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PathoPhys > Tutorial 7 - VD, Ath. & case studies > Flashcards

Tutorial 7 - VD, Ath. & case studies Flashcards

1
Q

Main forms of CVD (cardiovascular disease) (2)

A
  1. Ischemia

2. Hemorrhagic stroke

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2
Q

Define aneurysm?

A

excessive localized swelling of an artery

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3
Q

Main consequences of vascular disease? (3)

A
  1. Chest pain
  2. myocardial infarction
  3. heart failure
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4
Q

myocardial infarction AKA?

A

heart attack

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5
Q

State the major, early symptom of cardiovascular dysfunction?

A

Snoring!

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6
Q

Explain ‘OSA’?

A

Obstructive Sleep Apnea:

  • occurs due to collapsed airway
  • causes loud snoring, breathing ceases periodically
  • linked to CVS disease
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7
Q

t/f: if someone snores - but is yet to develop OSA, they are not at any greater risk of CVD.

A

false - the risk for CVS disease begins with snoring, before it develops into CVD

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8
Q

define atherosclerosis?

A

build up of fat/ cholesterol/ etc. in arterial walls, occluding lumen

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9
Q

What is the first sign of carotid artery disease?

A

Intima-media thickness

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10
Q

State the main means of detection, and progress tracking of atherosclerotic disease?

A

Carotid intima-media thickness

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11
Q

How do snorers compare to non-snorers, in carotid intima-media thickness?

A

snorers thicker

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12
Q

How do patients with CVD risk factors (smoking, diabetes etc.) compare to patients without, in carotid intima-media thickness?

A

not statistically different

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13
Q

State the SBP & DBP of:

a hypotensive person

A

SBP - < 90

DBP - < 60

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14
Q

State the SBP & DBP of:

Normal person

A 
SBP = 90-119
DBP = 60-79
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15
Q

State the SBP & DBP of:

Prehypertension

A 
SBP = 120-139
DBP = 80-89
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16
Q

State the SBP & DBP of:

Stage 1 hypertension

A 
SBP = 140-159
DBP = 90-99
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17
Q

State the SBP & DBP of:

Stage 2 hypertension

A 
SBP = 160-179
DBP = 100-109
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18
Q

State the SBP & DBP of:

Hypertensive urgency

A 
SBP = ≥180 
DBP =  ≥110
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19
Q

State the SBP & DBP of:

Isolated systolic hypertension

A 
SBP = ≥160
DBP = <90
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20
Q

State the main effects of high blood pressure?

A
  1. Damages wall of arteries - creating microscopic tears which turn into scar tissue
  2. Damaged arteries accumulate material (scar tissue provides lodging place) - cholesterol, platelets, fats and plaque build up. As the plaque builds, arteries narrow and harden.
  3. HBP speeds up hardening of arteries
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21
Q

Oxygen extraction from blood in the coronaries:

a. ) Depends on NO secretion
b. ) is maximal and can be modified by endogenous material
c. ) is maximal and cannot be modified by endogenous material
d. ) is not maximal

A

c

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22
Q

Stenosis of a coronary tract becomes symptomatic:

a. ) When is more than 70% of section area
b. )

A

a

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23
Q

Myocardial oxygen extraction from blood at rest is:

a. ) is very low (20-30%)
b. ) quite low (40-50%)
c. ) near max (60-80%)
d. ) maximal (99-100%)

A

c

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24
Q

Damage due of hypoxia in the myocardium:

a. ) Start always in middle layer
b. ) start often in endocardial layer
c. ) start always from epicardial layer
d. ) start always in endocardial layers

A

d

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25
Q

Maximal blood perfusion is achieved in the heart wall:

a. ) during systole
b. ) during diastole
c. ) toward end of systole
d. ) toward end of diastole

A

d

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26
Q

Stroke volume in heart failure is by definition:

a. ) Increased
b. ) Decreased
c. ) Normal
d. ) Decreased only in pulmonary circulation

A

b

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27
Q

Impaired NO-mediated vasodilation occurs:

a. ) Only in high blood pressure patients
b. ) Only during heart attack
c. ) Only in diabetic patients in peripheral arteries and later on in coronaries
d. ) in several diseases such as arteriosclerosis, diabetes, and high blood pressure

A

d

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28
Q

Distributing arteries:

a. ) are the major target of arteriosclerosis
b. ) have a minimal layer of SM cells
c. ) have biggest layer of SM cells
d. ) have a thin wall

A

???

