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Evidence Based Medicine > Week 2 > Flashcards

Week 2 Flashcards

Cardiovascular System

1
Q

What is thought to play a role in the development of essential hypertension?

A

systemic inflammation and oxidative stress

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2
Q

Secondary hypertension accounts for what percent of cases with an identifiable etiology?

A

5-10%

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3
Q

At what age does a blood pressure of 120/80 have a 90% lifetime risk of developing hypertension?

A

55

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4
Q

What percent of patients with hypertension will require 2 or more medications to control their blood pressure?

A

50-65%

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5
Q

What are the physiologic factors that affect blood pressure?

A
  • hydration status
  • sodium and potassium intake
  • sympathetic tone and arterial elasticity
  • cardiac contractility
  • renal function and hormonal factors
  • drugs
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6
Q

What are the 3 components that determine blood pressure?

A
  1. mean arterial pressure
  2. cardiac output
  3. peripheral resistance
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7
Q

What is the equation for mean arterial pressure?

A

MAP = SBP + 2(DBP)/3

MAP = Cardiac output x peripheral vascular resistance

cardiac output = the heart rate x stroke volume ejected with each heartbeat

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8
Q

What are the factors that most directly affect blood pressure?

there are 3

A

cardiac output, vascular resistance, and plasma volume

increased volume = increased pressure

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9
Q

What is the goal of the cardiovascular system?

A

To maintain a constant flow of blood to vital organs

pressure and volume are constantly adjusted to maintain homeostasis

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10
Q
A
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10
Q

What is the equation for cardiac output?

A

CO = Heart Rate x Stroke Volume

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11
Q

What type of fibers innervate the heart?

A

sympathetic: Beta-1 adrenergic fibers

SA node: increases heart rate; ventricles increase force of contraction

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12
Q

What nerve innervates the SA node via parasympathetic input?

A

Vagus nerve

works to modulate the sympathetic effects on heart rate

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13
Q

Where is calcium stored in cardiac muscle cells?

A

In the sarcoplasmic reticulum

releasing calcium leads directly to contraction

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14
Q

What changes lead to increased peripheral resistance?

an increase in peripheral resistance leads to increased blood pressure

A
  1. changes in arterial tone secondary to increased alpha-adrenergic synpathetic stimulation
  2. changes in vessel wall eslasticity produced by vascular smooth muscle contraction

blood viscosity, vessel length and vessel radius determine resistance

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15
Q

How does Poiseulle’s equation explain the relationship between vessel resistance, vessel length and vessel radius?

A

vessel resistance is directly proportional to the length of the vessel and the viscosity of the blood and inversely proportional to the vessel radius

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16
Q

What is blood viscosity dependent on?

A

hematocrit (the volume of RBC’s in the blood)

remember: blood viscosity is directly proportional to vascular resistance

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17
Q

How does vessel length contribute to vascular resistance?

A

blood passing through a longer vessel will encounter more friction

vessel length is directly proportional to vascular resistance

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18
Q

How is vessel radius related to peripheral resistance?

A

Resistance increases when vessels constrict

inversely proportional to vascular resistance

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19
Q

How does sodium regulate plasma volume?

A

in euvolemic and normotensive indivisuals, the kidneys clear excess sodium

people with hypertension are unable to fully clear sodium- as intake increases, higher blood pressure results; as intake decreases, blood pressure decreases

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20
Q

When is RAAS activated?

A

low blood volume or low sodium concentration

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21
Q

What do the juxtaglomerular cells secrete to activate RAAS?

A

renin

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22
Q

What does renin do?

A

cleaves angiotensinogen to produce angiotensin I, which is converted to angiotensin II by the angiotensin-converting enzyme (ACE)

angiotensin II is a potent vasoconstrictor

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23
Q

What categories of pharmaceutical agents act on the RAAS?

A
  • mineralcorticoid receptor blockers
  • ACE inhibitors
  • Renin inhibitors
  • Angiotensin II receptor blockers
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24
Q

How does atherosclerosis develop?

