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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?
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?
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?
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?
How does fiber act as an anti-carcinogen? (5)
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)
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?
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)
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
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
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
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)
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
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
What are compensatory mechanisms for heart failure? (3) Go into detail
- 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.
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!!)
1. What should you reduce intake of? 3
2. What minerals should you take? WHy?
- 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.
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.
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.
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