Module 1.1-1.3 Flashcards
What is atherosclerosis?
- Thick material that forms plaque on walls of arteries that causes stiff/hardening of arterial walls
- Highest cause of myocardial infarction
What are the risk factors for atherosclerosis?
Modifiable: obesity, smoking, diabetes, lifestyle
Non-modifiable: age, gender, genetics, dyslipidaemia
What is the pathophysiology for atherosclerosis?
- Endothelial injury occurs in artery, more things become prone to sticking
- Causes inflammation shown by an increase in c-reactive protein levels
- WBCs accumulate and stick to intima and media, endothelial cells retract and LDL moves into intima
- Smooth muscle cells proliferate, multiply and oxidize as monocytes absorb fat
- Lipid manifests into plaque
- Smooth muscles cells sit on top and secrete growth cells to build fibrous cap to stabilize fat but blocks blood flow
- Platelets adhere to damaged arterial wall surface creating thrombus, lining is unstable
- Lipids build up at site, prostaglandins released causing inflammation
- More platelets aggregate, enlarging clot
What is Peripheral Vascular Disease (PVD)?
any abnormality in the arteries or veins caused by disruption of peripheral perfusion due to stationary blockage of arteries causing increased pressure in veins
What is an arterial disorder and the cause?
- reduced perfusion in peripheral tissues leading to ischaemia and claudication (muscle pain)
Cause- atherosclerosis
What is a varicose veins and the cause?
-Superficial veins of the lower legs abnormally twisted and often appear raised which cause oedemas
Cause- increased BP in vein, venous valve insufficiency and excessive vessel wall dilation
What is Thrombophlebitis and the cause?
- Swelling of a vein which causes inappropriate thrombus formation (DVT)
Cause- sluggish blood flow, endothelial injury, increased blood coagulation, HTN
What are the differences in the degrees of hypertension?
Primary: arises spontaneously, unknown cause, due to slight vasoconstriction
Secondary: derived from renal/endocrine disease or pheochromocytoma (tumour in medulla oblongata)
Malignant: uncontrollable after treatment, extremely high diastole
How do beta blockers work (Examples)
- block cardiac output by blocking the beta receptors, slows heart and stops renin release (-olol)
How do ACE inhibitors work?
Prevent conversion of angiotensin I to angiotensin II by blocking ACE (-pril or -sartan)
How do A II receptor antagonists work?
blocks the affects of A II (vasoconstriction) (Candesartan)
How do Calcium Channel Blockers work?
Inhibit calcium entry into heart and smooth muscle cells (Nifedipine, Verapamil)
How do diuretics work?
Increase urine output through removing water from circulation to decrease blood volume (thiazide)
What are examples of ways to assess heart function?
- ECG
- Ultrasound
- Auscultation
- Stress test
- X-Ray
- Angiography
- Cardiac enzyme production record
What is Ischaemic heart disease (IHD)?
- Cardiac blood supply, therefore o2 supply is insufficient
- Closely linked with angina (aka chest pain)
What is the pathophysiology for angina?
- Caused by atherosclerotic plaque in coronary vessel
- Myocytes run low on blood and therefore O2, cause adenosine, BK and lactate release
- These sensitize nerve fibres inducing chest pain and irritation
What are the three types of angina?
(AS= Atherosclerotic/osis)
Stable: AS plaque in coronary vessels, predictable pain, relieved at rest
Unstable: AS plaque combined with thrombus, unpredictable and high severity
Variant: Vasospasm in coronary artery, leads to reduced blood flow, relieved by GTN
What is a myocardial infarction (MI)?
- consistent reduced blood flow causes myocardium to die due to plaque build up
- angina is ischaemia of cardiomyocytes, MI is necrosis of cardiomyocytes
- troponin and cardiac enzymes markers are assessment ways
What is the difference between a STEMI and an NSTEMI?
STEMI: ST segment elevation, entire muscle wall dies
NSTEMI: ST segment depression, partial muscle wall death
What is the pathophys of an MI?
The top of a plaque build up in a coronary vessel is ruptured, exposing contents and allowing platelets to aggregate, creating a clot and a full coronary arterial occlusion
What is the mechanism of action of aspirin?
Prevents COX enzyme producing thromboxane, which in turn prevents platelet aggregation
What is valve stenosis and the different types?
- valve doesn’t open enough, forward flow issue, higher pressure required
- Mitral valve stenosis: L atria increased pressure leading to AF, pulmonary HTN, SOB, blood backflowing into P. arteries causing RV hypertrophy, decreased CO
- Aortic valve stenosis: inc. afterload and LV hypertrophy causing stiffness, L atria overloads, heart muscles cannot get blood from stiffness and causes angina
What is valve regurgitation and the different types?
- valve is insufficient, does not fully close
MV regurg: MV closes on systole, vol. overload in LA and LV, LV hypertrophy and eventual L sided heart failure
AV regurg: Blood from aorta in LV pushed out in systole and leaks in diastole, inc. preload and LV hypertrophy
What are cardiac dysrhythmias?
- deviations from the normal sinus rhythm due to alterations in cardiac electrical conduction system
- caused by electrolyte imbalances,
infections, hypoxia, thyroid issues, stress, or post-myocardial infarction conditions
What are SA node dysrhythmias?
- abnormal impulse formation or disruption
Sinus bradycardia <60bpm (atropine)
Sinus tachycardia >100bpm (treat underlying cause)
What are atrial dysrhythmias?
Atria tachycardia: >100bpm can be focal or multifocal (single or multiple sites)
Atria flutter: 250-350bpm, persistence of electrical impulses in atria
Atrial fibrillation: >350bpm chaotic and rapid contractions, blood clot formation likely
What are AV node dysrhythmias?
- heart block, absence of depolarization down ventricles
1st degree: widened PR interval, impulse slowly gets to ventricles
2nd degree: impulse only makes it to lower heart chambers - Mobitz 1: lengthening of PR and no QRS
- Mobitz 2: noticeable QRS absence but multiple PR interval to make up, pacemaker required
3rd degree: no conduction between atria and ventricle
What are ventricle dysrhythmias?
V tachycardia: >100bpm, consecutive V contraction
V fibrillation: chaotic and rapid contractions, severe CO decrease causing death
- Verapamil, Adenosine, Lignocaine as treatment
