5.1 Fluids Flashcards
Osteoclasts are
Cells which promote bone resorption.
They are stimulated indirectly by PTH
Acidosis
affect on
K
Cl
Periperhal tone
?tetany
- why
An acidosis is associated with potassium retention and rise in chloride with maintanence of the anion gap.
Peripheral vasodilatation occurs in an effort to improve oxygen delivery to metabolising tissues.
In an effort to correct the acidosis, respiratory compensation occurs with an increased minute volume which consequently reduces arterial PCO2.
An alkalosis is associated with tetany due to a reduction in the ionised calcium concentration.
Where does 25 hydroxylation occur
where does 1 hydroxylation occur
What are the stimulation of 1 alpha hydroxy
What does 1 25 oh 2 vit d promote
what type of messneger is it
also known as
What happens in RF
25 hydroxylation occurs in the liver (not kidney).
1 hydroxylation is in the kidney.
Hypophosphataemia and hypocalcaemia are the main stimulants of 1 alpha hydroxylation.
1,25(OH)2 vitamin D promotes phosphate and calcium absorption from the gut, it is a steroid hormone and is an agonist for the calcitriol or vitamin D receptor (VDR) and also known as NR1I1 (nuclear receptor subfamily 1, group I, member 1), is a member of the nuclear receptor family of transcription factors.
It is decreased in chronic renal failure (not increased).
ECG changes - hypomag
simiar to what
chronic hypomag - what happens to pth
what can cause it
The ECG changes of hypomagnesaemia are almost the same as those of hypokalaemia:
Flattening of T waves ST segment depression Prominent U waves Prolonged PR interval, and Prolonged QT interval
There is a risk of atrial and ventricular ectopics and ventricular arrhythmias. There is an increased risk of digoxin toxicity.
In chronic hypomagnesaemia, there is impaired synthesis and release of parathyroid hormone (PTH), and target organ response to PTH is impaired. This produces secondary hypocalcaemia.
Hypomagnesaemia may result (like hypokalaemia) from the use of potassium ‘wasting’ diuretics (loop diuretics and thiazides, for example, furosemide).
Lactic acidosis -
Type A occurs with what:
examples
Type B
Lactic acidosis is a metabolic acidosis with a raised plasma lactate above 5 - 7 mmol/l, and may be either type A or type B.
Type A occurs in association with overt tissue hypoxia such as
Severe anaemia Shock Haemorrhage Hypotension Infections Cardiac/hepatic/renal failure.
Type B occurs in those without apparent initial hypoxia and may be drug induced, for example,
Biguanide therapy
Ethanol/methanol
Salycilates
Total parenteral nutrition.
Type I glycogenosis (von Gierke’s disease)
Metformin rather than chlorpropamide is associated with lactic acidosis.
The following are found in higher concentrations intracellularly than extracellularly:
Potassium Magnesium ATP Adenosine diphosphate (ADP) AMP, and Phosphate. Sodium is a primarily extracellular ion.
What is higher - standard base excess or actual base excess
Standard base excess (of ECF) is always higher than actual base excess (intravascular compartment).
because of less buffering capacity of haemoglobin. It gives a better reflection of the BE in the extracellular space rather than in the intravascular compartment only.
Prolonged vomiting leads to loss of -
what biochem might expect
Prolonged vomiting leads to loss of hydrochloric acid (HCl). As a result, one might expect the following, of varying degrees of severity:
Hypokalaemia
Hypochloraemia
Metabolic alkalosis, and
Increased bicarbonate to compensate for loss of chloride.
Buffers -
what contributes most
What else contributes
The bicarbonate ion (HCO3-) contributes most to the buffering capacity of whole blood.
Bicarbonate within the red blood cell contributes approximately 18% of total buffering capacity and that dissolved in plasma contributes 35% (total 53%).
When a strong acid is added to the bicarbonate buffer, the hydrogen ions released from the acid combine with the HCO3- to form carbonic acid (H2CO3). This then dissociates to H2O and CO2 under the influence of the enzyme carbonic anhydrase.
What is total body water of man
woman
divided how
ECF divided into what
A 70 kg man has total body water content of (70 × 0.6) = 42 litres. The calculation for a woman is (70 × 0.55) = 38.5 litres.
