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GMED5001 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Hypertension

Description, risk factors

A
  • 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

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2
Q

Hypertension

Types/PP, manifestations

A

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

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3
Q

Arteriosclerosis

Description, causes

A
  • 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
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4
Q

Atherosclerosis

Description, causes, PP

A
  • 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

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5
Q

Coronary heart disease

Description, causes, eval, treatment

A
  • 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

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6
Q

Angina

Description & manifestations

A
  • Chest pain caused by narrowing of the coronary arteries resulting in myocardial ischaemia
  • M:Causes pain, discomfort, breathlessness, indigestion-like symptoms
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7
Q

Acute coronary syndromes

+ process

A
  • 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
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8
Q

Unstable angina

Description, manifestations, treatment

A
  • Angina that occurs at rest due to reversible ischaemia & complicated plaque
  • Indication that infarction will occur
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9
Q

Silent ischaemia * infarction

A
  • 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
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10
Q

Thrombus

Description, causes, complications

A
  • 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
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11
Q

Emboli

Description, types, complications

A
  • 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
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12
Q

Peripheral artery disease

A
  • Atherosclerotic disease of arteries that perfuse limbs, causing ischaemia
  • Common in DM
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13
Q

DVT

Description, causes, complications

A
  • Blood clot that forms in the deep veins of the legs
  • Caused by blood stasis, endothelial damage, hypercoagulability
  • Causes oedema and pulmonary embolism
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14
Q

Congenital heart disease

Description, causes, classifications

A
  • 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)

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15
Q

Cyanosis & causes in congenital HD

A
  • Blue discolouration of the skin due to hypoxia
  • Usually caused by right-left shunt, moving blood away from the lungs
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16
Q

Cyanotic defects

+ Causes

A
  • Saturated and desaturated blood mix within the heart of vessels
  • Caused by truncus arteriosis, tetralogy of fallot, and transposition of great vessels
17
Q

Atrial septal defect

A
  • acyanotic, left to right shunt, increasing pulmonary blood flow (doesnt interfere with oxygenation)
18
Q

Tetralogy of fallot

A
  • Includes ventricular septal defect, pulmonary stenosis, overriding aorta, right ventricular hypertrophy
  • Cyanosis & hypertrophy occur due to restricted blood flow from RV
19
Q

Direct acting vasodilator drugs

A
  • Used to treat HTN, angina, peripheral vascular disease
  • Relax SM, act on arteries, veins or both
  • Types: nitrates, CCB, K channel activators
20
Q

Glyceryl trinitrate

A
  • Low dose: causes venodilation, reduced preload and stroke volume
  • High dose: vasodilation
  • Reduced work of heart and oxygen demand, improving angina
21
Q

Calcium channel blockers

A
  • Block inward movement of calcium ions through cell membrane of cardiac and SM
  • Reduced contraction, inducing vasodilation
  • Treats angina, HTN, arrythmias
22
Q

Indirect acting vasodilator drugs

A
  • Centrally acting drugs that inhibit sympathetic outflow and inhibit RAAS
  • ACE inhibitors such as captopril and ramipril
  • Angiotensin receptor blockers ARBs
23
Q

ACE inhibitors

A
  • 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
24
Q

Angiotensin receptor blockers

A
  • 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
25
Q

Dislipidaemia

Description, complications, treatment & management

A
  • 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
26
Q

Lipid lowering drugs

A
  • HMG-CoA reductase inhibitors (statins)
  • Bile acid-binding resins
  • Fibrates
27
Q

Statins

A
  • Reduce cholesterol levels by inhibiting the enzyme HMG-CoA reductase, that is required for cholesterol production
28
Q

Anticoagulants

A
  • Prophylactic preventing of blood clots by impeding on the coagulation cascade
  • Heparin & warfarin
29
Q

Heparin

A
  • 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
30
Q

Low-molecular weight heparins

A
  • 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
31
Q

Warfarin

A
  • Another anticoagulant, oral
  • Prophylactic treatment of DVT, pulmonary thromboembolism
  • Many interactions, INR must be monitored
32
Q

Thrombolytic drugs

A
  • 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
33
Q

Antiplatelet drugs

A
  • inhibit platelet aggregation, used to reduce the risk of a stroke
  • E.g. aspirin, clopidogrel

GMED5001 (13 decks)

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