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PMP 201 Patient-Centred Learning > Coronary Heart Diesase and Thromboembolic CV pathologies > Flashcards

Coronary Heart Diesase and Thromboembolic CV pathologies Flashcards

1
Q

Oxygen supply to myocardium

A
  • Hearts myocardium receives high levels of oxygen during diastole as blood is entering heart
  • When there is no contraction heart receives high amount of blood supply
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2
Q

Coronary circulation

A
  • Two tiny arteries leaving out of the aorta
  • Profuse blood to the myocardium
  • Handles high BP
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3
Q

Myocardial ischemia

A
  • Thickening of internal surfaces of arteries or progression of atherosclerosis lesions occlude oxygen supply cause CVD
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4
Q

Coronary artery flow angina

A
  • Atherosclerosis lesions narrow coronary artery and reduce ability for dilation
  • Lesions rupture and stimulate platelet aggregation causing thrombus to occlude artery restrict blood supply
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5
Q

Symptoms of angina

A
  • Reduced capacity in artery causes stress chest pains no change in troponin ECG
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6
Q

Unstable angina

A
  • Rapid reduction of blood flow due to rupture severe chest pain requiring urgent treatment
  • No change in troponin some ST depression in ECG
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7
Q

Antianginal drugs

A
  • Nitrates for acute attacks/ preventative measures - sublingual glyceryl trinitite
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8
Q

Nitric acid cytoplasmic guanylyl cyclase receptor

A
  • Nitric oxide endothelium derived vasodilator factor
  • Stimulate cytoplasmic guanylyl cyclase
  • Activate protein kinase G causing smooth muscle dilation
  • PDE isoform breaks down cGMP
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9
Q

Nitrates

A
  • Acute angina attacks/ Preventative measure
  • Isosorbide dinitrate (organic)
  • Isosorbide mononitrate (organic)
  • nitroglycerin
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10
Q

The effects of nitrates on Systemic vasculature

A
  • Increased venous dilation
  • decrease venous pressure
  • Decrease arterial pressure
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11
Q

The effects of nitrates on cardiac

A
  • Reduced preload and afterload
  • Decrease oxygen demand
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12
Q

The effects of nitrates on coronary

A
  • Prevents reverse vasospasm
  • Vasodilation
  • Improves subendocardial perfusion
  • Increased oxygen delivery
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13
Q

Beta-Blockers

A
  • Cardio specific depression of sympathetic activity
  • Reduce heart rate & lengthened diastole
  • Increased oxygen supply to myocardium
  • Patient with variant angina or HF are contraindicated
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14
Q

Calcium- Channel blocker

A
  • Verapamil and diltiazem cardiac specific
  • Amlodipine effective for patient with Prinzmetal angina
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15
Q

Second line inhibitors

A
  • Ivabradine selectively block hyperpolarization activated cyclic nucleotide gate in SA node
  • Lowers heart rate without effecting contractility of cardiac muscle
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16
Q

Class ID sodium channel blocker

A
  • Ranolazine blocks late inward sodium currents occurring during phase II of ventricular action potentials
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17
Q

Potassium channel activator

A
  • Nicorandil activate ATP sensitive K+ channels to enhance K+ efflux and hyperpolarization of vascular smooth muscle
  • Decrease calcium ion entry reduce cardiac contraction
18
Q

Progressive CVD

A
  • Narrowing transient occlusion or microembolization of thrombus
19
Q

Non-ST segment elevation MI

A
  • Myocardial ischemia and necrosis changes in troponin and no change in ECG
20
Q

Extreme CVD

A
  • Complete and prolonged exclusion of epicardial coronary blood vessel
21
Q

ST Segment elevation MI extreme

A
  • Dysfunction and death of cardiac myocytes
  • Troponin levels increase and elevation of ST levels and ECG
22
Q

Thrombosis

A
  • Blood clotting in artery
23
Q

Embolism

A
  • Blood clot materials moving in the blood vessel obstruct flow
24
Q

Cardiovascular atherosclerosis

A
  • Fat deposit and aggregation of thrombus ruptures and reaches small arteries causing ischemia
25
Q

Risk factors that lead to thrombus formation

A
  • Endothelial dysfunction - Smoking and hypertension
  • Hypercoagulability - Hereditary - Factor V Leiden, Protein C and S deficiency, Cancer
    Stasis - immobility polycythemia
26
Q

Artery

A
  • Thrombocytes (Platelets)
  • Contain no nucleus/ mitochondria and blood clotting
27
Q

Haemostasias - Vascular spasm

A
  • Rupture in Artery
  • Vascular spasm occurs prevent blood loss
  • Create signal for clotting factors chemicals and mediators released at sight of injury
  • Damage to collogen, endothelial cells and vascular smooth muscle cells
28
Q

Platelet activation plug

A
  • Platelet stick to exposed collogen
  • Platelets stimulate ADP, Thromboxane A2 and serotonin
  • Van-Wilbur factor stabilizes collogen and platelet adhesion
29
Q

Coagulation patch

A
  • Clotting factors in the liver, vitamin K and the biosynthesis of I to XIII
  • Prothrombin Activator to Prothrombin to Thrombin to fibrinogen to fibrin insoluble to fibrin mesh
30
Q

Platelet endothelial interaction

A
  • thrombin activate platelet by PAR
  • Platelets stick on exposed collogen
  • Protease activated receptor is mediated by the thrombin for platelets to interact with cell surface
30
Q

Clot regulation in a healthy individual

A
  • Endothelial cells in plasma membrane release heparin
  • Work as anticoagulant recruit antithrombin in circulation AT-III binding negatively inhibits thrombin activation on platelet
  • Clot formation prevented
31
Q

Atherosclerosis

A
  • Thrombin mediated platelet activation become abrupt and accelerated due to endothelial dysfunction and damage
31
Q

Platelet endothelial interaction (ADP - mediated process)

A
  • Activated platelets stimulates release of ADP which acts on P2Y 12 receptors activate positive feedback change platelet to start shape
32
Q

Negative feedback of ADP during Haemostasias

A
  • ADP binds P2Y1 receptor stimulates the release of prostacyclin and nitric oxide from endothelial cells to prevent plug formation
33
Q

Atherosclerosis

A
  • ADP meditated platelet formation become accelerated due to endothelial dysfunction damage
  • Smoking and hyperlipidemia damage endothelial and challenge negative feedback more clot
34
Q

Platelet fibrin plug formation

A
  • Von-Wilber factor bridge between collogen exposed in damaged blood vessels & glycoprotein receptor GPIIb expressed in activated platelets
  • GPIIb receptor binds fibrinogen and form platelet fibrin plug
35
Q

Clot and vessel healing

A
  • Clot retraction occurs actin and myosin in platelet contract pulls fibrin
35
Q

Platelet derived growth factor

A

Stimulate smooth muscle and fibroblast division

36
Q

Vascular endothelial growth factor

A
  • Rebuilds endothelial lining by multiplying endothelial cells
37
Q

Fibrinolysis

A
  • Plasminogen plasma protein trapped in clot converted and plasmin digest fibrin

PMP 201 Patient-Centred Learning (51 decks)

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