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1. What reduces vitamin E content?
2. What does absorption depend on? (2)
3. What interferes with absorption -1 and retention-1?
4. What is metabolism of vit E?
5. Where is it found in? (2)
6. What types of pools? Where is each found?
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1. What happens to vit E stores in adipose tissue during wieght loss?
2. What is function of vit E? (5)
3. What is the vit E paradox?
4. How is it recycled
5. Symptosm of vit E deficiency? (3)
6. Who does vit E def generally occur in?
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1. Which is least toxic fat sol vit?
2. What can high doses of vit E coutneract?
3. #1 risk associated with cancer? (%)? Followed by? (%)
4. Define cancerous cell. What is defective? Why don't they peter out?
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1. Six hallmarks of cancer?
2. Describe cellular changes
3. Describe stages of cancer (5)
4. How do vitamin A and D affect slow cycling?
5. What does S phase need?
6. Special checkpoint?
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How does fiber act as an anti-carcinogen? (5)
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1. What are the 4 carcinogens found in foods?
2. Describe exactly what foods they're found in.
3. What can vitamin C help with ?
4. What is cause of liver disease in Africa but not here?
5. Why does salt cause cancer?
6. Which requires phase I enzymes to activate it?
1. Nitrosamines (from spoiled food, beer, rubber nipples. Nitrites are found in fertilizers + amines --> nitrosamines)
Meats (polcyclic aromatic HCs from charbroiled fats; heterocyclic amines from meat cooked at high temp,)
Aflatoxin (moldy peantus and corn)
Salt --> preserved in high salty soln
3. Nitrosamines: prevents nitrates+amines in acidic environment --> nitrosamines
4. B/c of monitoring aflatoxin levels in peanuts and corn.
5. B/c it causes recurring injuries. Injuries have to go through cell cycling to heal wound --> increased risk for mutation.
6. Meats (polycyclic aromatic HCs and heterocyclic amines)
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1. What affects p450 phase 1 enzymes? (4)
2. What affects phase 2 enzymes? (2)
3. What activates phase 2 enzymes? (2) Where are these things found? (3)
4. What are 4 examples of free radicals involving DNA? Which is used to quantiate amount of damage?
5. what are oncogenes?
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What foods can function as antioxidants? 8
- 1. Vitamin E
- 2. Vitamin C
- 3. Colored foods (flavinoids, phenolics, carotenoids, lcopene, etc)
- 4. Selenium (GPx, Se-def are more likely to have DNA damage)
- 5. Soybeans (genistein inhibist tyrosine kinase, inhibiting growth signal) Estrogen-responding tumors may respond to this though :(
6. Monoterpenes from cherries, straw/blueberries contain perillyl alcohol & ellagic acid which blocks formation of farnesyl groups preventing EGF receptor from binding to G protein
- 7. Calcium - reduces colorectal cancer
- 8. Methionine folate & methyl donors (hypermethylation decreases expression - can increase/decrease risk of cance rin different places)
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1. What is difficult to separate?
2. What % of cancers are from obesity/lack of exercise?
3. What is the association b/t BMI and cancer?
4. BMI and breast cancer?
5. How does exercise affect cancer risk?
6. APoptosis --> which studies showed that for heavy smokers, increasing b-carotene intake increased lung cancer?
7. When should you take antioxidants?
- 1. Diets high in fat, high in calories, and low in fruits & veggies
- 2. 15-20%
- 3. Linearly positively associated
- 4. Obesity increases risk of first breast cancer and recurrence
- 5. Decreases it
- 6. CARET AND ATCB
- 7. when you're young and you don't have damage already
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1. What side of heart is high pressure system?
2. What is thing for CO?
3. What is cardiac reserve?
4. What is normal output? What can output increase to?
- 1. Left
- 2. Stroke volume x heart rate
- 3. Amount of capacity apart from at rest (at rest =40% of capacity)
- 4. 5L, 10L
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1. What are the two types of heart failure?
2. What are the 3 main causes?
3. What causes direct myocardial damage?
4. What is cor pulmonale
1. Systolic - loss of ventricular contraction --> less CO & diastolic failure --> loss of ventricular relaxation --> no filling and less CO
2. increased preload, increased afterload (increased pressure to push against) and direct mitochondrial damage
3. Myocardial infarction (decreased blood delivery to heart muscle/ischemic injury) and cardiomyopathy ---> (1) Coxsackievirus in Se-def and (2) Dilated cardiomyopathy (increases stretch of myocardium --> increases volume of ventricle --> decreases strength of myocardium --> inefficient blood ejection. Associated w/ chronic alcohol consumptino.
