W8 Fluid electrolyte and imbalances Flashcards

1
Q

Explain how water is distributed and balanced between body compartments.

A

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:

  1. Hydrostatic pressure: is the force generated by the pressure of fluid within or outside of capillary on the capillary wall.
  2. Oncotic or colloid osmotic pressure: is form of osmotic pressure exerted by proteins in the blood plasma.
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2
Q

Define third spacing and explain how it can cause cellular injury.

A

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.

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3
Q

Outline and describe the 5 ways oedema may arise, and exemplify with causes.

A

Excessive accumulation of fluid in interstitial spaces due to:

  1. Increased capillary hydostatic pressure: Sodium & water retention. Chronic heart failure, reneal failure, liver cirrhosis.
  2. Lowered plasma oncotic pressure. ↓ plasma proteins. Caused by liver disease, malnutrition, haemorrhage, burns.
  3. Increased capillary membrane permeability
  4. Venous obstruction
  5. Lymphatic vessel obstruction.
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4
Q

Describe the different types of oedema.

A
  • ↑ 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.
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5
Q

Define hypervolaemia and hypovolaemia.

A
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
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6
Q

Describe and explain the possible causes of hypovolemia.

A

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.

  1. Hypertnsion → due to overload
  2. Dilutional hyponatraemia: xcess water = ↓ Na+
  3. Water toxicity= intercranial pressure.

TX: → Diurtics are used but electrolyte balance must be monitored.

  1. Thiazides: eliminates K+
  2. Loop diuretics
  3. Potassium-sparring diuretics given as an adjuvant therapy
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7
Q

Describe the clinical manifestations of hypervolemia and its treatment.

A

Clinical manifestations: ↑ BP
Bradycardia ↓ HR.
- Swelling
- Discomfort in body.

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8
Q

Describe and explain the possible causes and clinical manifestations of hypovolemia.

A

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

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9
Q

Describe the aetiologies of Diabetes insipidus and how is causes hypovolemia.

A

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.

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10
Q

Compare and contrast Diabetes insipidus and SIADH.

A

PIC

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11
Q

Describe how fluid replacement therapy is performed in hypovolemia.

A

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

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12
Q

Explain why electrolyte balance is essential for homeostasis

A

Mainly: Na+, K+, Ca2+……
Electrolytes maintain precise osmotic gradient between cellular compartments. Disruption can lead to water accumulation or depletion in a compartment.

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13
Q

Define hypoNatremia and describe the main causes and manifestations.
↓Na+

A

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

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14
Q

Define hypernatremia and describe the main causes and manifestations.

A

↑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.

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15
Q

Define hypokalaemia and explain how it may develop.

A

(,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

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16
Q

Define hyperKalaemia and explain how it may develop

A

↑ 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.

17
Q

Describe the clinical manifestations of hypokalaemia and hyperkalaemia.

A

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

18
Q

Define hypocalcaemia and explain how it may develop.

A

(<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
19
Q

Describe clinical manifestations of hypocalcaemia.

A

Increased neuromuscular excitability, heart rate and contractility decreased.

20
Q

Define hypercalcemia and explain how it may develop.

A

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
21
Q

Describe the clinical manifestations of hypercalcemia.

A

Abdominal pain, bone pain, confusion, depression, weakness, kidny stones or abnormal heart rhythm,.

Can affct muscl tone, neurologic

22
Q

Describe the pH buffering systems in the body.

A

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

23
Q

Explain how the respiratory/renal systems regulate pH

A

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

24
Q

Explain how acidosis may arise and describe the compensatory responses

A

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.

25
Q

Explain how alkalosis may arise and describe the compensatory responses.

A

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.

26
Q

Describe the clinical manifestations of acidosis and alkalosis.

A

PIC