A

The mechanical shear forces from chronically elevated blood pressure cause stress on the arterial intia leading to damage

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25
Q

How does atherosclerosis lead to strokes and retinal infarctions?

A

Atherosclerosis casue cartoid plaques to occlude or embolize

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26
Q

How does cardiac ischemia develop?

A

Arterial plaque development leads to myocardial infarction when it occurs in the coronary arteries

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27
Q

Why do we see a decline in kidney function in patients with hypertension?

A

high pressure on the glomerulus and arterioles cuase kidney injury (hypertensive nephrosclerosis), leading to a decline in kidney function

28
Q

What is the mechanism of action of ACE inhibitors?

A

prevent the production of angiotensin II

leads to decrease in vascular tone, reducing afterload

29
Q

What is the mechanism of action of angiotensin receptor blockers?

A

block the receptors for angiotensin II

30
Q

Which organ do the angiotensin agents have a protective effect on?

ACE inhibitors and ARB’s

(-pril) and (-sartan)

A

kidney

31
Q

Which angiotensin agents are associated with better outcomes for myocardial infarction?

including reducing recurrence

A

ACE inhibitors

32
Q

How do beta blockers lower blood pressure?

A

They block the effects of sympathetic stimulation on renin production by the kidney to reduce vascular tone to lower blood pressure

33
Q

When do we need to use caution in prescribing topical beta-blockers?

A

when the patient is already on oral beta-blockers; or if the patient has baseline bradycardia, atrial fibrillation, lung disease or diabetes

diabetes is due to hypoglycemia unawareness

34
Q
A
35
Q

What are the ocular side effects of beta blockers?

A

dry eyes, diplopia, visual hallucinations, worsen ocular myasthenia

36
Q

How do calcium channel blockers work to lower blood pressure?

A

by inhibiting arterial contraction

37
Q

Which diuretics are most commony used for hypertension?

A

thiazides

38
Q

What other pharmaceuticals are commonly combined with diuretics?

A

ACE inhibitors, ARBs and beta-blockers can be found combined in a single pill with diuretics

39
Q

4 examples of loop diuretics

A
  1. furosemide
  2. bumetanide
  3. torsemide
  4. ethacrynic acid
40
Q

What is the patient profile for a central artery occlusion?

A

men>women in 6th decade of life

41
Q

What causes a central artery occlusion?

A

ateriosclerotic paque lodging at the level of the lamina cribrosa or at its posterior aspect

42
Q

What are the 3 types of emboli?

A
  1. cholesterol (74%)
  2. calcific (10.5%)
  3. platelet-fibrin (15.5%)
43
Q

What are the systemic associations with central artery occlusion?

A
  • diabetes mellitus
  • arterial hypertension
  • heart disease
  • renal disease
  • cerebrovascular accients
  • history of amaurosis fugax or TIAs
  • smoking
44
Q

What are the symptoms associated with central artery occlusion?

A
  • sudden onset severe (CF to LP), painless vision loss or visual field defect
  • typically unilateral
45
Q

What are the clinical signs of central artery occlusion?

A
  • presence of RAPD
  • Optic nerve edema and pallor
  • Thickened inner retina with increased reflectivity
  • decreased reflectivity of outer retina
  • cherry red spot (not seen in chronic)
  • Vessel attenuation and crossing changes
  • embolus
  • retinal hemorrhage not characteristic in acute cases
46
Q

What are the differentials for central artery occlusion?

A
  • commotio retinae
  • ophthalmic artery occlusion
  • necrotizing retinitis
  • r/o giant cell arteritis (older patients)
47
Q

Prognosis of central artery occlusion?

A
  • permanent vision loss (retinal damage occurs 90-120 minutes after complete occlusion)
  • RAPD, optic nerve pallor, attenuated vessels and retinal thinning typically persist (thinning- chronicity)
  • central vision spared in 10-20% of cases due to presence of cilioretinal artery
48
Q

What disorder is a chronic autoimmune, inflammatory condition that affects medium and large sized arteries of the aortic arch and its branches?

