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GI and Renal Exam 3 > 40 - Vascular Disease > Flashcards

40 - Vascular Disease Flashcards

1
Q

What is vascular disease?

A

Normal vessels
- thin intimal layer, smooth endothelium

Atherosclerotic vascular disease

  • Mild: small tears or fatty streaks present, with cellular immune response stimulated
  • Moderate: accumulation of cholesterol, calcium and cellular debris within the intima with bulging into arterial canal
  • Severe: thrombus formation after plaque rupture with platelet activation, causing a clot downstream
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2
Q

What are the causative factors of vascular disease?

A
  • Hypertension (vascular damage from shear effect)
  • Direct vascular effects of diabetes
  • Increased platelet aggregation (may be related to low fruit/vegetable/fish intake)
  • Hypercoagulable states related to obesity and high dietary fat
  • Cigarette smoking
  • Insufficient regular exercise
  • Diet ***
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3
Q

What is the effect of diet on vascular disease?

A
  • Deleterious effect-saturated fat and cholesterol
  • Protective effect-Higher intake dietary fiber, folate, anti-oxidants, Vitamin K, as well as lower sodium, higher intakes of potassium and magnesium
  • Fish intake (omega 3 FA) may also be protective
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4
Q

What are the primary organs affected by vascular disease?

A
  • Heart: coronary arteries
  • Aorta
  • Extracranial arteries (carotids/vertebral system)
  • Intracranial arteries
  • Renal arteries
  • Pelvic organs
  • Lower extremities
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5
Q

What is coronary artery disease?

A
  • Soft plaque vs hard plaque: hard plaque produces stable angina, soft plaques can rupture
  • Role of inflammation
  • Role of adrenergic hormones
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6
Q

Describe lipoproteins

A
  • Most fatty acids in blood come from dietary fats
    Uses: build membranes, precursor for more complex lipids, precursor for eicosanoids and provide for future energy needs
  • Lipids are transported in blood stream as lipoproteins; all contain cholesterol, cholesterol esters, triglycerides, apolipoproteins, and phospholipids

You need cholesterol for brain function, so anything below 70 can impair function

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7
Q

What are the classes of lipoproteins?

A
  • Chylomicrons and remnants
  • Low Density Lipoproteins (LDL)
  • High Density Lipoproteins (HDL)
  • Very Low Density Lipoproteins (VLDL)

VLDL and chylomicrons and HDLs are all okay

LDLs are bad

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8
Q

Describe atherogenic vs non-atherogenic lipoproteins

A

Present at some point daily in healthy people

  • Vary at time of day, correlate with meals
  • Relative concentrations create atherogenic potential

Atherogenic lipoproteins
- Chylomicron remnants, VLDL remnants and LDL

Non-atherogenic lipoproteins
- Chylomicrons, HDL, VLDL

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9
Q

What do you need to know about HDLs?

* KNOW THIS **

A

HDLs are ALWAYS OKAY ***

TEST QUESTION

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10
Q

Describe triglycerides

* KNOW THIS **

A
  • Ester made up of three fatty acids and a glycerol
  • Bi-directional transfer of adipose fat and blood glucose from the liver
  • *** Many triglycerides, which are more or less saturated, depending on oil source (saturation = carbon bonds “saturated” with/by hydrogen ions)
  • *** Chain lengths vary, most have even numbers of carbons, usually 16, 18, 20
  • ** Fatty acids derived from linolenic acid have 18 carbons: these are polyunsaturated

One of the way fat travels around in the body - more between the gut and liver (that’s what they are designed for)

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11
Q

Descrie chylomicrons

A
  • Function to transport fat-soluble molecules from intestine to other organs
  • Cleaved by lipoprotein lipase to release molecules to various sites
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12
Q

What do chylomicrons carry?

