Investigation of Salt/Water and Acid/Base Balance Flashcards
- How many litres is the total fluid in the body?
50 L
- We can break down the total body weight into extracellular and intracellular fluid.
What % does intracellular fluid make up of total body weight
40%
- What % of total body weight does extracellular fluid make up?
20%
4. Extracellular fluid makes up 20% of body weight Break that down into how much % for: -Interstitial -Intravascular -Transcellular -H20 in connective tissue
- Interstitial = 15%
- Intravascular = 5%
- Transcellular = 1%
- H20 in connective tissue = <1%
- What is our ‘intake’ of water? how do we get water?
Dietary intake by thirst mechanism
- What is our ‘intake’ of sodium? how do we get sodium?
Western diet has 100-200 mmol/day so our diet
unless vegan or no salt added to food
- What is our output of water and sodium that is obligatory( just happens, we cant control it)?
Water loss through skin and lungs
Sodium loss through skin
- What is our output of water that is controlled?
- Renal Function
- Vasopressin/ADH
- Gut (Most water gets reabsorbed)
- What is the redistribution of sodium determined by?
Intravascular volume
- Which hormones are involved in sodium balance?
- 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.
- Which hormones are involved in water balance?
• ADH/vasopressin (synthesised in hypothalamus and stored in posterior pituitary) 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
- What does a presence of osmotically active substances in the blood result in?
water redistribution to maintain osmotic balance but cause changes in other measured solutes.
- What does excess solute cause?
oExcess solute (hyperosmolarity) cause cells to shrink due to dehydration
- What does excess water cause?
hypoosmolality (excess water) causes cells to swell causing oedema.
- Fill in the blank:
Water will move from areas of **to ******areas.
Water will move from areas of hyporosmolarity to hyperosmotic areas.
- What is the physiological response to water loss?
Water loss increases osmolarity which triggers vasopressin release, water redistribution and stimulation of the thirst response to restore osmolarity.
- How does the stimulation of vasopressin release result in the restoration of ECF osmolarity?
Renal water retention
less water loss in kidneys
- How does the redistribution of water from the ICF ,result is the restoration of ECF osmolarity?
It causes increased ECF water
- How does the stimulation of the hypothalamic thirst centre result in the restoration of ECF osmolarity?
We take in more water- increased water intake
- Approx. what % of Na is filtered by the glomeruli (obligatory reabsorption by renal perfusion)
95-98%
- Where is the most of Na reabsorbed in?
PCT
proximal convoluted tubule
- What does the DCT to?
Fine tuning using aldosterone
- What is aldosterone produced by
Angiotensin II
- The Juxtaglomerular apparatus (JGA) produces renin, what is the result of this?
oJGA produces renin (hypo-osmolarity) which coverts angiotensinogen to angiotensin I (this is converted into II by ACE from the lungs).
- What is the difference between hypo-osmolarity and hyperosmolarity?
Hypo-osmolarity = Sodium is LOWER than normal (keeps water in) Hyper-osmolarity= Sodium HIGHER than normal (draws water out)
- What is the name for the device that measures osmotic strength?
Osmometry
- The osmometry can use a concept of freezing point depression and be called a freezing point depression osmometer. How do these work?
okay so your freezing point is the temp is which a liquid solidifies
So this osmometer using colligative properties (which means properties because of how much solute is in the sample) to determine osmolarity
More solute = LOWER the freezing point
- How would you measure sodium?
you can measure :
DIRECTLY or INDIRECTLY
Indirect Ion selective electrodes (main lab analysers)
Direct Ion selective electrodes (Blood gas analyser)
29. An 80yr old women comes in a drowsy/confused state, no previous history, tongue markedly dry, febrile (38.5 0C), BP 100/60 and pulse rate 90b/m Her results are shown below: o Sodium 163 mmol/L (133-146) Potassium 3.9 mmol/L (3.5-5.3) Urea 15.8 mmol/L (2.5-7.8) Creatinine 140 µmol/L (60-110) eGFR 31 mL/min/1.73m (>90)
What can you diagnose her with?
