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Week 6 Cardiovascular diseases(Clinical Science 1)
Terms in this set (20)
classification categories of hypertension
defined as blood pressure above 140/90, and is considered severe if the pressure is above 180/120.
risk factors associated with hypertension
Age(women >65 men >45)
not physically active
Distinguish between primary and secondary hypertension
Primary hypertension- cause by unknown symptoms or underlying disease 90% total population.
Secondary hypertension- cause by known disease Ex: adrenal disorder and kidney disorders
pathophysiological processes involved in the development of primary hypertension
-likely a multifactorial disorder
-due to genetic mutations in blood pressure regulation
-environmental factors (stress, sodium)
impact of chronic hypertension on the heart, kidneys, brain, retinas and medium to large arteries.
Heart- stroke, coronary heart disease, cardiac arrest, atrial fibrillation, tissue injury
Kidneys- reducing their ability to work properly
kidneys' blood vessels are damaged, they may stop removing wastes and extra fluid from the body.
Brain- confusion, hyperactive sympathetic nervous system
Eyes- retinal microvascular, hypertensive, retinopathy,retinal arteriolar narrowing, arteriovenous nicking, retinal hemorrhages, microaneurysms
nonpharmacological treatment strategies for hypertension
Maintain a normal body weight (i.e., body mass index less than 25 kg per m2).
Eat a diet high in fruits and vegetables and low in fat.
Consume less than 2.4 g of sodium per day.
Get 30 minutes of aerobic activity at least four days per week.
Men should have no more than two alcoholic drinks per day, and women no more than one alcoholic drink per day
pharmacological treatment strategies for hypertension and explain the mode of action of main drugs groups used.
risk factors for atherosclerosis
Hypertension- doubles risk due to endothelial damage
Smoking- direct endothelial damage, ↑LDL ↓HDL and ↑BP
High dietary intake of cholesterol/ saturated fats- ↑LDL ↓HDL →↑risk; genetic hyperlipidaemia associated with very high cholesterol (accounts for small proportion of cases)
Diabetes mellitus/insulin resistance- ↑LDL, ↑inflammation and endothelial damage
Obesity and sedentary lifestyle- central adiposity linked with insulin resistance, poor lipid profile and pro-inflammatory state
steps in development of atherosclerosis
Chronic endothelial injury
Increased endothelial permeability and inflammatory cell migration
Lipid accumulation and smooth muscle cell proliferation
cholesterol transport around the body contributes to atherosclerosis
Cholesterol travels in the blood transported in molecules called lipoproteins. High density lipoprotein (HDL good cholesterol) is quite dense and used to transport cholesterol from body tissues to the liver. Low density lipoprotein (LDL bad cholesterol) is slightly less denser and used to transport cholesterol from the liver to the cells of the body.
clinical manifestations of atherosclerosis
if plaque narrows or blocks these arteries (a disease called carotid artery disease), you may have symptoms of a stroke. These symptoms may include: Sudden weakness. Paralysis (an inability to move) or numbness of the face, arms, or legs, especially on one side of the body.
pharmacological treatments for atherosclerosis
Dietary- ↓cholesterol and saturated fats; ↑mono/polyunsaturated fats
↓Body weight; ↑exercise
Drug therapy considered when lifestyle changes are ineffective to lower cholesterol for individuals with high risk of coronary heart disease
Statins are most effective drugs (HMG-CoA reductase inhibitors)
aneurysm, its principle etiology and classifications
Arterial aneurysm- swelling of an arterial wall due to weakness from by trauma, infection (e.g. syphilis), congenital defect or atherosclerosis.
Classification: Aneurysms can also be classified by their location: Arterial and venous, with arterial being more common. ... The aorta, namely aortic aneurysms including thoracic aortic aneurysms and abdominal aortic aneurysms. The brain, including cerebral aneurysms, berry aneurysms, and Charcot-Bouchard aneurysms.
Causes Aneurysms have a variety of causes including high blood pressure and atherosclerosis, trauma, heredity, and abnormal blood flow at the junction where arteries come together. There are other rare causes of aneurysms. Mycotic aneurysms are caused by infections of the artery wall.
types of embolism
A condition in which one or more arteries in the lungs become blocked by a blood clot.
A serious condition that occurs when a blood clot blocks blood flow in an artery.
A blockage of blood supply caused by air bubbles in a blood vessel or the heart
risk factors for thrombus formation
Prolonged bed rest, such as during a long hospital stay, or paralysis.
Injury or surgery.
Being overweight or obese
Coronary heart disease
normally happens when cholesterol accumulates on the artery walls, creating plaques.
progression of coronary heart disease to acute myocardial infarction, including manifestations, diagnostic evaluation of myocardial infarction and management.
Build up of plaque in the endothelial tissues causing the accumulation is called atherosclerosis.
If pieces break off or rupture, platelets will clump in the area, attempting to repair the blood vessel. This clump can block the artery, reducing or blocking blood flow, causing MI.
drugs use in angina
prevent MI and death
reduce ischaemia, intensity, frequency of pain
If CHD: ↓cardiac O2 demand by ↓heart rate, contractility, afterload and/or preload
Three main types of drugs: organic nitrates, beta blockers (BBs), and calcium channel blockers (CCBs).
May need ACEIs, statins, antiplatelets, PCI, CABG
drugs use for MI
M Morphine (for pain)-↑SNS, ↑adrenaline/noradrenaline
O Oxygen-Augments the oxygen of inspired air
↑O2 saturation of haemoglobin
Arterial O2 levels may fall sharply after STEMI
Note: O2 usually only given if O2 saturation is low
N Nitrates- Nitroglycerin (glyceryl trinitrate)
Vasodilating effect, relieves coronary pain
↓venous return (preload) and arterial blood pressure (afterload)
↓ oxygen consumption
Platelets play major role in the thrombotic response to plaque disruption
Early inhibition of platelet aggregation is important early for acute coronary syndrome
Aspirin is preferred antiplatelet agent, acts by inhibiting the prostaglandin thromboxane A2
For people allergic to aspirin, clopidogrel or prasugrel is used
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