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29
Q

Sub-epicardial flow starts to decrease:

a. ) below mean coronary pressure of 35%
b. ) below mean coronary pressure of 45%
c. ) below mean coronary pressure of 25%
d. ) occurs across cardiac cycle irrespective MAP?

A

c

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30
Q

Sub-epicardial flow starts to decrease:

a. ) below mean coronary pressure of 35%
b. ) below mean coronary pressure of 45%
c. ) below mean coronary pressure of 25%
d. ) occurs across cardiac cycle irrespective MAP?

A

c

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31
Q

t/f: age causes hardening of arteries, irrespective of blood pressure

A

true (somewhat) - age does cause the hardening of arteries, but high blood pressure may accelerate this

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32
Q

Damaged arteries cause accumulation of plaque, hardening and narrowing.

a. ) What is the plaque composed of?
b. ) What pathologies may this give rise to?

A

a. ) Cholesterol, fats, platelets etc.

b. ) Peripheral artery disease, coronary artery disease

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33
Q

Mechanisms at play, following reduced exposure to CVD risk factors:

a. ) Oxidative stress?
b. ) NO availability?
c. ) Inflammatory processes?
d. ) Cyclic blood pressure?

A

a. ) Decreased; increased anti-oxidant defense
b. ) Increased
c. ) Decreased
d. ) Increased

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34
Q

Mechanisms at play, following reduced exposure to CVD risk factors:

a. ) Shear stress?
b. ) SNS activity?
c. ) Vascular tone?

A

a. ) Increased
b. ) Decreased
c. ) Decreased

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35
Q

Mechanisms at play, following increased exposure to CVD risk factors:

a. ) Oxidative stress?
b. ) NO availability?
c. ) Inflammatory processes?
d. ) Mean blood pressure?

A

a. ) Increased; more reactive O2 species
b. ) Decreased
c. ) Increased
d. ) Increased

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36
Q

Mechanisms at play, following increased exposure to CVD risk factors:

a. ) Shear stress?
b. ) SNS activity?
c. ) Vascular tone?

A

a. ) Decreased
b. ) Increased
c. ) Increased

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37
Q

Normal breaths per minute?

38
Q

Arteries are a ____ reservoir.

A

pressure reservoirs - this is why when the heart pumps out its SV, the arteries expand (temporarily storing the pressure) before contracting; thus maintaining the pressure

39
Q

Why are arteries considered a pressure reservoir?

A

As arteries are able to expand and recoil, due to elastic fibers in arterial wall

40
Q

What is systolic pressure?

according to MAURO

A

MAXIMUM pressure occurring during systole

41
Q

What is diastolic pressure?

A

Pressure occurring during diastole (not necessarily maximum)

42
Q

Stage 1 hypertension - does it call for drug administer?

43
Q

Does prehypertension call for drug administer?

A

No - monitor it over time, adapt in lifestyle hopefully

44
Q

t/f: atherosclerosis is an inflammatory disease

45
Q

Atherosclerosis:

a. ) Acute or chronic disease?
b. ) Is it deadly?
c. ) Occurs in veins or arteries? Of what size?

A

a. ) Chronic
b. ) Yes
c. ) Large arteries

46
Q

Not a question

Situation “John” is in assessment 3. Ensure to say that his BP must be monitored at least daily.

A

Not a question

Situation “John” is in assessment 3. Ensure to say that his BP must be monitored at least daily.

47
Q

Atherosclerosis:

a. ) Is a primary cause of what?
b. ) In westernized world, underlies _% of all deaths?

A

a. ) Heart disease, stroke

b. ) 50%

48
Q

CVD causes _% of all deaths in north america

49
Q

Best way to reduce BP?

A

Exercise; lose weight

50
Q

State the 4 main physiological complications of atherosclerosis, as developed chronologically?

A
  1. Endothelial dysfunction
  2. Fatty streak formation
  3. Advanced complicated lesion formation
  4. Unstable fibrous plaque formation
51
Q

State main risk factors for developing hypertension?

A
  1. Environmental - salt intake, tobacco, obesity, alcohol,
  2. Genetic
  3. Gene-environment Interaction - race, gender
52
Q

Explain how atherosclerosis begins (first main complication)?

A

Endothelial dysfunction:

  • increased permeability to lipoproteins/ other plasma constituents
  • migration of leukocytes into artery wall
53
Q

Endothelial dysfunction associated with atherosclerosis is partly characterized by increased permeability to lipoproteins and other plasma constituents. What mediates this?

