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Hypocalcemia
[Ca < 8.5 or ionized Ca level < 4.6mg/dL (1.2mmol/L)]
Hypocalcemia causes
Nutritional deficiencies
Lack of dairy or green leafy vegetables -Lack of Vitamin D needed for Ca absorption
Renal failure - decreased production of activated vitamin D & hyperphosphatemia
Hypoparathyroidism
Alkalosis decreased ionized Ca by binding more calcium to proteins, less
Ca available for stabilization of the neuromuscular membrane
Hypocalcemia Manifestations
increased excitability & repetitive responses to 1 stimulus
Neuro – paresthesia, muscle spasms, tetany, hyperactive reflexes
CV – hypotension, HF, long QT, cardiac arrhythmias
Skeletal - Fractures (chronic)
Hypocalcemia Assessment
Tapping on facial nerve, spazzing of lip/nose/face
Bp cuff above 10 mm - retraction of hand/fingers
Hypercalcemia
[Ca > 10.5]
Hypercalcemia Causes
Malignancy
cancer destroys bone thereby releasing calcium into body
tumors produce PTH which increase Ca levels
Hyperparathyroidism
Other causes – prolonged immobilization, excessive doses of vitamin D, and meds such as lithium & thiazide diuretics
Hypercalcemia Manifestations
decreased neuronal excitability & muscle function
Neuro – lethargic, behavioral changes, coma
CV – HTN, increased contractility, arrhythmias
GI – N/V, constipation
GU – high output, renal calculi
Hypokalemia
[K < 3.5 mEq/L] a lower than normal potassium level in your bloodstream
Hypokalemia causes
inadequate intake via diet – less than 40mEq/ day.
1. Fad diets, eating disorders & elderly who have difficulty chewing foods that are high in K (Foods high in potassium – broccoli, green beans, bananas)
ii. excessive loss
diuretic therapy, metabolic acidosis, excessive GI loss from
vomiting & diarrhea.
Primary aldosteronism caused by tumor of adrenal cortex will
abnormally excrete aldosterone into circulation.
Transcelluar shifts such as Treatment of DKA which will talk about
later. (insulin pulls K back into cells)
Hypokalemia manifestations
Neuro – weakness (mild), fatigue, paresthesia (mild)
CV - * ECG changes, peaked T waves (mild) lethal arrhythmias cardiac arrest
GI – Diarrhea, cramps (mild) Muscle weakness (severe)
GU - polyurea (kidneys are going to attempt to reabsorb K, so
sodium will be exchanged for K and water will follow → dilute
urine)
Hyperkalemia
a potassium level in your blood that's higher than normal
Hyperkalemia causes
1. Decreased renal elimination
GFR is less than 10ml/minute (90-120ml/minute)
Chronic Renal Failure
Acute Renal Failure with lactic acidosis or ketoacidosis
Aldosterone – mediated potassium elimination
a. Aldosterone is depressed causing sodium to be excreted + K retained.
b. Adrenal insufficiency & decreased renin release
Movement of K from ICF to ECF
Acidosis - K moves out of cell into the ECF for unknown reasons
tissue injury (burns & crushing trauma) release intracellular K into
ECF from cell death
Excessive rapid rate of administration
Hyperkalemia manifestations
Neuro – weakness (mild), fatigue, paresthesia (mild), tingling of
fingers
CV - * ECG changes, peaked +narrow T waves (mild) lethal
arrhythmias cardiac arrest, shortened QT interval
1. Severe - prolonged PR interval, widened QRS which will
delay repolarization of cells → Vbif → cardiac arrest
R – dyspnea (muscle weakness)
GI – Diarrhea, cramps (mild) Muscle weakness (severe), lost of muscle tone (severe)
c. Mild > 5.0 mEq/L ; severe > 6.0 mEq/L
Hyponatremia [sodium < 135 mEq/L]
[sodium < 135 mEq/L]
Hyponatremia Types
Hypotonic- dilution
Hypertonic-osmotic shift form ICF to ECF
Hyponatremia - Hypotonic
Excessive sweating, GI losses, SIADH, heart failure
Water is used as a replacement for electrolyte containing fluid
Hyponatremia- hypertonic
1. Hyperglycemia
2. Sodium in ECF becomes diluted as water moves out of body cells
in response to osmotic effects of elevated blood glucose levels
Hyponatremia manifestations
body is going to attempt to compensate by pulling water into the cell, so some of
the symptoms have to a lot to do with muscle bc sodium laters the ability of the cells to depolarize and repolarize normally
Depend on severity and onset
Muscle cramps
Motor weakness
Fatigue
Headaches
Confusion
Seizures (<120 sodium)
1. Cerebral edema from influx of fluids into the cells
Hypernatremia
[sodium > 145 mEq/L & Serum Osmolality >295]
Hypertonicity of ECF & intracellular dehydration
i. Intracellular water pulled into ECF component → cells shrink
Hypernatremia causes
Disproportionate loss of body H2O in relation to Na
1. At risk individuals - ventilator, elderly, babies (patients who have the inability to obtain a drink of water)
ii. sodium gain
Hypernatremia manifestations
Thirst - early symptom
Low urine output + increased urine osmolality
Weak, thready, elevated pulse
Low bp
Dry mucous membranes
Dry and rough tongue
Difficulty swallowing
Irritability
Restlessness
Headache
Muscle spasms
Seizures
Hypomagnesemia
[Serum Magnesium < 1.3 mg/dL + S&S occur when < 1.0 mg/dL]
-similar to hypocalcemia
Hypomagnesemia causes
Decreased intake or malnutrition
Loss – diarrhea, decreased absorption, NG output, diuretics
Hypomagnesemia Increased neuromuscular excitability:
Personality changes
Muscular weakness & tremors
Hyperactive reflexes
Seizures – increased irritability of nervous tissue
Hypomagnesemia cardiovascular effects
Tachycardia
Hypertension
Ventricular arrhythmias
Leads to a reduction in intracellular potassium and interferes the kidney’s ability to concentrate potassium
Hypermagnesemia
[Serum Magnesium > 2.1 mg/dL + S&S occur when > 4.0 mg/dL]
Hypermagnesemia causes
Renal insufficiency or failure
1. Can’t be excreted from body
ii. Injudicious use of magnesium containing drugs
Use antacids
Hypermagnesemia causes
Renal insufficiency or failure
1. Can’t be excreted from body
ii. Injudicious use of magnesium containing drugs
Use antacids
Hypermagnesemia neural and muscle effects
Lethargy
Hyporeflexia & muscle weakness – from decreased acetylcholine release
at myoneural junction
1. Myoneural junction – junction between a nerve fiber and muscle it
supplies
iii. Confusion, may lead to coma
Hypermagnesemia cardiovascular effects
Hypotension
Cardiac arrhythmias
Cardiac arrest
When hypomagnesemia occurs, it leads to reduction in intracellular K and impairs the ability of the kidneys to conserve K, leading to hypokalemia
When hypomagnesemia is present, hypokalemia is unresponsive to potassium replacement therapy.