Case 8 - HTN Flashcards
What is autonomic control of BP?
Through SNS and PNS
PNS is the vagus nerve
SNS is activated and vasodilates near the important organs, and vasoconstricts elsewhere
NAdr acts on alpha receptor in SMC > contraction of arterioles
SNS acts on beta receptors to vasodilate arteries, and increase contractility of the heart
Vasomotor centre split into three parts
- Sensory - CNIX and X input
- Vasoconstrictor
- Vasodilator
What is the function of the baroreceptors?
In the carotid bodies > hering’s nerve > CNIX > tractus solitarius
In arch of aorta > vagus nerve >tractus solitarius
When they sense high pressure, the signal from tractus solitarius to inhibit the vasoconstrictor centre
What is the function of the chemoreceptors?
2 in the carotid bodies, 1-3 in the arch of aorta
Stimulated by low O2, high Co2 and acidosis
When they are stimulated they excite the vasomotor centre
What is the atrial volume reflex?
When the atria are full, they stretch > signal sent to afferent arteriole in kidneys
Increased GFR > Increased fluid loss
Decreased secretion of ADH > less water reabsorbed > fluid loss
How does RAAS function?
Angiotensinogen produced by the liver
When the juxtaglomerular cells near the DCT sense low sodium, SNS input and low BP; release renin
Renin converts angiotensinogen to ATI
ATI converted to ATII by ACE
ATII:
-Increases SNS
-Increases salt resorption to increase water retention
-Increased release of aldosterone from adrenal cortex
-Increased vasoconstriction to increase BP
-Increases ADH
Aldosterone helps to retain salt
Risk factors for HTN
Increasing age CKD Decreased exercise Obesity DM Hyperlipidaemia Black Sleep apnoea Pyschosocial stress Smoking Alcohol Diet FHx
How do you diagnose HTN?
Take BP in both arms, use higher value arm if there’s a difference of more than 20 after a second reading
If different after 2 readings, take a third measurement, using 2 lower values as clinic BP
If over 140/90 should offer ambulatory BP monitoring - where BP taken every 2 hours for waking hours, need 14 readings
If not appropriate can do HBPM - need BD readings (2 at each sitting a couple of minutes apart) for 7 days, will discard the first day and take average of rest
What are secondary causes of HTN?
Kidneys - PKD, renovascular disease, gomerular disease Cushings Hyperaldosteronism Phaechromocytoma Drugs Sleep apnoea
How does renovascular disease cause HTN?
There is constriction of the renal arteries
To maintain eGFR, the efferent arteriole constricts, which increases glomerular pressure and causes HTN
But, ACE-i and ARBs cause vasodilation in the afferent arteriole, and the use of these will lead to dramatically reduced GFR
Treatment of HTN
In under 55y and non-black = start with ACE-i/ARB
In over 55y/black=Calcium channel blocker or diuretic
Then ACE-i/ARB plus one of the others
Then all three
Then other drugs including beta blockers, alpha blockers etc.
Should treat those with stage 2 HTN, or anyone in stage 1 with organ damage or comorbidities
Staging of HTN
1 - 140-159 / 90-99
2 - 160-179 / 100 - 109
3 - >180 / >110
Isolated systolic = diastolic under 90, but systolic >140
What are the LT complications of HTN?
Increased risk of IHD, MI, stroke, retinopathy, cognitive decline, premature death
What are hypertensive urgency and emergency?
Urgency is HTN >180 systolic but no signs of end organ damage
May have SOB, epistaxis, anxiety
Treat with oral anti-hypertensives
Emergency is the same but with signs of end organ damage - visual disturbances, chest pain, encephalopathy etc.
IV GTN, calcium channel blocker and beta blockers
SE of common antihypertensives
ACE-i - dry cough Beta blocker - bradycardia Calcium channel blocker - ankle swelling Thiazide diuretics - hyponatraemia Loop diuretics - gout
