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51 Cards in this Set

  • Front
  • Back

Body fluid and electrolyte imbalances are relatively uncommon in hospital practice.

relatively common

LT 1

Electrolyte and fluid imbalances usually present as chronic problems to the GP.

They usually present as ACUTE emergencies

LT 1
What % of the body weight is water (usually)?

What are its divisions?

40L in a 70Kg person

Intracellular - 25L - 30-40%
Extracellular - 15L - 20-30% (plasma - 3L and interstitial 12L )

LT 1
What is the normal volume of blood in a person?

(3L- plasma)

LT 1
Where is K+ and Na+ usually located?
K+ - intracelular

Na+, Cl- - Extracellular

Maintained byt the K/Na ATPase

LT 1
How/where is water lost from the body?
Obligatory Losses
Lungs, Skin, Stool

Kidney - only output that can be varied to achieve a balance between input and output - must also excrete waste

LT 1
What pathophysiological process leads to oedema?
1) Fluid retention from Kidney failure

2) reduced oncotic pressure of the plasma (hypoalbuminaemia - liver failure or protein loss in kidneys) or increased hydrostatic pressure (Heart failure, hepatic cirrhosis - ascites)

LT 1
What kind of Metabolic/electrolyte changes occur when drinking Sea Water?
Hypernatraemic overhydration

Gain of excess salt in excess water

LT 1
What are the clinical divisions of Hypovolaemia "dehydration" ?
4%, 7%, 10% loss of body weight

Mild moderate, severe dehydration

** at 10% fluid loss -- the reduction of water leads to a state in which life-threatening irreversible shock is the rule rather than exception.

LT 1
How do you clinically assess level of fluid loss?
Blood pressure - including postural drop
urine flow rate
accurate measurement of body weight
assessment of the peripheral circulatory state
state of tissue and mucosal hydration

LT 1
What is the main mechanism the kidney employs to control body fluids and electrolytes?
Sodium regulation + Regulation of Water reabsorption

Excess fluid - increased filtration or reduced reabsorption of sodium

Where is the tubular system is sodium reabsorbed?

What hormones regulate this?
The entire nephron

PRIMARILY - PROXIMAL TUBULE (60-65%) -- Na-H Countertransporter (AT-2)

Loop of henle - 25-30%

* Aldosterone - acts distally - enduces ENaC + Na/K-ATPase (enhancing K + acid excretion)
** - ANP (atrial naturetic peptide) - acts to inhibit sodium reabsorption in the terminal nephron - medullary collecting duct.

Where in the kidneys does Angiotension II act ?
Proximal tubule

Na-H countertransporter

Where does Aldosterone act ?

enduces ENaC and Na/K ATPase expression

Where in the kidneys is water reabsorbed?
Proximal tubule - along with sodium

but water ALONE is also reabsorbed in the descending limb of he loop of Henle

Also in the collecting tubule

What hormones effect water reabsoption?
ADH - acts in the collecting tubule to increase water permeability (water reabsorbed) by inserting aquaporins into the cell membrane, it also inserts urea transport proteins - increasing permeability to urea)

What is the amount of insensible water losses throughout the day?
skin, lungs, stool - 0.5L

+ kidneys + Sweating

Fluid losses may be visible or hidden. Give examples of these.
GIT (mouth, fistulae, stomata, anus), kidneys, skin (burns, sweating), blood stream

HIDDEN - Hard to quantitate
sequestered fluids around inflammation (pancreatitis) or tramua (rhabdomyolysis), so called third spacing, and into serosal cavities (pleural, peritoneal) or interstitial tissues (oedema)

Clinical Replacement of fluids depends on the type of fluids lost - hypo, iso, hypertonic.

Describe the composition of Sweat + Gastric Juices with regard tot he above terms.
Sweat - HYPOtonic

Gastric Juice - HYPO or ISOtonic
Depends on parietal (Acid, hypotonic) or non-parietal (plasma like) secretions.

Also Vomit - is HYPOKALAEMIC - but the associated hypokalaemia that occurs is due to kaliuresis (renal K+ loss accompanying HCO3-)

Pancreatic, bilary, intestinal - ISOTONIC, alkaline

*** Metabolic disturbances accompanying GIT fluid losses -- ALKALOSIS for lesions above the pylorus, ACIDOSIS for lesions below the pylorus --> but these may be corrected for by the kidneys if functioning and imbalance is not extreme

What are the physiological Responses to fluid and electrolyte loss?
Kidney - retains water and Na

HEART - cardiac inotropism and chronotropism (Force and rate), selective vasocontriction (non-vital organs - skin, GIT), Selective vasodilation (brain, heart)

** assessment of these things - indicated the severity and composition of fluid losses
Clinical Signs of Extracellular Volume Loss?
reduced skin turgor
Dry mucous membrances
Depressed JVP
Postural hypotension

Measurement of composition and volume of fluids lost, osmolality, electrolytes (plasma, urine)

These Guide severity and type of fluid replacement needed

What Type of Fluids are used as fluid replacement?

