Gastrointestinal Flashcards

1
Q

FLUID THERAPY

A
  • %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
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2
Q

Maintenance fluid

A

Wt mL/day Est mL/hr

<10kg – 100mL/kg – 4mL/kg

10-20 – 1000mL + 50mL/kg over 10kg

>20 – 1500mL + 20mL/kg over 20kg

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3
Q

Maintenance Fluids Constituents

A

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
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4
Q

Maintenance Fluids Tonicity: Isotonic

A

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
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5
Q

Hypotonic Fluids

A
  • 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
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6
Q

Hypertonic Fluids

A
  • 3% NaCl
  • Indications:
    • Severe hyponatremia with risk of seizures (120-125, 50% sz risk)
    • Increased ICP
  • CVL required
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7
Q

Sodium

A
  • 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
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8
Q

Potassium

A

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
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9
Q

Hypercalcemia

A

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
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10
Q

Hypocalcemia

A

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)
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11
Q

Magnesium

A
  • Helps regulate intracellular metabolism
  • Activates enzymes
  • Affects metabolism of proteins
  • Affects electrolyte balance
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12
Q

Hypermagnesemia

A

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)
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13
Q

Hypomagnesemia

A

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

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14
Q

Chloride

A
  • 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-
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15
Q

Histamine-2 Receptor Antagonists

A
  • Ranitidine (Zantac)
  • Famotidine (Pepcid)
    • 10-15x potency over ranitidine
    • Longer t1⁄2 = 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
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16
Q

Proton Pump Inhibitors

A
  • >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

17
Q

H2RAs vs PPIs

A

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
18
Q

Prokinetic Agents

A
  • 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
19
Q
A