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LMCC - Medicine > Endocrinology - Acid/Base Disorders > Flashcards

Endocrinology - Acid/Base Disorders Flashcards

1
Q

Discuss the definition and causes of hyponatremia

A
  • Na <135mEq/L
    Low Plasma Osmolality
  • low effective circulating volume (hypovolemia, heart failure, cirrhosis, thiazide)
  • Syndrome of inappropriate ADH secretion
    - CNS disease: stroke, hemorrhage, infection, trauma
    - Malignancy: lung, pancreatic
    - Medication: DDAVP, oxytocin
    - surgery
    - lung disease: TB, pneumonia, empyema
    - hormone deficiency
  • renal failure
  • primary polydipsia
    Normal Plasma Osmolality
  • high protein state: high triglyceride, multiple myeloma
  • absorption of mannitol
    High Plasma Osmolality
  • hyperglycemia
  • alcohol intoxication
  • renal failure
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2
Q

Discuss the investigations for hyponatremia

A

High Serum Osmolality
- hyperglycemia (confirmed with high serum glucose)
- azotemia (high BUN) from renal failure
- alcohol intoxication
Normal Serum Osmolality
- IV infusion of mannitol
- absorption of glycine, or amniotic irrigation
- hyperlipidemia (high triglycerides)
- hyperproteinemia for multiple myeloma
Urine Osmolality
- urine osmolality <100 and specific gravity <1.003 is appropriate response (ADH suppression) and primary polydipsia
- urine osmolality >100 and specific gravity >1.003 inappropropriate response (inadequate ADH suppression) inappropriate ADH secretion from: low effective circulating volume or euvolemia and SIADH
Urine Na and Cl concentration
- if high creatinine and hypervolemic then renal failure
- cannot use if on diuretic or salt wasting nephropathy
- urine Na <25 with hypervolemia then HF or cirrhosis
- urine Na <25 with hypovolemia then hypovolemia
- urine >40 and high fractional excretion of Na then SIADH

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3
Q

Discuss the risk stratification for hyponatremia

A 
Duration
- acute within 24hr
- chronic for 48hrs
Severity
- mild Na 130-135
- mod 121-129
- severe <120
Symptoms
- asymptomatic
- mild: headache, nausea, vomiting, fatigue, gait disturbance, confusion
- severe: seizure, obtunded, coma, respiratory arrest
Disposition
- asymptomatic and mild can be treated as outpatient
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4
Q

Discuss the management of hyponatremia

A
  • hyponatremia can lead to cerebral edema and brain herniation
  • fast correction of raising Na lead to osmotic demyelination disorder
    General
  • water restriction to 1L per day
  • diagnose and treat underlying cause
  • frequent monitor of urine output and serum Na
    Emergent Therapy (acute or severe)
  • increase serum Na by 4-6mEq/L over 6hrs but not to exceed 8mEq/L for 24hrs
  • serum monitoring Q2H and continuous urine output (urine output >100cc/h with osmolality <100 risk of rapid correction)
  • hypertonic saline (3% Na 1-2cc/kg/h)
  • Desmopressing 1-2mcg IV/SC Q8H
    - contraindicated: primary polydispsia and volume overload)
  • furosemide if volume overloaded
  • overly rapid correction treat with ADH/DDAVP or give water (D5W)
    Non-Emergent Therapy
  • increase by 3-6mEq/L within 24hrs
  • monitor Na Q4H and continuous urine output
  • water restriction and NS 0.9% with furosemide
  • Demeclocyline 300-600mg PO BID (ADH antagonist) if refractory to above
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5
Q

Discuss the definition and cause of hypernatremia

A 
- Na >145
Unreplaced Water Loss
- should not occur if pt alert, have intact thirst mechanism, access to water
- skin losses
- GI losses
- Urine Loss: hyperglycemia, loop diurectics, nephrogenic diabetes insipidus (kidneys do not respond to ADH) due to lithium toxicity, hypokalemia, hypercalcemia
Neurogenic Dysfunction
- hypothalamic lesion
- Centra diabetes insidious (lack of ADH)
Water Loss into Cells
- severe exercise/seizure
Sodium Overload
- intake of hypertonic sodium solution
Endocrine 
- Cushing's syndrome
- Hyperaldosteronism
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6
Q

