CVD 1 Flashcards

1
Q

pathophysiological events of atherosclerosis:
inflammation and activation of __ cells
__ deposition and modification (__ cell formation)

A

pathophysiological events of atherosclerosis:
inflammation and activation of endothelial cells
lipoprotein deposition and modification (foam cell formation)

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2
Q

pathophysiological events of atherosclerosis:
__ formation, __ core, thrombosis, and __
precipitation of __ events

A

pathophysiological events of atherosclerosis:
plaque formation, necrotic core, thrombosis, and remodeling
precipitation of acute events

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3
Q

when do atherosclerosis symptoms arise

A

only once the artery is severely blocked

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4
Q

when do atherosclerosis warning signs appear

A

sometimes days or weeks before a medical emergency

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5
Q

3 types of atherosclerosis symtpoms

A

neurological
pulmonary
cardiological

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6
Q

neurological symptoms of atherosclerosis

A

dizziness and fatigue

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7
Q

pulmonary symptoms of atherosclerosis

A

shortness of breath

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8
Q

cardiological symptoms of atherosclerosis

A

chest discomfort/pain

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9
Q

symptoms of stroke

A
  • Sudden numbness or weakness in face, arms, or legs (especially on one side of body)
  • Sudden trouble speaking or understanding others
  • Slurred or confused speech
  • Trouble seeing in one or both eyes
  • Severe dizziness or loss of balance
  • Trouble walking
  • Sudden and severe headache
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10
Q

symtpoms of stroke are typically located

A

only in one side of the body

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11
Q

symptoms of heart attack

A
  • Chest pain (mild discomfort or severe, crushing pain)
  • Pain in one or both arms or shoulders
  • Discomfort in neck or jaw
  • Nausea or vomiting
  • Heart palpitations
  • Anxiety or a feeling of “impending doom”
  • Sweating, dizziness, and/or fainting
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12
Q

what symptom can be both stroke and heart attack

A

dizziness

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13
Q

__ is causal of atherosclerosis

A

LDL is causal of atherosclerosis

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14
Q

3 steps of atherosclerosis

A
  1. initiation
  2. progression
  3. rupture
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15
Q

initiation:
__ dysfunction
atherogenic __ deposition
__ conditions
Injury/cell death, glycocalyx degradation, hyperpermeability, leukocyte adhesion

A

initiation:
endothelial dysfunction
atherogenic lipid deposition
proinflammatory conditions
Injury/cell death, glycocalyx degradation, hyperpermeability, leukocyte adhesion

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16
Q

progression:
__
formation of __
__ and necrotic cores

A

progression:
vasoconstriction
formation of fatty streak
plaques and necrotic cores

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17
Q

rupture:
impaired __
__ Atherothrombosis
intraplaque __/__

A

rupture:
impaired inflammation
resolution Atherothrombosis
intraplaque hemorrhage/neoangiogenesis

18
Q

immune system LDL steps

A
  1. cytokines oxidize LDL particles
  2. oxidized LDL particles are internalized by macrophages –> become foam cells
19
Q

3 steps of foam cell formation

A

capture
rolling
penetration

20
Q

foam cell formation: capture
__ capture by E-Selectins

A

foam cell formation: capture
leukocytes capture by E-Selectins

21
Q

foam cell formation: rolling
__ rolling, activation of __, adhesion to __
this all increases endothelial __

A

foam cell formation: rolling
leukocyte rolling, activation of chemokines, adhesion to endothelial cells
this all increases endothelial permeability

22
Q

foam cell formation: penetration
__ penetrates arterial intima

A

foam cell formation: penetration
monocyte penetrates arterial intima

23
Q

final step of foam cell formation
monocyte uptakes __ molecules via __ receptors and forms __ on __ wall

A

final step of foam cell formation
monocyte uptakes LDL molecules via scavenger receptors and forms plaque on arterial wall

24
Q

pathways that activate __ expression affect atherosclerosis by __ inflammation

A

pathways that activate NF-kB expression affect atherosclerosis by increasing inflammation

25
characteristics of vulnerable plaques
thickening and accumulation of lipids and foam cells --> rupture
26
4 therapeutic options to treat atherosclerosis
1. environmental factor modification 2. drug therapy 3. clinical intervention 4. gene therapy
27
environmental modification to treat atherosclerosis
1. smoking cessation 2. weight management 3. physical activity interventions
28
drug therapy for atherosclerosis
1. HMG-CoA reductase inhibitors 2. Ezetimbe 3. Fibrates 4. Anti-hypertensive agents 5. Anti-hyperglycemic agents
29
clinical interventions for atherosclerosis
1. intra-arterial catheterization balloon angioplasty 2. stenting 3. operation
30
gene therapy for atherosclerosis
1. genetic manipulation of scavenger receptors by delivering a transgene or gene blockade 2. EX: decoy oligonucleotides, siRNA
31
n-6 FA __ inflammation n-3 FA __ inflammation
n-6 FA **increase** inflammation n-3 FA **decrease** inflammation
32
general benefits of n-3 FA
1. inflammation 2. metabolic syndrome 3. some cancers 4. pregnancy 5. brain and CNS 6. CVD
33
n-3 FA help inflammation by improving __ function
n-3 FA help inflammation by improving **immune** function
34
n-3 FA help metabolic syndrome by improving __
n-3 FA help metabolic syndrome by improving **insulin sensitivity**
35
n-3 FAs help cancer by limiting __ and causing a better response to __
n-3 FAs help cancer by limiting **tumor growth** and causing a better response to **chemotherapy**
36
n-3 FA in CVD helps (3)
1. BP 2. plasma lipids 3. vascular/cardiac function
37
n-3 FA in atherosclerosis decreased arterial __ deposition decreased __ cytokines decreased __ cells increased __ __ mediators
n-3 FA in atherosclerosis decreased arterial **lipid** deposition decreased **pro-inflammatory** cytokines decreased **pro-inflammatory** cells increased **anti-inflammatory** **lipid** mediators
38
pro-inflammtory cytokines reduced by n-3 FA
monocytes macrophages dendritic cells (DC)
39
increased anti-inflammatory lipid mediators by n-3 FA
eicosanoids resolvins protectins
40
decreased arterial lipid depositon by n-3 FA
arterial LpL arterial macrophages
41
decreased pro-inflammatory cells
activation endothelium NE/MO recruitment DC maturation