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Final year semester 2 exam > cardiovascular > Flashcards

cardiovascular Flashcards

1
Q

Name the three layers of a typical blood vessel

A
  1. Tunica intima
  2. Tunica media
  3. Tunica adventitia
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2
Q

Which layer of a blood vessel will you find the endothelial cells?

A

Tunica intima

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3
Q

What is the tunica media made of? (type of muscle and including what else)

A

Made up of smooth muscle, with elastic and collagen

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4
Q

What kind of fibres are found on the tunica adventitia?

A

Sympathetic fibres

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5
Q

Why do we have tight junctions in the endothelium?

A

To allow the crossing of small molecules and water, but holding plasma and blood cells within the vessel

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6
Q

Which blood vessel layer creates nitric oxide?

A

Endothelium

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7
Q

What are the jobs of the glycocalyx?

A
  • to sense sheer blood stress against the walls of the vessel
  • lubricates the red blood calls as they prepare to go into a single file and cross the capillary
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8
Q

Name 2 condition that can damage the glycocalyx, and which disease does this start?

A
  • insulin resistance
  • inflammation
  • start of atherosclerosis
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9
Q

Name 3 key functions of the endothelium

A
  • Semi-permeable barrier (fluid balance, selective movement of substrates)
  • Homeostasis
  • Immune defense
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10
Q

What are 3 roles of nitric oxide in the cardiovascular system

A
  • Inhibits leukocyte adhesion
  • Apposes oxidation of LDLs
  • Regulates vascular tone
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11
Q

Where is nitric oxide secreted

A

The endothelium

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12
Q

What do PPAR’s do to HDL and triglycerides?

A

HDL - increase
triglycerides - decrease

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13
Q

What 2 places can we find PPAR’s?

A

In the cardiac tissue and in BAT (brown adipose tissue)

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14
Q

Which condition can PPAR gamma improve?

A

Insulin resistance

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15
Q

name 3 CVD risk factors

A
  • genetics
  • family history
  • ethnicity
  • gender
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16
Q

Why is elevated homocysteine a CVD risk factor?

A
  • associated with LDL oxidation
  • monocyte disfunction
  • causes endothelium disfunction
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17
Q

What can cause high homocysteine levels?

A
  • low B12 and folate (needed for remethylation of homocysteine to methionine)
  • ## genetic polymorphism (MTHFR)
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18
Q

How is nitric oxide generated?

A

from L-arginine via the enzyme eNOS (endothelial nitric oxide synthase)

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19
Q

What does PPAR stand for

A

Peroxisome proliferator-activated receptor

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20
Q

What do PPARs do?

A
  • decrease inflammation
  • promote ED health
  • balances lipid profile
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21
Q

How do PPARs balance lipid profiles?

A
  • enhances HDL
  • lowers triglycerides
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22
Q

How can you naturally enhance PPARs

A
  • green tea
  • oregano
  • thyme
  • roesmary
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23
Q

Name 3 genes that can cause cardio vascular disease if they have a SNP

A
  • MTHFR
  • NOS3
  • MnSOD
  • ACE
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24
Q

What does elevated Endothelin-1 (ET-1) lead to?

A

vasoconstriction leading to high BP

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25
Q

What are some CV symptoms of high Leptin?

A
  • high heart rate
  • high BP
  • Sodium retention
  • vasoconstriction of vessels
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26
Q

The thickness of which layers of the heart are directly impacted by insulin resistance?

A

Tunica media and tunica intima

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27
Q

Name some risk factors for cardiovascular disease

A
  • Dyslipidaemia
  • Family history
  • Genetics
  • Gender
  • Hypertension
  • Mitochondrial dysfunction
  • Elevated homeocystine
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28
Q

Which SNP is associated to CVD and how?

A
  • MTHFR: impacts supply of methyl groups
    needed to methylate B12 in the methionine cycle
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29
Q

How is obesity linked to CVD?

