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Nutrition and CMD > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What is the difference between arteries and veins?

A

Arteries take blood from the heart, veins take blood to the heart

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2
Q

What are the consequences of the increase in the surface of capillaries?

A
  • Larger surface (more options for transfer)
  • Slower speed (more time for transfer)
  • Lower pressure (capillaries are fragile)
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3
Q

What is the Bohr effect?

A

Heme-iron binds oxygen in the lung where the pH is high and releases in tissues where the pH is low.

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4
Q

What is the optimal BP?

A

Lower than 120/80

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5
Q

In which blood vessels is BP measured?

A

Large arteries in systemic circuit

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6
Q

What is pulse pressure?

A

systolic - diastolic

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7
Q

What is MAP?

A

Mean arterial pressure: diastolic + 1/3 pulse pressure

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8
Q

What is the immediate response to a change in BP?

A

baroreceptors in carotid arteries sense pressure -> ANS -> change in cardiac output or vascular resistance

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9
Q

What is the longer term response to a change in BP?

A
  • less vasopressin
  • RAAS: low BP -> renin (from kidney) -> angiotensinogen (from liver) into angiotensin I -> ACE converts I into II -> secretion of aldosterone -> aldosterone and angiotensin II: kidney, retain water and salt in the body. Angiotensin II also is a powerful vasoconstrictor.
  • Natriuretic peptides (ANPs): vessel dilation, decrease sodium reabsorption, supress RAAS, suppress ANS
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10
Q

What happens when there is a high water intake?

A

o Higher ECF volume -> kidneys excrete salt and water (slow) -> normal osmolarity
o Higher BP -> ANS lowers BP (rapid) -> normal osmolarity

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11
Q

What is excitation-contraction coupling?

A

Action potential spreads through transverse tubules to the sarcoplasmic reticulum -> release of calcium from the SR -> calcium binds to troponin to expose active sites on the actin filament -> cross-bridge cycling and muscle contraction.

Action potential
Calcium
Troponin
Expose actin
Contraction
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12
Q

What are the treatments of AF?

A 
Electrical cardioversion
Surgical ablation
Pharmacological cardioversion
Anticoagulation to avoid stroke
Symptom control
Lifestyle changes
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13
Q

What are the three types of AF remodelling?

A
  • electrical; reduced calcium transient (1 day)
  • metabolic; mitochondrial dysfunction/ oxidative stress (continuous)
  • structural; degradation of contractile proteins (long term)
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14
Q

What are possible compounds that could decrease cardiac diseases?

A

Vit B3 and vitamin C

Vit D3 and n-3 not much evidence

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15
Q

What is done for cardiac reperfusion?

A

PCI; go in arteries with a catheter

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16
Q

What are the mechanisms of IRI?

A
  • free radical damage
  • inflammation
  • influx of calcium
17
Q

Explain what ROS damage does in the mechanism of IRI

A

Free radical damage; damaged mitochondria produce ROS due to incomplete reduction of oxygen and by infiltrating leukocytes. Reperfusion -> more ROS -> lipid peroxidation and protein modifications (membrane damage, protein breakdown and DNA mutations).

18
Q

Explain what inflammation does in the mechanism of IRI

A

Inflammation; influx of leukocytes, plasma protein and cytokines

19
Q

Explain what calcium influx does in the mechanism of IRI

A

Influx of calcium; during ischemia, SR is damaged, so it doesn’t recycle calcium -> toxic amount of calcium in muscle cell -> hypercontraction.

20
Q

Explain the function of HIF1

A

Gene transcription (EPO, Slc2a1 and VEGF).

21
Q

What does VEGR do?

A

Angiogenesis

22
Q

What does EPO do?

A

Erythropoiesis

23
Q

What does Slc2a1 do?

A

Increase glucose supply

24
Q

What causes HIF1-alpha knock out mice to die?

A

Cardiac and vascular defects and decreased RBC production

25
Q

What increases and decreases low-grade inflammation?

A

Lower: weight loss, n-3 PUFAs
Higher: SAFAs, SSB

26
Q

What are markers of inflammation?

A

cytokines (TNF-alpha and IL-6), hsCRP and PAI-1

27
Q

Explain TNF-alpha

A

TNF-alpha; produced in AT. Increases insulin resistance in AT

28
Q

Explain IL-6

A

IL-6; produced in many different tissues. Both anti-pro inflammatory. Induction of insulin resistance

29
Q

Explain hsCRP

A

hsCRP; increased in inflammation. High sensitive CRP is predictive for future CVD

30
Q

Explain PAI-1

A

PAI-1; not a true marker but is still linked to inflammation. Secreted by fat and endothelial cells. Inhibits fibrinolysis -> atherosclerosis.

31
Q

What are the functions of the endothelium?

A
  • Control of vascular tone (release of NO in response to shear stress)
  • secretion of inflammatory factors and activation of adhesion factors when stressed -> atherosclerosis
  • coagulation control
32
Q

What happens with endothelial dysfunction?

A

Reduced NO and pro-inflammatory state
von Willebrand Factor (VWF) forms a bridge between the damaged surface and platelets
Atherosclerosis

33
Q

What nutritional factors are good for the endothelium?

A

n-3 PUFAs, antioxidants (vit C&E), folic acid, L-arginine, cacao and tea

34
Q

Explain the absorption of cholesterol

A

Liver secretes bile to facilitate absorption of dietary fat and cholesterol
TG and chol are packaged into cyclomicrons
Lipoprotein lipase (LPL) breaks down TGs (to be used by cells) and the resulting particle is taken back to liver
liver makes VLDL from resulting particle

35
Q

What does HDL do? What is the effect on CHD?

A

Removes chol that is trapped in arterial walls and transport it back to the liver. HDL is associated with lower incidence of CHD, but not causal, more a marker

36
Q

What is the effect of high TG on CHD/CVD?

A

Increased risk, causal role is unclear, maybe just markers for VLDL and IDL

37
Q

What is the effect of high lipoprotein a on CHD/CVD?

A

LPa increases stroke risk (probs causal), but is under strict control and constant

38
Q

What do phytosterols do?

A

Lower absorbtion of chol and lower LDL

39
Q

What are medications for high BP?

A
  • ACE inhibitors; vasoconstriction is reduced
  • Diuretics promote urinary excretion of water
  • Beta-blockers slow down heart rate and reduce cardiac output

Nutrition and CMD (7 decks)

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