Cardiovascular Flashcards
Hypertension
Description, risk factors
- Elevated systemic arterial BP due to increase in CO or peripheral resistance due to vasoconstriction (>140S, >90D, severe: >180, >110)
Risk factors
* low dietary minerals (retain sodium) & high Na
* Smoking (vasoconstrictor)
* Obesity and insulin resistance (less nitric oxide)
* Age
Hypertension
Types/PP, manifestations
Primary: idiopathic
* overactivity of the SNS and RAAS causing peripheral vasoC and sodium retention, decreased sodium excretion by kidneys & inflammation, endothelial injury and vascular remodelling = increased blood volume and shift in pressure-natriuresis relationship
* Secondary: caused by underlying disease (KD, hormone imbalance, drugs)
Manifestations:
* No early symptoms except high BP, long term damage causes HD, KD, CNS problems, MI, stroke, vision impairment, oedema
Arteriosclerosis
Description, causes
- Abnormal thickening and hardening of the vessel walls
- SM and collagen migrate, causing the walls to thicken and lumen becomes narrow
- Caused by changes in lipid and cholesterol metabolism, ageing, HTN, insufficient blood flow
Atherosclerosis
Description, causes, PP
- Most common form of arteriosclerosis
- Soft fat deposits and fibrin that harden that occur due to inflammation and cell damage
- Caused by smoking, HTN, DM, high LDL low HDL
PP
* injured cells are unable to prevent clotting and vasodiate
* SNS causes vasoC & ischaemia
* Macrophages engulf LDLs, migrates into intima, producing collagen a fibrous plaque, that may occlude vessel as a thrombus or become an emboli, causing MI, stroke or ischaemia
Coronary heart disease
Description, causes, eval, treatment
- Any condition that affects the coronary vessels, most often caused by atherosclerosis, leading to myocardial ischaemia, angina, MI
- High CRP (inflammatory marker that chronically causes unstable plaques)
- Usually find collateral circulation (arterial anastomoses) that occurs due to chronic ischaemia
Causes
* Dyslipidema: high LDL (atherosclerosis PP) & low HDL
* HTN (endothelial injury)
* Cigarettes (peripheral vasoC & inflam/thrombus formation)
* DM, insulin resistance, obesity: endo damage, low NO
* T: vasoD, BB, surgery
Angina
Description & manifestations
- Chest pain caused by narrowing of the coronary arteries resulting in myocardial ischaemia
- M:Causes pain, discomfort, breathlessness, indigestion-like symptoms
Acute coronary syndromes
+ process
- Syndrome of clinical presentations that encompass unstable angina without myocyte death to MI
- Atherosclerotic plaque - stable angina - thrombus & rupture - ischaemia & unstable angina - STEMI
- Decrease in 02 & increase in demand
Unstable angina
Description, manifestations, treatment
- Angina that occurs at rest due to reversible ischaemia & complicated plaque
- Indication that infarction will occur
Silent ischaemia * infarction
- Some people experience no chest pain (in DM)
- Cells canl last 20min without O2, by you will see hypoxic changes on ECG within 30-60 seconds
- This is because myoglobin binds to oxygen during D and releases it when O2 levels are low
Thrombus
Description, causes, complications
- Clot that remains attached to a vascular wall
- Caused by roughening/inflammation (arteriosclerosis), low BP, blood stasis, that activates coagulation cascade
- Can occlude the vessel or dislodge and form an emboli
Emboli
Description, types, complications
- Embolus is a bolus of matter that occludes a vessel
- Thrombus, air, fluid, fat, bacteria
- Can cause ischaemia when it blocks a vessel, causing infarction & necrosis
Peripheral artery disease
- Atherosclerotic disease of arteries that perfuse limbs, causing ischaemia
- Common in DM
DVT
Description, causes, complications
- Blood clot that forms in the deep veins of the legs
- Caused by blood stasis, endothelial damage, hypercoagulability
- Causes oedema and pulmonary embolism