A
  • Inflammation is linked with ↑ endothelin-1 (ET-1),
    a potent vasoconstrictor peptide. Elevated ET-1
    leads to fibrosis of VSMCs and ↑ ROS.
  • Adiponectin is decreased in obesity.
  • Adiponectin also ↑ insulin sensitivity, thus low
    levels contribute to insulin resistance.
  • Obesity is associated with high levels of leptin, which activates the
    SNS causing sodium retention, vasoconstriction & ↑ blood pressure.
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30
Q

How does insulin resistance cause CVD?

A

Generates chronic hyperglycaemia
leading to oxidative stress, inflammation and cellular damage.

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31
Q

Explain Advanced glycation end products (AGEs)

A

Harmful compounds
formed when protein or lipids becomes glycated after exposure to glucose.

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32
Q

In which 2 ways to AGEs exert their effects?

A

Receptor mediated: Bind to the RAGE receptor on cells (like endothelial cells, smooth muscle cells, and immune cells), leading to increased inflammatory cytokines and ROS

Non- receptor mediated: Increased EC matrix synthesis, trapping
ED LDL and cross binding with collagen (vascular stiffening).

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33
Q

What do AGEs lead to?

A

oxidative stress, vascular ED and immune cell dysfunction.

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34
Q

Name some causes of AGEs:

A
  • Highly refined carbs, processed foods, meat and dairy
  • High heat, grilling, roasting,
    searing / frying
  • Smoking and sedentary lifestyles
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35
Q

Alterations in the gut microbiota cause what leading to CVD?

A
  • increase in harmful metabolites such as trimethylamine-N-oxide (TMAO).
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36
Q

What is TMAO associated with in the ED?

A

TMAO is
associated with endothelial dysfunction and increased risk of CVD

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37
Q

Why is PRAL a dietary consideration in CV disease

A

Foods rich in protein (meat and cheese) may induce low grade metabolic acidosis

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38
Q

Why are trans fats a dietary consideration in CV disease

A
  • promote dyslipidaemia (high LDL and TGS, low HDL)
  • increase inflammation, contribute to ED disfunction
    -encourage visceral adiposity and increase risk of IR
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39
Q

Why is fructose a dietary consideration in CV disease

A
  • increase risk of de novo lypogenesis
  • increase fatty acids (palmitic acid)
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40
Q

Which nutritional defiencies are a dietary consideration in CV disease

A
  • vitamin C
  • D
  • E
  • CoQ10
  • Mg
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41
Q

Why is increased palmitic acid a risk for CV disease

A

it’s a major driver of atherosclerosis and coronary artery disease

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42
Q

Explain the cardiac risk tools (CV test)

A

calculate score based
on CV risks e.g., age, BMI, smoking.

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43
Q

Explain cardiac troponin (CV test)

A

Cardiac troponin proteins hs-cTnT and hs-cTnI are released into the blood when heart muscle is damaged

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44
Q

Explain Lp-PLA 2 (CV test)

A

Enzyme produced by monocytes, macrophages, T-cells. Upregulated in atherosclerotic plaques and vascular inflammation.

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45
Q

Explain hsCRP (CV test)

A

Inhibits NO and e-NOS and is involved in plaque deposition.

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46
Q

Explain MPO (CV test)

A

Released by macrophages and measures the body’s response to damaged arterial walls. High MPO is associated with inflammation / oxidative stress and a poor prognosis.

