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Patho Wk 5: Ch.

3

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FLUID DISTURBANCES
Objective: Identify the major consequences/manifestations of abnormal levels of water.
FUNCTIONS OF WATER (it’s 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 body’s water)

Extracellular (ECF) = 20% ( ~1/3 of body’s 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 = 1500–2500 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 concentrationLOW 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 HIGHLOW

Ex: Lipid insoluble substances cannot cross plasma membrane (needs glucose carrier)
Active Transport = mvmt of substance across the cell membrane from LOW concentrationHIGH 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
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Patho Wk 5: Ch. 3

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 ¼ liter to ECF & adds ¾ 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 – don’t know they’re thirsty
o Senility (dementia), Psychosis, Confusion – can’t 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

4

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

o

5

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)

Cushing’s Syndrome:
o Exogenous (outside body)
o Endogenous (problem with cortisol excretion)

Patho Wk 5: Ch. 3

6

o

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

o

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

o

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)

o

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

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

o

Results in :

 in capillary pressure

 in oncotic pressure

 in serum aldosterone

o

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

o

8

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 ½NS)
o Saline (0.9% NS, ½ NS, ¼ 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 Henle’s loop

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

s ECF volume
o Examples:

Furosemide (Lasix)

Patho Wk 5: Ch. 3

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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

o

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

o

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 Cushing’s 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

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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

o

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

o

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 doesn’t 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 Trousseau’s sign

Inflate BP  spasm of hand, wrist, fingers
o Chvostek’s 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 Fleet’s 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)