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Integrative Nutrition and Pathophysiology > CVD 1 > Flashcards

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
Q

characteristics of vulnerable plaques

A

thickening and accumulation of lipids and foam cells –> rupture

26
Q

4 therapeutic options to treat atherosclerosis

A
  1. environmental factor modification
  2. drug therapy
  3. clinical intervention
  4. gene therapy
27
Q

environmental modification to treat atherosclerosis

A
  1. smoking cessation
  2. weight management
  3. physical activity interventions
28
Q

drug therapy for atherosclerosis

A
  1. HMG-CoA reductase inhibitors
  2. Ezetimbe
  3. Fibrates
  4. Anti-hypertensive agents
  5. Anti-hyperglycemic agents
29
Q

clinical interventions for atherosclerosis

A
  1. intra-arterial catheterization balloon angioplasty
  2. stenting
  3. operation
30
Q

gene therapy for atherosclerosis

A
  1. genetic manipulation of scavenger receptors by delivering a transgene or gene blockade
  2. EX: decoy oligonucleotides, siRNA
31
Q

n-6 FA __ inflammation
n-3 FA __ inflammation

A

n-6 FA increase inflammation
n-3 FA decrease inflammation

32
Q

general benefits of n-3 FA

A
  1. inflammation
  2. metabolic syndrome
  3. some cancers
  4. pregnancy
  5. brain and CNS
  6. CVD
33
Q

n-3 FA help inflammation by improving __ function

A

n-3 FA help inflammation by improving immune function

34
Q

n-3 FA help metabolic syndrome by improving __

A

n-3 FA help metabolic syndrome by improving insulin sensitivity

35
Q

n-3 FAs help cancer by limiting __ and causing a better response to __

A

n-3 FAs help cancer by limiting tumor growth and causing a better response to chemotherapy

36
Q

n-3 FA in CVD helps (3)

A
  1. BP
  2. plasma lipids
  3. vascular/cardiac function
37
Q

n-3 FA in atherosclerosis
decreased arterial __ deposition
decreased __ cytokines
decreased __ cells
increased __ __ mediators

A

n-3 FA in atherosclerosis
decreased arterial lipid deposition
decreased pro-inflammatory cytokines
decreased pro-inflammatory cells
increased anti-inflammatory lipid mediators

38
Q

pro-inflammtory cytokines reduced by n-3 FA

A

monocytes
macrophages
dendritic cells (DC)

39
Q

increased anti-inflammatory lipid mediators by n-3 FA

A

eicosanoids
resolvins
protectins

40
Q

decreased arterial lipid depositon by n-3 FA

A

arterial LpL
arterial macrophages

41
Q

decreased pro-inflammatory cells

A

activation endothelium
NE/MO recruitment
DC maturation

Integrative Nutrition and Pathophysiology (22 decks)

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