Discuss the presentation and investigations for hypernatremia

A

Presentation
- thirst, polyuria >1.5L
- acute: altered mental status, coma, seizure, focal neurological deficit
- signs of hypovolemia
Investigation
- if hypervolemic then Cushing’s syndrome or hyperladosteronism
Urine Osmolality
- urine osmolality >600mOsm/kg and output <500 then
- urine Na <25 then unreplaced water loss
- urine Na >100 sodium overload
- urine osmolality <300mOsm/kg then
- administration of ADH/DDAVP cause 50% increase in urine osmolality then central diabetes insipidus
- administration of ADH/DDAVP does not cause 50% increase in urine osmolality then nephrogenic diabetes insipidus or osmotic diuresis or loop diuretic
- total urine >1000mOsm/day then loop diuretics

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7
Q

Discuss the management of hypernatremia

A
  • examine for underlying cause
    - central require DDAVP
    - hypovolemic then fluid resuscitation
    Lowering Sodium Regimen
  • too fast correction lead to cerebral edema and encephalopathy with seizure and possible permanent brain damage
  • oral free water or IV dextrose if PO not tolerated
    - chronic D5W 1.35mL/kg/hr with lowering Na by no more than 10mEq/L in 24hrs
    - acute D5W 3-6mL/kg/hr with lowering Na 1-2mEq/L per hour until serum Na 145 then reduce to D5W 1-2mL/kg/hr
    - 2mL/kg/hr D5W will correct Na by 0.5mEq/hr or 12 mEq/d
  • monitor Na Q4-6H and urine output
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8
Q

Discuss the definition and signs of hypokalemia

A 
- serum K <3.5mEq/L
Redistribution into Cells
- metabolic alkalosis
- insulin
- beta-agonist
- increased RBC production
GI Loss
- vomiting
- diarrhea
- NG tube drainage
Renal Loss
- diuretics
- diabetic ketoacidosis
- Hypomagnesium
- Increased mineralocorticoid - aldosterone activity (steroids, Cushings)
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9
Q

Discuss the presentation and investigation for hypokalemia

A

Presentation
- asymptomatic
- nausea/vomiting
- muscle cramps
- constipation
- muscle necrosis, paralysis, arrhythmia when severe
Investigation
- most diagnosed through hx of Gi loss or medications
- negative hx suggest renal loss
- renal loss have urine K >30mEq/d
- BP: where mineralcorticoid-aldosterone have hypertension and metabolic acidosis/congenital renal disease have normal or hypotension
- VBG: acidosis suggest DKA or renal tubular acidosis where alkalosis suggest congenital tubular lesion

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10
Q

Discuss the treatment for hypokalemia

A 
Address underlying cause
- hypomagnesium
Replace K
- mild-mod asymptomatic start with 20-80mEq/d of KCl IV
- severe or symptomatic 10-20mEq/hr
- if acidosis KHCO3 IV
- Q2-4H checks with continuous telemetry if severe or symptomatic
Caution
- diabetic
- elderly
- impaired renal function
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11
Q

Discuss the definition and causes of hyperkalemia

A
  • serum K >5
    Laboratory Artifact
  • hemolysis
  • prolonged tourniquet
  • exercise
  • extreme leukocytosis >70 or thrombocytosis >500
    Increased Intake
  • KCl IV or PO
    Cellular Release
  • Cell lysis: intravascular hemolysis, rhabdomyolysis, tumor lysis syndrome
  • Insulin deficiency
  • Hyperosmolar state: hyperglycemia
  • Metabolic acidosis: all except DKA or lactic
  • Beta blocker, succinylcholine
    Decreased Renal Excretion of K
  • renal failure
  • decreased renin-aldosterone activity
    - decreased aldosterone secretion: ACEi/ARB, heparin
    - reduced response to aldosterone: K sparing diuretics
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12
Q

Discuss the presentation and management of hyperkalemia

A 
Presentation
- asymptomatic
- nausea
- palpitation
- muscle weakness
- muscle stiffness
- paresthesia
- arrhytmia
Investigation
- Rule out/in Lab Artifact
- Rule out/in increased intake
- Determine acute vs chronic
      - acute due to cell shift
      - also trauma, chemotherapy
- Chronic due to decreased renal secretion
      - high creatinine
      - ACEi/ARB/heparin/K-sparing diuretic
      - plasma renin activity, serum aldosterone, and serum cortisol
               - normal plasma renin and low serum aldosterone suggest decreased aldosterone secretion
               - normal plasma renin and normal aldosterone suggest reduced response
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13
Q