Colloids - macromolecular solute confined to the intravascular compartment

Crystalloids (electrolytes which will initially be distributed in the ECS)

Dextrose based solutions (water without electrolytes)

Crystalloids may be altered in osmolality by altering glucose, dextrose, saline levels
Which electrolytes are the most important to replace?
Na + K

also - Ca, Mg, phosphate --

** parenteral nutrition may contain dextrose, AA, fats and trace elements
what is important to consider when giving fluid replacement?
rate and severity of fluid loss

vital organ function
cardiac status
What can be the consequences of to rapid / excessive fluid replacement?
cardiac decompensation in Pt with congestive heart failure, electrophysiological effects of potassium replacement (arrhythmias), osmotic cell shrinkage with hypertonic saline (brain function)
What are the 2 processes of the kidneys?
Glomerular filtration
Tubular transport (mainly Na and water reabsorption)

What is Glomerular Filtration?
Production of a plasma ultra filtrate (free of protein and large molecules)

Driven largely by hydrostatic pressure

How is Glomerular filtration regulated?
Constriction (NA - SNS) and relaxation (PGE2) of afferent arterioles to the glomerular apparatus

Efferent constrictors (AT-II - released locally) action maintain or increase the single nephron filtration rate

TUBULOGLOMERULAR FEEBACK - local feeback mechanism which relates the filtration rate of an individual nephron to the adequacy of sodium reabsorption (in tubules)

* AUTOREGULATION - GFR is stabilised over the entire kidney despite a wide range in mean arterial pressure MAP (100ml/min/1.73 sq m)

What percentage of glomerular filtrate is excreted as urine?

99% is reabsorbed - because GF is around 150L/24hr

What is the main mechanism of of fluid reabsorption from the tubules in the kidneys?
Na is actively reabsorbed and due to the osmosis of water, water is passively reabsorbed with the Na - PROXIMAL TUBULE (65% of Na reabsorption)

Further reabsorption occurs further along the tubules - although not as closely linked

What is absorbed in the proximal tubule?

How are wastes excreted in the urine?
Either filtered at the glomerulus and NOT reabsorbed (Creatinine)


They are actively secreted into the tubular lumen (organic acids + bases, hydrogen ions)

What are the cardiac/ECG consequences of hypokalaemia?
(following cardiac insult - MI or cardiac surgery)

Increased risk of arrhythmia with more severe hypokalaemia, aswell as potentiating the arrhythmia risk associated with DIGITALIS and THIAZIDE diuretics

ECG Changes
T wave flattening, Depression of ST segment, appearance of U waves

LT 5
Does increased extracellular K cause hyper or de-polarisation of cells?

due to the [K=] effecting the Nerst potential

Hypokalaemia = hyperpolarisation

LT 5
How does Hyperkalaemia result in arrhythmias?
hyperkalaemia = depolarisation of cells

This prevents the sinoatrial node firing because it depends on Na current for signal generation --> BUT with depolarisation caused by hyperkalaemia - the cell is stuck in a depolarised state - never repolarising and losing the Na current which generated the AP for contraction.

>8mM plasma [K+] = asystole = death

LT 5
How does hypokalaemia lead to arrhythmias?
Not entirely understood - hyperpolarisation

Duration of the AP is prolonged/ventricular repolarisation is delayed (due to low [K+]) which renders the heart liable to re-entrant arrhythmias:
1) ventricular tachycardia
2) ventricular fibrillation

* same mechanism as with genetic "Long QT Syndrome" - which various channels are mutated (K, NA, Ca)

LT 5
Which causes Arrhythmias:

Hypokalaemia or hyperkalaemia?

hyperkalaemia - heart block, bradycardia, ventricular fibrillation, asystole - SA cannot initiate AP due to high [k] - partial depolarization which causes the opened Na channels to become refractory and hence - it is harder to depolarize the cell (depolarisation)

Hypokalaemia - Ventricular tachycardia + Ventricular fibrilliation
hyperpolarisation - inhibitory in most cells (neurons)
Low K makes the heart hyper excitable. Due to the lower membrane potentials allowing faster recovery of Na channel inactivation (arrhythmias) - also delayed ventricular repolarisation may promote reentrant arrythmias