Est w/ tritium 3H
For a man this is subdivided into:
Extracellular fluid (ECF) = 14 litres (1/3)
Thio / Inulin used
cross capil but not cell membranes
Intracellular fluid (ICF) = 28 litres (2/3). cant be measured - derived
The ECF volume is subdivided into:
Interstitial fluid = 10.5 litres (70%) -calc subtract plasma vol from ECF Plasma = 3 litres (~25) Transcellular fluid (CSF/synovial fluid) = 0.5 litres. (5%) Fluid compartments directly measured:
TBW can be measure how
Plasma measured how
Erythrocyte measure how
what are measured indirectly
Total body water can be measured using heavy water (deuterium), which is freely distributed.
Plasma volume can be measured by labelling albumin with a radioactive isotope or using a dye called Evans blue. They remain in the plasma and do not diffuse into erythrocytes.
Total erythrocyte volume can be measured using radiolabelled (Cr-51) red blood cells.
ECF volume can be measured using inulin as the tracer as it is freely distributed to the interstitial and plasma volumes.
Fluid compartments indirectly measured:
Total blood volume can be calculated with knowledge of the haematocrit and the total circulating red cell volume.
Intracellular fluid volume can be calculated by subtracting ECF volume from measured TBW.
How much sodium excreted / day
mmol /kg
in ARF how what is urinary Na conc
Intrisnic
osmolality / osmolarity is what
Normal Ur:Pl osmolality ration
The normal amount of sodium excreted in the urine is 1-2 mmol/kg per day.
In acute renal failure due to a prerenal cause the kidney is still able to conserve sodium, consequently the urinary sodium concentration is <10 mmol/l.
In acute renal failure due to intrinsic renal disease the urinary sodium concentrations are >20 mmol/l.
Osmolality is expressed as milliosmoles per kilogram of solvent and
osmolarity is expressed as milliosmoles per litre of solution.
The normal urine:plasma osmolality ratio is >2:1;
in intrinsic renal failure it is <1:1;
and in prerenal causes it is >1:1.6.
Where is most of the water reabsorbed in kidney
what drives this
Loop of henle
collecting ducts
Perecentage of water reabsoprtion
Most of the water of the glomerular filtrate is reabsorbed by the proximal convoluted tubule (65-70%) and is termed “obligatory” absorption.
Sodium is the main osmotic driving force for the reabsorption of water and other solutes as it enters the tubular cell via the apical membrane and subsequently actively transported out across the basolateral membrane. The filtrate remains isosmotic.
Loop of Henle:
Descending limb is freely permeable to water. The countercurrent exchange and multiplier arrangements of the vasa recta and the loop of Henle produce a hyperosmolar filtrate as water passively moves into the interstitium in the inner medullar. 20-25% of water is reabsorbed.
Thick ascending limb impermeable to water (Na-K-2Cl co-transporter).
In the distal convoluted tubule 5-10% of the filtrate is further reabsorbed passively down a concentration gradient driven by a Na+/K+ ATPase pump.
In the collecting ducts under the influence of antidiuretic hormone (ADH) a further 1-3% of water can be reabsorbed
SIADH
a/w
Syndrome inappropriate antidiuretic hormone (SIADH) is associated with:
Pneumonia Bronchial small cell carcinoma Pulmonary tuberculosis Subarachnoid haemorrhage Head injuries Meningitis, etc. Patients are hyponatraemic with an elevated urine osmolality, a urine sodium above 20 mmol/l, and a low plasma osmolality.
Transient SIADH commonly occurs post-operatively.
ADH stored where
Factors stimulating secrtion
Agonist for what subtypes
Antidiuretic hormone or vasopressin is stored in the posterior pituitary. It is a nonapeptide (a nine amino acid protein chain).
Principle factors stimulating secretion include:
Osmotic factors: Osmoreceptors in the paraventricular nuclei and supraoptic nuclei of the hypothalamus respond to increases in plasma osmolarity
Hypovolaemia: Low pressure receptors in the atria and to a lesser extent the baroreceptors in the carotid sinus and aortic arch stimulate ADH
Other factors influencing secretion include: Stress, exercise, atrial natriuretic peptide (inhibition) and drugs (opioids and nicotine).
ADH is an agonist for two receptor subtypes:
V1: Mediates a powerful vasoconstrictor effect
V2: Mediates an increase in water permeability of the apical membrane of the cells of the distal tubule and collecting ducts in the cortex and medullar. A rise in cyclic-AMP following a sequence of events on the cell membrane of metabotropic receptors. This in turn triggers the opening of aquaporin-2 channels thus allowing water reabsorption.
ADH does not directly affect the glomerular filtration rate (GFR). It will eventually return the GFR back to normal in a hypovolaemic patient.
acts camp
