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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