4. Cor pulmonale - ventricular dilation and hypertrophy due to resistance and high BP in lung
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1. What causes increased preload? (3) - increased speed of blood delivery back to heart, increased peripheral need for nutrients
2. What causes increased afterload? (3) - impaired outflow, increased pressure in large arteries and increased blood volume.
1. Arterio-venous fistula, hyperthyroidism b/c of incrased need for additional nutrient and O2 delivery and vitamin deficiency same reason as above.
2. Hypertension, obesity, valvular disease (mitral valve prolapse - b/c of regurgitation of blood into left atria increasing workload on heart)
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1. conseq of heart failure? (4)
2. What are the 2 types of heart failure? where does congestive heart failure go?
1. Decreased perfusion to tissues, loss of cardiac reserve!!!, increased venous pressure --> peripheral edema and pulmonary edema.
2. Left-sided (Cong) and right-sided
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1. What happens in congestive heart failure?
2. WHat are risk factors for left-sided heart failure HF?
3. What is the most common symptom of the above? Main consequences of the above? (2)
4. Most common cause of right-sided HF?
- 1. Blood cannot pump enough blood to support body
- 2. Obesity, hypertension, diabetes, high cholesterol
- 3. Fluid in lungs. Decreased cardiac output and pulmonary congestion!!!
- 4. Left-sided
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What are compensatory mechanisms for heart failure? (3) Go into detail
1-5
2-5
3-
- 1. Sympathetic nerve stimulation
- - Decreased cardiac output --> increased b-adrenergic tone --> increases contraction force --> increases peripheral vasoconstriction to increase perfusion pressure (short-term); long-term can lead to damage.
- 2. Increased fluid retention
- - Less cardiac output is sensed by JGA in kidneys --> releasese renin.
- -Renin-angiotensin-aldosterone system is activated leading to increased Na+ resorption in kidneys
- - Increased water retention and incrased fluid volume
- -Angiotensin II causes peripheral vasoconstriction pushing CO back to normal levels
- -Can disrupt normal electrolyte balance by increasing Na+ resorption and K excretion
- 3. Cardiac muscle remodeling
- - Long-term effects of increased load on heart or adrenergic nerve stimulation
- - cardiac hypertrophy
- - results in decreased ventricle volume (diastolic failure) --> propagates cardiac insufficiency.
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Treatment strategies for heart failure? 4
1. Vasodilation (ACE inhibitors or angiotensin II blockers)
- 2. Myocardial relaxation using B-blockers, also blunts renin secretion
- 3. Fluid reduction (diuretics)
- 4. Digitalis (decreases activity of Na/K pump --> makes muscle contract b/c it is a positive inotrope!!)
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1. What should you reduce intake of? 3
2. What minerals should you take? WHy?
3. Vitamins?
- 1. Na+, trans/sat fats, LDL:HDL ratio
- 2. Calcium - muscle contraction, magnesium, potassium - sinus rhythm has increased clearance w/ diuretics, selenium (GPx), def associated w/ cardiomyopathy
3. B1 (TCA for energy), Vitamin C, vitamin E antioxidants.
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1. Diagnostic values of hypertension?
2. What leads to hypertension? (5)
3. Consequences of hypertension 4
4. Treatment? (4)
- 1. >140 mm Hg and >90 mm Hg
- 2. High Na+, low K+, high BMI, low exercise, alcohol
- 3. Storke, heart failure, kidney damage, retina damage.
4. Diuretics, ACE inhibitors - targets angiotensin, exercise, and weight management.
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What do compensatory mechanisms cause short-term and long-term? 1, 5
- 1. Acute hemodynamic improvement
- 2. Increased cardiac preload, increased cardiac afterload, increased myocardial workload, arrythmia, and decreased myocardial rxn in those with heart failure.
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Describe pathway of renin --> angoitensin II.
What does it do? (3)
1. Renin (kidney ) --> angiotensiongen -- cleaved into > angiotensin I --> ACE in the lung --> angiotensin II
Vasoconstrictor, increases ADH, increases aldosterone
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