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47
Q

Which diet is associated with CVD

A

Plant based and Mediterranean diet

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48
Q

Why is the mediterranean diet helpful with CVD

A
  • lowers inflammatory mediators
  • reduces adiposity
  • reduces risk of thrombosis
  • increased SCFAs
  • improved insulin sensitivity
  • increased adiponectin
  • improved ED function
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49
Q

how does vitamin C promote CV health

A
  • down regulates NADPH oxidase
  • up regulated endothelial nitric oxide synthesis
  • lowers tendency for platelet aggregation
50
Q

how does vitamin E promote CV health

A
  • Mixed tocotrienols and tocopherols plus vitamin C will protect the endothelium from NOS and support NO synthesis
  • reduces oxidation of LDL
  • anti-thrombotic
51
Q

how does vitamin D promote CV health

A
  • modulates the production of NO
  • Modulates RAAS system (BP control)
  • anti-inflammatory
52
Q

how do omega-3 fatty acids promote CV health

A
  • improve lipid and lipoprotein profiles
  • EPA and DHA are anti-inflammatory
  • DHA supports membrane fluidity
53
Q

how does magnesium promote CV health

A
  • vasodilator
  • regulates iron transporters
  • reduces platelet aggregation
  • helps regulate vascular tone and stabilise heart rhythm
54
Q

how does CoQ10 promote CV health

A
  • needed for ATP production
  • supports mitochondrial health
  • major antioxidant
  • reduces oxidation of LDL
  • increases levels of superoxide dismutase which preserves activity of NO
55
Q

how does Hawthorne promote CV health

A
  • natural ace inhibitor
  • natural diuretic
  • natural beta-blocker
  • Antioxidant
  • improves BP
  • Inhibits vasoconstrictive endothelin-1
  • increases NO
56
Q

how does garlic promote CV health

A
  • antioxidant
  • anti-hypertensive by promoting NO in endothelium
  • lowers homocystine
  • regulated lipid profile
  • anti-platelet effect
  • enhances SOD and glutathione
57
Q

What is lipoprotein A?

A

A form of LDL with a high risk of clotting

58
Q

why is linoleic acid (LA) a problem in CV disease?

A
  • easily oxidised, causing it to be easier for LDL to cross into the endothelium, causing atherosclerosis.
59
Q

How do you reduce LA?

A
  • reduce intake of high LA vegetable oils (replacing some vegetable oil with saturated fat)
60
Q

How does exercise protect us from CVD

A
  • improves lipid profile (lowers triglycerides)
  • improves insulin sensitivity and insulin signalling in the ED
  • lowers resting BP
61
Q

Nutrient depletions: Statins

A

CoQ10 synthesis

62
Q

Nutrient depletions: Cholestrymine

A
  • lowers cholesterol: fat soluble vitamins and beta-carotene
63
Q

Nutrient depletions: diuretics

A
  • increase excretion of potassium, calcium, thiamine (B1 = heart failure) and zinc
  • drive T2DB
64
Q

Nutrient depletions: ACE inhibitors

A
  • binds with zinc preventing utilisation (major anti-inflammatory and gut integrity)
65
Q

Nutrient depletions: Beta blockers

A
  • causes fatigue, nightmares from melatonin deficiency
  • decreases CoQ10 production
66
Q

Nutrient depletions: PPI

A
  • depletes B12, Mg
67
Q

Hypertension symptoms:

A

fatigue, dizziness, headaches, visual disturbances

68
Q

define systolic BP

A

pressure of blood on arterial walls during heart compression

69
Q

define diastolic BP

A

force of blood when the heart relaces

70
Q

What is the UK definition of hypertension:

A

140/90 mmHg minimum (naturopathically, 110-115 and above is indicative)

71
Q

Hypertension risk factors

A
  • genetic
  • obesity
  • alcohol
  • stress
  • nutritional deficiencies (Mg, K)
  • high table salt
  • inactivity
  • drugs
  • smoking (NSAIDS, corticosteriods)
72
Q

How will increasing potassium lower hypertension:

A
  • increase NO leading to vasodilation
  • increases sodium excretion
  • reduces sensitivity to the vasoconstrictor angiotensin 2
  • antioxidant and anti-inflammatory
73
Q

What does the DASH diet include?

A

fruit and veg, grains, low fat or no fat dairy foods, lean meat and fish, nuts seeds and beans and fats and oils.

