Patho Wk 5: Ch.

FLUID DISTURBANCES
Objective: Identify the major consequences/manifestations of abnormal levels of water.
FUNCTIONS OF WATER (its role in our body)

Solvent things can dissolve in H2O

Chemical imbalance altered H2O can lead to altered chemicals

Transports nutrients in/out/to the cell & wastes away from cell

Helps eliminate wastes

Cushions, protects

Lubricates, insulates
WATER = comprises ~60% of the total body weight

ECF+ICF = total body water (sum of all fluids in all compartments)

o Varies with: Age, Weight, & Gender
o Distributed among compartments and spaces moves freely
o Distributed and maintained by osmotic and hydrostatic forces

Intracellular (ICF) = 40% ( ~2/3 of bodys water)

Extracellular (ECF) = 20% ( ~1/3 of bodys water)

o Interstitial = 15% (trans-cellular fluids: lymph, synovial fluid, interstitial fluid, sweat, urine, biliary, hepatic,
CSF, intraocular, peritoneal, pericardial, pleural, etc)
o Intravascular = 5% (in blood/plasma)
WATER REQUIREMENTS

Amount of water necessary to maintain health = 15002500 ml/day

Sources:
o Liquids = 1200 ml; Foods = 1000 ml; Oxidation of food = 300 ml
ROUTES OF WATER LOSS

Kidneys (most) 1-2 liters/day = 1400 ml

Lungs 300-400 ml/day = 300 ml

Skin 0-1000 ml/hr = 600 ml (varies d/t sweating, febrile, etc)

Gastrointestinal tract 100-200 ml/day = 200 ml

WATER LOSS
Sensible
o Urine (MAIN way pee)
o Stool
Insensible
o Lungs breathing
o Skin
OBLIGATORY WATER LOSS

Amt of urine/pee necessary to maintain kidney function = ~300-500 ml/day

Water balance ideally intake = output (happens in euvolemic person)

o 2500 ml intake == 2500 ml output
CAUSES OF WATER LOSS: any work of body or metabolic demand leads to water loss!

Fever (sweating)

Diarrhea, Vomiting

Diaphoresis

Gastric suctioning

Pneumonia ( RR)

Tachypnea
CAUSES OF WATER GAIN

Na+ intake or Na+ retention (Na+ and H2O travel together!)

Patho Wk 5: Ch. 3

Excessive intake of water

Excess secretion of ADH

BODY FLUID COMPARTMENTS

When thinking about labs, the values correlate with ICF vs ECF (would expect high Na+ in ECF, not ICF)

Intracellular (ICF) (40% or ~2/3 of body weight)

o Inside the cells
o Large amounts of K+, PO4 - -, Mg++

Extracellular (ECF) (20% or ~1/3 of body weight)

o Intravascular PLASMA (5% of the body weight)
o Interstitial fluid (15% of the body weight)
o Large amounts of Na+, Ca++, Cl -, and HCO3

Osmosis = movement of H2O DOWN the concentration gradient

HIGH concentrationLOW concentration

Semipermeable membrane Membrane must be more permeable to water

A greater concentration of solutes on one side of the membrane water moves to equal out concentration
Diffusion = movement of SOLUTE molecule from HIGH solute concentration LOW solute concent.
Facilitated Diffusion

Requires a carrier molecule

No energy/ATP required moves HIGHLOW

Ex: Lipid insoluble substances cannot cross plasma membrane (needs glucose carrier)
Active Transport = mvmt of substance across the cell membrane from LOW concentrationHIGH concentration
o ATP is expended
o Ex: Na+/K+ pump
Filtration = mvmt of a fluid through a semipermeable membrane from HIGH pressure area LOW pressure
Hydrostatic Force = the mechanical force of water pushing against cellular membranes
In vascular system hydrostatic pressure = the blood pressure pushing against vascular walls.
Colloid Osmotic Pressure = tendency of plasma proteins to hold water in the intravascular spaces (maintains water in ECF)

Albumin is the plasma protein which exerts the greatest osmotic pressure
o Albumin is formed in the liver
o Most abundant plasma protein
o Binds to hormones and transports them
o Acid-base balance

Globulin
o Antibodies (IgG)
o Humoral immunity
o Transport of iron and fats

Fibrinogen
o Blood coagulation/clotting cascade
Osmolality = a measure of the concentration of molecules per kilogram of water (mOsm/kg weight measurement)

