HTN and the kidneys Flashcards
What affects arteriolar radius and therefore TPR?
Neural controls
Hormonal controls
Local controls
What affects blood viscosity and therefore TPR?
Haematocrit
What factors increase ECF volume?
Fall in GFR
RAAS (ATII) - salt reabsorption
Symp activation - salt reabsorption
What factors increase VC?
RAAS (ATII)
Symp activation
Endothelin
Renal PG’s (+ other vasodilators)
What is RAAS released in response to?
Proteolytic enzyme released from the kidneys in response to:
- Symp nerve activation - mediated by baroreceptor feedback
- Renal artery hypotension -independent of baroreceptor feedback
- Decreased sodium in kidney distal tubules
What does RAAS do?
Renin released from kidney juxtaglomerular cells
Ang II acts on resistance vessels - inc TPR
Ang II causes release of aldosterone from adrenal glands - na and water reabsorption
Ang II stimulates release of ADH from pituitary
Why do people with kidney disease get HTN?
Activation of renin-angiotensin-aldosterone system
Retention of salt and water with reduced excretory function
In later stages of renal disease the latter mechanism becomes dominant and high BP is often volume dependent
Differentiate stage 1, 2 and severe HTN
S1 - Clinic 140/90, home 135/85
S2 - Clinic 160/100, home 150/95
Severe - 180/110 clinic
ABPM
Ensure at least two measurements per hour during the person’s usual waking hours, average of at least 14 measurements to confirm diagnosis
HBPM
Two consecutive seated measurements 1 min apart
BP recorded twice daily for at least 4 days and preferably for a week
Measurements on first day are discarded - av value of remaining used
For all HTN patients offer to…
test urine for presence of protein
take blood to measure glucose, electrolytes, Cr, eGFR and cholesterol
- examine fundi for HTN retinopathy
- 12 lead ecg
Secondary HTN causes
Renal disease
Coarction of aorta
Endocrine - Cushing’s (excess cortisol), Conn’s (excess aldosterone)
