Lytes acid and base Flashcards
All lytes are measured in
mEq/L
Sodium level
135-145
K+ level
3.5-5.0
Ca2+ level
4.5-5.5
Phosphate level
2.5-4.5
Mg level
1.5-2.5
Sodium function
90% of ECF cations Regulates osmotic forces and H20 balance For muscle and nerves with K and Ca Helps with pH through sodium bicarb and sodium phosphate Particaptes in cell reactions
Hypernatremia
> 145
From extra sodium or too little water
It causes intracellular dehydration and movement of water to ECF which may cause hypervolemia
Hypernatremia etiology
1. Excessive water loss from Diabetes insipidus Fever Resp infections (tachypnea) Diarrhea (osmotic) 2. Too little water 3. Too much sodium too much Nabicarb Saltwater near drowning Over secretion of aldosterone
ADH
Vasopressin
Increases solute free water reabsorption
Constricts arteries
Released from hypertonicity
Clinical manifestations
- Thirst and signs of high ADH (polydipsia, oliguria, anuria)
- Intracellular dehydration
- H20 out of cells (headache, agitation, restlesness, decreased reflexes, seizures)
- Decreased vascular volume - tachy, weak and thready pulse, low BP
Hyponatremia
<135
Vomiting, diarrhea (inflammatory) GI suctioning, burns, sweating, lack of salt intake
Some diuretics
Hormone imbalances (low aldosterone high ADH)
Too much water
Kidney failure
Hypeglycemia as it draws water into ECF, lowering serum Na
Clinical manifestations of hyponatermia
Cramps, weakness, headache, depression, apprehension, impending doom, personality changes, lethargy, stupor, coma (from nerves not being able to depolarize)
GI - anorexia, nausea, vomting, cramps, diarrhea
Increased ICF causing pitting edema and hypotension
Potassium function
Maintaining RMP
Predominant ICF cation
Regulation of K+
Kidneys via diffusion, distal tubular cells determines whether it will be secreted into urine or reabsorbed into distal tubules
K+ and diuretics
increase flow rate of K+ through distal tubules increasing K+ secretion
There are K+ sparing diuretics which can counter this
K+ and pH
H+ accumulate in ICF and kick K+ out of cell
decreased ICF decreases secretion of K+ by distal tubular cells creating a state of hyper K
Hyper K causes
> 5.5 mEq/L
From increased K+
or a shift out of cells from
Trauma, burns, crush injuries, acidosis, insulin deficiency, hypoxia
Also decreased renal excretion from renal failure, aldosterone deficit, K+ sparing diuretics, ACE inhibtors, Angiotensin II receptor blockers
Hyper K clinical manifestation
GI -nausea, vomiting, cramps, diarrhea Muscles -paraesthesia -muscle weakness Cardiovascular -arrythmias, cardiac arrest Oligura Acidosis
Hypo K
<3.5 from
- Inadeqaute intake
- Renal loss (non K+ sparing, cushings, aldosteronism, steroids)
- Vomiting, diarrhea, GI suction, draining GI fistula
- Transcompartmental shift from ventolin, alkalosis, insulin
Hypo K presentation
Impaired ability to concentrate urine (polyuria nocturia)
Anorexia, nausea, vomiting, constipation, abdo distension, paralytic ileus
Muscle flabbiness, weakness, fatigue, paresthesia, paralysis, cramps
ECG changes, postural hypotension
Confusion, depression
Alkalosis
Where is calcium
99% in bone
.4 ionized
.6 non ionzed (bounded to albumin)
Calcium is needed for
Structure (bone teeth) Clotting Hormone secretion, cell function Plasma membrane stability Transmission of nerve impulses Contraction of muscles
Calcitonin
Opposes PTH, and REDUCES blood calcium
Calcium/phopshate mediated by
PTH
Vit D
Calcitonin
Hypercalcemia
<12mg/dl
From:
Too much D or calcium
Milk-alkali syndrome
Increased bone resporption (hyperPTH, bone metasis from cancer, immobility)
Decreased elim from thiazides or lithium
Acidosis (decreases Ca binding to albumin)
Hypercalcemia clinical manifestations
Polyuria, dipsia, flank pain, renal failure, kidney stones
Anorexia, N/V, constipation
Muscle weakness, atrophy, ataxia, loss of tone
