Long Term Control of BP, Oedema and Dehydration Flashcards
1
Q
Why must ECF volume and osmolality be maintained?
A
Volume:
- to maintain BP
- important for tissue perfusion and function
- maintained by adjusting total body content of NaCl
Osmolality:
- to maintain cell volume
- important for cell function
- maintained by adjusting total body H20 content
2
Q
Describe how the ECF volume is controlled
A
- changes in ECV is sensed by carotid sinus, aortic arch, renal afferent arteriole, or atria
- activates hormonal transducers (RAAS, SNS, ANP, AVP (arginine vasopressin))
- short term: exerts effects in the heart and blood vessels to adjust BP
- long term: exert effects on the kidney causing Na+ excretion
3
Q
Describe how ECF osmolality is controlled
A
- changes in plasma osmolality sensed by hypothalamic osmoreceptors
- activates hormonal transducers (AVP and thirst)
- exerts effects on the kidney to cause renal H20 excretion
- exerts effects on brain to cause drinking behaviour resulting in H20 intake
4
Q
What level is extrarenal Na+ output?
A
- usually negligible
- unless large fluid loss such as:
- GI tract (vomiting and dairrhoea)
- skin (excessive sweating, burns)
- causes kidneys to respond by reducing Na+ excretion
5
Q
What is effective circulating volume?
A
- functional blood volume
- reflects extent of tissue perfusion in specific regions
- changes in ECV paralelel to changes in total ECF volume
6
Q
In what circumstances will changes in ECF not be parallel to ECF volume?
A
- in disease states
- congestive heart failure, nephrotic syndrome, liver cirrhosis
- total ECF grossly expanded (oedema/ascites)
- but ECV is low so increasing Na+ retention
- can exacerbate systemic congestion as there is a mismatch in Na+ intake and excretion
7
Q
Describe volume expansion
A
- when Na+ persists in face of impaired Na+ excretion
- body retains isosmotic fluid
- expansion of plasma fluid volume and interstitial fluid compartment
- in severe cases, interstitial volume increase so severe that subepidermal tissues swell (causes pitting oedema)
8
Q
Describe volume contraction
A
- excessive loss of Na+ into urine
- dramatic shrinkage of ECF volume
9
Q
What states cause a shrinkage of ECF volume?
A
- hypovolaemic shock
- prolonged use ot diuretics
- osmotic diuresis in poorly controlled diabetes mellitus
- adrenal insufficiency
- recovery phase after AKI/urinary obstruction
10
Q
Describe the RAAS mechanism
A
- angiotensinogen is converted to angiotensin I by renin
- angiotensin I is converted to angiotensin II by the angiotensin converting enzyme (ACE)
- angiotensin II acts on AT1 receptors
11
Q
What is renin and its function?
A
- proteolytic enzyme released by granular cells in juxtaglomerular apparatus
- cleaves angiotensinogen to angiotensin I
- cleared by plasma
12
Q
Where is the angiotensin converting enzyme found?
A
vascular endothelium in lungs and renal afferent and efferent arterioles
13
Q
Describe the effect that angiotensin II has
A
- increases vasoconstriction and TPR in vascular smooth muscle cells of blood vessels
- increases release of ADH, reabsoprtion of H20 in kidneys, and ECV
- increases stimulation of secretion of aldosterone from adrenal glands, Na+ reabsorption and ECV in renal tubules of kidney
14
Q
Describe the sympathetic NS mechanism
A
- enhanced activity of renal sympathetic nerves directly causes:
- increased vascular resistance
- increased Na+ reabsorption by tubule cells
- indirectly causes:
- enhanced renin release from granular cells
- together decrease GFR and enhance Na+ reabsorption
- increases Na+ retention and ECV
15
Q
Describe the arginine vasopressin (AVP) mechanism
A
- ADH
- released by posterior pituitary in response to increases in extracellular osmolality
- promotes water reabsorption in distal nephron
- also released in response to large reductions in ECV (eg. haemorrhage)
- also causes vasoconstriction and increases renal Na+ retention