74
Q

what are the limitations of the DASH diet

A

potential high levels of fructose from hydrogianted fats, vegetable oils

75
Q

Name some supplements for hypertension

A
  • vitamin D
  • L-argenine
  • Magnesium
  • B6
76
Q

How can the glucocalyx be damaged?

A
  • inflammation
  • oxidised LDL
  • oxidative stress
  • hyperglycaemia
  • endotoxaemia
77
Q

What are inflammasomes?

A

macrophages in the subendothelial space that release inflammatory cytokines and activate IL-6

78
Q

what are some ways to prevent atherosclerosis?

A
  • low intake of saturated fats
  • increase omega-3 (avocado and EVOO)
  • red yeast rice
  • increase dietary fibre
  • Hawthorne berries
  • Beetroot
  • blueberries
  • L-theanine
79
Q

How do you reduce homocytine?

A

increase B6 B12 and folate, and trimethylglycine.

80
Q

How do you reduce fibrinogen levels?

A

Mediterranian diet, and garlic. Also exercise.

81
Q

How does L-citrulline prevent/manage atherosclerosis?

A

L-citrulline is converted to arginine, which NO is synthesised from via eNOS. Arginine is involved in lowering BP in the kidneys.

82
Q

How does B3 prevent/manage atherosclerosis?

A
  • reduces LDL, LDL-P, TGs, VLDL.
  • can also decrease fibrinogen
83
Q

How does B5 prevent/manage atherosclerosis?

A
  • Increasing HDL
84
Q

How does omega-3 prevent/manage atherosclerosis?

A
  • anti-inflammatory
  • anti-thrombotic
  • lowers BP
  • lowers heart rate
  • lowers IR
85
Q

How does pomegranet prevent/manage atherosclerosis?

A
  • powerful antioxidant
  • reduces levels of oxidised LDL
  • improves HDL function
  • reduces macrophages ability to uptake oxidised LDL (as this carries on to create foam cells)
  • reverses cholesterol transport
86
Q

How does pine bark extract prevent/manage atherosclerosis?

A
  • anti-inflammatory
  • antioxidant
  • falvonoid
  • anti-thrombotic
  • Enhances NO and ED function
87
Q

What is myeloperoxidase (cardiovascular inflammatory marker)?

A

An enzyme secreted from macrophage cells that increases oxidation of lipoproteins

88
Q

How does lycopene prevent/manage atherosclerosis?

A
  • It suppresses intestinal cholesterol absorption
  • powerful antioxidant
  • decreases LDL
  • increases HDL
89
Q

Name some practical strategies for CVD and HTN

A
  • sauna
  • dry skin brushing
  • stress management
  • exercise
  • yoga
  • acupuncture
90
Q

what is the main cause of ischaemic heart disease

A

atherosclerosis

91
Q

define ischaemic heart disease

A

an imbalance between myocardial oxygen supply and demand, associated with inadequate arterial supply via the coronary arteries

92
Q

define angina

A

chest pain caused by insufficient blood supply to the myocardium via coronary arteries

93
Q

What’s the difference between stable and unstable Angina?

A

Stable: predictable chest pain, symptoms resolved once oxygen levels are stable
Unstable: Unpredictable, pain occurs at rest. More sever and serious.

94
Q

Angina symptoms

A
  • SOB
  • constricting chest pains (neck, L shoulder arm and jaw)
  • worsened by exertion, relieved at rest
  • sweating
  • nausea
95
Q

Angina risk factors

A
  • smoking
  • vitamin D deficiency
  • family history
96
Q

Allopathic diagnosis tests for angina

A
  • ECG
  • cardiac stress test
  • angiogram
97
Q

what are some medications prescribed for angina?

A
  • nitrates
  • calcium channel blockers
  • beta blockers
98
Q

define a myocardial infarction

A

Acute blockage of the coronary artery usually due to a thrombus, resulting in death of myocardial tissue

99
Q

What enzymes do ischaemic myocardial cells release?

