Systemic Arterial Hypertension Study

Damage to blood vessels caused by high blood pressure (HTN).

Sustained/severe high blood pressure leads to changes in blood vessels (e.g., thickening, damage).

High blood pressure damages vessels, leading to changes like hyaline or hyperplastic arteriosclerosis.

Heart, large arteries, brain, eyes, and kidneys are commonly affected by high BP.

High blood pressure that doesn't respond to standard treatments.

High blood pressure caused by another underlying condition.

Factors like age, obesity, family history, diet, and lifestyle habits.

Changes in the structure of blood vessels, such as thickening, narrowing, and damage.

Pathologic buildup of LDL within artery walls, causing narrowing.

Formation of plaque involving foam cells, fatty streaks, and atheromas; potentially leading to rupture and thrombosis.

Factors influencing atherosclerosis development, including genetic predisposition, lifestyle choices, and comorbidities.

Atherosclerosis progresses through stages, with distinct morphological changes (e.g., fatty streak, plaque build-up).

Common arterial locations include coronary, carotid, and peripheral arteries.

Reduced blood flow due to atherosclerosis damages organ function downstream the affected area.

Symptoms arise from plaque rupture, clot formation, or narrowing impacting blood circulation.

Diagnosis involves various tests (e.g., lipid profiles, imaging) depending on the suspected location and symptoms

Aortic aneurysm is caused by inflammation and degeneration of connective tissues (collagen, elastin, smooth muscle) leading to weakened vessel walls, dilation, and potential rupture. Weakened areas may further get affected by increased blood flow stress.

Aortic aneurysm risk factors include host variables (age, genetics, obesity, diabetes, smoking, family history), vascular diseases (atherosclerosis, cystic medial degeneration, vasculitis), and infections.

Aortic aneurysms often present asymptomatically, but some can present with pain (especially radiating back pain, if it's a thoracic or abdominal aneurysm), dyspnea, hoarseness, dysphagia, edema, or a pulsatile mass.

Diagnosis of an Abdominal Aortic Aneurysm (AAA) usually involves physical examination (pulsatile mass), imaging studies (x-rays to CT scans), and potentially blood tests to evaluate underlying disorders.

Treatment for AAA depends on the size, symptoms, and rate of expansion. If over 5cm, symptomatic, or the rate of expansion is rapid, surgery or an endovascular procedure might be needed. Surveillance/elective repair might be used for asymptomatic patients.

Aortic aneurysm treatment is often guided by size measurements (>5cm) and symptom presence or rapid expansion.

Vasculitis refers to inflammation and weakening of the blood vessel walls that can cause aortic aneurysms. This includes conditions like giant cell arteritis and Takayasu arteritis.

Aortic aneurysm prognosis is impacted by vessel size, symptoms, rate of expansion, the underlying cause, and overall patient health.

A tear in the aortic wall that allows blood to flow between the layers, causing a false lumen that can grow and cause serious problems

Dissection involves a tear in the arterial wall, while an aneurysm is a bulge or widening of the artery.

High blood pressure (hypertension), atherosclerosis (hardening of the arteries), and connective tissue disorders are leading causes.

High blood pressure, weakening arterial walls, and a pre-existing condition (like a tear or weakness) increase the risk.

Intraluminal pressure (blood pressure), wall tension (related to pressure and vessel size), shear stress (from blood flow), and vascular compliance (ability to stretch and accommodate changes) affect the aorta.

High blood pressure, aging, genetics, and certain connective tissue disorders increase the risk.

Symptoms vary but can include severe chest pain, radiating pain, unequal pulse, and shortness of breath.

Techniques to diagnose aortic dissection include imaging studies (e.g., CT scans), ultrasound, and physical assessments.

Medication classes used to treat high blood pressure.

Treatment for abnormal blood lipids (fats).

Class of drugs that lower cholesterol by inhibiting cholesterol production.

Processes of moving cholesterol and lipids through the body.

Side effects from antihypertensive medications.

Unwanted side effects caused by statins.

Effects of combining antihypertensive drugs with other medications.

Effects of combining statins with other medications.

Fibrates (like gemfibrozil) increase lipoprotein lipase activity, which breaks down triglycerides in the blood, leading to lower triglyceride levels and increased HDL cholesterol.

Niacin (vitamin B3) reduces LDL cholesterol and triglycerides by inhibiting their production in the liver and increasing HDL cholesterol levels.

Omega-3 fatty acids reduce triglyceride levels and may slightly increase HDL cholesterol by lowering the production of triglycerides in the liver and reducing inflammation.

Non-statins are used to lower LDL cholesterol and triglycerides in patients with high cholesterol or triglycerides, particularly those with mixed dyslipidemia, high triglycerides, or low HDL.

Calcium channel blockers (like amlodipine) reduce the heart's workload by relaxing blood vessels and slowing the heart rate, decreasing oxygen demand and relieving angina symptoms.

Nitrates (like nitroglycerin) act as vasodilators, relaxing blood vessels and improving blood flow to the heart, reducing chest pain by improving oxygen supply.

Ranolazine reduces sodium current in heart cells, slowing the heart's electrical activity and decreasing oxygen demand, relieving angina by regulating heart rhythm.

Antianginal drugs can interact with other medications. For example, some antianginals can enhance the effects of other vasodilators or interact with diuretics.