Disorders of fluid, electrolyte and acid base CHAPTER 8 Flashcards Preview

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Flashcards in Disorders of fluid, electrolyte and acid base CHAPTER 8 Deck (20):

Describe the control of cell volume and the effects of isotonic, hypotonic, and hypertonic solutions on cell size

-cell volume is controlled by diffusion and osmosis
-movement of high to low gradient

-no difference in solute concentration = same cell

-high solute concentration inside cell = swollen cell

-low solute concentration inside cell = crenated cell/shrink


Differentiate intracellular from extracellular compartments in terms of distribution and composition of water, electrolytes and other osmotically active solutes

-contains 2/3 of body water and is larger compartment than extracellular
-lots of K and MG, low NA, CL

-1/3 body water
-fluid outside cell, tissue spaces, blood vessel
-lots of NA, CL, bicarbonate


Describe factors that control fluid exchange between the vascular and interstitial fluid compartments and relate them to the development of edema and third spacing in extracellular fluid

4 factors:
Capillary filtration - water is pushed from capillary to interstitial

Capillary colloidal osmotic pressure (proteins) - water is pulled into the capillary (decreased protein causes edema)

Interstitial hydrostatic pressure - which opposes the movement of water out of the capillary

Interstitial colloidal osmotic pressure - water pulls out of the capillary into the interstitial space


Describe the consequences and treatment of edema

Increases distance for diffusion of oxygen, nutrients and wastes
Tissues more susceptible to injury
Pressure ulcers
Compresses blood vessels and nerves (tourniquet)
Self-concept disturbances
Improper fitting of clothes

Elastic support stockings
Range of motion exercises


describe the cause, manifestation and treatment of psychogenic polydipsia

-compulsive water drinking in those with psychiatric disorders
-drinks large amount of water and urinates a lot
-cause unknown, idiopathy

-drink a lot, pee a lot

-water restriction
-behaviour control to decrease water consumption


Describe the relationship between body water and the extracellular sodium concentration

-the distribution of body fluids between the ICF and ECF compartments relies on the concentration of ECF sodium and water


Describe pathophysiology, manifestations, and treatments of diabetes insipidus

-deficiency of a decreased response to ADH
-neurgenic (not secreting enough ADH)
-nephrogenic (kidney not responding)
-unable to concentrate urine, during periods of water restriction and they excrete large volumes of urine

-intense thirst, craving ice water, excess urination
-hypernatremia, dehydration

-give ADH


pathophysiology, manifestations, and treatment of syndrome of inappropriate antidiuretic hormone

-failure of the negative feedback system that releases ADH which causes continued ADH secretion

-water retention
-urine output decreases despite increase water intake
-water intoxication
-extremely low sodium level

-fluid restriction
-lithium and antibiotics inhibits the action of ADH


State the causes and manifestations of hypokalemia

-inadequate intake, excessive loss (GI tract, diuretics)

-movement of K from bloodstream into cell
-increased insulin, alkalosis

MANIFESTATION (usual gradual)
- GI: anorexia, N&V, constipation
-CNS: muscle weakness, fatigue, parathesia, paralysis
-CVS: ventricular arrhythimas, ECG changes, digoxin toxicity (if taking)


State the causes and manifestations of hyperkalemia

-decreased excretion
-adrenal insufficiency, ACE inhibitors
-chronic kidney disease
-increased intake
-increased movement of K from cells into blood stream
-acidosis, tissue injury, decreased insulin, bblockers

-CVS: bradycardia, cardiac arrest
-CNS: weakness, paresthsia, paralysis
GI: cramps, diarrhea, n&v


describe hypocalcemia and hypercalcemia and their causes and manifestation

causes of hypo - decreased intake, abnormal loss, hypoparathyroidism, vitamin D deficiency

-muscular: tetany, muscle cramps. carpopedal spasm (trouseau's sign)
CNS: chvostek's sign, paresthesia, confusion, lethargy, anxiety
CVS: prolonged QT. reistance to digitalis, hypotension

causes of hyper - neoplasms of parathyroid glands, immobilization, poor absorption

