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TI2 > Investigation of salt and water and acid/base balance > Flashcards

Investigation of salt and water and acid/base balance Flashcards

1
Q

What is water balance determined by?

A
  • Intake
  • Output - obligatory losses (sweat, exhaling), controlled losses (renal function, ADH, gut absorption)
  • Redistribution (between compartments)
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2
Q

How does water redistribute?

A
  • Osmotically active substances in the blood may result in water distribution to maintain osmotic balance
  • Water will transfer into a compartment with much higher solute levels
  • Excess solute in ECFV -> cell shrinkage
  • Excess solute IC -> cell swelling
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3
Q

What are the physiological responses to water loss?

A
  • Stimulation of ADH release - renal water retention
  • Stimulaiton of hypothalamic thirst centre - increase intake
  • Redistribution of water from ICF - increased ECF water
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4
Q

What is sodium balance determine by?

A
  • Intake - dietary

- Output - obligatory losses (skin), controlled excretion (kidneys, aldosterone, GFR, gut absorption/pathological loss)

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5
Q

What hormones are involved in salt and water balance?

A

Sodium

  • Aldosterone from adrenal cortex - regulates Na and K homeostasis
  • Natriuretic hormones (ANP and BNP) - promote Na excretion and decrease BP (look for n-terminus of both when looking at heart failure)

Water

  • ADH - synthesised in hypothalamus and store in posterior pituitary. Release causes increase in water absorption in CDs
  • Aquaporins - AQP1 in PCT, AQP2 and 3 in CD under control of ADH
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6
Q

Briefly describe the RAAS system

A
  • Juxtoglomerular cells recognise hypotension and macula densa recognises sodium depletion
  • These signal juxtoglomerular cells to release renin
  • renin released, converts angiotensionigen to angiotensin I
  • This is converted to angII by ACE
  • AngII acts on adrenal cortex to release aldosterone
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7
Q

What is freezing point depression osmometry?

A
  • Looks at the colligative properties of a solution
  • If you increase the number of particles in a soln, the osmotic pressure will increase
  • Increasing more solute will increase the boiling point
  • Decreasing the solute will decrease the boiling point
  • Can decrease the freezing point with more solute
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8
Q

Case 1 - drowsy and confused, dry tongue, low BP and high pulse.
Blood results - high sodium, urea and creatinine

A

Renal impairment

  • dry tongue = dehydration
  • BP low and pulse fast = dehydration
  • Na high = dehydration
  • Urea and creatinine high = poor renal perusion -> increased reabsorption
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9
Q

Case 2 - confusion, drinking lots of water

- lab results - v low sodium

A
  • Very low sodium - cause confusion, can become violent and have other psychiatric problems
  • Psychogenic polydipsia - drink lots and lots of water
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10
Q

What clinical questions do you have to ask when looking at a sodium related case?

A
  • Are they euvolaemic, or hypo-/hyper-?
  • What is the underlying cause of the hyponatraemia?
  • What other lab tests might help interpret the data?
  • What is the kidney doing with sodium etc
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11
Q

How do you assess a pt with possible fluid/electrolyte disturbance?

A
  • History - fluid intake/output, vomiting/ diarrhoea, past history, medication
  • Examination - lying and standing BP, pulse, oedema, tongue, JVP/ CVP
  • Fluid chart
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12
Q

What brain probs can sodium probs cause?

A
  • Hyponatraemia - over-rapid correction may lead to central pontine myelinolysis
  • Hypernatraemia - over-rapid correction may lead to cerebral oedema - too much water in brain causes it to start pushing down through the foramen magnum
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13
Q

Sodium balance summary

A
  • BP/ volume sensed - baroreceptors and renal perfusion pressure
  • Aldosterone produced from renal cortext
  • Causes action at DCT - sodium reabsorption and loss of H+/K+
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14
Q

Why do we have to balance acid-base?

A
  • Large amounts of hydrogen ions are a by-product of ATP production
  • Maintenance of EC H+/ pH is essential to maintain protein/ enzyme function
  • Depends on the relative balance between acid production and excretion (CO2 production and excretion - respiration; and H+ production and excretion - renal)
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15
Q

What i significant about the pH being a log scale?

A
  • Changes in H+ ions doesnt seem that much

- A drop in 40mM from 80 to 40mM is only a drop in 0.3 pH from 7.4 to 7.1

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16
Q

What is the henderson-hasselbalch equation?

A

CO2 + H20 H2CO3 H+ + HCO3

17
Q

What happens in metabolic acidosis?

A

The H+ generation exceeds the excretion - H+ goes up

  • Try to get equilibrium to bring back normality
  • increase bicarbonate levels and remove CO2
  • Kussmaul respiration is deep sighing breahing to get rid of CO2 to compensate for metabolic acidosis
18
Q

What happens in respiratory acidosis?

A
  • Rate of CO2 excretion < generation
  • Ability to excrete CO2 is impaired, but still producing a lot
  • H+ conc goes up because of the CO2 retention
  • Have to try and improve the renal excretion od H+ and regeneration of bicarb
  • Metabolic compensation takes longer than respiratory
19
Q

What are the 3 main buffer systems we have in the body?

