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SEARCH RESULTS FOR: Hypomagnesemia

Approach to Arterial Blood Gases ABGs

Approach to Arterial Blood Gases (ABGs) Normal pO2 should be FiO2 x 4-5 (FiO2 in room air= 21%) pH >7.40 = Alkalemia 1. Adequate oxygenation? 2. Define the acid-base disturbance Diarrhea (Loss of electrolytes not reabsorbed through bowel) Normal ABG on Room Air = 7.40 / 40 / 90 / 24 pO2 ↓ than expected Possible hypoxemia See slide on Hypoxemia: Pathogenesis and Clinical Findings (pH) (Loss of acidic fluids from stomach) (HCO3-) (pCO2) (pO2) Renal Tubular Acidosis (RTA) pH <7.40 = Acidemia Metabolic derangement (Due to poisons, infection, or ketones) Gain of acid (H+) Brain unable to promote respiratory drive (ex. drugs, trauma) Inability for chest wall to expand (ex. obesity, neuromuscular weakness, pleural or chest wall abnormalities) Vomiting or nasogastric suction Impaired tubular transport of H+ (Due to loop/thiazide diuretics, hypomagnesemia, congenital abnormalities) 1o Hyperaldosteronism = ↑ H+ ion secretion at distal tubule (Due to tumours, congenital abnormalities , malignant hypertension, etc) Type II RTA = HCO3- not reabsorbed Type I or IV RTA = H+ not secreted GI or renal loss of HCO3- Hypoventilation ↑ CO2 from ↓ exhalation Respiratory Acidosis Acute= ↑10:↑1, Chronic= ↑10:↑3 GI or renal loss of acid (H+) ↑ HCO3- from ↓ H+ to bind with Metabolic Alkalosis ↑7:↑10 ↑ Ventilation from stress, trauma, infection ↓ CO2 from ↑ exhalation Respiratory Alkalosis Acute= ↓10:↓2, Chronic= ↓10:↓4 3. Identify the primary (1o) process 4. Compensatory mechanisms in lungs and kidneys attempt to lose/retain CO2 or HCO3- to maintain normal pH. Determine if compensation is appropriate (approximate normal ratio of change in pCO2 : HCO3- is shown in green boxes). If inappropriate, there is a secondary (2o) process occurring HCO3- binds with extra H+ ↓ HCO3- Metabolic Acidosis ↓12 :↓10 Less CO2 than expected, due to ↑ exhalation = Less acid in serum 2o Respiratory alkalosis More CO2 than expected, due to ↓ exhalation = More acid in serum 2o Respiratory acidosis Less HCO3- than expected, due to 2o gain of H+ or loss of HCO3- 2o Metabolic acidosis More HCO3- than expected, due to 2o loss of H+ 2o Metabolic alkalosis Less CO2 than expected, due to ↑ exhalation = Less acid in serum 2o Respiratory alkalosis ↑ CO2 than expected, due to ↓ exhalation = More acid in serum 2o Respiratory acidosis Less HCO3- than expected, due to 2o gain of H+ or loss of HCO3- 2o Metabolic acidosis More HCO3- than expected, due to 2o loss of H+ 2o Metabolic alkalosis 5. Calculate anion gap (AG) to determine the presence and type of metabolic acidosis. This is done regardlessofthe1o or2oprocess, as there may also be a hidden metabolic acidosis 6. HAGMA only: In normal blood buffer system, acid gain should match bicarbonate lost. If not, identify if another process is causing an inappropriate loss or gain of HCO3- Gain of acid (∆AG) = AG-12 LossofHCO3- (∆HCO3-)=24-HCO3- 7. Calculate Osmolar Gap (for HAGMA) or Urine net charge (for NAGMA) to narrow the etiology Authors: Sravya Kakumanu Reviewers: Huneza Nadeem, Ben Campbell *Adam Bass, *Yan Yu * MD at time of publication (normal is ~12) Calculate AG = Na+- Cl- - HCO3- If a metabolic acidosis is present, ↓ HCO3- is compensatedby↑otherserumanionstomaintain neutral charge If no metabolic acidosis was identified in steps 2-4: No Metabolic acidosis present Classically, the compensating anion is Cl-,maintaininganormalAG AG ≤ 12 If a 1o or 2o metabolic acidosis was identified in steps 2-4: Normal Anion Gap Metabolic Acidosis (NAGMA) In this scenario, a normal distal nephron should be excreting excess acid Excess acid is normally excreted as ammonium (NH +) with Cl- 4 The more Cl- in the urine relative to cations, the more acid is being excreted Calculate urine (U) net charge to determine cause of NAGMA = UNa+ + UK+ - UCl- When the cause is addition of an abnormal acid, HCO3- is used up asabuffer,andthecompensatinganionistheabnormalacid's conjugate base – which is not measured in the AG calculation ↓ HCO3- is compensated by unmeasured anionsà the AG ↑ AG>12 High Anion Gap Metabolic Acidosis (HAGMA) Calculate ∆AG = AG-12 Calculate ∆HCO3- = 24-HCO3- ∆HCO3- > ∆AG Loss of HCO3- > Gain of acid Additional process causing further loss of HCO3- HAGMA + NAGMA ∆HCO3- = ∆AG Loss of HCO3- = Gain of acid Only acid gain from HAGMA causing HCO3- loss HAGMA only ∆HCO3- < ∆AG Loss of HCO3- < Gain of acid Additional process causing gain of HCO3- despite losses due to HAGMA HAGMA + Metabolic alkalosis See slide on Metabolic Alkalosis: Pathogenesis -ve U net charge Appropriately large Cl- excretionà Toxic alcohol ingestion ↑ serum osmolality (and H+) from metabolites produced, so osmolality helps identify etiology Calculate osmolar gap to determine cause of HAGMA = (measured serum osm) – (expected serum osm) = (measured serum osm) – (2(Na+) + urea + serum glucose) +ve U net charge Inappropriately small Cl- excretionà impaired acid excretion is the issue Type IV or Type I RTA See slide on Normal Anion Gap Metabolic Acidosis: Pathogenesis and Laboratory Findings HCO3 GI losses or Type II RTA - loss is the issue Osmolar gap > 10 (extra osmoles present) Toxic alcohol poisoning Osmolar gap ≤10 (normal) Test for other causes See slide on High Anion Gap Metabolic Acidosis: Pathogenesis and Laboratory Findings Legend: Disease State Mechanism Lab Finding/Calculation Published January 29, 2023 on www.thecalgaryguide.com