Her creatinine level is too high and her eGFR is too low
Indicates water deficiency - dehydration
20. A 38 year old female, confused, known psychiatric history, can’t remember eating, drank lots of water. oResults: • Na 106mmol/L (high) • K 4.8 mmol/L • Urea 3.2 mmol/L • Creatinine 71 umol/L • Glucose 5.6 mmol/L • Serum Osmolality 245 mosm/Kg (low) • Urine Osmolality 227 mosm/Kg • Urine Na <20 mmol/L Whats you diagnoses
Sodium and serum osmolarity is LOW
indicates a lot of water so water excess
As patient has psychiatric history we call this psychogenic polydipsia, is a form of polydipsia characterised by excessive fluid intake in the absence of physiological stimuli to drink.
or caused by medication such as Prozac
- What is the difference between Euvolemic, hypovolemic or hypervolemic Hyponatremia
Hypovolemic hyponatremia: decrease in total body water with greater decrease in total body sodium.
Euvolemic hyponatremia: normal body sodium with increase in total body water.
Hypervolemic hyponatremia: increase in total body sodium with greater increase in total body water.
- What does osmolality mean? In a practical sense what is high osmolality and what is low?
“Osmolality” refers to the concentration of dissolved particles of chemicals and minerals – such as sodium and other electrolytes – in your serum. Higher osmolality means more particles in your serum. Lower osmolality means they’re more diluted.
- Does prozac increase or decrease Na?
decrease
- How would you assess a patient who has possible fluid/electrolyte disturbances?
oFluid chart (input and output measured hourly): usually not done very well.
oHistory: Fluid intake / output, Vomiting/diarrhoea, Past history, Medication (Prozac reduces Na).
oExamination - Assess volume status
•Lying and standing BP, Pulse, Oedema, Skin turgor/Tongue
•Jugular and Central Venous Pressures.
- If a patient has Hyponatraemia , what can rapid over correction lead to?
may lead to central pontine myelinolysis (myelin destruction).
- If a patient has Hypernatremia , what can over rapid correction result in?
cerebral oedema
- Its important to correct sodium at the same speed, what speed would this be?
- no more than 10mmol/L per 24 hours sodium change.
- Why is the urea/creatinine ratio useful?
Urea increase shows dehydration
- What does serum osmolality indicate?
Indicates if other osmotically active substances are present
- What does urinary sodium tell us?
<20 mmol/L = conservation and >20 mmol/L = loss
- What does urine/serum osmolality tell us?
> 1 = water conservation and < 1 = water loss.
- What is the serum osmolality calculation and when is it useful?
(only useful if you think something else is present)
•2 x Na + urea + glucose (+/- 10) 290 = (2 x 140 = 280) + 5 + 5
- What is meant by “overriding control is intravascular volume”?
salt + water in ‘wrong place’, intravascularly volume deplete, this activates renin-angiotensin-aldosterone (RAAS ) to promote Na +H20 retention.
- We can break down hyponatraemia into :
-Hypertonic
-Hypotonic
-Pseudo
What do all of these mean?
- Hypotonic is when there is low plasma osmolality- (too much water, not enough solutes).
- Hypertonic is when there is increased glucose (too concentrated) and so increased reabsorption of water
- Pseudo is when it seems sodium levels are low when in fact they are not, because of an increase in serum proteins and lipids , there is less water content (so seems less sodium) but actually sodium is the same!
- What does hypovolaemic hyponatraemia result in?
- Cirrhosis (liver does not function properly)
- Cardiac Failure
- Nephrotic Syndrome (kidneys usually + diuretic (pills that make you release more water) prescription
- What does Euvolemic hyponatremia mean?
SIADH (too much ADH released)
Hypothyroidism
Glucocorticoid deficiency (low cortisol)
- What is psychogenic beer potomania? What can it result in
excessive intake of alcohol, particularly beer, together with poor dietary solute
- what is meant by “Iatrogenic medication”, what can it cause?
sometimes adverse effects of a medical treatment are iatrogenic.