A
  • NO
  • prostacyclin
  • PDGF
  • ANG II
  • endothelin
  • up-regulation of leukocyte adhesion molecules (L-selectin, integrins, platelet-endothelial-cell-adhesion-molecule-1, vascular-cell-adhesion-molecule-1)
54
Q

Endothelial dysfunction associated with atherosclerosis is partly characterized by migration of leukocytes into artery wall. What mediates this?

A
  • oxidized low-density lipoprotein
  • monocyte chemotactic protein 1
  • IL-8
  • PDGF
  • macrophage colony-stimulating factor
  • osteopontin
55
Q

The second stage of atherosclerosis is fatty-streak formation:

a. ) What do the fatty streaks initially consist of?
b. ) What are the fatty streaks later joined by?

A

a. ) Monocytes, macrophages and T lymphocytes (all lipid laden).
b. ) smooth muscle cells

56
Q

The second stage of atherosclerosis is fatty-streak formation:
What are the steps involved in this process?

A
  1. Smooth muscle cell migration
  2. T-cell activation
  3. Foam cell formation
  4. Platelet adherence and aggregation
57
Q

The second stage of atherosclerosis is fatty-streak formation:
What stimulates the first step in this stage?

A

Smooth muscle cell migration - stimulated by:

  • PDGF
  • Fibroblast Growth Factor 2
  • transforming growth factor b
58
Q

The second stage of atherosclerosis is fatty-streak formation:
What mediates the second step in this stage?

A

T cell activation - mediated by:

  • tumor necrosis factor A
  • IL-2
  • granulocyte-macrophage colony-stimulating factor
59
Q

The second stage of atherosclerosis is fatty-streak formation:
What mediates the third step in this stage?

A

Foam cell formation - mediated by:

  • tumor necrosis factor A
  • IL-1
  • macrophage colony-stimulating factor
  • oxidized low density lipoprotein
60
Q

The second stage of atherosclerosis is fatty-streak formation:
What stimulates the fourth step in this stage?

A

Platelet adherence and aggregation - stimulated by:

  • integrins
  • P-selectin
  • fibrin
  • thromboxane A2
  • tissue factor
61
Q

HDL are (protective/ unprotective), at (a certain range/ any amount).

A

HDL is protective; within a certain range

62
Q

Provide an explanation as to how the third stage of atherosclerosis takes place?

A

Formation of advanced, complicated lesions:

  1. fatty streak forms fibrous cap walling off lesion from lumen (healing/ fibrous response to injury)
  2. Leukocytes, lipid & debris contained within lesion may form necrotic core
  3. Lesion expands as mediating factors enter and more leukocytes/ macrophages adhere
63
Q

The third stage of atherosclerosis is formation of advanced, complicated lesions:
What factors stimulate macrophage accumulation?

A
  • macrophage colony-stimulating factor
  • monocyte chemotactic proteins 1
  • oxidized low density lipoprotein
64
Q

The necrotic core forming during atherosclerosis:

a. ) Forms during which stage & step of the disease?
b. ) Is the result of what?

A

a. ) Stage 3 (formation of advanced, complicated lesions). Step 2 of this stage (necrotic core formation).
b. ) Necrotic core is result of apoptosis, necrosis, increased proteolytic activity & lipid accumulation

65
Q

The fibrous cap forming during atherosclerosis:

a. ) Forms during which stage & step of the disease?
b. ) Is the result of what?

A

a. ) Stage 3 (formation of advanced, complicated lesions). Step 1 of this stage (fibrous cap formation).
b. ) Fibrous cap is result of:
- increased activity in PDGF, transforming growth factor b, IL-1, tumor necrosis factor a, osteopontin
- decreased CT degradation

66
Q

The fourth stage of atherosclerosis is unstable fibrous plaque formation:
Describe the steps involved in this stage?

A
  1. The rupture/ ulceration of the fibrous cap at areas where it is thinning
  2. This leads to thrombus formation
67
Q

The fourth stage of atherosclerosis is unstable fibrous plaque formation:
Why does the fibrous cap thin in this fourth stage, and what are other complications as a result?

A
  1. Continued influx and activation of macrophages, leading to release of:
    - metalloprotinases
    - other proteolytic enzymes
  2. These enzymes cause degradation of matrix
  3. Degradation of matrix leads to hemorrhage from vasa vasorum/ lumen of artery
  4. This can result in thrombus formation and occulsion of artery
68
Q

State triggers (risk factors) for atherosclerosis?

