Examples of ACE inhibitor
Ends in pril
Captopril
Prindopril
Examples of ARB
Sartan
Olmesartan
Valsartan
Example of Ca channel blocker
Ends in pine Amlodipine Felodipine Or Verepamil
Example of thiazides
Chlorathiildone
Hydrochlorothiazide
Indapimide
Examples of Beta blocker
End in lol
Propranolol
Metoprolol
Side effects of ACE inhibitor
Cough
Hyperkalemia
Renal Impairment
Angiodema
Side effects of ARB
Hyperkalemia
Renal impairment
Rare- cough and angiodema
Side effect of Ca channel blocker (dihydropiradine)
Peripheral vasodilation —> odema (don’t treat with diuretic) Postural hypertension Tachycardia Chest pain Palpitation Gingival hyperplasia
Side effects of Ca channel blocker (non-dihydropyradine)
Bradycardia - because reduces HR and cardiac contractility
Constipation (severe with verapamil)
AV block
Heart fail
Side effects of Thiazides
Hypokalemia Hyponatremia Postural hypertension Dizziness Hyperuricalcemia Hyperglycemia
Side effects of Beta blocker
Bradycardia Postural hypertension Worsening HF Bronchospasm Cold extremities
Contraindications of ACE/ARB
Pregnancy
Hyperkalemia
Bilateral renal artery stenosis
Contraindication for thiazides
Gout
Age
Contraindication for Beta blocker
Asthma
Bradycardia
AV block
Combination for hypertension and diabetes
ACE/ARB and Ca channel blocker
Combination for hypertension post stroke or HF
ACE/ARB + diuretic
Combination post MI or HF
ACE/ARB + Beta blocker
Combinations to avoid
ACE + ARB —> renal impairment
Verapamil + beta blocker —> risk of heart block
What is more dangerous, high systolic or high diastolic
High systolic - indicates left ventricular hypertrophy esp if patient >50 years old
End organ damage in HT
Heart - ischemic heart disease, congestive heart failure CNS - TIA, stroke Kidney- hypertensive nephropathy Eyes - hypertensive retinopathy Vessels - athrosclorosis
Prehypertensive range
120-139/80-89
Risk management in prehypertensive range
Change in lifestyle Physical activity increase smoking avoidance hyperlipidemia mangement stress mangement weight mangement salt reduction more fruits and veggies relax
Types of HT
- Essential/Idiopathic HT (Primary)
2. Secondary HT
What determines the systolic BP (CO or TRP)
cardiac output
BP=
CO x TRP
Systolic BP relation to heart
ventricular squeeze in presence of open valves = systolic BP, because no resistance, the BP can be read in arteries
Diastolic BP relation to the heart
no relationship, because valve closed. related to TRP and the amount of blood left
Changes in systolic indicate
changes in CO
Changes in diastolic indicate
changes in TRP or vessel dilation/contriction
What influences CO
- Blood volume
2. Cardiac factors
What influences BV
Na intake
mineralocorticoid like aldosterone
atriopeptides ANP = vasodilation
What cardiac factors influence CO
Heart rate
contractility
anxiety (increases symp = increase HR and contractility)
What influences TRP
Humoral factors - dilators
Neural factors
What causes the release of Renin
Reduced renal perfusion can be due to reduced BP or due to stenosis
Overall - reduced Na in macular densa in DCT (because slowly flowing waste = increases Na retention)
Where is Renin released from
Juxtaglomerulo apparatus, which is modified afferent from arterioles and macular densa from DCT
What happens to Renin
converted to angiotensin 1 by angiotensinogen (from the liver)
What happens to Angiotensin I
converted to angiotensin 2 by ACE (angiotensin converting enzyme) from the lungs
What are the effects of Angiotensin II
Thirst - hypothalamus
Vasoconstrictor - Arterial = increase TRP, venous increases CO
Aldosterone release - from zonaglomulosa –> acts on principle cell to increase H2O and Na rentention thus increasing CO