*PREFERRED measure of osmotic activity in clinical assessment

Indicates hydration status, body fluid concentrations

Can measure serum or urine osmolality

Normal osmolality = 285-295 mOsm/kg

Osmolality = 2 (Na) + K + BUN + Glucose

3
18

Patho Wk 5: Ch. 3

Osmolarity = a measure of the concentration of molecules per liter of solution (mOsm/L)

NOTE: Difference btwn osmolality and osmolarity matters what types of solutes you are measuring
o Na & K vs. proteins, glucose lipids present also

Tonicity = describes the effective osmolality of a solution (term interchangeable with osmolality !!)
ISOtonic Solutions has the SAME osmolality as the ECF

Examples
o D5W

Distributes evenly in the body compartments

Used to replace deficits of total body water

o Normal Saline (0.9% NS)

NOTE: Each liter adds liter to ECF & adds liter to interstitial fluid
HYPERtonic Solutions have a HIGHER concentration of solute and are MORE CONCENTRATED than ECF

Examples
o 3% saline
o 5% saline

Net movement (PIC) = ICF ECF

HYPOtonic Solutions have a LOWER concentration of solute and are MORE DILUTE than ECF

Examples
o 1/2 NS
o 1/4 NS

Net movement (PIC): ECF ICF

THIRST = A desire for water

Regulated by osmoreceptors in the hypothalamus

Angiotensin II plays a role

Symptom: Dryness of the mouth

CAUSES:
O d OSMOLARITY

Hypertonicity occurs (Na+ higher)

Water is drawn from the cell (crenation)

Water is ingested Cell returns to normal

O

d FLUID VOLUME

Loss of fluid (ex hemorrhage)

d circulation (CHF: H2O moves from ICF to ECF look swollen but actually depleted)

Dryness of the mouth Thirst triggered replace fluids resolves

ALTERED THIRST MECHANISMS:

o Coma dont know theyre thirsty
o Senility (dementia), Psychosis, Confusion cant comprehend thirst
o Psycogenic Polydipsia drink way too much water water intoxication, hypoNa+

REGULATION OF BODY FLUID KIDNEYS!! (review in book)

Filtration r/t hydrostatic pressure

Secretion Mvmt from blood to renal tubules

Reabsorption Mvmt from renal tubules to the blood

Excretion - Mvmt from kidney to the environment

KIDNEYS how well are they working?

o Glomerular filtration rate (GFR) rate of urine production

indicates stage of kidney dz

o Renal perfusion

Cardiac output ( CO, hypoTN - s renal perfusion)

Patho Wk 5: Ch. 3

o
o

o In shock state, body shunts blood to heart/brain 1st

Ex: Renal artery stenosis

Hydration status Dehydration not filtering or sending water/fluids to kidneys
RAAS SYSTEM

*Renin-Angiotensin-Aldosterone System* (RAAS) negative feedback loop!

Regulates BP, fluid status, everything!

STIMULUS = BP, GFR, Na+, or renal perfusion

o stimulates kidneys to release renin
o stimulates conversion of angiotensin I to
angiotensin II via ACE
o tells BP to rise tells adrenal gland to produce
aldosterone
o aldosterone tells kidneys to hold onto Na+ (and in
turn, H2O), so BP rises

ALDOSTERONE = mineralocorticoid (steroid) hormone

Produced and secreted by the adrenal cortex

GOAL = conserve Na+, restore blood volume and H2O

Promotes Na+ & H2O reabsorption by the proximal tubule in the kidney
Stimulates secretion/excretion of K+ by the distal tubule of the kidney ( thus ing K+ in the ECF)

Aldosterone = End product of RAAS system!!

o Stimulus received (DECd BP, renal blood flow, Na+)
o Renin secreted by juxtaglomerular cells of the kidney stimulates formation of angiotensin I.
o ACE (angiotensin converting enzyme) in the pulmonary vessels converts Angiotensin I to II.
o 2 functions of angiotensin II: vasoconstriction (elevates BP) + stimulates the secretion of aldosterone
o When blood volume is restored, feedback loop turned off inhibits renin release.

