The Renal & Urological System - Water, Electrolyte and Acid-base balance Flashcards
Function of RAAS
Rapid pressor response
CNS effects
Slow pressor reposne
Where are AngII receptors located
Vascular smooth muscle
Rapid pressor response - RAS
AngII activates receptors and contracts the pre capillary arterioles
Weak vasoconstrictor action in brain, lung and skeletal
Where is vasoconstriction maximum in rapid pressor response
Kidneys (efferent arteriole)
Lesser in splanchnic
CNS effects of RAS
Increase in central sympathetic outflow
Attenuation of baroreceptors mediated reduction in sympathetic discharge from brain
Slow pressor response of RAS
Produced by effect on kidneys
AngII reduces urinary excretion of Na+ and water and increases excretion of K+
Effect of AngII on adrenals
Stimulaltes synthesis and secretion of aldosterone
What does aldosterone act on
Collecting and distal tubule to cause retention of Na and excretion of K+ and H+
Source of aldosterone
Zona glomerulosa
What increases secretion of aldosterone
AngII
K+
ACTH
What acts as an aldosterone antagonist
Loss of Na and water
Hyperkalaemia
Risk of acidosis
Role of AngII
Vasoconstriction of vascular smooth muscle
Vasoconstriction of efferent arteriole
Stimulates thirst
Stimulates aldosterone and ADH release
Increase proximal Na+/H+ activity
How does constriction of mesangial cells affect GFT
Increases
Which drugs reduces renin secretion
Beta blockers
NSAIDs
Cicl;osporin
Tacrolimus
Aldosterone and cardiac remodelling
1’ aldosteronism stimulates increased ECM production by vascular smooth muscle and fibroblasts
Resulting in cardiac myocyte hypertrophy
Inhibitors of RAS
ACEi
ARBs
Na channel blockers
Impaired aldosterone metabolism
Aldosterone receptor blockers
Impaired release renin
What may cause impaired aldosterone metabolism
Adrenal disease
Heparin
Ketoconazole
Examples of Na channels blockers inhibiting RAS
Amiloride
Trimethoprim
Classification of hyponatreamia
Mild: SNa+ 130-135 mmol/L
Mod: 125-129
Severe <125
Clinical features of a/c hyponatraemia (48hrs)
Seizures
Coma
Resp distress
Severe cerebral oedema (if untreated)
MEDICAL EMERGENCY
Clinical features of c/c hyponatraemia (>48hrs)
Frequently mild or no sx
Headache, restlessness, muscle cramps
What can rapid correction of hyponatraemia lead to
Central pontine myelinolysis (osmotic demyelination syn)
At risk if Na is corrected faster than 12mmol/L/ day
Causes of hypovolaemia hyponatreamia - low urinary Na (<20)
Burns
Sweating
Diarrhoea
Vomiting
Fistuale
Causes of hypovolaemia hyponatreamia - high urinary Na
Diuretics - thiazides, loop diuretics
Addisons (mineralocorticoid deficency)
Causes of euvolaemic hyponatremia - low urinary Na
Severe polydipsia
Inappropriate fluid admin
Causes of euvolaemnic hyponatraemia - high urinary Na
SIADH
Hypothyroidism
Causes of hypervolaemic hyponatraemia
Nephrotic syn
Cirrhosis
Cardiac failure
Renal failure (high urinary Na)
Drugs commonly causing hyponatreamia
Thiazides
Amiloride
Carbamazepine
PPi
ACEi/ ARBs
Opiates
Causes of pseudo hyponatraemia
Hypertriglyceridaemia
Hyperproteinameia e.g MM
Cause of hypertonic hyponatreamia - increased serum osmolality
Hyperglycaemia
How can the causes of hypotonic hyponatreamia be divided
Assessing volume status
Hypervolaemic
Euvolameic
Hypovolameic
Initial ix for hyponatremaia
Measure serum Na
Measure serum osmolality
Perform fluid status assessment
Measure urinary Na
May measure TFTs and AM cortisol/ ACTH
Causes of SIADH
Malignancy - small cell lung, pancreas, GI, bladder
Chest disease - TB, pneumonia, lung abscesses
CNS - head injury, CVA
Drugs - carbamazepine, TCAs
Mx of hypovolaemic hyponatraemia
IV normal saline
Treat underlying cause
Mx of SIADH causing hyponatraemia
Fluid restriction
ADH receptor antagonists (deomeclocycline)
Oral sodium and furosemide
Mx of hypothyroidism causing hyponatraemia
Levothyroxine
Mx of hypervolaemia hyponatraemia
Fluid restriction
Salt restriction
Diuretics
Sx of central pontine myelinolysis
Occurs after 2/7
Dysarthria
Dysphagia
Paraparesis
Coma
‘Locked-in syn’
Hypernatraemia values
Serum conc >145mmol/L
What does hypernatraemia represent
Deficit of water relative to Na
What can cause hypernatraemia
Free water losses
Inadequate free water intake
Rarely, sodium overload
What is hypernatraemia almost always associated w/
Hyperosmolality
Risk factors for hypernatraemia
Inability to drink water - ventilated pts