-muscular: weakness, ataxia
CNS: lethargy, personality changes, stupor, coma
CNS: hypertension, short QT, AV blocks
GI: Anorexia, n&v, constipation
GU: interferes with ADH so can't cncentrate urine


Describe hypomagnesemia and hypermagnesemia their causes and manifestation

causes of hypo - insufficient intake, excessive loss, movement between ECF and ICF

-manifestation are ususally due to related electrolyte disorders
-increased in neuromuscular excitability
-hyperactive deep tendon reflex
-paresthesias, muscle fasciculation, and muscle contraction
-positive chvostek or trousseau sign present
-ataxia, vertigo, disorientation

causes of hyper - renal insufficiency or excessive intake (antacids, laxatives)

-hypocalcemia may accompany hypermagnesemia
-muscle weakness, hyporeflexia
-low bp
-ECG increase in PR interval, shortening of QT, t wave abnormal and prolong QRS
-severe is muscle respiratory paralysis. heart block and cardiac arrest


Describe the three forms of carbon dioxide transport and their contribution to acid-base balance

-in circulation as dissolved base (pCO2)

-as bicarbonate (HCO3)

-as carbaminohemoglobin


List the three major mechanisms of pH regulation

-chemical buffer systems
-respiratory control mechanism
-renal control mechanism


compare the role of the kidneys and respiratory system in regulation of acid-base balance

-Kidneys regulates pH by secreting of excess H and re-absorption of HCO3 (bicarbonate) by the renal tubules. Each bicarbonate that s reclaimed requires the secretion of H, a process that is tightly coupled with sodium reabsorption.

-increased ventilation decreases carbon dioxide in the blood. While decreased ventilation increases. Chemoreceptors in the brain and in the carotid sense changes in the blood CO2 and pH and alters the ventilatory rate

-if cause of an acidosis or alkalosis is respiratory, the kidney will compensate
-if the cause is renal, the lung will compensate


Causes of metabolic acidosis and manifestation

-causes loss of bicarbonate via kidney or GI tract
-excess production/accumulation of acids (liver disease, ketoacidosis, drugs, rhabdomyolysis
-inability of kidney to excrete excess acid
CNS: head ache, lethargy, kussmaul breathing
RESP: hyperventilation

CVS: hypotension
GI: anorexia


Causes of metabolic alkalosis and manifestation

-causes is increase in plasma bicarbonate(HCO3)
-excess H ion loss: vomitting, gastric suctioning
-excess bicarbonate (HCO3): ingestion of alkali
-loss of K ion d/t renal excretion: diuretics hyperaldosteronism

CNS: hyperactive reflexes, tetany, confusion, seizures, trousseau's sign

RESP: bradypnea, shallow

CVS: hypotension, arrhthimias

GI: n&v

pH >7.45
HCO3 >26


Causes of respiratory acidosis and manifestation

-causes increased CO2
-over production of CO2 from sepsis, burns, hyperthermia
-inspiration of CO2
-decreased expiration of CO2:
obstruction, lung chest wall damage, hypoventilation, asphyxia, devervation of muscle, damage to muscles

CNS: headache, restlessness, confusion, depressed reflexes, comnolence, coma

RESP: dyspnea, tachypnea, hypoxemia

CVS: tachycardia, arrythmias, hypertension or hypotension


Causes of respiratory alkalosis and manifestation

-decrease in pCO2 (hypocapnia)
-hyperventilation from anxiety, pain, fever, anemia, high altitude, medularry stimulation, mechanical ventilation, disease processes
Medication: salicylate OD

CNS: dizzy, agitated. circumoral and peripheral paresthesia, tetany, twitching, muscle weakness

RESP: deep, rapid respiration

CVS: increased in HR


Explain the purpose of arterial blood gas analysis

-assessing respiratory and metabolic function

-venous blood gases unreliable because it varies