A
  • Triglycerides (for fuel and essential fatty acids)
  • Cholesterol (membrane synthesis, bile acids, hormones)
  • Vitamin A and β-carotene (vision pigments and growth)
  • Vitamin D (calcium metabolism and growth)
  • Vitamin E (antioxidants)
  • Vitamin K (blood coagulation, calcium metabolism)

ADEK = fat soluble vitamins

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13
Q

Describe VLDLs

A
  • Lipoproteins that transport lipids from liver to muscles and other organs
  • Transport cholesterol, triglycerides and Vitamin E
  • Lipoprotein lipase cleaves off portions to deliver to those organs (but more slowly than with chylomicrons)
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14
Q

Describe VLDL remnants

A
  • Remnants that are left are recirculated to the liver to make LDL cholesterol
  • VLDL remnant clear less easily after consumption of a typical American high fat meal
  • VLDL remnants are atherogenic ****
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15
Q

Describe LDL

A
  • ALWAYS BAD
  • Derived from VLDL
  • Cholesterol-rich and promotes atherosclerosis
  • Carry Vitamin E (anti-oxidant)
  • Taken up by liver via LDL receptors on hepatocytes
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16
Q

Describe LDL in terms of a high and low cholesterol diet

** KNOW THIS ***

A

***** High cholesterol diet: fewer receptors expressed and more circulating LDL

**** Low cholesterol diet: more receptors expressed and less circulating LDL

Some cholesterol is needed to synthesize cell membranes, adrenal steroid hormones, bile acids and bile

Can move cholesterol from arteries (not as well as HDL)

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17
Q

Describe HDL

A
  • Relatively small and dense
  • Contain more proteins and phospholipids than other lipoproteins
  • Contain enzymes and proteins such as LCAT and apoE **** (these enzymes are important **)
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18
Q

What are the funcitons of HDL?

A
  • Transfer apoCII and apoE to chylomicrons and VLDL to regulate their metabolism
  • Take up cholesterol from LDL and VLDL and phospholipids from VLDL
  • Reverse transport of cholesterol (removal from peripheral tissues)
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19
Q

What is LOW HDL associated with?

** KNOW THIS **

A

KNOW THIS

***** Low HDL levels are associated with increased cardiovascular risk. Targets are > 40 mg/dl for men and > 50 mg/dl for women.

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20
Q

What are the BAD types of dietary fats?

A
  • Poly-unsaturated fats (N6) ω 6: corn, soy, sunflower, safflower oils
  • Poly-unsaturated fats (N3) ω 3: oily ocean fish, flax seed oil, 10% in canola and soy oils
  • “Trans” fats (partially hydrogenated poly-unsaturated N6): baking and cooking oils, margarine
21
Q

What are the BAD saturated fats?

A

All of the carbon atoms have single bonds, free bonds are “saturated” with hydrogen atoms

Include dietary fats myristic (14:0), palmitic (16:0) and stearic (18:0) acids

22
Q

Know the chart on slide 27

A
  • Cholesterol raising fats
  • Neutral fats
  • Cholesterol fats
23
Q

Describe trans fats

A
  • Dyslipidemia: LDLꜛ, HDLꜜ, triglyceridesꜛ, Lp(a)ꜛ
  • Abdominal fat deposition
  • Systemic inflammation: Interleukin-6 (IL-6)ꜛ, TNF-αꜛ, C-reactive protein (CRP)ꜛ
  • Endothelial dysfunction
  • Diabetes
  • Membrane effects
24
Q

Describe mono-unsaturated fats

A
  • Have only one carbon with a double bond
  • Often called MUFAs
  • Have a higher melting point than PUFAs (liquid at room temperature)
  • Specific fatty acids: palmitoleic 16:1 and oleic acid 18:1
  • Neutral to cholesterol synthesis
  • Most common source is the olive oil found in the Mediterranean diet
25
Q

Describe poly-unsaturated fatty acids

A
  • Class of animal or vegetable fats with multiple carbon double bonds, unsaturated with hydrogen atoms
  • Also called PUFAs
  • They exist in cis or trans isomers, depending on the geometry of the double bond (trans-straight, cis-angled)
  • Position of the double bond is designated by Greek letters and named from relationship to the carboxyl group
  • Can be liquid at room temperature
  • Generally will not raise cholesterol content
  • Easily oxidized by free radicals (increased rancidity AND increased risk for atherosclerosis) due to multiple unsaturated bonds (less stable)
26
Q

What are eicosanoids?

