Biochemistry Hypo and Hyper natraemia Flashcards Preview

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Flashcards in Biochemistry Hypo and Hyper natraemia Deck (48):
1

2 interfaces:

• Cell membrane between intra and extra cellular
• Capillary epithelium between plasma and interstitial space

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Cell membrane:
Balance of osmotic pressures →

• Intracellular potassium and associated anions balanced against the extracellular osmolality due to Sodium and its associated anions.
• It is this Osmotic balance that retains 2/3 of water insides cells.
= Osmi (k+) = Osmo (Na+)

3

Acute hyponatraemia Description





If there was an acute fall in extracellular Osmolality due to an acute fall in plasma Na concentration.
Fall in Na = fall is osmolality
Water → Will move towards the direction of higher osmolarity → Shift of water into the cells

4

Acute hyponatraemia Clinical features

Cerebral cellular oedema:
1. Confusion (mild) – first sign
2. Stupor
3. Convulsions (most important)
4. Coma
5. Death (tentorial shift – coning)

5

Acute hyponatraemia Chronic Hyponatraemia

Sodium and extracellular osmolality falls slowly over weeks/months then there is a capacity to compensate by shifting the osmolar constituents to adjust for change.

6

Acute Hypernatraemia Description




Acute rise in extracellular Osmolality due to a rise in NA. Water will move towards the direction of higher osmolality → water leave cells

7

Acute Hypernatraemia Clinical features

Cerebral cellular dehydration accounts for acute hyernatraemia:
1. Confusoin
2. Stupor
3. Convulsions (less often0
4. Coma

8

Capillary endothelium function

Retain Plasma volume and interstial volume at the right levels

9

Governed by

Frank starling forces

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Arterial end

Hydrostatic – water and electrolytes out arterial

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Venous end

Colloid osmotic pressure drawing water back in at venous end
→ Small residual pressure exerted by large molecules (proteins mainly albumin)

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Pathology

Reduction in albumin – nephrotic syndrome
Congestive cardiac failure – abnormal hydrostatic pressure gradient (accumulation of fluid in interstial space- oedema
Liver cirrhosis – abnormal albumin production and hydrostatic changes

13

Sodium and Water balance:
Obligatory loss (unregulated inout)

1. Skin (500 lm)
2. Lungs (400 ml)
3. Gut (100 ml)
4. Kidney (UO) 500 m

14

Typical sources (regulated output): sodium and water

1. Oxidation 400 ml
2. Dietary 1100 ml

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Increased Fluid loss:

• Burns
• Fever
• Exercise
• Diarrhoea
• Vomiting
• Stomas
• Diabetes mellitus/insipidus

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Pseudo Hyponatraemia explanation








Normally when we measure substance in plasma we assume that 1 L of plasma = 1 L of water.
→ E.g. Na in plasma 140 mmol/L
→ Homeostatic mechanisms regulates Na in plasma water

If patient has a negligible non water but with high lipid or immunoglobulin percentage of plasma not water will go up –less water per unit volume of plasma – less solvent for NA.
 In plasma water 140 mol/L (still)
 Total volume lower

17

If pseudo is suspected Measure

Osmolality – reflection of number of particles in the water. Despite the NA appearing low

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ABG measurement of NA

Directly sense sodium concentration in plasma water (via electrode)

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Compensated Hyponatraemia:
Description


If a patient has diabetes with a high extracellular glucose concentration. Not taken up to cells and not metabolism – how will this effect water?
Water moves out – dilutes other solutes present in plasma – therefore Na reduction

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How does this effect Na levels

The high extracellular water dilutes other solutes present in plasma – therefore Na reduction

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Compensated hyponatraemia always check

Glucose

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Volume Depleted: Volume Expanded:

Renal Loss
Extra-Renal

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Renal Loss




1. Over diuresis
→ Thiazide diuretics – disproportionate loss of sodium - Intravascular volume depleted (excessive it can trigger ADH – this only protects WATER loss not Sodium loss)

2. Addison’s disease

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Extra-Renal

Vomiting
Diarrhoea

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Volume Expanded:

No oedema
Oedema

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No oedema


SIADH
Hypothyroid
UNa>20
Rx – Normal Saline

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Oedema

Nephrotic Cirrhosis
CCF
UNa <10

Rx – fluid restriction

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SIADH

Inappropriate action of ADH

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Causes of Inappropriate ADH Secretion (SIADH) →

Neoplasia
Pulmonary disorders
Neurological disorders 0 dsmage hypothalamus

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Neoplasia

Bronchogenic carcinoma
Pancreatic carcinoma
Lymphoma

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Pulmonary disorders

Pneumonia
Tuberculosis
Bronchiectasis
Positive pressure ventilation
Acute exacerbation of COPD (reduction with sodium)

32

Neurological disorders - damage hypothalamus

Encephalitis (basal)
Meningitis (basal)
Head Injury
Porphyria (toxic)

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Causes of Hypernatraemia →

Inadequate water intake
Impaired water retention
Loss of hypotonic fluids
Excessive sodium intake
Increased sodium retention

34

Inadequate water intake

• Lack of water (not available)
• Inability to drink (coma)
• Loss of thirst

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Impaired water retention

Diabetes insipidus
Osmotic diuresis (very common due to hyper glycaemia)

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Loss of hypotonic fluids

Sweat
Hyperventilation
Watery diarrhoea
Burns

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Excessive sodium intake

Intravenous fluids
Drugs (e.g. IV antibiotics)

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Increased sodium retention

Primary hyperaldosteronism (Conn’s Syndrome)

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Diabetes insipidus:

→ Deficiency in ADH

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Causes if Diabetes Insipidus →

Cranial
Nephrogenic

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Cranial types

Idiopathic
Secondary

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Idiopathic

Familial (autosomal dominant)
Sporadic

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Secondary

Trauma (accidents, surgery)
Tumours (craniopharyngioma, pit, adenoma)
Granuoma (sarcoid, histocytosis X)
Infection (encephalitis, meningitis)
Vascular (aneurysm, hypoxia, vasculitis)
Autoimmune

44

Idiopathic

Familial (autosomal dominanant)
Sporadic

45

Secondary:

Drugs/Toxins
Metabolic
Vascular
Pyelonephritis
After ATN

46

Secondary: Drugs and Toxins

Demeclocycine – used to treat SIADH
Lithium

47

Metabolic

Hypercalcaemia
Hypokalaemia
Amyloid

48

Vascular

Sickle cell disease

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