Discuss the ECG findings for hyperkalemia

A

Usually at K 6.5

  • Peaked and narrow T waves, taller than QRS
  • decreased amplitude and loss of P wave
  • prolonged PR
  • widened QRS
  • AV block, VFib, asystole
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14
Q

Discuss the management of hyperkalemia

A

Lower Hyperkalemia to Stabilize

  • emergency if ECG changes or symptomatic
  • ECG Changes: Calcium gluconate 1-2amp (10mL) IV to stabilize cardiac membrane for 30-60min
  • Cell shift
    - Insulin Regular 10-20 units IV with 1-2 am D50W
    - onset 15-30 min last 1-2 hrs
    - Beta2-agonist Ventolin nebulized 10mg or 0.5mg IV
    - onset 30-90 minutes
    - NaHCO3 1-3amps
    - onset 15-30 minutes
  • Eliminate K
    - kidney function intact then furosemide 40mg IV
    - renail failure: dialysis
    - Kayexalate to increase bowel excretion of K
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15
Q

Discuss the definition and signs of hypocalcemia

A 
- total corrected Ca <2.25mmol/L
Low PTH
- hypoparathyroidism
      - iatrogenic: neck surgery, iodine ablation
      - primary: idiopathic, autoimmune, infiltrative
- hypomagnesemia
- hemachromatosis
Vitamin D Related
- vitamin D deficiency: decreased intake, malabsorption, nephrotic syndrome medication
- renal failure
Other
- PTH resistance
- Calcitonin, loop diuretics
- Acute pancreatitis
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16
Q

Discuss the presentation of acute and chronic hypocalcemia

A

Acute
- neurologic: delirium, psychiatric symptoms, paresthesia, hyperreflexia
- Trousseau sign: tetany of the hand and forearm resulting in flexion of wrist and MCP as well of extension DIP/PIP when blood pressure cuff inflated
- Chvostek’s sign: tetany of facial nerve when tapped at jaw angle, resulting in twitch of nose/lips
Chronic Hypocalcemia
- neurologic: seizures, Parkinson’s dystonia, papillaedemia
- prolonged QT
- steatorrhea
- dry, scaling, alopecia, brittel and transveresely fissure nails
- cataract
- lethargy, generalized muscle weakness and wasting

17
Q

Discuss the diagnostic approach to hypocalcemia

A

Low Ca Initial Investigations
- PTH
- PO4
- Mg
- Urine Ca
- Creatinine
High PTH
- Normal PO4
- pseudohypoparathyroidism
- acute pancreatitis (release of pancreatic caldecrin decrease bone resorption)
- Drugs (loop diuretic, calcitonin)
- Low PO4
- decrease calcidiol
- decrease intake or malabsorption
- nephrotic syndrome
- drugs: phenobarbitol, phenytoin
- decrease calcitriol
- chronic renal failure
- Vit D dependent Rickets type 1
- increase calcitriol
- hereditary vit D resistant rickets type II
- secondary hyperparathryoidism
Normal or Decreased PTH
- low MG: drugs (antineoplastic) or alcoholism
- liver dysfunction: hemachromatosis
- parathyroid gland destruction: iatrogenic or primary hypoparathyroidism

18
Q

Discuss the treatment of hypocalcemia

A 
Mild/Asymptomatic
- ionized Ca >0.8
- increase dietary intake by 1000mg/day
Acute/Symptomatic
- ionized Ca <0.7
- IV Calcium Gluconate 1-2g over 10-20min
- treat hypomagnesium and low vitamin D
19
Q

Discuss the definition and causes for hypercalcemia

A
  • total corrected Ca >2.62 or ionized >1.35
    - total corrected: measured Ca + 0.02(40-albumin)
    - for every decrease in albumin by 10 increase Ca by 0.2
    Primary Hyperparathyroidism
  • adenoma
  • hyperplasia
  • carcinoma
    Tertiary Hyperparathyroidism
  • secondary: increase PTH due to hypocalcemia from renail failure
  • tertiary: increase in PTH after prolonged secondary hyperparathyroidism from renal failure
    Malignancy
  • skeletal
  • hematologic
  • paraneoplastic syndrome
    Vitamin D Related
  • excessive intake
  • excessive calcitriol
  • granulomatous disease: TB, sarcoid
    High Bone Turn over
  • immobilization
  • vitamin A intoxication
  • hyperthyroidism
  • Paget
    Medication
  • Thiazide
  • estrogen
  • lithium
20
Q