Can result in Euvolaemic hyponatraemia
- What can cause hypovolaemic hyponatraemia?
GI LOSS ( replacement with hypotonic fluid) through vomiting or diarrhoea
SKIN LOSS through burns and sweating
Lastly HAEMORRHAGE
- What can Hypovolaemic hyponatraemia result in?
- Addisions
- Diuretic Rx
- Salt losing nephritis
- Solute Diuresis
- Cerebral Salt wasting
- What is the reference range for sodium?
133- 145 mmol/L
- What is the low and high life threatening level for sodium?
<115
>160
- What is blood pressure/volume sensed by?
Baroreceptors
Renal perfusion pressure
- What is aldosterone produced by?what cause it cause?
oAldosterone is produced by the adrenal cortex- causes sodium reabsorption and the loss of H+/K+ at the DCT.
- Whats an inevitable by-product of ATP production
large amounts of protons and hydrogens
- Why is it important to maintain extracellular pH / {H+} ?
to maintain protein/enzyme function as it depends on balance between acid production and excretion
- Through what biological process is carbon dioxide produced/excreted?
Respiration
- Through which physiological compartment is H+ ions produced and excreted?
Renal
- Fill in the blanks
“H+ can be carbonic (carbohydrate burning) or non-carbonic (amino acid metabolism), most of it is removed by the* and the rest is closely regulated by the*.
Lungs
Kindney
- What two equations can you use to find pH using H+ conc?
pH = -log(10)[H+]
or
pH = log(10)1/[H+]
(10) is small right hand side
- On a pH/{H+} graph, what is the range for pH and {H+}?
pH ranges from 7.4-7.1 and [H+] ranges from 40-80 so when [H+] is doubled, the pH falls by 0.3.
- What is pH proportional to and inversely proportional to?
pH is proportional to HCO3- and inversely proportional to the partial pressure of CO2
- What is the henderson Hasselbalch equation?
pH =pKa + log 10 ( A- / H+)
- Using henderson Hasselbalch equation, what would it be for when
CO2 + H2 —> (K hydration) H2CO3 —-> (K dissociation) (H+) + HCO3
pH = pK + log10 [HCO3] / {pC02)
- How does the body respond to metabolic acidosis?
compensated for by the removal of CO2 (Kussmaul respiration: deep, laboured breathing) and the buffering action of HCO3- (increased consumption).
- How does the body compensate for respiratory acidosis?
increased renal H+ excretion and increased HCO3- regeneration.
- Explain the three steps of trying to return acid / base status to normal
?
- Buffering
- Compensation
- Treatment
- Explain the buffering step?
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
- Explain the step compensation?
Diametric opposite of original abnormality
Never overcompensates
Delayed and limited
- Explain the step Treatment
By reversal of precipitating situation
- Compare the speed of compensation for respiratory and metabolic disturbances?
Respiratory compensation for a primary metabolic disturbance can occur very rapidly.
• Kussmaul breathing (respiratory alkalosis) in response to DKA.
Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur.
• Limited because it requires enzyme induction (needs increased genetic transcription and translation etc).
• No compensation seen in acute respiratory acidosis such as asthma.
• Requires more chronic scenario to include compensation mechanism.
- What is the mechanism of renal bicarbonate regeneration?
o H2O and CO2 produce carbonic acid which dissociates into H+ and HCO3-.
o The HCO3- is reabsorbed in exchanged for Cl- ions. PCT reclaims bicarbonate and DCT regenerates bicarbonate.
o The H+ ions are excreted by an Na/H exchanger. When H+ is being excreted, K+ can’t be excreted simultaneously.