LT 5
What are the neuromuscular complications associated with hypokalaemia?
GI - reduced motility --> S&S range from constipation to ileus

3.0-3.5mmol/L [K+] - asymptomatic, Malaise, weakness, leg cramps, myalia

<2.5mmol/L - rhabdomyolysis, paralysis

Muscle - is susceptible to damage due to reduced blood flow and reduced intracellular K+ reduces intracellular glycogen synthesis --> thus low energy stores

LT 5
What are the Renal consequences of hypokalaemia?
Does not usually cause symptoms but does:

1) renal vaso constriction
2) reduced renall blood flow
3) reduced GFR
4) increased ammonia production - may in part account for the metabolic alkalosis observed in severe hypokalaemia

If symptoms are present - they are likely to be polyuria and secondary polydipsia due to a defect in concentrating ability.

*** may lead to interstitial nephritis

LT 5
What are the endocrine effects of hypokalaemia?
Glucose intolerance - reverses with correction of K imbalance

Decreases plasma Aldosterone - independent of volume status

LT 5
What is the main distinction between potassium sparing or losing diuretics?
Where they act in the tubule system.

K sparing diuretics act later in the system (late-distal)

K lossing diuretics - act earlier in the nephron (EDT - thiazides; loop of henle - frusemide)

This is due to the fact that delivery of NA to the distal parts of the nephron is one factor which ENHANCES K secretion --> therefore Diuretics which act before will have more Na reaching the distal parts and MORE K secretion, where as diuretics acting later will have relatively less Na and therefore less secretion of K+

Is frusemide a low or high potency diuretic?

Thiazides are low potency

What are some the adverse effects of Potassium losing diuretics?
Excessive Fluid loss (hypovolaemia) - hypotension, dizziness, collapse

Hyponatraemia - weakness, muscle cramps, confusion, drowsiness, seizures (esp Thiazides)

Hypokalaemia - weakness, muscle cramps, cardiac arrhythmias, polyuria (esp. in Pt with congestive heart failure)

Alkalosis - commonly associated with hypokalaemia

More common with THIAZIDES (than Loop):
Hypercalcaemia - reduce calcium excretion
Hyperuricaemia - may lead to gout
Hyperglycaemia - may unmask previously unDx diabetes, or worsen control in diabetic Pts
Hyperlipidaemia - dose-dependent increase in cholesterol and TAGs

Loop --> in very high dose or IV --> Deafness

Eg - Frusemide (loop), Thiazides (Early distal tubule)

Note: mixed drugs have a combination of electrolyte imbalances

What are some SE of Potassium sparing diuretics?
hyperkalaemia (leading to cardiac arrhythmias + muscle weakness)

- care must be taken with using these drugs in renal failure and with ACEI (which may also elevate potassium)

Eg. - spironolactone, amiloride

Spironolactone -- may cause gynocomastia, GI upset, impotence

What are some example of Diuretic Misuse and Abuse?
Diuretic prescription for ankle swelling associated with cyclical menstration or from standing all day --> may lead to dependence on drugs (because without them the swelling is worse)

Weight loss (dependence + long term use)

Athletes - dilute illicit drugs

** Clinical Presentation - Hypokalaemia, hyponatraemia + metabolic alkalosis -- take history of Diuretic use, if suspected but not Hx - do urine screen

What is the normal plasma sodium range?

What are the main clinical feature associated with hyponatraemia?

Hyponatraemia may occur in low or high ECF states - how can you distinguish them?
High ECF State
Raised JVP, Peripheral and sacral oedema

Hypotension, postural hypotension, tachycardia

** clinically an understanding of this - indicated the appropriateness of ADH secretion (Low ECF, shock, pain, nausea = ADH secretion is normal; high ECF = ADH secretion is abnormal - SIADH)

What may cause ADH release?
1) Real or apparent fall in "effective" circulating blood volume

2) shock, pain, nausea

3) inappropriately - SIADH

Pathophysiologically Hyponatraemia can be of 4 types. What are these?
SURIOUS (false reading of low levels, hyperlipaemia, hyperproteinaemia, hyperglycamia, mannitol)

DILUTIONAL - congestive heart failure, cirrhosis, nephrotic syndrome, water overload, SIADH
DEPLETIONAL - adrenocortical failure, vomitting, diarrhoea, nasogastric or GIT fistula loss, diuretic abuse

** therapy should target the specific cause

What cancer is associated with SIADH>
small cell carcinoma of the lung