A
  • Bicarbonate in the serum, phosphate in the urine
  • Skeleton - good at taking up H+
  • IC accumulation/ loss of H+ ions in exchange for K+ - proteins and phosphate act as buffers
20
Q

What are the differences in compensation speeds between resp and metabolic?

A
  • Respiratory can occur very rapidly - kussmaul breathing in response to diabetic ketoacidosis
  • Metabolic takes around 36-72 hrs
    . need enzyme induction for increased genetic transcription and translation
    . no compensation seen in acute resp acidosis such as asthma
    . requires more chronic scenario to include compensation mechanism
21
Q

What is the mechanism of renal bicarb regeneration?

A
  • We reclaim most bicarb in PCT, and only generate bicarb in the DCT
  • Sodium goes into the cell in exchange for K which gets excreted
  • Carbonic acid dissociates to form bicarb and H+ which are excreted
  • When we excrete H+ ions, we dont excrete sodium ions to regulate the electrochemical gradient
22
Q

How do we interpret ABG?

A
  • pO2 - have to also check FiO2
  • pH - is it normal?
  • pCO2 - primary resp, or compensatory response?
  • HCO3 - metabolic component (dont measure on ABG< we calculate using H-H)
23
Q

What are some causes of resp acidosis?

A
  • Airway obstruction - bronchospasm, COPD, aspiration, strangulation
  • Resp centre depression - anaesthetics, sedatives, cerebral trauma, tumours
  • Neuromuscular disease - Motor neurone disease, Gullain-Barre syndrome
  • Pulmonary disease - pulmonary fibrosis, respiratory distress syndrome, pneumonia
  • Extrapulmonary thoracic disease - flail chest
24
Q

Case 3 - RTA, flail chest, unable to oxygenate, cant blow off CO2

A
  • Low O2, low pH (acidotic), high pCO2, normal bicarb

= Uncompensated acute respiratory acidosis + impaired oxygenation

25
Q

What are the main causes of respiratory alkalosis?

A
  • Hypoxia - high altitude, severe anaemia, pulmonary disease (oedema or embolism)
  • mechanical overventilation
  • Increased respiratory drive - resp stimulants (salicylates), cerebral disturbance (trauma, infection, tumours), hepatic failure, G-ve septicaemia, primary hyperventilation syndrome, voluntary hyperventilation
26
Q

Case 4 - increasingly anxious, tingling in fingers and toes

A
  • Tingling from change in ionised ca levels
  • more is bound to protein because you are trying to release H+ from protein
  • high pH (alkalotic)
  • Low pCO2
  • normal bicarb
  • uncompensated, acute respiratory alkalosis
    (should compensate by decreasing bicarb)
27
Q

What are the main causes of metabolic acidosis?

A
  • Increased H+ formation - ketoacidosis, lactic acidosis, posioning, inherited organic acidosis
  • Acid ingestion
  • Decreased H+ excretion - renal tubular acidosis, renal failure, carbonic dehyrdratase inhibitors
  • Loss of bicarbonate - diarrhoea, pancreatic, intestinal or biliary fistulae
28
Q

Case 5 - type 1 diabetes, not taken isnulin for 24 hrs

A
  • normal pO2
  • acidotic low pH
  • Normal pCO2
  • Low bicarb
  • uncompensated acute metabolic acidosis
29
Q

What are main causes of metabolic alkalosis?

A
  • Increased addition of base
  • Decreased elimination of base
  • Increased loss of acid - GI loss - hypovolaemia from persistent vomiting (loss of HCl, loss of K and loss of fluid)
  • renal loss (diuretics, K depletion, mineralocorticoid excess)
30
Q

Case 6 - vomiting last 48 hrs

A
  • normal PO2 and CO2
  • alkalotic high pH
  • High bicarbonate
  • uncompensated metabolic alkalosis
31
Q

Acid base clinical scenarios summary

A

Resp acidosis

  • CO2 retention
  • Compensation is metabolic alkalosis

Resp alkalosis

  • Increased CO2 loss
  • Compensation is metabolic acidosis

Metabolic acidosis

  • Acid ingestion
  • Increased acid production
  • Reduced acid excretion
  • Compensation is resp alkalosis

Metabolic alkalosis

  • very difficult primary disturbance to produce and maintain - very specific factors required
  • Compensation is resp acidosis
32
Q

Why is it that when you are acidotic, you tend to also have hyperkalaemia?

A
  • Exchange of cations to keep neutral charge
33
Q

Hyper vs hypokalaemia

A

Hyper

  • increased intake
  • Decreased loss - reduced GFR, reduced tubular loss (K+ sparing diuretics, ACEIs, mineralocorticoid deficiency)

Hypo

  • increased loss - gut, kidney (diuretics, Mg deficiency, mineralocorticoid excess, renal tubular abnoralities)
  • Decreased intake - alcohol, anorexia
34
Q

Why would you get K+ redistribution?

A

Can get redistribution between ICF and ECF

  • Alkalosis, insulin and beta agonists into the cell
  • Acidosis, decreased insulin and tissue damage - out of the cell

TI2 (20 decks)

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