys promote diuresis
  • When Na+ increases, kidneys retain water
• Maintenance depends on thirst mechanism & kidneys

Question 8

Potassium

Answer 8

Managing HyperK

• Correct underlying issue
• Calcium to alter cardiac effects – stabilize heart

Drive serum K+ back into the cells

• IV insulin with glucose
• Albuterol neb
• Sodium bicarbonate

Remove excessive serum K+

• Sodium polystyrene sulfonate (Kayexalate PO/PR)
• Loop, thiazide diuretics
• Dialysis
• Patiromer (Veltassa®) - not currently approved for children
  • MoA: Increases fecal potassium excretion through binding of potassium in the lumen of GI tract
    
    • AE: Hypomagnesemia
      
      • Interactions: Binding to other medications in the GI tract, decreasing GI absorption

Question 9

Hypercalcemia

Answer 9

Hypercalcemia

Results from:

• Immobilization
• Medications
• Malignancy
• Renal failure

Signs & symptoms:

• Constipation, dehydration, dry mouth
• Muscle hypotonicity

Treatment - Decrease levels

• Treat underlying condition
• Fluid therapy to dilute serum level

Question 10

Hypocalcemia

Answer 10

Hypocalcemia

Results from:

• Acute pancreatitis
• Excessive infusion of citrated blood
• Malabsorption
• Cow’s milk given to newborns
• Vitamin D deficiency
• Infants at higher risk
  • Stress increases growth hormone secretion increasing deposits of Ca²⁺ into bone
  • Infants already have low stores
  • Unable to keep up with the demand to deposit Ca²⁺ into bones
  • CHARGE, DiGeorge syndrome need 2x Ca²⁺

Signs & symptoms:

• Tingling of fingers and toes
• Abdominal & muscle cramps
• Seizures

Treatment:

• PO or IV supplementation (CaCl, Ca gluconate IV push; Tums)

Question 11

Magnesium

Answer 11

• Helps regulate intracellular metabolism
• Activates enzymes
• Affects metabolism of proteins
• Affects electrolyte balance

Question 12

Hypermagnesemia

Answer 12

Results from:

• Renal failure
• Overuse of antacids/laxatives
• Adrenal insufficiency

Signs & Symptoms (correlate to levels):

• Lethargy
• EKG changes
• Respiratory depression
• Hypotension (*SE of giving Mg IV too fast)

Treatment

• Administration of Ca²⁺ to stabilize heart
• Hydration to enhance excretion
• Hemodialysis (severe)

Question 13

Hypomagnesemia

Answer 13

Results from:

• Decreased intake
• Decreased intestinal absorption
• Diuretic therapy (thiazides, loops waste all e^-s)
• Gastric losses (severe diarrhea)

Signs & Symptoms

• AMS
• Seizures
• Muscle spasms
• EKG Changes, arrythmias (Torsades)

Treatment – IV or PO supplementation

Question 14

Chloride

Answer 14

• Imbalances seen as acid-base disturbances
• Metabolic Acidosis
  
  • Loss of bicarbonate in diarrheal stools
• Metabolic Alkalosis
  
  • Loss of acid from vomiting or excessive gastric suction
  • Common with diuretic therapy
    
    • Losses of Na⁺ Cl^- & H₂O w/o a proportional loss of HCO₃^-

Question 15

Histamine-2 Receptor Antagonists

Answer 15

• Ranitidine (Zantac)
• Famotidine (Pepcid)
  
  • 10-15x potency over ranitidine
  • Longer t_1⁄2 = less frequent IV dosing
• Indication: GERD, mild esophagitis
• MoA: Reduce acid secretion stimulated by histamine and gastrin
  
  • Histamine released from ECL cells by gastrin or vagal stimulation is blocked from binding to the parietal cell H2 receptor (blocks histamine<>histamine receptor = less acid)
  • Direct stimulation of the parietal cell by gastrin/Ach to secrete acid doesn’t work as well in the presence of H2-receptor blockade (blocks gastrin<>parietal cell)
• PK: rapidly absorbed from the intestine
  
  • Undergo first-pass hepatic metabolism resulting in a bioavailability of approximately 50%
  • Hepatically/renally cleared (reduce dose in renal impairment)
• AE: HA, irritability, somnolence, thrombocytopenia, agranulocytosis; *tolerance* after 6wk, not overcome by dose increase

Question 16

Proton Pump Inhibitors

Answer 16

• >1m esomeprazole
• >1y omeprazole, lansoprazole
• >5y pantoprazole

Indications:

• First line therapy for chronic heartburn
  
  • 2-4w diagnostic trial + lifestyle; if improves, continue for 8-12w
• Reflux esophagitis
  
  • mucosal healing seen in 70-100% of patients within 12 weeks
  • heals more severe grades of esophagitis and cases refractory to H2RAs

MoA: irreversibly inhibit final common pathway for acid production within the parietal cells, the H+/K+ ATPase/proton pump

• acid secretion can only return once parietal cell makes new pumps
• decrease volume of reflux bu decreasing 24h intragastric volume
• Discontinuation: rebound acid secretion
  
  • Taper off over 4w when therapy is complete

PK: 15-30m before first meal of day; delayed onset of action up to 4 days; duration of action 15 hours

• Hepatic metabolism – substrate of CYP2C19, 3A4
  
  • Omeprazole inhibits 2C19
• Reduced metabolism is preterm infants, NBs
• Increased clearance in children

AE: HA, n/v/d/c, chronic therapy: bone loss, nephritis, B12 deficiency

Question 17

H2RAs vs PPIs

Answer 17

PPIs have superior efficacy because:

• Longer duration of action for acid suppression
• Inhibit meal-induced acid secretion
• Are not associated with development of tolerance

Long-term acid suppression complications

• Gastric acid is protective to GI system as bacterial flora inhibited
  
  • both H2RAs and PPIs can lead to bacterial overgrowth
  • Increased risk in children of:
    
    • Community-acquired pneumonia
    • Acute gastroenteritis
    • C. diff infections
  • Increased risk in premature infants of:
    
    • NEC
    • Candidemia

Question 18

Prokinetic Agents

Answer 18

• Reglan/metoclopramide:
  
  • MoA: dopamine/D2 receptor antagonist
    
    • Blocks GI tract dopamine receptors, therefore enhancing Ach response
    • Modest decrease in daily symptoms
    • AE: Extrapyramidal rxn, tardive dyskinesia, QT prolongation
• Erythromycin:
  
  • MoA: directly stimulates motilin receptors in GI sm. muscle
    
    • AE: lower doses than antibiotic, less SE
      
      • GI upset, hepatotoxicity, arrythmias, ABX resistance, QT prolongation