Causes of d secretion
o HypoNa+
o HyperK+ (must get rid of it!)
o Activation of the RAA

Causes of d secretion
o HyperNa+
o HypoK+

Patho Wk 5: Ch. 3

Inhibition of the RAA mechanism

ANTIDIURETIC HORMONE (ADH) [arginine vasopressin (AVP)]

Formed in the supraoptic and paraventricular nuclei of the hypothalamus

Released by posterior pituitary

FUNCTION = INCs H2O reabsorption in the distal convoluted tubule and

collecting ducts of the kidneys
O tells kidney to hold onto more H2O!

PROCESS:
o d plasma osmolality d/t d H2O or d Na+
o Stimulates osmoreceptors in hypothalamus which tells post.
pituitary to release ADH
o ADH tells kidneys to permeability of renal tubular cells to water
o restores plasma volume, BP rises
o move towards euvolemic state
Factors INHIBITING RELEASE of ADH (s ADH)
o Hypotonicity of the ECF (d osmolality)
o Ethanol
o INCd ICP (intracranial pressure)

Factors STIMULATING RELEASE of ADH (s ADH)

o Hyperosmolality of the ECF
o Hypovolemia (ex bleeding)
o HypoTN
o d body temperature ( dehydration d/t fever)
o Medications:

Narcotics

Antineoplastics

Oral hypoglycemic

Beta adrenergic drugs

o Stress, Pain
o Trauma
Anything that makes body work harder!!
o Surgery

PROSTAGLANDINS = Fatty acids widely distributed in the cells of the body

MOA: Interferes with the renal tubules response to ADH

BODY FLUID REGULATION VIA:

o s Na+ & H2O excretion
o Renal vasodilation to protect kidney from ischemic injury

FUNCTIONS:
o Inflammatory process
o Blood pressure
o Uterine contractions
o Increased GI motility
o Bronchoconstriction

GLUCOCORTICOIDS (CORTISOL)

Hormones produced by the adrenal glands

Promotes Na+ and H2O retention (weak effect)

Cushings Syndrome:
o Exogenous (outside body)
o Endogenous (problem with cortisol excretion)

Patho Wk 5: Ch. 3

S/S: Edema, HTN (volume overloaded), HyperNa+, HyperK+

ETIOLOGY = Excess cortisol (which helps regulate blood sugar)

ATRIAL NATRIURETIC PEPTIDE (ANP)

Released from myoendocrine cells in the atria

STIMULUS = atrial stretch (d/t d atrial pressure, intra-atrial volume, CHF, volume overload, etc)
o Turned off when atrial pressure lowers (a negative feedback loop)

PHYSIOLOGIC EFFECTS:
o s Na+ & H2O excretion by kidneys
o Renal vascular dilation
o Antagonist of RAAS Inhibits release of aldosterone & ADH

ALTERATIONS IN WATER BALANCE

ISOTONIC FLUID IMBALANCE changes in total body water are accompanied by proportional changes in electrolytes

Na+ or H2O or in the SAME proportion

Na+ and osmolality are WNL

Types: Hypovolemia, Hypervolemia

HYPOVOLEMIA = Fluid Volume DEFICIT (contraction of ECF)

O Na+ or H2O in the SAME proportion
o

CAUSES:

Inadequate intake

GI/GU losses

Skin losses

Third-space losses

SIGNS (classic sign of dehydration):

d Body weight

Mild deficit = 2% loss

Moderate deficit = 4% loss

Severe deficit = 6% loss

d UOP

Oliguria little bit

Anuria NO urine

d Urine and Serum osmolality (more concentrated)

Poor skin turgor

Dry mucous membranes

Postural hypotension

d HR (Tachycardia)

MAJOR COMPLICATIONS:

d CO

Shock, Death

HYPERVOLEMIA = Fluid volume EXCESS (ECF excess)

O Na+ or H2O in the SAME proportion
O

CAUSES:

Patho Wk 5: Ch. 3

Excessive administration of IV NS
Over-secretion of aldosterone (kidneys retain Na+ and H2O)
Drug effect of cortisone
Renal failure

Results in :

in capillary pressure

in oncotic pressure

in serum aldosterone

SIGNS/SYMPTOMS:

Acute weight gain

Edema, HTN

Pulmonary edema

SOB, Crackles, Dyspnea, Cough

Venous distention

d HCT, d plasma protein concentration (dilution)

MAJOR COMPLICATIONS:

Pulmonary edema BAD!

