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Pemeriksaan laboratorium

dehidrasi

Prihatini

Departemen Patologi KlinikFK-UWKS

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Mengenal Cairan dan elektrolit

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Bagian cairan dipisahkan dgn

membran yg bebas dilaluiair Gerakan cairan tgt tekanan

(hydrostatic pressure )& (

osmotic pressure)

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Solutesd isso lved part ic les

Electrolytes charged particles Cations positively charged

Na+, K+ , Ca++, H+

Anions Cl-, HCO3

- , PO43-

Non-electrolytes - Uncharged

Proteins, urea, glucose, O2, CO2

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Cairan tubuh terdiri :

Muatan elektrik netral (Electr ical lyneutral)

Pemeliharaan osmotik (Osmotical ly

maintained) Jumlah partikel per volume

cairan(Speci f ic number of part ic les

per volume of f lu id)

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MW (Molecular Weight) =

sum of the weights of atoms in a molecule

mEq (milliequivalents) = MW (in mg)/ valence

mOsm (milliosmoles) =

number of particles in a solution

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Tonicity

Isotonic

Hypertonic

Hypotonic

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Cell in a

hypertonicsolution

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Cell in a

hypotonicsolution

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Movement of body fluids

Where sodium goes, water follows.

Diffusion movement of particles down a

concentration gradient.

Osmosis diffusion of water across a

selectively permeable membrane

Active transport movement of particles

up a concentration gradient ; requires

energy

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ICF to ECF osmolality changes

in ICF not rapid

IVF ISF IVF happens

constantly due to changes in fluid

pressures and osmotic forces at

the arterial and venous ends ofcapillaries

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Regulation of body water

ADH antidiuretic hormone + thirst

Decreased amount of water in body

Increased amount of Na+ in the body

Increased blood osmolality

Decreased circulating blood volume

Stimulate osmoreceptors in

hypothalamus

ADH released from posterior pituitary

Increased thirst

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Result:

increased water consumption

increased water conservation

Increased water in body,increased volume and decreased

Na+ concentration

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Decreased amount of water in body

Increased amount of Na+ in the body

Increased blood osmolalityDecreased circulating blood volume

Can also be due to dysfunction or trauma

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Edema is the accumulation of fluid

within the interstitial spaces

increased hydrostatic pressure

lowered plasma osmotic pressure

increased capillary membrane

permeability

lymphatic channel obstruction

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Hydrostatic pressure increases due to:

Venous obstruction:

thrombophlebitis (inflammation of veins)

hepatic obstruction

tight clothing on extremitiesprolonged standing

Salt or water retention

congestive heart failure

renal failure

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Decrease plasma osmotic pressure:

plasma albumin (liver disease orprotein malnutrition)

plasma proteins lost in :

glomerular diseases of kidney

hemorrhage, burns, open

wounds & cirrhosis of liver

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Increased capillary permeability:

Inflammation

immune responses

Lymphatic channels blocked:

surgical removal

lymphedema

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Fluid accumulation:

increases distance for diffusion

may impair blood flow

= slower healingincreased risk of healing

pressure sores over bony

prominences

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Edema of specific organs can be

life threatening (larynx,

brain, lung)

Water is trapped, unavailable for

metabolic processes. Can result

in dehydration & shock. (severeburns)

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Electrolyte balance

Na + (Sodium)

90 % of total ECF cations

136 -145 mEq / L

Pairs with Cl- , HCO3- to neutralize charge

Low in ICF

Most important ion in regulating waterbalance

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Regulation of Sodium

Renal tubule reabsorption affected by

hormones:

Aldosterone

Renin/angiotensin

Atrial Natriuretic Peptide (ANP)

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Potassium

Major intracellular cation

ICF conc. = 150- 160 mEq/ L

Resting membrane potential

Regulates fluid, ion balance

inside cell pH balance

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Isotonic alterations in water balance

Occur when TBW changes are accompanied

by = changes in electrolytes

Loses plasma or ECF

Isotonic fluid loss ECF volume, weight loss, dry skin and

mucous membranes, urine output, and

hypovolemia ( rapid heart rate, flattened

neck veins, and normal or B.P.

shock)

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Isotonic fluid excess

Excess IV fluids

Hypersecretion of aldosterone

Effect of drugs cortisone

Get hypervolemia weight gain, decreasedhematocrit, diluted plasma proteins,

distended neck veins, B.P.

Can lead to edema ( capillary hydrostatic

pressure) pulmonary edema and heart

failure

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Electrolyte imbalances

Sodium

Hypernatremia

Plasma Na+ > 145 mEq / L

Due to Na + or water

Water moves from ICF ECF

Cells dehydrate

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Due to:

Hypertonic IV soln.

Oversecretion of aldosterone

Loss of pure water

Long term sweating with chronic fever

Respiratory infection water vaporloss

Diabetes polyuria

Insufficient intake of water

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Clinical manifestations

Thirst

Lethargy

Neurological dysfunction due todehydration of brain cells

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Treatment

Lower serum Na+

Isotonic salt-free IV fluid

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Hyponatremia

Overall decrease in Na+ in ECF

Two types: depletional and dilutional

Depletional

Na+ loss:

diuretics, chronic vomiting

Chronic diarrhea

Decreased aldosterone

Decreased Na+ intake

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Dilutional

Renal dysfunction with intake of

hypotonic fluids Excessive sweating increased thirst

intake of excessive amounts of pure water

Syndrome of Inappropriate ADH (SIADH)

oroliguric renal failure, severe congestive

heart failure, cirrhosis all lead to:

Impaired renal excretion of water

Hyperglycemia attracts water

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Clinical manifestations

Neurological symptoms

Lethargy, confusion, apprehension,

depressed reflexes, seizures and coma

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Hypokalemia

Serum K+ < 3.5 mEq /L

Beware if diabetic

Insulin gets K+ into cell

Ketoacidosis H+ replaces K+, which is

lost in urine

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Causes of hypokalemia

Decreased intake of K+

Increased K+ loss

Chronic diuretics

Acid/base imbalance

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Clinical manifestations

Neuromuscular disorders

Weakness, flaccid paralysis, respiratoryarrest, constipation

Dysrhythmias

Postural hypotension

Cardiac arrest

Treatment-

Increase K+ intake, but slowly

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Clinical manifestations

Early hyperactive muscles

Late - Muscle weakness, flaccid paralysis

Change in ECG pattern

Dysrhythmias

Bradycardia , heart block, cardiac arrest

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Treatment

Insulin + glucose

Bicarbonate

Ca++ counters effect on heart

Calcium Imbalances

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Calcium Imbalances

Most in ECF

Regulated by:

Parathyroid hormone

Blood Ca++ by stimulating osteoclasts

GI absorption and renal retention

Calcitonin from the thyroid gland

Promotes bone formation

renal excretion

Hypercalcemia

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Hypercalcemia Results from:

Hyperparathyroidism Hypothyroid states

Renal disease

Excessive intake of vitamin D Malignant tumors hypercalcemia of

malignancy

Tumor products promote bone breakdown

Tumor growth in bone causing Ca++release

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Hypocalcemia

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Hypocalcemia Hyperactive neuromuscular reflexes and

tetany differentiate it from hypercalcemia

Convulsions in severe cases

Caused by:

Lack of vitamin D Suppression of parathyroid function

Hypersecretion of calcitonin

Malabsorption states

Abnormal intestinal acidity

Widespread infection or peritoneal

inflammation