Hypomagnesemia

Hypomagnesemia: Physiology Hyperglycemia An increased amount of glucose enters renal tubules as glomerulus performs blood filtration ↑ [Solute] in renal tubules from ↑ glucose content exerts osmotic force that pulls water & electrolytes, including Mg2+, into renal tubules ↑ Urinary Mg2+ excretion Lack of insulin Lack of insulin receptor signaling in distal convoluted tubule (DCT) ↓ glucose uptake from renal tubules Hypercalcemia Ca2+ binds to Ca2+ sensing receptors on thick ascending limb (TAL) of loop of Henle, where resorption of Ca2+ & Mg2+ occurs Receptor activation ↓ Na-K- 2Cl (NKCC) transporter activity which maintains electro- chemical gradient in TAL Passive paracellular resorption of Ca2+ and Mg2+, dependent on electrochemical gradient, ↓ ↑ Extra- cellular fluid ↓ Resorption of Na+ & H2O from renal tubules Genetic disorders (e.g. Bartter syndrome, familial hypomagnesemia) Medications (e.g. loop & thiazide diuretics, certain antibiotics, calcineurin inhibitors) Some metabolic byproducts of these drugs are nephrotoxic Inability to absorb free fatty acids (FFAs) Mg2+, which associates with FFAs, is not absorbed through the gut Steatorrhea (fat in the stool) Mal- absorption (often due to inflammation or infection) & diarrhea Acute pancreatitis ↓ Lipase secretion from pancreas ↑ levels of undigested fats in small intestine ↓ Passive Mg resorption from tubules Mg saponification in necrotic fat 2+ Varying mechanisms causing defective Mg2+ re-absorption (e.g. impacts to PCT, TAL, DCT disrupting transporters and ion shifting; ↓ gut resorption of Mg2+) Nutrients & 2+ electrolytes are lost in stool undergoes Renal loss of magnesium Gastrointestinal loss of magnesium Hypomagnesemia Serum [Mg2+] < 0.7 mmol/L Impairs production and release of parathyroid hormone responsible for ↑ blood Ca2+ Hypocalcemia Muscle cells are unable to activate Mg2+ dependent ATP hydrolysis Impairs muscle relaxation and reduces the ability to stop muscular contraction Lack of Ca2+ disrupts neurotransmitter release and neuronal signaling Impairs rapid depolarization and repolarization during muscle contraction Neuromuscular excitability (large, rapid change in membrane voltage due to small stimulus) Delirium Apathy QRS widening and peaking of T waves on ECG Torsade de Pointes Constant muscle contraction compresses blood vessels Reduced blood supply to hands, wrists, feet, and ankles Trousseau sign (carpopedal spasm with inflation of BP cuff) Authors: Caroline Kokorudz Reviewers: Shyla Bharadia Allesha Eman Michelle J. Chen Dr. Adam Bass* * MD at time of publication Chvostek sign (facial muscle twitch with cheek touch) Seizures Tetany Weakness Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Oct 4, 2024 on www.thecalgaryguide.com