A

Giant cell arteritis

primarily affects the internal elastic lamina of blood vessels

49
Q

How does vessel occlusion occur in GCA?

A

inflammatory mediators cause proliferation, thickening and fibrosis of the walls of the affected arteries

occluded arterial wall is often infiltrated by lymphocytes, plasma cells and multinucleated giant cells

50
Q

What happens if treatment for GCA is not initiated immediately?

A

more than 70% will lose vision in the contralateral eye within 1 week

51
Q

What conditions can GCA lead to?

A
  1. AAION
  2. CRAO
  3. Amaurosis fugax
  4. diplopia
52
Q

What condition is a vascular optic nerve disease, but is not inflammatory?

Characterized by poor perfusion in the posterior ciiary circulation to the optic nerve secondary to either transient drop in mean blood pressure OR sharp rise in IOP and arteriosclerosis or thromboembolic event (very rare)

A

NAION

53
Q

What are the risk factors for NAION?

A
  • small cup with crowded disc (disc at risk)
  • hypertension
  • diabetes
  • hypercholesterolemia
  • cerebrovascular disease
  • nocturnal arterial hypotension
  • migraine or other vasospastic disorders
  • increased blood viscosity (polycythemia, thrombocytopenia, sickle cell anemia)
  • obstructive sleep apnea syndrome
  • phosphodiesterase type 5 drugs
54
Q

Ocular Perfusion Pressure (OPP) equation

A

OPP = BP-IOP

BP is mean arterial pressure, diastolic BP, or systolic BP

55
Q

What does mean perfusion pressure best reflect?

A

mean perfusion pressure

56
Q

What is the main clinical sign of NAION?

A

wake up with unilateral vision loss

other signs and symptoms: dyschromatopsia proportionate to vision loss, presence of RAPD, inferior altitudinal, inferior nasal, or cecocentral visual defects

57
Q

Acute NAION signs

A
  • Optic disc edema (sectoral or total)
  • small flame-shaped hemorrhages
  • juxtopapillary arteriolar attenuation and sheathing
  • prelaminar capillary telangiectasia
  • small cup in same/ fellow eye
58
Q

Chronic NAION signs/ symptoms

A
  • optic disc edema resolves over several weeks
  • optic atrophy will appear rapidly (within one months) with RNFL loss on OCT
  • ateriolar attenuation at disc margin
  • no cupping changes
59
Q

What conditions should be ruled out when NAION is suspected?

A

AAION, normal tension glaucoma, optic neuritis

60
Q

What testing should be done when diagnosing NAION?

A

CBC with diff, plasma glucose, serum lipid profile, ESR, CRP, OCT, FA, MRI, OCTA

61
Q

What is the treatment for NAION?

A

none

62
Q

Ocular Ischemic Syndrome average age?

A

65; rarely seen younger than 50

63
Q

What leads to ocular hypoperfusion in ocular ischemic syndrome?

A

90% stenosis of the ipsilateral ICA

64
Q

Systemic associations of ocular ischemic syndrome

A
  • atherosclerotic disease
  • Behcet’s disease
  • GCA
  • Aortic arch syndrome
  • Takayasu arteritis
  • Carotid artery dissecting aneurysm
  • Fibrovascular dysplasia
65
Q

What are the risk factors for OIS?

A
  • laterality and degree of stenosis
  • absence or presence of collaterals
  • associated systemic vascular diseases
  • chronicity of carotid artery disease
66
Q

What is the triad for ocular ischeic syndrome?

A
  1. midperipheral dot hemes
  2. dilated non-tortuous retinal veins
  3. iris neovasculariation
67
Q

What are the signs and symptoms of ocular ischemic syndrome?

A
  • gradual vision loss over weeks to months
  • abrupt vision loss d/t severe hypoperfusion of the retinal artery system
  • amaurosis fugax
  • ocular or periocular pain (suspected to be due to anterior segment ischemia)

Evidence Based Medicine (4 decks)

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