A
  • Signaling molecules: used in growth during and after physical activity, in immunity and inflammation, and as messengers in the central nervous system (CNS)
  • Made from oxidation of 20 carbon fatty acids (FA)
    Eicosanoids derived from FA with N6 (ω-6) oils are pro-inflammatory; those from FA with N3 (ω-3) are less so

**** N6 are pro-inflammatory and N3 are not

27
Q

Describe N3 and N6

A

N3 FA include Eicosapentaenoic (EPA) and Docosahexaenoic (DHA)

N6 FA include arachidonic acid (AA)

28
Q

Describe atherosclerosis

A
  • Free radicals**** attack PUFAs and apoB in LDL creating fragments
  • Fragmented LDL is not recognized by the liver LDL receptor so it binds to other receptors
  • Scavenger receptor on macrophages binds LDL and creates foam cells
  • LDL is more likely to be oxidized the longer it stays in circulation
  • High levels of LDL in blood also increase amount of uptake into the endothelium of arteries
  • Macrophages take up the oxidized LDL becoming foam cells
  • Dead and dying foam cells deposit cholesterol creating atherosclerosis
  • Oxidized lipids also stimulate an inflammatory response
29
Q

Describe free radicals

A
  • Free radicals are atoms or groups of atoms with an odd (unpaired) number of electrons and can be formed when oxygen interacts with certain molecules
  • Often called Reactive Oxygen Species and include superoxides, hydroxyl anions, hydrogen peroxide and singlet oxygen.
  • These are very unstable
  • Free radicals can arise from excess iron and copper
  • Targets of free radicals include all kinds of molecules in the body. Among them, lipids, nucleic acids, and proteins are the major targets
30
Q

What are the defense mechanisms against free radicals?

A

Super foods - antioxidants

  • Protective cellular enzymes inactivate free radicals as they are generated: superoxide dismutase, catalase
  • Fat-soluble anti-oxidants protect membranes, lipid rich organelles and lipoproteins: alpha-tocopherol (form of vitamin E), carotenoids (vitamin A derivatives)
  • Proteins and metabolites protect against aqueous environments within and outside cells: albumin, uric acid, ascorbic acid
  • Different antioxidants are interdependent and have complementary free radical scavenging activity; sources such as fruits, vegetables, seeds and nuts provide that complementary activity better than supplements
  • Example: ascorbic acid regenerates alpha tocopherol after the latter has scavenged a free radical
31
Q

Where can you find antioxidants?

A
  • Different antioxidants are interdependent and have complementary free radical scavenging activity
  • Sources such as fruits, vegetables, seeds and nuts provide that complementary activity better than supplements
  • Example: ascorbic acid regenerates alpha tocopherol after the latter has scavenged a free radical
32
Q

What foods in the US diet give us antioxidants?

A
  • Fruits: berries, cherries, citrus, prunes, and olives
  • Vegetables: potato, spinach, tomatoes, and legumes
  • Green and black tea

Others
- Indian medicinal herbs: including cinnamon, turmeric, holy basil, onion, curry leaf

33
Q

Describe marine oils

** KNOW THIS ****

A

Study of 22,000 male physicians x 12 years showed that those who ate at least 1 serving/week of cold water fish decreased their risk of cardiac arrest by 50%

Other sources of 0mega-3 fatty acids (primary alpha linolenic acid), is from seeds, oils and vegetables

** Primary fatty acids are EPA and DHA **

34
Q

Describe the recommendation with fish consumption

A
  • Healthy people should consume 2 servings/week of cold water fish
  • Target consumption: 1.1 gm/day for women, 1.6 gm/day for men

The concern with this is mercury

35
Q

Describe hypertension

A
  • Defined as BP > 140/90; over age 60: 150/90

- Blood pressure (BP) regulation is via the renin-angiotensin system, residing in the kidney

36
Q

Describe the RAAS regulation of hypertension

A
  • Renin catalyzes first of series of steps to release hormone aldosterone
  • Aldosterone maintains BP by conserving sodium
  • Renin release triggered by: low arterial BP, low plasma volume, low plasma Na, edema, activation of renal nerve
  • Renin catalysis of angiotensinogen to angiotensin eventually causes effects at blood vessels (vasoconstriction), brain (thirst and release of anti-diuretic hormone) , kidneys (Na conservation at proximal tubule increasing BP) and adrenals (aldosterone raises BP)

Not going to test on the names here

37
Q

What do you NEED to know about RAAS?

