W8 Fluid electrolyte and imbalances Flashcards
Explain how water is distributed and balanced between body compartments.
Water is found in: intracellular space - ICF fluid contained within cells.
Extracellular fluid ECF- the fluid environmnt in which cells live outside the cells.
Interstitial space and intravascular space.
Electrolyte and fluid is maintained by an electric chemical gradient (Na+/ K+ pump).
- *More Na+ in ECF
- *More K+ in ICF.
COMPARTEMENT: 1. Between the interstitial spac and plasma: regulated by osmosis and hydrostatis fluid pressure.
2: Between interstitial and intercellular spaces: regulates by osmosis
Interstitial space:
- Hydrostatic pressure: is the force generated by the pressure of fluid within or outside of capillary on the capillary wall.
- Oncotic or colloid osmotic pressure: is form of osmotic pressure exerted by proteins in the blood plasma.
Define third spacing and explain how it can cause cellular injury.
Third-spacing occurs when too much fluid moves from the intravascular space (blood vessels) into the interstitial or “third” space-the nonfunctional area between cells.
Outline and describe the 5 ways oedema may arise, and exemplify with causes.
Excessive accumulation of fluid in interstitial spaces due to:
- Increased capillary hydostatic pressure: Sodium & water retention. Chronic heart failure, reneal failure, liver cirrhosis.
- Lowered plasma oncotic pressure. ↓ plasma proteins. Caused by liver disease, malnutrition, haemorrhage, burns.
- Increased capillary membrane permeability
- Venous obstruction
- Lymphatic vessel obstruction.
Describe the different types of oedema.
- ↑ diffusion distance for nutrients and wastes: leads to poor wound haling, ↑ infection risk, ↓ gas exchang in the lungs.
- Locaised: to site of trauma
- Generalised: more uniform throughout the body due to renal failure.
- Dependant: Fluid accumulates in gravity dependant areas.
- Pitting oedema: fit left in the tissue.
Define hypervolaemia and hypovolaemia.
Hypervolamia: fluid overload. - xcessive water intake, or water retention. Causes: - excessive watre drinking - acute kidney injury = ↓ urine formation - Severe congestive heart failur - Liver cirrhosis - Excess ADH secretion Hyporvolaemia: low fluid volum
Describe and explain the possible causes of hypovolemia.
Inappropriate ADH secretion.
↑ levels of ADH without normal physiological control. ECF fluid ↑ resulting in dilutional hyponatraemia.
Most common cause is ectopic production associated with cancer.
- Hypertnsion → due to overload
- Dilutional hyponatraemia: xcess water = ↓ Na+
- Water toxicity= intercranial pressure.
TX: → Diurtics are used but electrolyte balance must be monitored.
- Thiazides: eliminates K+
- Loop diuretics
- Potassium-sparring diuretics given as an adjuvant therapy
Describe the clinical manifestations of hypervolemia and its treatment.
Clinical manifestations: ↑ BP
Bradycardia ↓ HR.
- Swelling
- Discomfort in body.
Describe and explain the possible causes and clinical manifestations of hypovolemia.
Loss of fluid volume from the body,
- Vomiting
- Diarrhoea
- Sweating/fever
- Diabetes
Clinical manifestations: Fluid loss → low BP, tachycardia reflex can lead to hypovolaemic shock
Describe the aetiologies of Diabetes insipidus and how is causes hypovolemia.
Hypovolemia→ Diabetes insipidus = large amounts of dilute urine and increased thirst.
Caused by: Neutogenic: problem with pituitary gland.
- Absence of ADH
Nephrogenic (problem with kidney,
Gestational diabetes.
Compare and contrast Diabetes insipidus and SIADH.
PIC
Describe how fluid replacement therapy is performed in hypovolemia.
Alcohol inhibits the secretion of ADH = more urine.
Caffeine: acts as a diuretic: ↑ filtration rate and inhibits Na+ reabsorption in the kidneys.
Need to use ISOTONIC fluids via infusion or orally methods
Explain why electrolyte balance is essential for homeostasis
Mainly: Na+, K+, Ca2+……
Electrolytes maintain precise osmotic gradient between cellular compartments. Disruption can lead to water accumulation or depletion in a compartment.
