Biochemistry Hypo and Hyper natraemia Flashcards

1
Q

2 interfaces:

A
  • Cell membrane between intra and extra cellular

* Capillary epithelium between plasma and interstitial space

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2
Q

Cell membrane:

Balance of osmotic pressures →

A

• 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+)

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3
Q

Acute hyponatraemia Description

A

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

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4
Q

Acute hyponatraemia Clinical features

A

Cerebral cellular oedema:

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

Acute hyponatraemia Chronic Hyponatraemia

A

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.

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6
Q

Acute Hypernatraemia Description

A

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

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7
Q

Acute Hypernatraemia Clinical features

A

Cerebral cellular dehydration accounts for acute hyernatraemia:

  1. Confusoin
  2. Stupor
  3. Convulsions (less often0
  4. Coma
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8
Q

Capillary endothelium function

A

Retain Plasma volume and interstial volume at the right levels

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9
Q

Governed by

A

Frank starling forces

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10
Q

Arterial end

A

Hydrostatic – water and electrolytes out arterial

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11
Q

Venous end

A

Colloid osmotic pressure drawing water back in at venous end

→ Small residual pressure exerted by large molecules (proteins mainly albumin)

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12
Q

Pathology

A

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

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13
Q
Sodium and Water balance:
Obligatory loss (unregulated inout)
A
  1. Skin (500 lm)
  2. Lungs (400 ml)
  3. Gut (100 ml)
  4. Kidney (UO) 500 m
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14
Q

Typical sources (regulated output): sodium and water

A
  1. Oxidation 400 ml

2. Dietary 1100 ml

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15
Q

Increased Fluid loss:

A
  • Burns
  • Fever
  • Exercise
  • Diarrhoea
  • Vomiting
  • Stomas
  • Diabetes mellitus/insipidus
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16
Q

Pseudo Hyponatraemia explanation

A

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

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17
Q

If pseudo is suspected Measure

A

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

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18
Q

ABG measurement of NA

A

Directly sense sodium concentration in plasma water (via electrode)

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19
Q

Compensated Hyponatraemia:

Description

A

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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20
Q

How does this effect Na levels

A

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

21
Q

Compensated hyponatraemia always check

A

Glucose

22
Q

Volume Depleted: Volume Expanded:

A

Renal Loss

Extra-Renal

23
Q

Renal Loss

A
  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
24
Q

Extra-Renal

A

Vomiting

Diarrhoea

25
Q

Volume Expanded:

A

No oedema

Oedema

26
Q

No oedema

A

SIADH
Hypothyroid
UNa>20
Rx – Normal Saline

27
Q

Oedema

A

Nephrotic Cirrhosis
CCF
UNa <10

Rx – fluid restriction

28
Q

SIADH

A

Inappropriate action of ADH

29
Q

Causes of Inappropriate ADH Secretion (SIADH) →

A

Neoplasia
Pulmonary disorders
Neurological disorders 0 dsmage hypothalamus

30
Q

Neoplasia

A

Bronchogenic carcinoma
Pancreatic carcinoma
Lymphoma

31
Q

Pulmonary disorders

A
Pneumonia
Tuberculosis
Bronchiectasis
Positive pressure ventilation
Acute exacerbation of COPD (reduction with sodium)
32
Q

Neurological disorders - damage hypothalamus

A

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

33
Q

Causes of Hypernatraemia →

A
Inadequate water intake
Impaired water retention
Loss of hypotonic fluids
Excessive sodium intake
Increased sodium retention
34
Q

Inadequate water intake

A
  • Lack of water (not available)
  • Inability to drink (coma)
  • Loss of thirst
35
Q

Impaired water retention

A
Diabetes insipidus
Osmotic diuresis (very common due to hyper glycaemia)
36
Q

Loss of hypotonic fluids

A

Sweat
Hyperventilation
Watery diarrhoea
Burns

37
Q

Excessive sodium intake

A

Intravenous fluids

Drugs (e.g. IV antibiotics)

38
Q

Increased sodium retention

A

Primary hyperaldosteronism (Conn’s Syndrome)

39
Q

Diabetes insipidus:

A

→ Deficiency in ADH

40
Q

Causes if Diabetes Insipidus →

A

Cranial

Nephrogenic

41
Q

Cranial types

A

Idiopathic

Secondary

42
Q

Idiopathic

A

Familial (autosomal dominant)

Sporadic

43
Q

Secondary

A
Trauma (accidents, surgery)
Tumours (craniopharyngioma, pit, adenoma)
Granuoma (sarcoid, histocytosis X)
Infection (encephalitis, meningitis)
Vascular (aneurysm, hypoxia, vasculitis)
Autoimmune
44
Q

Idiopathic

A

Familial (autosomal dominanant)

Sporadic

45
Q

Secondary:

A
Drugs/Toxins
Metabolic
Vascular
Pyelonephritis
After ATN
46
Q

Secondary: Drugs and Toxins

A

Demeclocycine – used to treat SIADH

Lithium

47
Q

Metabolic

A

Hypercalcaemia
Hypokalaemia
Amyloid

48
Q

Vascular

A

Sickle cell disease