Loop diuretics

Loop Diuretics: Mechanism & side effects Inhibit Na+/K+/2Cl- (NKCC) symporter at thick ascending limb of Loop of Henle (aLOH) Authors: Andrew Wu, Rafael Sanguinetti Reviewers: Luiza Radu, Adam Bass* * MD at time of publication Over-inhibition of ion symporter in ear at high concentrations Damage to tight junctions in the blood vessel epithelium in the ear Disruption of the blood- cochlear barrier Hearing loss Opening of ATP-sensitive K+ channels on pancreatic β- cells causes efflux of K+ ↓ Intracellular K+ causes a negative intracellular charge ↓ Ability for pancreatic β- cells to depolarize & release insulin Hyperglycemia (rare) Stimulation of prostaglandin E2 (PGE2) synthesis in the cortical & medullary aLOH Stimulation of endothelial nitric oxide synthase releases nitric oxide Systemic venodilation (dilation of veins) ↓ Systemic vascular resistance ↓ Blood pressure ↓ Na+ in renal interstitium ↓ Water reabsorption (water follows Na+) Interstitial washout (↑ NaCl & water wasting in interstitium) ↓ Sodium (Na+) reabsorption ↑ Positive luminal charge at thick aLOH ↓ Electrochemical gradient reduces cellular transport of cations ↓ Ca2+ & Mg2+ reabsorption in the aLOH Hypocalcaemia & hypomagnesemia ↑ Na+ delivery to the distal convoluted tubule (DCT) ↑ Intracellular Na+ at collecting duct ↑ K+ efflux via renal outer medullary potassium channel (ROMK) ↓ Fluid status ↓ Serum Na+ ↓Serum Cl- ↑ Luminal K+ at alpha intercalated cell Chemical gradient ↑ K+/H+ antiporter activity ↑ K+ excretion Hypokalemia Chemical gradient shifts K+ into cells creating a charge gradient to shift H+ out Hyponatremia Hypovolemia Hypochloremia ↓ Volume status activates angiotensin II, which plays a role in sodium and volume retention ↑ Na+/H+ antiporter 3 (NHE3) activity in the proximal tubule Kidneys excrete & conserve ions to preserve intracellular charge gradient ↑ H+ loss in the urine ↓ Serum H+ ↑ Proximal Na+ reabsorption causes ↑ urate reabsorption via urate-hydroxyl exchangers Hyperuricemia Contraction alkalosis (loss of Na+-rich, HCO3- low fluid) & hypokalemia ↑ Serum HCO3- Metabolic alkalosis (systemic pH > 7.45 due to metabolic process) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Nov 18, 2024 on www.thecalgaryguide.com

Hypocalcemia Pathogenesis

Hypocalcemia: Pathogenesis Malnutrition ↓ Oral intake Acquired (e.g. neck surgery) Autoimmune (e.g., autoimmune polyglandular syndrome) Infiltrative (e.g., hemochro matosis, Wilson’s disease) Congenital (e.g., DiGeorge) Hypomagnesemia Magnesium is needed to produce PTH Malabsorption ↓ Small bowel surface area ↓ Absorption of 25-OH Vitamin D (calcidiol) ↓ Conversion of calcidiol to 1-25 (OH)2 Vitamin D (calcitriol) by 1-α- hydroxylase ↓ Calcitriol (impacts GI absorption of calcium) Chronic Renal Failure ↓ Renal parenchymal mass (site of 1-α- hydroxylase production) Vitamin D Dependent Type 1 Rickets Mutation in the gene that encodes 1-α- hydroxylase ↓ Sun exposure ↓ 1-α-hydroxylase Pancreatitis Destruction or atrophy of parathyroid gland ↓ Parathyroid hormone (PTH) Calcitriol resistance (e.g., Vitamin D Type 2 rickets) Inflammation of pancreas ↑ Release of lipase enzyme into serum ↑ Breakdown of fat by lipase ↑ Free fatty acids in serum ↑ Ca2+ binding to negatively charged tail of free fatty acids ↑ Parathyroid hormone (PTH) PTH resistance Genetic mutation causes body to not respond to PTH ↓ Renal calcium reabsorption ↑ Calcium excretion ↓ Osteoclast activity ↓ Calcium release from bone ↓ Action of PTH on intestinal cells ↓ Absorption of calcium in the small intestine ↑ Serum phosphate (PO4) (e.g. tumor lysis, rhabdomyolysis) ↑ Ca2+ binding to negatively charged PO4 ↑ Serum pH ↓ H+ in serum binding to proteins ↑ Ca2+ binding to proteins Calcium sequestration ↓ Absorption of calcium in the small intestine Hypocalcemia Author: Breanna Fang Reviewers: Gurreet Bhandal, Raafi Ali, Luiza Radu Samuel Fineblit* * MD at time of publication Serum calcium levels below 2.10mmol/L Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Nov 22, 2024 on www.thecalgaryguide.com