**Pink, frothy sputum

Hypoxia, Dyspnea, SOB, Pleural effusion

HR
EDEMA = Expansion or accumulation of interstitial fluid volume (ECF)

First-space cellular

Second-space intravascular

Third-spacing interstitial (ex swelling in ankles, ascites in abd)

o

CAUSES:
o d hydrostatic force
o d colloid osmotic pressure (low albumins, nephrotic syndrome, end-stage liver failure)
o d capillary permeability (sepsis)
o Obstruction of a lymphatic vessel
o Na+ and H2O excess

DISTRIBUTION of Edema: (mostly r/t condition of pt)

o Localized = Venous or lymphatic obstruction (lymphedema d/t mastectomy)
o Generalized = Hypoproteinemia (low protein/low albumin states)
o Dependent = Heart failure (d EF)

Edema Terms:
o Ascites = Fluid within the peritoneal cavity (abdomen)
o Pleural effusion = Fluid within the pleural space
o Pericardial effusion = Fluid within the pericardium
o Pulmonary edema = Fluid within the alveoli

CONCEPTS R/T FLUID INTAKE

All foods which are liquids at room temperature fluid!

One fluid ounce = 30cc or 30 ml

Fever (insensible fluid loss)

o 101o 103o: s 24-hr fluid needs by at least 500 ml
o >103o: s 24-hr fluid needs by at least 1000 ml

Normal urinary output = = 1 ml/kg/hr (1 ml of urine per kilogram of body weight per hour)
o Anuria = NO urine output
o Oliguria = urine output

Patho Wk 5: Ch. 3

Polyuria = urine output

CONCEPTS R/T FLUID OUTPUT

Includes: Urine, Vomitus, Diarrhea, Drainage (ex: chest tube, abdominal fistula), Perspiration
CONCEPTS R/T FLUID VOLUME DEFICIT

d UOP

d Urine specific gravity (i.e. high urine osmolality more concentrated d/t body holding onto water)

Poor skin & tongue turgor

Dry mucous membranes

d or absence of tearing and/or salivation

d Body weight

d Thirst (if intact thirst mechanism)

Skin may be warm and flushed in moderate FVD

Skin may be cold and clammy in severe FVD

d intraocular pressure

Sunken fontanels
getting worse, entering SHOCK STATE, body attempting to compensate for FVD:

HR, BP, CVP

Neck & Hand veins flat

o What happens to CO and perfusion?? Both suffer if not corrected/reversed

BP and warm is better than BP and cold (means not perfusing extremities)

TYPES OF FLUID REPLACEMENT

Crystalloids
o Dextrose (D5, D5 NS)
o Saline (0.9% NS, NS, NS, 3%, 5%)

Colloids (Proteins)
o Albumin Plasma protein fraction

Colloid substitutes (volume expanders)

o Dextran
o Hetastarch

Blood transfusions
o Packed red blood cells (PRBCs)
o Whole blood
DIURETICS: GETTING RID OF FLUID (can also limit fluid intake! Duh.)

Thiazide Diuretics
o Actions:

Inhibit Na+ resorption in the kidney (thus, getting rid of water)

Causes LOSS of Na+, Cl-, Mg++ and K+

s ECF volume
o Examples:

Chlorothiazide (Diuril)

Hydrochlorothiazide (HCTZ, Esidrix)

Loop Diuretics
o Actions:

Acts in the limbs of Henles loop

Causes LOSS of Na+, Cl-, and K+

s ECF volume
o Examples:

Furosemide (Lasix)

Patho Wk 5: Ch. 3

Ethacrynic acid (Edecrin)

Bumetanide (Bumex)

Potassium-Sparing Diuretics (weaker diuretic effect)

o Actions

Inhibit Na+ reabsorption

Cause LOSS of Na+, K+ (lose some K but not as much)

Cause an in Clo Examples:

Spironalactone (Aldactone)

Amiloride

Triamterene (Dyrenium)

Osmotic Diuretics
o s osmotic pressure and causes intracellular and interstitial fluids to enter the vascular spaces
o *Used frequently in neuro for d ICP
o Actions:

s Na+ and Cl- Hyponatremia, Hypochloremia

s ECF volume (VOLUME EXPANDER)

o Example: Mannitol

ELECTROLYTE DISTURBANCES
SODIUM (NA+) == 135 145 mEq/L
Main extracellular cation

FUNCTIONS:
o Maintains osmolality
o Participates in active transport (Na/K ATP pump)
o Helps regulate body fluids
o Participates in the action potential
o **where sodium goes, water will follow**
HYPONATREMIA: HYPO-OSMOLAR IMBALANCE