- How does an ABG work? What are some pitfalls? What are errors due to?
o Errors in blood gas analysis are dependent more on the clinician than on the analyser.
o All air has to be expelled and the sample mixed well - analyse ASAP
o Plastic syringes are OK at room temp for for 30mins, ensure there is no clot in the syringe tip.
o Ice is not required
- How do we interpret the results of an ABG?
o pO2 remember to check FiO2 (fraction of inspired oxygen – oxygen concentration inhaled).
o pH – is it normal or does it show an acidosis or alkalosis
o pCO2 – primary respiratory or compensatory response
o HCO3 – metabolic component
- What are some causes of respiratory acidosis (co2 retention)
Airway obstruction
•Bronchospasm (Acute), COPD (Chronic), Aspiration (breathing)/Strangulation (circulation cut off by constriction).
Respiratory centre depression
•Anaesthetics, Sedatives, Cerebral trauma, Tumours
Neuromuscular disease (respiratory muscle weakness- shallow breathing). •Guillain-Barre Syndrome, Motor Neurone Disease
Pulmonary disease
•Pulmonary fibrosis, Respiratory Distress Syndrome, Pneumonia (inflamed lungs filled with pus).
Extrapulmonary thoracic disease
•Flail chest (trauma breaks part of rib cage – rib detached from the rest of the chest wall).
76. What is the : compensation correction and features of RESPIRATORY ACIDOSIS?
oCompensation: Increased renal acid excretion (metabolic alkalosis, 36-72 hrs delay)
oCorrection: Requires return of normal gas exchange
Features
acute: low pH (Increase[H+]), increased pCO2, ->[HCO3-],– i.e. no compensation.
chronic: low pH (increased[H+]), increased pCO2, increased [HCO3-],– i.e. Compensation.
77. Case study: 21 yr old male with RTA flail chest: pO2 8.0 kPa Low pH 7.24 Acidotic pCO2 8.0 kPa High HCO3 25 Normal Diagnosis?
oUncompensated acute respiratory acidosis + impaired oxygenation.
oHCO3 is normal: uncompensated.
- What are the causes of respiratory alkalosis (low pCO2- C02 removal)
Hypoxia:
•High altitude, Severe anaemia, Pulmonary disease
Pulmonary disease:
•Pulmonary oedema, Pulmonary embolism
Mechanical overventilation.
Increased respiratory drive
•Respiratory stimulants e.g. salicylates
•Cerebral disturbance e.g. trauma, infection and tumours
•Hepatic failure or G-ve septicaemia
•Primary hyperventilation syndrome or Voluntary hyperventilation
- What is the :
-Compensation
-Correction
-Features
of RESPIRATORY ALKALOSIS?
oCompensation: Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)
o Correction: Of cause
Features
•acute: high pH, low [H+], normal [HCO3-], low pCO2 – no compensation
•chronic: high pH, low [H+], low [HCO3-], low pCO2
- Case study:
: Anxious student with tingling in fingers/toes who is giving a blood sample.
pO2 12.8 kPa Normal
pH 7.52 Alkalotic
pCO2 3.5 kPa Low (due to hyperventilation)
HCO3 23 Normal
Diagnosis?
o Uncompensated acute respiratory alkalosis.
- What are some causes of metabolic acidosis?
1.Increased acid addition:
o Increased H+ formation: Ketoacidosis, Lactic acidosis, Poisoning (methanol, ethanol, ethylene glycol, salicylate), Inherited organic acidosis.
o Acid ingestion: Acid poisoning or XS parenteral administration of amino acids e.g. arginine.
2.Reduced H+ excretion:
o Renal tubular acidosis or failure
o Carbonic dehydratase inhibitors
3.Loss of bicarbonates:
o Diarrhoea
o Pancreatic, intestinal or biliary fistulae/drainage
- What is the:
-Compensation
-Correction
-Features
of METABOLIC ACIDOSIS?
o Compensation: hyperventilation, hence low pCO2
o Correction of cause and increased renal acid excretion
o Features: low pH, high [H+], low [HCO3-], low pCO2
- Case study:
: 7 year old Type 1 diabetic who hasn’t taken insulin for 24 hours – build-up of acidic ketone bodies.
pO2 12 kPa Normal
pH 7.20 Acidotic
pCO2 5.0 kPa Normal
HCO3 15 Low
Diagnosis?
o Uncompensated acute metabolic acidosis.
