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Week 5 Flashcards

1
Q

What are modifiable and non modifiable CVD risk factors

A

Mod: hypertension, smoking, high LDL, sedentary lifestyle, obesity, poor nutrition, excessive alcohol consumption
Non-mod: increased age, gender (male more likely before menopause), family Hx, ethnicity

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2
Q

Determinants of BP

A 
BP = CO x SVR/TPR (systemic vascular resistance) 
CO = HR x SV
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3
Q

Normal regulation of blood pressure

A
  1. Short term: baroreceptors (found in carotid arteries) and endocrine. Baroreceptors reduce sensitivity with age. Baroreceptors stimulate SNS (adrenaline binds to alpha receptors in vessels = vasoconstriction) (noradrenaline binds to beta 1 receptor in heart = increase HR/contractility) or PNS activation

Long term: renal system - RAAS

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4
Q

What are the alpha 1/ beta 1/beta 2 located, MOA

A

Alpha 1: located on blood vessel - lead to vasoconstriction/dilated pupils
Beta 1: located on cardiac cells - increases rate and force of contraction. Increase contractility
Beta 2: found on smooth muscles in bronchioles and blood vessels: bronchodilation + vasodilation

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5
Q

What is hypertension and what are the risk factors

A

Hypertension: SBP>140mm/Hg or DBP > 90mmHg. Primary: no specific cause, secondary: due to specific cause

Risk factors: genetics, age, high sodium, glucose intolerance, smoking, obesity, alcoholic

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6
Q

Clinical manifestations of hypertension and it’s complications

A

Silent killer - no early symtpoms.
Later: due to damage of organs/vascular: heart disease, renal insufficiency, brain dysfunction, impaired vision, impaired mobility, vascular occlusion

Complications: organ disease in heart, brain, PVD, kidney, eyes

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7
Q

Pathophysiology of primary hypertension

A
  1. Genetic + environmental factors
  2. Leads to (1) defects in renal sodium haemostatis (poor sodium excretion —> sodium/water retention), (2) functional vasoconstriction (3) defects in vascular smooth muscle growth/structure.
  3. Leads to increase in CO and TPR = hypertension
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8
Q

Non-pharmacological management of hypertension

A

Lifestyle changes: dietary restriction (Na), increase K intake. Weight loss, exercise, smoking cessation, relaxation.

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9
Q

Pharmacological management of hypertension

A
  1. beta blockers: beta adrenergic antagonist - olol. Work against beta 1 and 2. To reduce heart rate/contractility = reduce CO and BP. Adverse: bronchospasm (block b2)
  2. Alpha 1 blockers: -sin. Block vasoconstriction = vasodilation = reduce TPR.
  3. ACE inhibitors: effect the RAAS -pril. Inhibit ACE = no conversion of Ag 2 = no release of aldosterone = no Na/h20 retention = reduced BP
  4. Diuretics - furosemide. Each drug Work differently ~ reduce sodium retention/absorption = decrease BP
  5. Angiotensin 2 blockers - blocks vasoconstriction / aldosterone = reduced fluid retention
  6. Calcium channel blockers - prevent Ca in cardiac cells = reduce contractility
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10
Q

What is coronary artery disease

A

Prolonged ischemia leading to chronic stable angina or acute coronary syndrome (unstable angina/NSTEMI or STEMI)

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11
Q

Risk factors for CAD

A 
C-HAM-FOLDS
Cocaine 
Hypertension
Age
Male
Family Hx 
Obese
Lipids 
Diabetes 
Smoking
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12
Q

How does CAD most likely develop

A

Atherosclerosis - narrowing and stiffening of the arteries that perfuse the myocardium - loss of recoil in BV
Oxygen demand vs oxygen supply

  1. Environment + free radicals = arterial wall injury
  2. Free radicals + LDL enter damaged artery wall and oxidise
  3. Injured arteries/oxidised LDL signal monocytes that turn into macrophages, engulf LDL and form foam cells. Foam cells signal for more monocytes/backup = Build up of foam cells - fatty streak
  4. Smooth muscle cells within arterial wall produce collagen to form a fibrous plaque cap. Calcium is also deposited = stiffened BV.
  5. Narrowing BV = reduced perfusion & Increases demand = ischemia = angina
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13
Q

Management of CAD

A

Lifestyle: smoking cessation, diet changes, exercise,
Pharmacological: statin (lipid lowering med), ace inhibitors, beta blockers, anti platelet therapy
Angioplasty, standing, bypass

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14
Q

What is angina and what causes the chest pain?

A

Angina = chest pain when myocardial O2 demand > O2 supply = ischemia

Patho:

  1. Atherosclerosis
  2. Myocardium becomes hypoxic within 10 sec of occlusions
  3. Anaerobic metabolism
  4. Lactic acid accumulation
  5. Lactic acid irritates myocardial nerve fibres = pain
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15
Q

Symptoms of angina

A

Usually 3-5 min with no permanent damage
Pain: heaviness/pressure can radiate to neck/jaw/left arm
SNS: pallor/diaphoresis
Dyspnoea can occur

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16
Q

Chronic stable angina vs unstable angina

A

Chronic stable angina

  • cause: myocardial ischemia usually to CAD
  • characteristic: episodic pain lasting 5-15min, provoked by exertion,/ relieved by GTN

Unstable angina

  • cause: rupture of thickened plaque
  • characteristic: new onset angina, chronic stable angina that increases frequency, duration, severity. Occurs at rest/minimal exertion. Not responsive to GTN
17
Q

Goal for management of angina and it’s management

A

Goal: restore a balance between myocardial O2 demand and supply

Management
1. Nitrates (GTN) = metabolism and converted into nitric oxide in vessel walls —> NO causes vasodilation of peripheral blood vessels (reduces TPR = decreases preload and afterload = decreases SV = decreases CO = decreases O2 demands) + dilates coronary arteries = increase blood flow ischemic area

  1. ACE inhibitors, beta blockers, Ca+ channel blockers, antiplatelet/anticoagulants, statins, opioids
18
Q

How CAD develops from stable to unstable/NSTEMI

A
  1. Deterioration of once stable plaque
  2. Rupture
  3. Platelet aggregation
  4. Thrombus

Unstable: (partial occlusion) chest pain that is new onset, occurs at rest, worsening pattern
NSTEMI: (partial occlusion) no ST elevation, severely occluded artery, partial thickness damage of heart
STEMI: (complete occlusion) ST elevation, sudden complete occlusion, full thickness damage of heart

19
Q

What is an MI and it’s complications

A

NSTEMI/STEMI

Result of sustained ischemia causing irreversible myocardial cell death = loss of contractile function

Damage to myocardial cells release adrenaline/noradrenaline
Adrenaline: short term then reduces BP due to reduced contractility of necrotic tissue = decreased perfusion
Noradrenaline: vasoconstriction= cool/clammy/pale skin

Complications: arrhythmia, HF, cardiogenic shock, pain, diaphoresis, N/V,

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