Congenital heart disease
Description, causes, classifications
- Birth defects due to environmental and genetics (8th week)
- Maternal conditions: viral infections, DM, PKU, alcoholism, age
Classifications
* Anatomical (obstruct blood from ventricles)
* Haemodynamic alterations (changes to blood flow)
* Status of tissue oxygenation (cyanosis)
Cyanosis & causes in congenital HD
- Blue discolouration of the skin due to hypoxia
- Usually caused by right-left shunt, moving blood away from the lungs
Cyanotic defects
+ Causes
- Saturated and desaturated blood mix within the heart of vessels
- Caused by truncus arteriosis, tetralogy of fallot, and transposition of great vessels
Atrial septal defect
- acyanotic, left to right shunt, increasing pulmonary blood flow (doesnt interfere with oxygenation)
Tetralogy of fallot
- Includes ventricular septal defect, pulmonary stenosis, overriding aorta, right ventricular hypertrophy
- Cyanosis & hypertrophy occur due to restricted blood flow from RV
Direct acting vasodilator drugs
- Used to treat HTN, angina, peripheral vascular disease
- Relax SM, act on arteries, veins or both
- Types: nitrates, CCB, K channel activators
Glyceryl trinitrate
- Low dose: causes venodilation, reduced preload and stroke volume
- High dose: vasodilation
- Reduced work of heart and oxygen demand, improving angina
Calcium channel blockers
- Block inward movement of calcium ions through cell membrane of cardiac and SM
- Reduced contraction, inducing vasodilation
- Treats angina, HTN, arrythmias
Indirect acting vasodilator drugs
- Centrally acting drugs that inhibit sympathetic outflow and inhibit RAAS
- ACE inhibitors such as captopril and ramipril
- Angiotensin receptor blockers ARBs
ACE inhibitors
- Block angiotensin converting enzyme that converts angiotensin I to II
- Prevents II from vasoC and raising BP, and releasing aldosterone that retains Na and water
- Treats HTN, HF, MI
Angiotensin receptor blockers
- Antagonists of angiotensin II receptor, acting specifically on it
- Prevents unwanted side effects that can occur with ACE inhibitors
- Like ACEs, they prevent vasocontriction and treat HTN
Dislipidaemia
Description, complications, treatment & management
- metabolic disorder with high concentrations of cholesterol and triglycerides (lipids)
- Implicated in atherosclerosis, where lipids are then deposited in the linings of arteries, causing damage and inflammation, leading to CAD, angina, HF, MI
- Management is based on cholesterol levels, current HD, HTN, smoking (target all of these)
- If not effective use drugs to lower lipids
Lipid lowering drugs
- HMG-CoA reductase inhibitors (statins)
- Bile acid-binding resins
- Fibrates
Statins
- Reduce cholesterol levels by inhibiting the enzyme HMG-CoA reductase, that is required for cholesterol production
Anticoagulants
- Prophylactic preventing of blood clots by impeding on the coagulation cascade
- Heparin & warfarin
Heparin
- Bings with antithrombin III to form a complex that inactivates multiple clotting factors
- Inactivating Xa of intrinsic and extrinsic pathway prevents conversions of prothrombin to thrombin, thus and inhibits formation of fibrin from fibrinogen
- Risk of bleeding
Low-molecular weight heparins
- fragments of standard heparins that inactivate factor Xa more potently than other factors, and have a minor effect on APTT
- This makes them safer, easier to administer and required less monitoring
- Enoxaparin
- Risk of bleeding
Warfarin
- Another anticoagulant, oral
- Prophylactic treatment of DVT, pulmonary thromboembolism
- Many interactions, INR must be monitored
Thrombolytic drugs
- Used to disolve clots that have already formed, such as in thromboembolitic disorders
- IV reteplase is given when there is a blockage in the coronary artery in MI
Antiplatelet drugs
- inhibit platelet aggregation, used to reduce the risk of a stroke
- E.g. aspirin, clopidogrel
