Hypertension Flashcards
Describe the relationship between blood pressure and blood flow
BP = CO x TPR and Blood flow = Arterial BP / TPR
Excessive arteriole constriction ⇡TPR and switches off blood flow to tissues. Increases BP
Decrease in blood volume (hypovolemia) ⇣CO. e.g. haemorrhage or dehydration will reduce BP and produce poor blood flow to tissues
State normal blood pressures
What is the definition of hypertension?
High blood pressure that doesn’t have a known cause is called essential or primary hypertension. Secondary hypertension has a known cause, usually other medical conditions
140/90 mmHg is hypertension for < 50 years
160/95 mmHg is hypertension for older individuals
Draw a table to describe and classify hypertension
What factors are believed to cause primary hypertension?
Increased sympathetic NS, Increased renin-angiotensin-aldosterone system (RAAS)
Obesity / Insulin resistance, endothelial dysfunction, defect in vascular smooth muscle contraction and renal Na handling.
Increased salt intake, Age, Ethnicity
How do we treat Hypertension?
Three main treatment pathways:
Non-pharmacological, e.g. Life-style modifications.
Pharmacological treatment
Surgical for some secondary causes e.g. Conn’s syndrome: This is excessive aldosterone release from adrenal glands, so you can get surgery on adrenal glands
How do ACE inhibitors reduce hypertension? Use diagrams to support your answer
ACEi: Blocks ACE which blocks Ang II production. Less Ang II= less vasoconstriction and aldosterone release which means it can’t increase blood volume/SV
Ang II receptor blockers: block the ATR1 receptor and act as a competitive antagonist for Ang II. Ang II can’t bind, it can’t vasoconstrict blood vessels or release aldosterone which can’t increase blood volume
What are the side affects of ACEi and Ang II receptor blockers (ARB) which can cause non compliance?
Bradykinin is an inflammatory molecule broken down by ACE. If ACE is inhibited, Bradykinin is not broken down; it causes a dry cough.
Rarely causes angioedema (throat swelling to prevent breathing)
Hyperkalaemia: Reducing aldosterone ⇣ Na reabsorption but also ⇣ K excretion. K levels in the blood thus increase
ACEi/ARB cause fetal problems so not used in pregnancy
Renal stenosis: reduced renal blood perfusion. Ang II maintains proper renal function.
How do voltage dependent calcium channel blockers work?
Voltage-dependent Ca2+ channel blockers target VGCCs in vascular smooth muscle cells (vsmcs)
Reduction in Ca influx in vsmcs leads to less Ca-CaM-MLCK activity. This causes more relaxation and vasodilatation of vsmcs, lowering TPR and BP
What are side affects of Ca2+ channel blockers?
Increased heart rate in response to lowering BP
Headache/ankle swelling/flushing due to excessive vasodilation
Contraindications: Don’t use in patients who already have heart failure. This is bc we need Ca2+ influx to produce cardiac muscle contraction. So these drugs could make the heart aun worse
How do diuretics lower BP? What are the side affects?
Diuretics increase Na and H2O excretion from the kidneys. This reduces blood volume → reduces CO → reduce BP (BP = CO x TPR). Also produce vasodilatation which lowers TPR.
Side effects: Reducing salt levels too much causes loss of K from the blood, causing Hypokalaemia (from Loop and thiazide diuretics)
Can cause less insulin release leading to Hyperglycemia (high blood glucose bc the body lacks insulin).
Briefly explain the consequences of stimulating alpha 1 vs B1 adrenoreceptors
Stimulate β1 increases HR and Contractility → Increase CO → Increase BP
Stimulate α1 causes vasoconstriction → Increase TRP → Increase BP
Which drugs decrease Sympathetic Activity and therefore hypertension?
α2 receptors are on the presynaptic terminal of the symp synapse. α2 adrenoceptor agonists, eg Clonidine stimulate these receptors. This causes less NA to be released, reducing effect of NA on the heart.
Ganglion blockers: NIC blockers, e.g. Trimethapan cause less ganglion transmission in the pre and post sympathetic neurones. This reduces the effect of the symp ns.
Both drug classes are used in hypertensive crises
Describe how adrenoreceptor blockers work
α1 blockers cause relaxation of vascular smooth muscle. Used in hypertensive crisis, drug-resistance hypertension.
β1 blockers cause reduction in CO and renin release, e.g. atenolol
When selecting a drug treatment what do you consider?
Essential/primary vs. Secondary hypertension
Evidence of efficacy
Side effects of drug, drug interactions
Individual demographics- eg black/Caribbean not given ARBs or ACEi, instead they’re 1st given CCBs
Co-existing diseases, quality of life
Economic considerations