- Metabolic Alkalosis causes?
o Increased addition of base: Inappropriate Rx of acidotic states and Chronic alkali ingestion
o Decreased elimination of base
o Increased loss of acid
1. GI loss:
• Gastric aspiration (technique for collecting gut contents) or Vomiting with pyloric stenosis (increased HCL loss).
2. Renal:
• Diuretic Rx (not K+ sparing)
• Potassium depletion
• Mineralocorticoid excess (stimulate ENaC and H+ ATPase) e.g. in Cushing’s or Conn’s.
• Drugs with mineralocorticoid activity – carbenoxolone
- What is the ;
-Compensation
-Correction
-Features
of metabolic alkalosis?
oCompensation: hypoventilation with CO2 retention (respiratory acidosis)
oCorrection: increased renal bicarbonate excretion and reduce renal proton loss.
oFeatures: high pH, low [H+], high [HCO3-], N/high pCO2.
- Case study:
56 year old female who has been vomiting for the last 48 hours.
pO2 13 kPa Normal
pH 7.48 Alkalotic
pCO2 5.8 kPa Normal
HCO3 33 High
o Uncompensated acute metabolic alkalosis.
- What are some clinical scenarios of Metabolic Alkalosis?
o Hypovolaemia from persistent vomiting: Loss of HCl, Loss of potassium, Loss of fluid
o Diuretics: Chronic K+ depletion
o Response to fluid loss is aldosterone activation:
• Reabsorb NaCl/H2O at distal convoluted tubule in kidney in exchange for K+ /H+
- Summarise the clinical scenarios of :
- Respiratory Acidosis
- Respiratory Alkalosis
- Metabolic Acidosis
- Metabolic Alkalosis
o Respiratory acidosis (CO2 retention): Compensation is metabolic alkalosis
o Respiratory alkalosis (increased CO2 loss): Compensation is metabolic acidosis
o Metabolic acidosis (Acid ingestion, Increases acid production, Reduced acid excretion):
• Compensation respiratory alkalosis
o Metabolic alkalosis: compensation is respiratory acidosis.
• very difficult primary disturbance to produce and maintain in proton producers! (Very specific factors required)
- Acidosis causes hyperkalaemia, how?
- Causes K+ movement to the plasma for exchange on H+ ions.
* Insulin corrects hyperkalaemia as it causes a reduction in serum K+ levels by causing influx into cells.
- Alkalosis causes hypokalaemia, how?
- Causes K+ movement out of the plasma into the tubules in exchange for H+.
- Catecholamines increase cellular uptake of K+ so reduces plasma concentration
- Case study:
76 year old male with a long history of prostatism and 24 hour anuria (failure of urine production).
o Results: • Na 137 mmol/L • K 6.7 mmol/L • HCO3 10 mmol/L • Urea 59 mmol/L • Creat 470 µmol/L • eGFR <5
o Hyperkalaemia (reduced loss as kidneys aren’t working) - AKI leading to failure of K excretion. o Redistribution across the cells (effect of acidosis).
92. Case Study: 23y female nurse, several A&E visits due to malaise, generalised muscle weakness etc. Results: • Na 137 mmol/L • K 2.6 mmol/L • HCO3 36 mmol/L • Urea 6.5 mmol/L • Creat 100 µmol/L
o Mild hypokalaemic alkalosis given oral potassium supplements.
o Renal potassium loss - Diuretic abuse.
- Hypokalaemia is either due to increased loss or decreased intake - give examples of how each would occur?
Increased Loss:
Gut (diarrhoea, laxatives)
Kidney (diuretics, magnesium deficiency, mineralocorticoid XS, renal tubular abnormalities)
Decreased Intake:
- Alcholol
- Anorexia
94.Hyperkalaemia is either due to increased intake or decreased loss - give examples of how each would occur?
Decreased loss:
- Reduced GFR
- Reduced tubular loss (potassium sparing diuretics anti-inflammatories, ACEIs, mineralocorticoid deficiency)
Increased Intake:
Usually parenteral