A
  1. Hemodynamic forces and vortices (turbulent flow)
  2. High blood pressure
  3. Fat and cholesterol levels in blood
  4. Genetic background (LDL, HDL, platelet reactivity)
  5. Specific microbes (Chlamydia pneumoniae, CMV)
  6. Microbiota in the gut (TMAO)
69
Q

How may the following factor(s) change to INCREASE risk of atherosclerosis:
LDL/ HDL levels

A

LDL - increased

HDL - decreased

70
Q

How may the following factor(s) change to INCREASE risk of atherosclerosis: blood pressure

71
Q

How may the following factor(s) change to INCREASE risk of atherosclerosis: fat and cholesterol levels

72
Q

How may the following factor(s) change to INCREASE risk of atherosclerosis: gender and age

A

male, risk increases at 45 for men and 60 for female

73
Q

t/f: most trigger mechanisms for atherosclerosis are self-maintained, and do not expand over time

A

false - trigger mechanisms for athersclerosis are self maintained but expand over time

74
Q

what is the largest ‘characterizable factor’ of athersclerosis - what’s the biggest risk factor?

A

LDL levels (if high = bad bad)

75
Q

Effectors of atherosclerosis - what cells?

A
  • smooth muscle cells
  • endothelial cells
  • macrophages
  • T cells (CD4, CD8, Th17)
  • platelets
76
Q

Effectors of atherosclerosis - what soluble mediators?

A
  • NO
  • ANG II
  • IL-1, 8
  • PDGF
  • CD40L, Gamma-interferon, osteopontin, MMP, MCP-1
77
Q

what is the ‘critical point’ in atherosclerosis mechanism?

A

fibrous capsule rupture

78
Q

platelet reactivity is a critical factor in the (beginning/ middle/ late) stage of athersclerosis

A

middle to late

79
Q

what causes the fibrous caps of lesions formed during atherosclerosis to become thin and vulnerable?

A
  1. proteinases - collagenases, gelatinases, stromolysin

2. inhibition of matrix secretion

80
Q

How may the following factor(s) change to INCREASE risk of atherosclerosis: infection.

How does this occur?

A

Increased infection increases atherosclerosis.

Infection causes:

  1. systemic effects - induction of acute phase proteins
  2. local effects - increased tissue factor expression, decreased plasminogen activator (PA)
81
Q

Actions of fibrinogen?

A

Increased…

  1. endothelial permeability
  2. monocyte transmigration
  3. LDL accumulation
  4. platelet reactivity
  5. inflammation
82
Q

Define Pleiotropic?

A

producing multiple effects from a single gene

83
Q

What is the “biological modifier” of atherosclerosis?

A

Platelet activation - this is a plieotropic effector mechanism

84
Q

how do platelets and their activation effect atherosclerosis?

A

platelets release inflammatory and mitogenic substances into the microenvironment - altering proteolytic, chemotactic and ADHESIVE properties of endothelium

85
Q

t/f: platelet inhibition and/or modulation is a means of controlling atherosclerotic events in the late stages

86
Q

what are “foam cells”, and how do they relate to atherosclerosis?

A

foam cells are macrophages which localize to fatty deposits on BV walls, they ingest LDL here and become laden with lipids giving them a foamy appearance

they are an important step in fatty-streak formation

87
Q

what is TMAO?

A

Trimethylamine N-oxide:

  • gut microbiota-derived metabolite
  • microbiome produces it when eat choline (meat, egg, fish etc.)
  • makes resting platelets become hyper-reactive and enhances atherosclerosis (increases thrombus formation)
88
Q

arteriosclerosis vs atherosclerosis?

A

Both involve impeded BF in arteries - atherosclerosis is a type of arteriosclerosis, which occurs due to fatty deposit.

arteriosclerosis - thickening, hardening and loss of elasticity in artery walls
atherosclerosis - build up of fats/ cholesterol and other substances which can impede blood flow

89
Q

how may a diet high in red meat, poultry and other choline rich food affect atherosclerosis and why?

A

these foods contain choline which results in TMAO formation (microbiome), which increases platelet responsiveness and thrombus formation - increasing risk of atherosclerosis

90
Q

how are platelets effected by TMAO - why is it they become hyperreactive?

A
  • increases thrombin, ADP, collagen levels

- stimulates release of intracellular Ca+2

91
Q

what do gut microorganisms turn choline into?

A

TMA, which is then converted to TMAO in the liver (trick question TMA)

92
Q

what main complication may arise from chronic atherosclerosis?

A

cardiovascular problems - myocardial infarction

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