Electrolyte Osmolarity Regulation

Electrolyte

Any ion that can hold a charge

Osmolarity

Measures concentration per volume (kg)

Osmolality

Measures concentration per weight (kg)

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Produces excess antidiuretic hormone leading to water retention and Na loss, dropping osmolarity

Antidiuretic hormone (ADH)/ Vasopressin

Regulates water and electrolyte balance; synthesized in hypothalamus and released from posterior pituitary gland

Dehydration

Involves ADH and SIADH, causing retention of ALL water in tissues

Renin Angiotensin Aldosterone System

Controlled by aldosterone, allows Na reabsorption but K loss, with water following Na

Hyponatremia

Weakness, fatigue, muscle paralysis, coma due to low Na <135 mmol/L

Hypokalemia

Weakness, fatigue, muscle paralysis, coma due to low K <3.5 mmol/L

Hypernatremia

Confusion, twitching, numbness, cardiac arrhythmia due to high Na >145 mmol/L

Hyperkalemia

Confusion, twitching, numbness, cardiac arrhythmia due to high K >5.5 mmol/L

Divalent cations

Ions with a 2+ valence, e.g., Ca2+ and Mg2+, contributing to neurologic, muscle function, and bone development

Hypomagnesemia

Symptoms include seizures, weakness, and tetany (involuntary muscle contraction)

Hypermagnesemia

Symptoms include nephrolithiasis, diabetes insipidus, depression, weakness, and gastrointestinal issues

Chloride (Cl)

Most abundant extracellular anion, follows Na; important in osmotic pressure

Cl shifts

Cl exchanges for HCO3 to regulate pH and electrical neutrality

Bicarbonate (HCO3)

Large factor in osmotic pressure, linked to chloride shifts

Lactate

Balances and maintains electrical neutrality; produced during anaerobic glycolysis

Lactate prescence

anaerobic glycolysis, insulin 0, insulin insensitivity high

Anion Gap (AG) ratio

High insensitivity, reflects unmeasured anions balancing cations in blood

AG ratio formula

cation-anion

Elevated AG ratio

more unmeasured anions in blood, something is not being measured

Mercury (Hg)

No identified use in human physiology, poisoning leads to neurologic side effects targeting the CNS

Lead (Pb)

Exposure leads to neurologic damage, coma, rashes, and death; around 10 microliters can poison a child

Blood Lead Level (BLL)

Measures Pb in a sample using mass spec method

Ferrous

Fe2+ is what we absorb and use for biochemical reactions

Copper (Cu)

Reduces Fe to aid heme synthesis; excess leads to various pathologies

Arsenic (As)

Common in seafood, exposure causes acute and chronic issues; treated with activated charcoal or chelating agents

Vitamins ADEKB12

Stored in the liver, fat soluble

Thiamine

Stored in erythrocytes

Ferric

Fe3+ is used for storage in the body

Fe deficiency anemia (IDA)

not enough Fe to put in centers of protoporphyrin ix, cannot make heme to provide O2

Fe overload

trying to turn Fe into abundance, resulting in Fe in tissues, DNA damage, carcinogens, neurologic damage

Wilsons disease

increased ceruloplasmin, not necessarily Cu

vitamin b12

bind with intrinsic factor to keep it safe in intestine to bind to receptors that recognize only the b12 intrinsic factor complex

vitamin C

water soluble antioxidant blocks free radicals

vitamin c folate (B9)

lipid chains are clipped by 2 via beta oxidation, this clips the remaining one in cases of odd chains

folate deficiency

causes megaloblastic anemia just like B12 without the neurologic damage

calcitonin

puts Ca in bones, drops Ca levels

Vitamin D

increases total Ca levels and conserves Ca in kidneys to absorb more in gut to increase body Ca

PTH serum

increases [Ca] by taking it Ca from bones, great short term, increases osteoporosis chance long term

mechanisms for hypercalcemia malignancy

tumors release PTH related peptides and osteolytic metastases

acidic

rich in hydrogen ions

hypoxia

general term that we are breathing less oxygen

hypoxemia

have low levels of oxygen in blood, can have it even when breathing normal amounts

alkalosis

pCO2 is decreased or HCO3 is increased

ratio of bicarbonate to carbonic acid in normal pH

1:20

pH range

7.35-7.45

metabolic acidosis with respiratory compensation

too much H+, breathe quicker so more CO2 escapes, decrease pCO2

metabolic alkalosis with respiratory compensation

lacking H+, breathe slower, H+ accumulates, drops pH

Respiratory compensation

lungs response to stabilize acid base disturbance by controlling pCO2 in blood

Respiratory acidosis with metabolic compensation

increase HCO3, kidneys increase secretion of H+ to bind NH3 to become NH4

Respiratory alkalosis with metabolic compensation

decrease HCO3, breathe to fast to lose CO2 and pass out, breathing returns to normal before kidneys compensate

metabolic compensation

kidneys response to acid base disturbance by controlling HCO3 in blood

O2 dissociation curve

affinity changes between o2 and hemoglobin to release O2

alkylosis O2 dissociation curve

goes left, o2 binds more readily

acidosis o2 disassociation curve

peripheral tissues curve goes right, facilitates O2 unloading

blood gases measures:

pO2, pCO2, and pH, HCO3 is calculated

metabolic compensation controls

bicarbonate concentration

metabolic compensation occurs

a few days

respiratory concentration controls

pCO2 concentration

respiratory compensation occurs

immediately