fluid and electrolyte balance Flashcards

1
Q

what electrolytes and anions in ECF

A

Na+, Cl- and HC03

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2
Q

what electrolytes and anions in ICF

A

K+, proteins and phosphate

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3
Q

how is water excreted and what controls it? what secretes what controls it

A

Water excretion by the kidney is very tightly controlled by arginine vasopressin (AVP) also called ADH secreted from the posterior pituitary gland according to the osmolality.
A rising osmolality promotes the secretion of AVP, causing water to be retained by the kidney.
A declining osmolality switches the secretion off.

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4
Q

concentration of sodium in circulation

A

135-145mmol/L maintains serum osmolality

100-300mmol per day intake in the west

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5
Q

how is na+ lost

A

kidneys, sweat, poo, vommit( OTC diaralyte has electrolytes.

Na needs to be regulated otherwise hypotension

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6
Q

what controls na urinary output homeostasis

A

Aldosterone: na and water retention and k+ excretion

Atrial natriuteric peptide: secreted from cardiocytes of the right atrium of the heart. It increases urinary sodium excretion

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7
Q

explain RAAS system

A

at the end : increase reabsorption of na and h20 and decrease cardiac output

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8
Q

what is the science name for low sodium and what are the causes, clinical symptoms and clinical signs?

A

hyponatraemia
Loss of Sodium; e.g. vomiting diarrhoea, loss from burns, fistulae, Addison’s disease.
Water retention; inappropriate secretion of ADH (SIAD), e.g. post trauma or inappropriate treatment with iv dextrose

Clinical symptoms: nausea, malaise, headache, lethargy and a reduced level of consciousness. Seizures and coma are not seen usually until Na+ Conc. < 110-115 mmol/l.
Clinical signs: signs of volume depletion e.g. hypotension, decreased urine output, decreased consciousness, decreased skin turgor, soft/ sunken eyeballs, dry mucous membrane, increased pulse
-demeclocycline- for hyponatraemia

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9
Q

toxicity of which drug is made worse by hyponatraemia

A

Lithium- causes lithium retention and causes toxicity bc narrow therapeutic index.

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10
Q

what is hypernatraemia and what causes it

A

Water depletion:
water intake e.g. post-op ( due to unconciousness or nil by mouth) or dysphagia.
Excessive water loss, diabetes insipidus (failure of ADH), sweating, hyperventilation
Sodium retention
Excessive intake e.g. over infusion of saline, salts etc.
Excessive adrenocortical hormones e.g. Conn’s syndrome and Cushing’s syndrome

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11
Q

potassium serum levels

A

K+ is the major ICF cation, 2% of body content being in the ECF (serum level is 3.5-5mmol/l)
Potassium intake is variable, 30-100mmol/day in the UK.
The kidney excretes the bulk of ingested potassium (20-100mmol/day), with some lost in the faeces (~5mmol/day).
Serum potassium conc. does not vary appreciably in response to water loss or retention. However, factors that cause even a small or sudden shift of intracellular potassium will cause a big change in the ECF K+ conc.

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12
Q

how does k+ move, cellular paths and in acids and alkaline situations?

A

Cellular uptake of potassium is stimulated by insulin.
A reciprocal relationship exists between K+ and H+ ions. In acidosis, H+ ions conc. , K+ ions are displaced from the cells into ECF to maintain electroneutrality. The opposite occurs in alkalosis. Hence, H+ ions changes cause marked alteration in serum K+ conc.
One of the main functions of potassium is to maintain excitability of neuromuscular tissue.

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13
Q

what’s name for high k+ and what’s the causes

A
Is caused by:
Renal failure
Mineralocorticoid deficiency (hypoaldosteronism (Addison’s disease))
Acidosis
Hormonal effects-low plasma insulin
Severe tissue damage
Excessive doses of K+ sparing diuretics, what others?
Excessive doses of K+ supplements
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14
Q

how k+ clinical symptoms

A

Clinical symptoms;
Hyperkalaemia results in an enhanced state of excitability of cells. The main effects are on cardiac and skeletal muscle. In many cases, cardiac signs appear and lead to death before skeletal muscle symptoms appear.
Cardiac toxicity manifests as the sudden development of cardiac irregularity, tachycardia, ventricular fibrillation and asystole. Sudden death from cardiac arrest is common.

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15
Q

name for low k+? and what are causes?

A

hypokalaemia may be caused by:

  • gastrointestinal losses eg. vomiting, diarrhoea or surgical fistula
  • renal losses in renal tubular failure
  • drug induced: diuretics, corticosteroids

patients with hypokalaemia may have sever muscle weakness, neurological and cardiac arrhythmia

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16
Q

what is the calcium serum level

A

2.2-2.6mmol/l

17
Q

factors that control calcium homeostasis

A

vitamin d and parathyroid hormone PTH

PTH is secreted from the parathyroid glands in response to low unbound plasma calcium. It causes an;
Increase in osteoclastic resorption of bone
Increase in renal tubular reabsorption of calcium
Increase synthesis of 1,25-(OH)2D3
Increase intestinal absorption of calcium

18
Q

Calcium calculation

A

About half of serum calcium is bound to proteins, mostly to albumin.
Unbound calcium is the biologically active fraction of the total calcium in plasma and maintenance of its concentration within tight limits is required. It is this fraction that is recognised by the parathyroid gland.
Laboratories routinely measure total calcium concentration (both bound and unbound).
This may give to problems in interpreting results, as changes in serum albumin concentration cause changes in total calcium concentration.
E.g. if albumin concentration falls, total serum calcium is low because the bound fraction is decreased.

Corrected calcium (mmol/L)= Total measured calcium + 0.02 (40-albumin)

19
Q

hypocalcaemia causes

A
  • vit d deficiency: malabsorption, inadequate diet, lack of sun
  • renal disease: unable to synthesise 1,25-DHCC
20
Q

Hypocalcaemia symptoms and management

A
  • numbness and tingling and burning in extremities
  • tetany occurs when levels are 1.5-1.6mmol/l
  • prolonged hpocalcaemia can interfere with metabolism of the lens and cause cataracts

management:

  • calcium supplemets
  • calcitriol or alfacacidol can be given
21
Q

hypercalcaemia causes and clinical signs

A

causes of high calcium:

  • vitamin d oversode
  • hyperparathyroidism
  • neoplasms
  • Bone disease: pagets

clinical signs of hypercalcaemia:

  • heart: cardiac arrhythmias
  • neurological and physc: legsrthy, confusion, dementia, depression
    renal: thirst, polyuria
  • gi: anorexia, constipation, n and v
22
Q

what are the functions of the kidney

A
  • regulation of water, electrolytes and acid base balance
  • excretion of urea, creatinine and uric acid
  • produced hormones eg renin and erythop
23
Q

Cockcroft and Gault equation for egfr

A
GFR= A X (140 – age(years)) X weight (kg)
		      Serum Creatinine (µmol/L)

Where A=1.23 for males, A = 1.04 for females

24
Q

considerations for obese patients for egfr calculations?

A

To normalise the calculation, use ideal body weight where fat is likely
to be the major contributor to body mass

	IBW male = 50 + (2.3 x height in inches over 5 feet)
	IBW female= 45.5 + (2.3 x height in inches over 5 feet)

Many other formulas used:

Ideal body weight (kilograms) = Constant + 0.91 (Height - 152.4)
Where:
Constant = 50 for men; 45.5 for women
Height in centimetres

25
Q

limitations in GFR calculations

A
  • not valid in pregnancy
  • not valid in elderly
  • amputees
  • vegans
  • bodybuilders