Infancy and older age
Severe watery diarrhoea or vomiting
Renal concentrating defect
Diabetes insipidus
Large salt intake
Renal concentrating defects that may cause hypernatreamia
Osmotic diuresis
Renal failure
Obstructive uropathy
What do sx of hypernatraemia depend on
Underlying cause and whether a/c or c/c
Sx of hypernatraemia
Neuro disturbances - lethargy, weakness, irritability, seizure
Impaired thirst
May see signs of hypovolaemia
Signs of hypovolaemia
Orthostatic hypotension
Decreased JVP
Tachycardia
Dry mucous membrane
Tx of hypernatraemia
Review med and closely ,monitor fluid chart
Oral or IV fluids
Can be given desmopressin of central diabetes insipidus
Can give thiazide diuretics if nephrogenic diabetes insipidus
5 R’s of IV fluid therapy
Resus
Routine maintenance
Replacement
Redistribution
Reassessment
What are resus fluids aimed at
Rapid restoration of perfusion and expansion of circulating volume
Preferred ways of meeting routine daily fluid and electrolyte requirements
Eating and drinking sufficiently is 1st and TPN is 5th
How long is short term cover required for routine fluid maintenance
Less than 3/7
Examples of continuing losses after any initial resus
High-output stomas
Post-AKI polyuria
Losses through vomiting
Surgical drains
What does redistribution incl in IV fluid resus
Redistributing fluid into large-volume ascites
Pleural effusion
Trapped in non-motile gute w/ SBO or ileus
Leaking into interstitial in sepsis
Most important R in IV fluid resus
Reassessment - adjusting composition and preventing complications from fluid therapy
When might a pt need immediate fluid resus
Hypovolaemic shock
What is shock
Inadequate perfusion to tissues
Clinical signs of shock
Low SBP (<100mmHg)
Tachycardia
Tachypnoea
Delayed CRT
Cool peripheries
High or deteriorating EWS
Response to PLR
Confusion/ decreased LOC
PLR
Pssive leg raise
Bolus doses and admin
500ml over 15mins - short, fat tube in larger peripheral veins
If venous access is difficult, consider interosseous access
What is the max vol of bolus that can eb given
2000ml
>2000ml requires ICU
What can excessive NaCl in fluid therapy cause
Hyperchloraemic metabolic acidosis but since no K, risk of hyperkalemia (AKI, rhabdo)
Can you resuscitate a pt w/ hyperkalemic solution
No
What is the routine maintenance of electrolyte daily
Na/K/ cl intake should be equal
Water ~25-30ml/kg/ day
When can human albumin solution be used in fluid resus
In pts w/ severe sepsis
Used for large-volume paracentesis and hepato-renal syn
Potassium rich foods
Tomato
Banana
Baked potato
Orange
Where is the majority of total body K stored
Mainly intracellular - 95%
In muscle, liver and interstitial fluid
What causes movement of K from ICF to ECF
Acidosis
Hyperosmolality
beta-adrenergic antagonists
Cell damage
What causes movement of K from ECF to ICF
Alkolosis
Insulin
Aldosterone
beta-adrenergic agonists
How does K enter body
Oral intake causes K in ECF to increase
Loses K through urine and stool
What may increase free serum K
Hyperglycaemia
Exercise
Where is the majority of K absorbed
PCT
What increases the secretion of K+
Aldosterone
Increased delivery of Na and water
High K
Who is most likely to get hypokalaemia
Elderly and pts w/ reduced oral intake
Hypokalaemia definition
Serum K conc <3.5mmol/L
Clinical features of hypokalaemia - neuromuscular
Weakness
Constipation
Confusion
Clinical features of hypokalaemia - cardiac
Arrhythmias, ECG changes, dig toxicity
HTN
Why does hypokalaemia cause HTN
Increased vascular reactivity and Na retention
Clinical features of hypokalaemia - renal
Polydispia/ polyuria
Metabolic alkalosis
Tubulointersitial fibrosis/ cystic changes
Why does hypokalaemia cause polydipsia
Impaired renal concentrating ability
What does hypokalaemia cause metabolic alkalosis
Increased acid excretion
ECG changes in hypokalaemia
ST-segment depression
Flattened T-wave
U wave
Aetiology of hypokalaemia
Pseudohypokalaemia
Decreased K intake/ reduced absorption
Increased entry into cells (usually caused by drugs)
Increased GI losses (D + V)
Increased urinary losses
Cause of pseudo hypokalaemia
Blood sample w. large no. abnormal white cells (e.g. AML) - take up intracellular K —> reduced conc
Why does alkalosis cause hypokalaemia
Metabolic or resp
H+ moves out of cell to reduce pH and K+ is moved in
Upper vs lower GI losses causing hypokalaemia