A

adenosine and lactate, into nerve endings causing pain

100
Q

What is the main risk of a MI?

A

prolonged ischaemia causing myocardial necrosis, leading to scar tissue, causing the heart to grow in size leading to lowered efficiency. This can lead to heart failure.

101
Q

MI risk factors:

A
  • sex
  • physical factors such as stress, sudden life events
  • drug induced (cocaine)
  • severe hypotension
  • severe anaemia
102
Q

What is the potential link with males being more likely to have a MI

A

low testosterone

103
Q

Complications of a MI

A
  • arrhythmia
  • death
  • heart failure
  • cardiogenic shock; rapid reduction in blood flow to rest of the body, leading to multiple organ failure (rare)
104
Q

name some naturopathic approaches to IHD

A
  • vitamin D status
  • warming herbs and spices to aid blood flow (cayenne, ginger)
  • increasing movement
  • address stress
105
Q

How is L-carnitine a natural approach to IHD

A
  • improves utilisation of fatty acids (hearts main source of energy)
  • shuttles out toxins from mitochondria
  • major antioxidant
106
Q

How is Magnesium a natural approach to IHD

A

Mg deficiency has been shown to cause coronary artery spasms. It also controls movement of calcium into smooth muscle cells leading to smooth muscle contraction

107
Q

How is CoQ10 a natural approach to IHD

A
  • increases ENOS and NO
  • stabliser of calcium ion channels
  • increases inflammatory effects by lowering TNF and IL-6
  • Improved ED function and vascular elasticity
108
Q

How is L-arganine a natural approach to IHD

A

precursor to NO

109
Q

How is Ginko biloba a natural approach to IHD

A

inhibits platelet activating factor by blocking the receptors

110
Q

Signs and symptoms of heart failure

A
  • nocturnal apnoea
  • breathlessness
  • fluid retention (ankle and abdomen oedema)
  • fatigue
  • lightheadedness
  • tachycardia
111
Q

Name some causes/risk factors of heart failure

A
  • coronary heart disease
  • IHD
  • hypertension
  • cardiomyopathy
  • pulmonary hypertension (thickening of the heart making right side work harder)
  • thyroid dysfunction
112
Q

how can IR cause heart failure?

A
  • decreased production of myocardial glucose (25% of myocardial ATP is glucose)
  • enhances fatty acid oxidation (75% of myocardial ATP is fatty acids)
113
Q

How can obesity cause heart failure?

A

Obesity causes changed to heart structure

114
Q

How can vitamin D deficiency cause heart failure

A

vitamin D is needed for calcium absorption, and calcium is needed for muscle contraction.

115
Q

Name some supplements that can help HF

A
  • CoQ10 (mitochondrial help)
  • D-ribose (regulates low myocardial ATP)
  • Mg (needed for ATP, vasodilator)
116
Q

Name some causes/risk factors for haemorrhoids and varicose veins

A
  • high abdominal pressure (pregnancy, constipation, childbirth, obesity)
  • being sedentary
  • low fibre diet
  • dehydration (blood viscosity)
  • inherited valve defects
  • smoking
  • vitamin C deficiency
  • abdominal bloating
117
Q

Name some naturopathic approaches for varicose veins/haemorrhoids

A
  • vitamin C (collagen synthesis)
  • bioflavonoids (buckwheat, grapes, apples, cranberries)
  • optimise liver function
  • reduce weight
  • Raising feet above heart
118
Q

which foods are phlebotonic foods?

A

flavonoids

119
Q

How are vitamin C and bioflavonoids a natural approach to varicose veins and haemorrhoids?

A

supports connective tissue integrity by increasing collagen synthesis and

120
Q

according to TCM, what will the tongue look like if there is blood pooling?

A

purple tongue with a think yellow brown covering

Final year semester 2 exam (9 decks)

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