** KNOW THIS ***

A
  • Renin is bad (need some, but excess is bad)
  • Aldosterone is bad (need some, but excess is bad)
  • Norepinephrine can increase BP
  • NO (nitric oxide) drops blood pressure
  • Vascular stiffness raises BP
38
Q

What populations are at risk for hypertension?

A
  • Obese
  • Diabetes
  • Advanced age
  • Lower socioeconomic status
  • Sedentary lifestyle
  • African-Americans, Hispanics
  • Alcohol abuse
  • Family history of hypertension
  • Prevalence:1in 3 Americans
39
Q

What is the role of sodium in hypertension?

A
  • Sodium: highest concentration is in processed food, lowest is in fresh foods
  • High salt intake predisposes to higher BP
40
Q

What are the recommendation for daily intake?

** KNOW THIS ***

A
  • *** Current recommendations for EVERYONE are 2300 mg per day
  • *** For people with established high BP, 1500 mg per day
41
Q

What is the role of potassium in hypertension?

A
  • Our ancestors consumed much more dietary potassium and less dietary sodium than the typical modern Western diet
  • Low potassium increases BP and risk of stroke by stimulating renin secretion and causing vasoconstriction

** WE NEED dietary potassium ** Fruits and vegetables, fresh meats and milk are good sources of dietary potassium

42
Q

What is the role of calcium in hypertension?

A
  • Adequate calcium maintains normal blood pressure
  • 2-4 servings per day of low-fat dairy is effective
  • Adults need 1000-1200 mg/day
43
Q

What is the role of magnesium in hypertension?

A
  • Adequate dietary magnesium intake helps maintain normal blood pressure
  • Evidence lacking for magnesium supplements
  • Magnesium rich diet is achieved via whole-grain foods, legumes, nuts, dark-green vegetables
  • Suggested intake for adults 310-420 mg/day
44
Q

Describe the role of alcohol in hypertension

A

Alcohol: limit intake to no more than 2 drinks/day for men and 1 drink/day for women (women absorb alcohol more efficiently than men)

45
Q

Describe the role of obesity and weight reduction in hypertension

A
  • Obesity: 2-6 fold increase risk for hypertension (probably salt-sensitivity and hyperinsulinemia)
  • Weight reduction: with every 10 kg loss in an overweight patient, the systolic BP drops 5-20 mmHg

HOW you lose weight is important
- PREDIMED study (2013): in people with high CV risk factors, a higher total protein intake was associated with a 90% greater risk of GAINING weight if they were used as a substitute for carbohydrates (but not for fats) AND overall mortality is increased with a high protein intake (59-66% higher)

46
Q

Describe the role of exercise in hypertension

A
  • Exercise: to lower BP, adults should engage in moderate to vigorous exercise 3-4x/week for 40 minutes
  • Aerobic or resistance (build muscle)
47
Q

Describe the role of caffeine in hypertension

A
  • Caffeine: minor and temporary effect; a small minority are more sensitive and should limit intake to 1 serving/day
  • Black coffee is what has been studied NOT high calorie coffee drinks
  • Moderate consumption: 3-5 cups/day
  • Lower risk of cardiovascular disease, stroke, congestive heart failure
  • Also decreases risk of liver cancer, ? breast cancer
  • Lower risk of Parkinson’s disease, possible protection against Alzheimer’s disease
48
Q

Case study

A
  • 27 yo medical student whose BP has been elevated at her admission physical and at several occasions subsequently
  • BPs range 140-150 systolic and 90-100 diastolic
  • She wants to avoid BP medication if possible

How do you counsel her re:

  • Diet
  • Exercise
  • Alcohol
  • Caffeine
  • Stress

GI and Renal Exam 3 (15 decks)

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