Discuss the approach to hypercalcemia

A
  • assess for PTH, PO4, Mg, Urine Ca, and creatinine
    Low PTH
  • Low PO4
    - humoral medication
  • Normal or high PO4
    - high calcidiol: hypervitaminosis D
    - High calcitriol: Granulomatous disease or excessive calcitriol intake
    • Low Vit D metabolite: immobilization, malignancy, high bone turnover, milk alkali syndrome, drugs
      Normal or Elevated PTH
  • Drugs: lithium
  • Familial hypocalciuric hypercalcemia
  • Primary hyperparathyroidism
  • tertiary hyperparathyroidism
21
Q

Discuss the presentation of hypercalcemia

A 
Moans
- abdominal pain
Groans
Stones
- nephrolithiasis
Bones
- bony pain
Psychiatric overtones
- psychosis
Others
- hypertension, arrhythmia, short QT
- pancreatitis
- polyuria, polydispsia
- pseudogout, chondrocalcinosis
Hypercalcemia Crisis
- total corrected >4 presenting with oliguria/anuria and mental status change
22
Q

Discuss the acute management of hypercalcemia

A

Volume Expansion
- normal saline IV 300-500cc/h and adjusted to maintain urine output 100-150mL/hr
- if HF, then furosemide
Lower Calcium Levels
- Calcitonin 4 units/kg SC/IM Q12H to transiently decrease Ca
- bisphosphonate pamidronate IV 60-90mg IV single dose over 2hrs
- Prednisone 20-40mg PO OD if vit D toxicity, granulomatous disease or hematological malignancy
- dialysis

23
Q

Discuss the normal range for arterial and venous blood gas

A 
Arterial
- pH 7.35-7.45
- pO2 80-100
- HCO3 22-26
- pCO2 35-45
Venous
- pH 7.32-7.42
- pO2 28-48
- HCO3 19-25
- pCO2 38-52
24
Q

Discuss interpretation of acid base disorders

A

pH <7.35
- pCO2 >45 then respiratory acidosis
- pCO2 <45 and HCO3 <19 then metabolic acidosis
pH 7.35-7.45
- pCO2 and HCO3 are in opposite direction then mixed disturbance
pH >7.45
- pCO2 <45 then respiratory alkalosis
- pCO2 >45 and HCO3 >26 then metabolic alkalosis

25
Q

Discuss compensation for acid base disorders

A

Metabolic acidosis
- fall in HCO3 have equal fall in pCO2
Metabolic Alkalosis
- every 10 increase in HCO3 have 6 increase in pCO2
Respiratory Acidosis
- acute: every 10 increase in pCO2 have 1 increase in HCO3
- chronic every 10 increase in pCO2 have 3 increase in HCO3
Respiratory Alkalosis
- acute every 10 decrease in pCO2 have 2 decrease in HCO3
- chronic: every 10 decrease in pCO2 have 5 decrease in HCO3

26
Q

Discuss the presentation and management of metabolic acidosis

A

Presentation
- nonspecific: headache, altered mental status, n/v
- Kussmaul breathing as respiratory compensation
- arrhythmia
Management
- Underlying cause (MUDPILESCT)
- DKA: insulin
- Aspirin: alkaline diuresis
- Alcohol: ethanol and dialysis
- Renal failure: dialysis
- lactic acidosis: address decreased perfusion
- Correct co-existing hyperkalemia
- Reverse acidosis with bicarbonate
- 50mL 7.2% if pH <7, HCO3 <8 or salicylate/alcohol poisoning

27
Q

Discuss the presentation and management for metabolic alkalosis

A 
Presentation
- hypovolemia
- hypokalemia
Management
- treat underlying cause
      - vomiting or NG suction then PPI
      - for diuretics then discontinue
- Address electrolyte abnormality
      - replinish K and Mg deficit
- Reverse alkalosis
      - normal saline at 100mL/h for hypovolemia
- KCl and K sparing diuretics if volume overloaded
28
Q

List the equation for correcting hyponatremia

A

Change in Na = [infusate Na - serum Na]/(TBW+1)

- TBW: 0.6xkg for men and 0.5xkg for women

29
Q

List the equation for H2O deficit for correcting hypernatremia

A

H2o Deficit: TBW x [Na plasma - 140)/140]

- Hourly infusion rate is H20 deficit in mL/hr

30
Q

Discuss how to calculate osmolar gap

A

Osmolality: 2xNa + (Urea+Glucose)

Osmolar gap <10

LMCC - Medicine (40 decks)

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