Define hypoNatremia and describe the main causes and manifestations.
↓Na+
Low sodium due to gain of water or loss of sodium.
Common causes: potassium-sparring diuertic, inappropriate ADH secretion, hypervolaemia.
Clinical manifestations: neurologic due to osmotic shift into brain cells - hadaches, confusion and seizures.
Other manifiestations: loss of energy
Define hypernatremia and describe the main causes and manifestations.
↑Na+
High sodium concerntration surrounding the cells. Results from either loss of water or gain of sodium in ECF.
Main symptom is thirst.
Clinical manifestations: neurological including headche, neuromuscular excitability.
Impaires thirst mechanism for elder. Diabetes.
TX: water replacement.
Define hypokalaemia and explain how it may develop.
(,3.5 mEq/L)
↓ K+ in ICF. Potassium loss in the ECF is compensated by K+ coming out the cells. Acid-base and potassium homeostasis are linked, cells can exchange potassium ions & hydrogen ions → aids to buffer acidosis.
- H+ions causing acidosis in plasma (ECF) are moved into cells in exchange for K+ This reduced plasma pH but ↑ plasma K+
- Alkalosis causes hydrogen ions to be moved out of cells in exchange for potassium. This normalises plasma pH but ↓ plasma potassium
Define hyperKalaemia and explain how it may develop
↑ K+ (>5 mEq/L) gain of potassium. Excessive K+ in blood plasma.
Causes: cell damage, burns, trauma, renal failure, potassium sparring diuretics
Acidosis → H+ moves into cells in exchang for K+ to return plasma pH to normal but producd hyperkalaemia.
Describe the clinical manifestations of hypokalaemia and hyperkalaemia.
K+ is required for maintenance of resting potential and generation of action potentials. Disruptions in K+ manifest as a problem with muscle function.
Hypokalaemia: repolarisation is delayed this may cause dysrhythmias.
Hyperkalaemia: cardic conduction is decreased and repolarisation mor rapid = may cause ventricular fibrilation and arrest
Define hypocalcaemia and explain how it may develop.
(<8.6 mEq/L) Low level of calcium in the blood due to inadequate intestional absorption, dietary deficiency, ↑ calcium exertion/deposition.
- Parathyroidisim,
- Nutritional deficiencis
- Calcification of tissues
Describe clinical manifestations of hypocalcaemia.
Increased neuromuscular excitability, heart rate and contractility decreased.
Define hypercalcemia and explain how it may develop.
High concerntration of calcium in the blood due to calcium release from bone or increasd absorption.
- Hyperparathyroidism: excess parathyoid hormone acts to release calcium from bone
- bony metastasis
- ectopic secretion of PTH
- excess vit D
Describe the clinical manifestations of hypercalcemia.
Abdominal pain, bone pain, confusion, depression, weakness, kidny stones or abnormal heart rhythm,.
Can affct muscl tone, neurologic
Describe the pH buffering systems in the body.
Th body buffers against dangerous changes in pH by taking advantage of the chemical properties of weak acids and weak bases.
Carbonic acid-bicarbonate buffer system: ECF
Protein buffer system:
Phosphate buffer system: ICF
Explain how the respiratory/renal systems regulate pH
Red blood cells use this systm (and protein buffering with Hb) to both transport CO2 and acid from issues to lung elimination.
In the lungs: the body compensates for ↑ acidity H+ by producing more CO2, breathing rate increases.
The body compensates for ↓ acidity by producing less CO2: breathing rate decreases
Explain how acidosis may arise and describe the compensatory responses
Carbon dioxide retention as a result of COPD, CNS depression, pneumonia. Compensation to correct the pH happns in kidneys. ↑ H+ excretion. Retain bicarbonate ions.
Respiratory acidosis: carbon dioxid retention,
Metabolic acidosis: eh lactic acid. Deep
and rapid sustain breathing.
Explain how alkalosis may arise and describe the compensatory responses.
Respiratory alkalosis. Hyperventiation due to anxiety ↑ pH. To correct the pH excretion happens in the kidnys.
Metabolic alkalosis: xcess antacid. Compensation: respiratory retention of CO2.
Describe the clinical manifestations of acidosis and alkalosis.
PIC