LABS: d serum osmolality, chloride, hematocrit, and BUN (dilution)

*Most common electrolyte imbalance in hospitalized patients

Cellular effect
o Cells become swollen (Na+ and H2O move INTO cell)
o Amt of Na+ has d inside the cell

CAUSES of ABSOLUTE hyponatremia ( pure Na+ deficit)

o Extra-renal losses: Sweating, GI losses (V/D), GI suctioning, burns,
o Diuresis
o Adrenal insufficiency

CAUSES of RELATIVE hyponatremia ( dilutional water exceeds Na+)

o Excess intake of plain water
o Tap water enemas
o Absorption of water from irrigating fluids used in a TURP (trans-urethral prostectomy)

Patho Wk 5: Ch. 3

o
o

10

Long-term IV therapy with D5W

d ADH levels

SIADH Syndrome of Inappropriate Anti-Diuretic Hormone

o Inappropriate in ADH secretion retain H2O FVE !
o ETIOLOGY: acute infections, brain trauma, surgery, ADH-secreting tumors
o

CAUSE: NOT excess H2O intake, but d renal reabsorption of H2O d/t inappropriate ADH secretion
Note: ADH normally secreted in hyperosmolar or hypovolemic state

Secretion is stimulated by factors other than the norm

SIGNS/SYMPTOMS:

Blood #s - dilutional effect Na+ (kidneys continue to excrete), serum osmolality

Urine #s - urine Na+ and urine osmolality

Volume: blood vol s, UOP s, Concentrated urine

Common underlying disorders:

Tuberculosis

Pneumonia

Cancer: Oat cell carcinoma, Pancreatic CA

Encephalitis

Meningitis

Some medications

MAJOR COMPLICATIONS: THINK NEURO

o *Neurological disturbances
o Cerebral edema
o Headache, lethargy
o Depression, confusion
o Seizures, Convulsions, Coma
o Cardiovascular disturbances

Postural hypotension

Shock
HYPERNATREMIA: HYPER-OSMOLAR IMBALANCE
Cellular effect
o Cells shrink; Cellular dehydration
o d Na+ levels outside the cell

CAUSES: (acute Na+ or loss of H2O) (NOTE: if both occur, will have ICF and ECF dehydration)
o Excessive oral or parenteral (IV) Na+ intake
o Near-drowning in salt water
o Hypertonic tube feedings without free water
o Inability to respond to thirst
o d water losses
o Diabetes insipidus (DI)
o Over-secretion of aldosterone (primary hyper-aldosteronism)
o Cushings syndrome excess secretion of ACH

MANIFESTATIONS: (DRY!)
o Thirst; Dry, sticky mucous membranes
o Tongue dry and swollen
o d temperature
o Agitation, Confusion
o Convulsions
o d HR
o d UOP (Oliguria or anuria)
o d urine specific gravity

Patho Wk 5: Ch. 3

11

MAJOR COMPLICATIONS:
o Net osmotic diuresis!!
o Water (& Na+) moves out of the cells into the circulation/ECF hypervolemia/FVE
o Cellular dehydration
o Circulation s
o Cell function is impaired
o Brain cells are particularly susceptible
o *Neurologic changes EARLY sign!

POTASSIUM (K+) == 3.5 to 5.0 mEq/L

Main intracellular cation

FUNCTIONS:
o Transmission of nerve impulses
o Resting membrane potential
o Acid-base balance
o Promotes myocardial, skeletal, and smooth muscle contractility

FACTORS AFFECTING REABSORPTION/SECRETION OF K+

o Sodium balance Na+ deficit results in d K+ loss (inverse relationship)
o Acid-base balance:

Acidosis results in excretion of H+ and retention of K+

Metabolic acidosis treating acidosis will K+ - i.e. must lower the CO2

Alkalosis results in retention of H+ and excretion of K+

o Use of diuretics Results in d K+ loss
o Loss of gastric secretions Result in d K+ loss
o
o
o
o

Aldosterone = promotes K+ excretion

Epinephrine = promotes K+ reabsorption
Anabolism = K+ enters the cell
Catabolism = K+ leaves the cell

Movement of K+ INTO the cell is dependent on:

Oxygen
Tx hyperkalemia by giving insulin and glucose moves K+ INTO cell

Glucose

Insulin

HYPOKALEMIA == <3.5 mEq/L

ETIOLOGY:
o Poor nutrition
o Diuretic therapy ***
o Vomiting, diarrhea, GI suctioning
o Burns
o Alkalosis
o Hyperaldosteronism

MAJOR COMPLICATIONS: (THINK muscle contractility, action potential and ATP pump)
o Cardiovascular T wave abnormalities

Dysrhythmias, hypoTN, digitalis toxicity exacerbation, myocardial damage, cardiac arrest

o Neurological

Lethargy, confusion, depression

o Gastrointestinal

Paralytic ileus
o *Skeletal muscle MAJOR!

Weakness, flaccid paralysis, weakness of respiratory muscles, respiratory arrest

o *Renal system

d ability to concentrate urine, water loss, kidney damage

o *Acid base balance

Patho Wk 5: Ch. 3

12

Metabolic alkalosis

HYPERKALEMIA == >5.0 mEq/L

ETIOLOGIES:
o Taking in too much K+ & kidneys unable to compensate
o Retention of K+

Renal failure, potassium-sparing diuretics, adrenocortical insufficiency

o *Cell lysis = Major release of K+ from the cells

Trauma, burns, transfusions of old blood, metabolic acidosis

o Rapid IV K+ administration

TREATMENT: insulin & glucose (acute tx), calcium chloride, albuterol, kayexalate (takes longer)

MAJOR COMPLICATIONS: can kill!

o Nervous system

Paraesthesia
o Neuromuscular

Muscle twitching, muscle weakness, paralysis

o Cardiovascular

Bradycardia

Cardiac arrest

*Peaked T waves on EKG

Tombstone waves dead heart

CALCIUM (CA+) == 8.5 to 10.5 mg/dl or 4.5 to 5.8 mEq/L

FUNCTIONS:
o Formation of bone and teeth
o Contraction of muscle
o Blood coagulation
o BLOCKS Na+ transport INTO the cell
o Transmission of nervous impulses

Three Types of Calcium:

o Bone
o Ionized Calcium
o Protein Bound (*primarily to albumin)

REGULATION OF CALCIUM negative feedback loop

o Parathyroid hormone (PTH)

Bone to plasma

Intestinal absorption
o Calcitonin

Patho Wk 5: Ch. 3

13

Plasma to bones and teeth

Calcitrol (activated vitamin D 25-hydroxy Vit D)

Calcium absorption from intestines

Aids in mobilization of bone calcium to where it is needed

CORRECTING TOTAL CALCIUM LEVELS FOR ALBUMIN

o If calcium level, must check albumin level!

If albumin level normal correct calcium deficit

If albumin level low correct albumin deficit

o *When total calcium is the only calcium level you have, the level has to be corrected for albumin level
o *CALCULATION: For every 1 gram in albumin below normal level, the measured total serum
calcium should be adjusted up by 0.8 mg/dl

EXAMPLE of Calcium Correction:

o Ca+ = 7.0
o Albumin = 2.3
o Normal albumin = 4
o 4 2.3 = 1.7(.8) = 1.36
o 7.0 + 1.36 = 8.36 Corrected Calcium

= 8.0
= 2.0

4 2 = 2(.8) = 1.6
8.0 + 1.6 = 9.6 corrected
o
thus, Ca level not as low as you thought!

HYPOCALCEMIA

ETIOLOGIES: (think of feedback loop!)

O Hormone-dependent (body doesnt know that it needs to keep calcium)

Hypoparathyroidism (d PTH)

d calcitonin

Vitamin D deficiency (d vit D)

o Renal-dependent

Renal failure

Hyperphosphatemia (not excreting phos from kidneys)

Loop diuretics
o Acid-base imbalance

Alkalosis
o Nutritional

Malnourishment; Malabsorption syndromes (intestinal)

Multiple blood transfusions (d/t preservative)

Neonatal hypocalcemia
o Deposition of ionized calcium in bone or soft tissue

*SPECIAL SIGNS OF HYPOCALCEMIA (PIC)

o Trousseaus sign

Inflate BP spasm of hand, wrist, fingers

o Chvosteks sign

Tap on side of face in front of earlobe twitching

MAJOR COMPLICATIONS:
o Nervous system

Paraesthesia
o Muscular system LATE signs

Tetany, laryngeal spasms

o Cardiovascular system (PIC)

