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Fundamentals of P > Investigation of Salt & Water and Acid/Base Balance > Flashcards

Investigation of Salt & Water and Acid/Base Balance Flashcards

1
Q

Distribution of body fluids - describe

A 
Extracellular Fluid Compartment = 20%
Interstitial = 15%
Intravascular = 5%
Transcellular = 1%
H2O in connective tissue = <1%

Intracellular Fluid Compartment = 40%

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2
Q

Water balance are determined by what? (w/sodium)

A 
Intake
 - Dietary intake (Thirst)
Output 
 - Obligatory losses
         Skin
         Lungs
- Controlled losses – these depend on:
         Renal function
         Vasopressin/ADH (anti-diuretic 
         hormone)
         Gut (main role of the colon)
         Redistribution
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3
Q

Sodium balance are determined by what? (w/water)

A

Intake

  • Dietary (unless vegan and doesn’t add salt)
  • Western diet 100-200 mmol/day

Output
- Obligatory losses
Skin

- Controlled losses – these depend on:
      Kidneys     
      Aldosterone
      GFR
      Gut - most sodium is reabsorbed; loss 
       is pathological

Determined by intravascular volume

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4
Q

Hormones involved in water and salt balance for sodium

A

Aldosterone produced in the adrenal cortex: regulates sodium and potassium homeostasis

Natriuretic hormones (ANP cardiac atria, BNP cardiac ventricles) promote sodium excretion and decrease blood pressure

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5
Q

Hormones involved in water and salt balance for sodium for just water

A

ADH/vasopressin: synthesised in hypothalamus and stored in posterior pituitary. Release causes increase in water absorption in collecting ducts

Aquaporins (AQP1 proximal tubule and not under control of ADP) AQP2 and 3 present in collecting duct and under control of ADH

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6
Q

Effect of osmotically active substances in blood

A

Osmotically active substances in the blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes

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7
Q

Define osmometer and its action

A

An osmometer is a device for measuring the osmotic strength of a solution, colloid, or compound.

Freezing point depression
Uses colligative properties of a solution
More solute – lower the freezing point

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8
Q

List methods for analysing sodium

A

Indirect Ion selective electrodes (main lab analysers)

Direct Ion selective electrodes (Blood gas analyser)

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9
Q

How to assess a patient with possible fluid/electrolyte disturbance using history

A

History

=

Fluid intake / output
Vomiting/diarrhoea
Past history
Medication

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10
Q

How to assess a patient with possible fluid/electrolyte disturbance using examination

A

Examination - Assess volume status

=

Lying and standing BP
Pulse
Oedema
Skin turgor/Tongue
JVP / CVP
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11
Q

How to assess a patient with possible fluid/electrolyte disturbance using examination apart from history + examination

A

Fluid chart

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12
Q

Action at DCT

A

Sodium reabsorption

Loss of H+/K+

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13
Q

By-prod of ATP prod

A

Large amounts of protons/hydrogen ions are an inevitable by-product of energy/ATP production

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14
Q

Maintenance of extracellular [H+]/pH depends on what ?

A

depends on the relative balance between acid production and excretion
carbon dioxide production and excretion (respiration)
hydrogen ion production and excretion (renal)

maintain protein/enzyme function

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15
Q

Effect of decreased buffering

A

Decr. Buffering – consumption of HCO3

= Removal of CO2

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16
Q

Define metabolic acidosis

A 
Metabolic acidosis
(rate of H+ generation > excretion)
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17
Q

Effect of increased renal excretion

A

🡩 renal excretion of H+ & regeneration of HCO3

=

🡩retention of CO2
(H20 + CO2 ⮀ H2CO3)

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18
Q

pH equation in terms of HCO3 and CO2

A

pH = HCO3/CO2

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19
Q

Describe attempt to return acid / base status to normal by buffering

A

Bicarbonate buffer in serum, phosphate in urine (for excretion)
Skeleton
Intracellular accumulation/loss of H+ ions in exchange for K+ , proteins and phosphate act as buffers

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20
Q

Describe attempt to return acid / base status to normal by compensation

A

Diametric opposite of original abnormality
Never overcompensates
Delayed and limited

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21
Q

Describe attempt to return acid / base status to normal by treatment

A

By reversal of precipitating situation

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22
Q

Describe the speed of respiratory compensation with an example

A 
Respiratory compensation for a primary metabolic disturbance can occur very rapidly
Kussmaul breathing (respiratory alkalosis) in response to DKA
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23
Q

Describe the speed of metabolic compensation + its requirements

A

Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur

=

requires enzyme induction from increased genetic transcription and translation etc

Requires more chronic scenario to include compensation mechanism

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24
Q

When is compensation absent

A

No compensation seen in acute respiratory acidosis such as asthma

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25
Q

Mechanism of renal bicarbonate regeneration

A

H+ moves out from tubular cell into renal lumen, Na+ moves in
- H+ from H20 + CO2 ⮀ H2CO3

K+ movement stopped

HCO3- from H20 + CO2 ⮀ H2CO3
- Regenerated and reclaimed bicarbonate

26
Q

Pitfalls of ABG

A 
Expel air
Mix sample
Analyse ASAP
Plastic syringes OK at room temp for  ̴ 30mins
Ice not required
Ensure no clot in syringe tip
27
Q