Upper causes metabolic alkalosis and volume depletion due to loss of HCl –> 2’ hyperaldosteronism - renal K wasting
Lower causes metabolic acidosis due to loss of bicarb
How do beta2-agonist cause increased K entry into cells
Stimulates Na-K ATPase, NaClK cotransporter
Increased urinary losses causing hypokalaemia
Increased mineralocorticoid activity - hyperaldosteronim
Diuretics
Renal tubular acidosis
Barrier and Gittelman’s syn
1’ vs 2’ hyperaldosteronismm
1’ - adrenal adenoma, hyperplasia or carcinoma
2’ - heart failure, nephrotic syn
Why do diuretics cause hypokalaemia
Volume depletion activates hyperaldosteronism, increased distal delivery of Na and water
Renal causes of hypokalaemia
Urine K+ > 20
Diuretics
Hypomagnesia
Endocrine - hyperaldosteronism, Cushing’s
Renal tubular acidosis (type 1 or 2)
Batter’s and Gitelman’s syn
Extra renal causes of hypokalaemia
Inadequate oral intake
Gut losses
Redistribution into cells (e.g. beta-agonist, insulin, theophylline, alkalosis)
Assessment of hypokalaemia
ECG
Bloods - U&E’s, chloride, bicarb, glucose
Urinary potassium and chloride
Mx of mild to moderate hypokalaemia (3.0 - 3.5)
Oral slow release KCl
Treat causes e.g aldosterone antagonists for hyperaldosteronism
Check K regularly
Mx of severe hypokalaemia (<2.5)
Continuous cardiac monitoring
Check and correct Mg
IV infusion of 1L 0.9% saline w/ 40mmol KCl - 10mmol/hr via peripheral line
Treat causes
Causes of hypokalaemia w/ HTN
Cushings
Conn’s synd (1’ hyperalodsteronism)
Liddle’s syn
Causes of hypokalaemia w/ alkalosis
Vomiting
Thiazides
Cushing’s
Conn’s
Causes of hypokalaemia w/ acidosis
Diarrhoea
Renal tubular acidosis
Acetazolamide
Partially treated DKA
What is hyperkalaemia defined as
K > 5.5
Clinical features of hyperkalaemia
Non-spp
Arrhythmias
N & V
Muscle weakness
SOB
ECG changes in hyperkalaemia
Tall tented T waves
Widened QRS
Small/ flattened P waves
Causes of pseudohyperkalaemia
Thrombosis (K leaks out of platelets during clotting)
Severe leucocytosis (CLL)
Haemolysis (tourniquet use, fist clenching)
How can we divide causes of hyperkalameia
Impaired excretion - AKI/ CKD, drugs, RTA type 4, Addisons
Increased release from cells - Insulin deficiency, rhabdo, tumour lysis, BB
Common causes of hyperkalaemia
3 A’s RMD
AKI
Acidosis (metabolic)
Addisons
Rhabdo
Massive blood transfusion
Drugs
Drug that may induce hyperkalemia
K-sparing diuretics e.g. amiloride
ACEi
ARBs
Spiro
Ciclosporin
Heparin
Treating hyperkalaemia w/ ECG changes
IV calcium gluconate (10% over 10mins) - stabilse cardiac membrane
Insulin/ dextrose infusion - shifts from ECF to ICF
Nebulised salbutamol - shifter
Classification of hyperkalemia
Mild: 5.5. - 5.9
Mod: 6.0 - 6.4
Sev: >6.5
When can sodium bicarb be given for hyperkalaemia
Controversial
High K w/ metabolic acidosis (HC03 <16) and volume depletion
Removing K from body in hyperkalaemia
Diuretics - urinary K wasting
Dialysis - if refractory
Calcium resins - gut wasting
Hormones affects Ca homeostasis
PTH
Vit D (calcitriol)
Organs involved in Ca homeostasis
Intestines
Bone
Kidney
What happens to PTH when Ca is low
Increased
Bone release Ca2+ and PO4-
Kidney increase PO4- production, Ca reabsorption, increased calcitriol formation (increased intestinal absorption)
Foramtion of active vit D
UVB –> vit D3
25-hydroxylase in liver —-> 25 OHD (circulating form)
1alpha-hydroxylase in kidney –> 1, 25 (OH)2D (active hormonal form)
Defence against hyperCa
Increased plasma Ca
Decreased PTH and increased calcitonin
Increased renal Ca excretion
Decreased conversion from 25 OHD to calcitriol
Decreased intestinal absorption
Calcitonin vs calcitriol
Calcitriol is active form of vit D
Calcitonin is a hormone released from thyroid when Ca is low - inhibits osteoclasts (bone resorption)
Sources of vit D
Sunlight
Fish
Cheese
Milk
Fortified cereal
What form can vit D be stored in
24,25 D
What is the metabolically active form of Ca
Ionised
Causes of hyperCa w/ increased PTH
Hyperparathyroidism (1’. 3’)
Familial hypocalciuric hyperCa - do 24-hr urinary Ca
Malignancy (MM, PTHrP from solid tumours, bone mets)
Excess Vit A
Thyrotoxicosis
Causes of hyperCa due to increased Ca absorption
Milk-Alkali syn
Excess vit D
Increased intake
Non-spp causes of increased Ca
Lithium - increases pTH
Thiazide diuretics - reduce urinary Ca excretion
Rhabdo - Ca released from muscle
Ix for hyperCa
ECG
LFTs
U&Es
PTH
Boine profile