Osteopenia (low density but not porosis low), osteoprosis
Lethargy, personality and behaviour changes, stupor coma
hypertension, QT shortening, AV block
Hypocalcemia
<8.5mg/dl
HypoPTH, hypomag, resistance to PTH
Decreased intake from vit d deficiency, liver or renal failure
Abnormal loss from too much phosphate or renal failure
Hypocalcemia etiology
increased protein binding or chelation
Increased pH increases serum albumin increases fatty acids or rapid transfusion of citrated blood
Pancreatisi
Hypocalcemia clinical manifestations
Paraestehsia, cramps, gi spams, carpopedal spasm, tetany (intermittent spasm from PTH), laryngospasm
Hypotension, arrythmias
Osteomalacia, bone pain, fractures, deformities
Phosphate overview
Mainly in bone
Serum it exists in phospholipids and inorganic compounds
Acts as a buffer and role in high energy stores
Hyperphosphatemia
<4.5mg/dl
Laxatives or enemas with phosphates
Intracellular to extra shift from trauma, heat stroke, seziures, rhabdo, tumor
Impaired elimination (renal failure or hyperthyroidism)
Clinical manifestations
same as low calcium
Hypophosphatemia
<2mg/dl Severe diarrhea Lack of D Antacids binding phosphates Increased renal secretion HyperPTH, DKA, alkalosis malnutrtion Total parental hyperalimentation, insulin from DKA
Hypophosphatemia manifestations
Reduced O2 capacity by RBC
ATP issues
2,3 diphospho used to release oxygen, so decrese will shift to left (causing hypoxia)
Hemorrhage from altere leukocyte and platelet function
Irritability, confusion, numbness, weakness, chest pain, convulsions
Mg
Major intracellular cation
Cofactor in intracellular enzymatic reactions (ATP?)
Hypomag
<1.5 From absorption issues (ETOH, starvation, bowel bypass or increased losses (diuretics, hyperPT, hyperaldost, DKA)
Hypomag clinical manifestations
Similar to hypo calc and hypo K because they occur in conjucation
Tachy, hypertensive, arrythmias
Hypermag
> 2.5
Too much mag sulfate, or kidneys can’t excrete
N/V lethargy, HYPOreflexia, confusion, hypotension, brady, cardiac arrest, resp depression
Osmolality definition
Refers to concentration of solutes in soluction, term used in reference to extracellular space
Isotonic imbalance
Changes in body water equal with lytes. No cell shape changes
Isotonic volume depletion causes
Inadequate fluid
Excessive GI fluid loss, renal loss, skin loss, third space loss
Hypertonic imbalance
> 0.9% Na+ causes ECF to attract water from intracellular space (ICF dehydration) cells shrink due to water loss
Hypotonic imbalance
Hypo-osmalar ECF less than 09% from sodium deficinecy or excess water causes edema and decreased plasma volume so symptoms of hypovolemia
Metabolic acidosis causes
Lactic acid build up from poor perfusion
Kidney failure
DKA
Ingestion of ammounium chloride, salicylates
Loss of bicarb from diarrhea or renal failure
Metabolic acidosis clinical
Neuro, resp, GI, CV issues Headache Kussmauls Anorexia dysrhythmias Resp increases CO2 exhalation to compensate
Metabolic alkalosis
Increases in bicarb or loss of acid from GI suctioning or vomiting
Too much bicarb
Diuretics
Causes weakness cramps hyperactive reflexes and tetany
CO2 retained to compensate
Resp acidosis
Hypercapnia (retained CO2) from depressed vent or decreased alveoli diffusion, chronic or acute
Trauma or oversedation
Resp muscle paraylsis
Kyphoscoliosis, flail, pneumonia, pulmonary edmea, emphysema, asthma, bronchitis
Kidneys compensate by retaining bicarb (HCO3-) and pissing out H+ but takes hours to days
Resp acidosis clinical
Restlessness, apprehension, lethargy, muscle twitching, tremors, convulsions, coma
CO2 can cross blood brain and drop CSF pH and cause vasodilation
Resp alkolosis
Hypoxemia (pulmonary disease, CHF, high altitudes) fever, anemia, sepsis, salicyate OD (EARLY) hysteria, improper vent use
Irritates CNS and PNS, dizziness, convulsions
Carpopedal spasm