Errors in blood gas analysis are dependent more on what

A

Errors in blood gas analysis are dependent more on the clinician than on the analyser

28
Q

Causes of respiratory acidosis

A 
Airway obstruction
Neuromuscular disease
Pulmonary disease
Extrapulmonary thoracic disease
Respiratory centre depression
29
Q

Respiratory acidosis - describe compensation

A

Increased renal acid excretion (metabolic alkalosis, 36-72 hrs delay)

30
Q

Respiratory acidosis - describe correction

A

Requires return of normal gas exchange

31
Q

Respiratory acidosis - features (acute and chronic)

A

Features
acute: 🡻pH (🡹[H+]), 🡹pCO2, 🡺[HCO3-],– ie. no compensation

chronic: 🡻pH (🡹[H+]), 🡹pCO2, 🡹[HCO3-],– ie. compensation

32
Q

Causes of respiratory alkalosis

A

Hypoxia
Pulmonary disease
Mechanical overventilation
Increased respiratory drive

33
Q

List what would cause increased respiratory drive

A 
Respiratory stimulants eg salicylates
Cerebral disturbance eg trauma, infection and tumours
Hepatic failure
G-ve septicaemia
Primary hyperventilation syndrome
Voluntary hyperventilation
34
Q

List what would cause respiratory centre depression

A

Anaesthetics
Sedatives
Cerebral trauma
Tumours

35
Q

List what would cause airway obstruction

A

Bronchospasm (Acute)
COPD (Chronic)
Aspiration
Strangulation

36
Q

List what would cause pulmonary disease

A

Pulmonary fibrosis
Respiratory Distress Syndrome
Pneumonia

Pulmonary oedema
Pulmonary embolism

37
Q

List what would cause an extrapulmonary thoracic disease

A

Flail chest

38
Q

List what would cause neuromuscular disease

A

Guillain-Barre Syndrome

Motor Neurone Disease

39
Q

List what would cause hypoxia

A

High altitude
Severe anaemia
Pulmonary disease

40
Q

Respiratory alkalosis - describe compensation

A

Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)

41
Q

Respiratory alkalosis - describe features (acute and chronic)

A

acute: high pH, low [H+], n[HCO3-], low pCO2 – no compensation
chronic: high pH, low [H+], low [HCO3-], low pCO2

42
Q

Causes of metabolic acidosis

A 
Increased addition of acid 
Increased H+ formation
Acid ingestion
Decreased H+ excretion
Loss of bicarbonate
43
Q

List what would cause increased H+ formation

A

Ketoacidosis
Lactic acidosis
Poisoning – methanol, ethanol, ethylene glycol, salicylate
Inherited organic acidosis

44
Q

List what would cause acid ingestion

A

Acid poisoning

XS parenteral administration of amino acids eg arginine

45
Q

List what would cause decreased H+ excretion

A

Renal tubular acidosis
Renal failure
Carbonic dehydratase inhibitors

46
Q

List what would cause loss of bicarbonate

A

Diarrhoea

Pancreatic, intestinal or biliary fistula/drainage

47
Q

Metabolic acidosis

- describe compensation

A

hyperventilation, hence low pCO2

48
Q

Metabolic acidosis

- describe correction

A

of cause

increased renal acid excretion

49
Q

Metabolic acidosis

- features

A

low pH, high [H+], low [HCO3-], low pCO2

50
Q

Causes of metabolic alkalosis

A

Increased addition of base
Increased loss of acid
Negative effects on renal system
Decreased elimination of base

51
Q

List what would cause increased addition of base

A

Inappropriate Rx of acidotic states

Chronic alkali ingestion

52
Q

List what would cause increased loss of acid

A

GI loss

  • Gastric aspiration
  • Vomiting with pyloric stenosis
53
Q

List what would cause negative effects on the renal system that would lead to metabolic alkalosis

A

Diuretic Rx (not-K+sparing)
Potassium depletion
Mineralocorticoid excess- Cushing’s, Conn’s
Drugs with mineralocorticoid activity – carbenoxolone

54
Q

Metabolic alkalosis

- describe compensation

A

Hypoventilation with CO2 retention (respiratory acidosis)

55
Q

Metabolic alkalosis

- describe correction

A

increased renal bicarbonate excretion

reduce renal proton loss

56
Q

Metabolic alkalosis

- features

A

high pH, low [H+], high [HCO3-], N/highpCO2

57
Q

Hypovolaemia from persistent vomiting

leads to

A

Loss of HCl
Loss of potassium
Loss of fluid

58
Q

Diuretics lead to

A

Chronic K+ depletion

59
Q

Describe response to fluid loss

A

Response to fluid loss is aldosterone activation

  • Reabsorb NaCl/H2O at distal convoluted tubule in kidney in exchange for K+ /H+
60
Q

Hyperkalaemia causes

A

If increased intake:
Usually parenteral

if decreased loss:

Reduced GFR
Reduced tubular loss (potassium 
      sparing diuretics
      anti-inflammatories, ACEIs, 
      mineralocorticoid deficiency)
61
Q

Hypokalaemia causes

A

If increased loss:

Gut (diarrhoea, laxatives)
Kidney (diuretics, 
      magnesium deficiency, 
      mineralocorticoid XS
      renal tubular abnormalities)

if decreased intake:

Often alcohol
Anorexia

Fundamentals of P (62 decks)

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