Congestive heart failure

d CO

Cardiac dysrhythmias r/t QT interval (hyper = shortened, hypo = elongated)

TREATMENT:
o Oral calcium TUMS
o Vitamin D replacement
o IV Calcium gluconate (preferred)

Patho Wk 5: Ch. 3

o
o
o

14

IV Calcium chloride (VERY toxic to vessel need central line)

IV Calcium gluceptate
Thiazide diuretics

HYPERCALCEMIA == >12.5

ETIOLOGIES:
O Hormone imbalance

Hyperparathyroidism (NOTE: 4 parathyroid glands near thyroid)

Vitamin D excess
o Thiazide diuretic use
o *Bony cancers, malignancies
o Sarcoidosis in lungs
o Resorption from bone

Prolonged immobilization

Multiple fractures

Bone tumors

Multiple myeloma

MAJOR COMPLICATIONS:
o Neurological manifestations

Lethargy, confusion, coma

o Skeletal manifestations

Deep bone pain

Pathological fractures
o Renal manifestations

*Kidney stones, renal failure

o Gastrointestinal manifestations

Constipation

Anorexia

Nausea and vomiting

o Cardiovascular manifestations

Shortened QT interval

Bradycardia

Cardiac arrest

TREATMENT Dilute the calcium!

o Loop diuretics & IVF 1st line therapy
o Oral or IV phosphate preparations
o Plicamycin or Calcitonin (slows bone resorption)

MAGNESIUM (MG+) == 1.5 to 2.5 mEq/L

Primarily regulated by PTH

Interacts with Calcium at cellular level!

FUNCTIONS:
o Aids in neuromuscular transmission
o Aids in heart muscle contraction
o Activates enzymes for cellular metabolism of carbohydrates and proteins
o Aids in transmission of hereditary information to offspring
HYPOMAGNESEMIA

ETIOLOGIES:
o Malnutrition
o Chronic alcoholism
o Loop diuretics
o Diarrhea
o Severe dehydration
o Malabsorption syndrome (Crohns disease)

Patho Wk 5: Ch. 3

MANIFESTATIONS:
o Severe respiratory muscle depression
o Apathy, depression, confusion
o Muscle weakness, tremors, tetany
o Life-threatening cardiac arrhythmias (PIC)

TREATMENT:
o IV Magnesium sulfate

2 Grams over 2-3 hrs/ 4gms over 4 hours

12 Grams over 12 hours

HYPERMAGNESEMIA (rare; often r/t renal failure)

ETIOLOGIES:
o Chronic renal failure
o Laxatives or Antacids that contain magnesium

MANIFESTATIONS:
o Severe muscle weakness
o Depression of respirations
o Inability to swallow
o Hyporeflexia
o Hypotension
o Cardiac dysrhythmias

TREATMENT:
o 1st d/c all magnesium-containing drugs
o Fluid therapy
o Calcium gluconate to counteract the effects of magnesium
o Mechanical ventilation if needed

PHOSPHORUS == 2.7 to 4.5 mg/dl

FUNCTIONS:
o Aids in structure of cellular membrane
o Contributes to the metabolism of glucose, fat, and protein
o Helps maintain bone hardness
o Acid-base balance
HYPOPHOSPHATEMIA

ETIOLOGIES:
o Alcoholism
o Malnutrition
o Diabetic ketoacidosis (DKA)
o M/C intestinal malabsorption or INC renal excretion of phos

MANIFESTATIONS:
o Hemolytic anemia
o Muscular weakness (respiratory esp)
o Paraesthesia
o GI distress d/t reduced energy and oxygen stores in cells

TREATMENT:
o Fleets Phospho-soda enema
o IV or oral phosphate
HYPERPHOSPHATEMIA

ETIOLOGIES:
o *Chronic renal failure
o Rapid cell catabolism
o Excessive intakes of phosphates

TREATMENT:

15

Patho Wk 5: Ch. 3

o
o
o
o
o
o

16

Dietary restriction of phosphates

Aluminum-containing antacids
Hydration
Correct hypocalcemia
Renagel , Phosrenol (non-calcium-based phosphate binders bind phos with meals & excrete in stool)
Tums, Phoslo (calcium-based phosphate binders bind & excrete in stool)