Pharmacological treatment in Cardiovascular Disease Flashcards
what is the role/functions of the vascular endothelium
vascular endothelium, a monolayer of endothelial cells (EC), constitutes the inner cellular lining of arteries, veins and capillaries and therefore is in direct contact with the components and cells of blood;endothelium is not only a mere barrier between blood and tissues but also an endocrine organ. It actively controls the degree of vascular relaxation and constriction, and the extravasation of solutes, fluid, macromolecules and hormones, as well as that of platelets and blood cells
functions:
* controls vasular permeability, vascular tone, coagulation/thrombosis/ fibrinolysis.
*leukocyte activation/adhesion/transmigration
*angiogenesis
*direction; inflammatory cells to foreign bodies; sites requiring repair
*metabolism; Endothelial cell (EC) metabolism is important for health and disease. Metabolic pathways, such as glycolysis, fatty acid oxidation, and amino acid metabolism, determine vasculature formation
define heart failure + describe its treatment
heart failure is caused by structural and/or functional abnormality that produces raised intracardiac pressure and/or inadequate cardiac output at rest and/ or at exercise
basically it’s
when cardiac output is insufficient to meet body’s metabolic requirements
heart failure can be grouped into:
*reduced ejection fraction (HFrEF= systolic failure) {EF including and less than 40%} treatment; ACEi/ARB, beta blocker/ARB, SGLT2 inhibitors, 2nd line; antiplatelet, antistatin
*preserved ejection fraction (HFpEF= diastolic failure) {EF above and including 50%} treatment wld be diuretics, SGLT2 inhibitors, 2nd line; antiplatelet, antistatin
ejection fraction= % of blood leaving the heart during each contraction
EF= (stroke volume/end diastolic volume) x 100
define vascular tone
Vascular tone, the contractile activity of vascular smooth muscle cells in the walls of small arteries and arterioles, is the major determinant of the resistance to blood flow through the circulation
what is rheumatic heart disease
Rheumatic heart disease is a condition where the heart valves have been permanently damaged by rheumatic fever. The heart valve damage may start shortly after untreated or undertreated streptococcal infection, such as strep throat or scarlet fever. An immune response causes an inflammatory condition in the body
how is hypertension classified?
stage 1 hypertension= clinic blood pressure ranging from 140/90mmHg to 159/99mmHg and subsequent ABPM (ambulatory blood pressure monitoring)
stage 2 hypertension= clinic blood pressure of 160/100 mmHg or higher less than 180/120 mmHg and subsequent ABPM daytime average or HBPM average blood pressure of 150/95 mmHg or higher
stage 3/ SEVERE HYPERTENSION =clinic systolic blood pressure of 180mmHg diastolic of 120mmHg or above n.b. this high usually means u refer to same day specialist review
what is AMBP vs HBPM
AMBP= ambulatory BP monitoring ; monitors blood pressure + heart rate at fixed time intervals for 24hours
HBPM - home BP monitoring over 2 weeks
ABPM assesses daytime and nighttime blood pressure during routine daily activities typically during one 24-hour period, whereas HBPM assesses blood pressure at specific times during the day and night over a longer period of time while the patient is seated and resting
what is a normal blood pressure reading (range)
As a general guide: normal blood pressure is considered to be between 90/60mmHg and 120/80mmHg (this applies if it’s measured at home or at a pharmacy, GP surgery or clinic)
The blood pressure is written as the systolic pressure over the diastolic pressure
n.b. if BP measured in clinic= cld have white coat hypertension. This condition occurs when blood pressure readings at a health care provider’s office are higher than they are in other settings, such as at home (factors like stress, time of day)
how does renal artery hypotension/renal artery stenosis wrongly trigger the RAAS system
renal artery stenosis (narrowing of blood vessels causing less blood flow) this means reduced perfusion pressure is detected by kidney by the baroreceptors in the afferent arteriole
= the body will raise blood pressure thinking there’s not enough= u can die
where are the following enzymes made + stored
* angiotensinogen
*renin
*angiotensin converting enzyme (ACE)
*angiotensin II
The angiotensinogen substrate is produced in the liver, while renin is produced in the kidney and Ang II in the vascular tissue
where is ADH released from and what triggers its release
hypothalamus produces ADH; storing it in pituitary gland.
hypothalamic osmoreceptors then initiate the release of ADH from the** posterior pituitary gland**. ADH primarily acts on the kidneys to increase the amount of water reabsorbed from the kidney filtrate back into the blood
ADH release stimulated by angiotensin II which stimulates posterior pituitary gland to release more ADH
ACE inhibitor (meds always end in -pril) + most common side effect
angiotensin coverting enzyme inhibitor; if u inhibit ACE u inhibit the formation of angiotensin II= lower bloow pressure
Bradykinin is cause of dry cough and may occur in patients taking ACE inhibitors
Angiotensin II receptor blocker (ARB) (meds usualy have an ‘ar’ or -artan in them)
Angiotensin II receptor blocker= inhibits VAASt effects of RAAS system
Aldosterone antagonists e.g. spironolactone
aldosterone antagonists block the action of aldosterone, which is a hormone your adrenal glands make. By stopping aldosterone; your kidneys put extra water and salt (Na+) into your pee. These medicines also keep your body from getting rid of potassium
what medications for CVD(cardiovascular disease) do not act on the RAAS system?
*thiazide diuretics (meds end in -thiazide) (block the Na+/Cl- symporter in the early DCT! so decrease Na+ in blood= decrease water going into blood= decrease flow= decrease blood pressure
*loop diuretics e.g.flurosemide (DEcrease sodium reabsorption at loop of henle) by blocking the Na+/K+/2Cl- co-transporter kidney epithelial cell in the thick ascending limb of loop of Henle= so decrease Na+ in blood= decrease water going into blood= decrease flow= decrease blood pressure
N.B. these meds block one symporter meaning other ions are affected= these meds can cause hypocalcaemia (low calcium) or hypokalemia(low potassium) {or sometimes these meds cause increases as messes w function}
“iur”= urine/ smth to do w kidneys
alpha 1 blockers + beta blockers (meds end in -ol or -lol)
alpha-1 adrenergic receptor antagonists (also called alpha-blockers) are a family of agents that bind to and inhibit type 1 alpha-adrenergic receptors and thus inhibit smooth muscle contraction= inhibit vasoconstriction i.e. cause vasodilation which decreases TPR= decreases blood pressure
beta blockers= block both beta-1 receptors that are present in cardiac muscle and beta-2 receptors found in bronchial+ smooth muscles. This decreases RENIN release which reduces cardiac output and lowers blood pressure= reduced RAAS activity
BOTH A + B blockers inhibit SNS, decrease contractile force (ionotropy) and decrease heart rate (chronotropy)
