Term
|
Definition
| hardening of the arteries (loss of elasticity) |
|
|
Term
1)aging
2)damage (diffuse distribution along vessels)
3)collagen replaces elastic fibers
4) increase in systolic pressure |
|
Definition
| what are the causes of arteriosclerosis? |
|
|
Term
|
Definition
|
|
Term
cholesterol buildup
calcified plaques
high glucose(diabetes) damaging arteries
LDL (fatty materials)
high pressure damaging arteries
inflammatory response |
|
Definition
| what are the causes of atherosclerosis? |
|
|
Term
| alter flow, rupture and cause clots, ischemia, infarction |
|
Definition
|
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Term
|
Definition
| transport lipids in plasma, composed of various amounts of cholesterol, triglycerides, phospholipids, and proteins |
|
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Term
|
Definition
| causes fibrosis, calcification, clot formation |
|
|
Term
high sat fat diet (high LDL/cholesterol)
lack of excercise
obesity
diabetes
HTN |
|
Definition
| risk factors for atherosclerosis |
|
|
Term
HDL
oat bran (sucks up cholesterol to be excreted)
statins (decreased cholesterol by increasing LDL receptors) |
|
Definition
|
|
Term
|
Definition
| when is a murmur heard for aortic valve stenosis? |
|
|
Term
|
Definition
| when is a murmur heard for aortic regurgitation? |
|
|
Term
|
Definition
| when is a murmur heard for mitral valve stenosis? |
|
|
Term
|
Definition
| when is a murmur heard for mitral regurgitation? |
|
|
Term
|
Definition
| narrowing of the aortic valve, slow to open, LV hypertrophy |
|
|
Term
|
Definition
| blood flow back into the LV, LV chamber enlargment, LV hypertrophy |
|
|
Term
|
Definition
| obstruction of blood moving from LA to LV, LA expands, pulmonary edema |
|
|
Term
|
Definition
| blood flows back into the LA from the LV, LA expands |
|
|
Term
arteriosclerosis: increase in P(cannot distend to compensate with volume)
aortic stenosis: cannot get blood out of the valve, so less blood out to aorta, less pressure
aortic regurgitation: pressure increases normally, but drops down low because blood squirts back in (backflow) |
|
Definition
| what happens to aortic pressure in arteriosclerosis? aortic stenosis? aortic regurgitation? |
|
|
Term
atherosclerosis (plaques) -> thrombus
coronary vasospasms |
|
Definition
| list the causes of coronary ischemia |
|
|
Term
| collateral circulation of the coronary arteries |
|
Definition
| what helps prevent damage in MILD ischemic attacks (according to wacker but not rinaldi) |
|
|
Term
1)heart failure
2)hypertrophy
3)cardiac shock
4)ventricular fibrillation |
|
Definition
| list the problems associated with myocardial ischemia/infarction |
|
|
Term
|
Definition
| heart is not pumping so blood backs up into atria and veins |
|
|
Term
|
Definition
| areas around infarction do this which is pathological over time |
|
|
Term
|
Definition
| if bad enough damage, heart cannot pump enough blood to the rest of the body |
|
|
Term
|
Definition
| areas of the heart become hyperexcited, increased extracellular K+, ishcemic area is negatively charged and doesnt repolarize, sympathetic response, dilation of injured muscle-circus movements of depolarization |
|
|
Term
|
Definition
| increase in size of heart muscle (HW to BW ratio) |
|
|
Term
physioligcal is good like lance armstrong
pathological is bad because the muscle is big and weak |
|
Definition
| what is the difference between physiological hypertrophy and pathological hypertrophy? |
|
|
Term
1) decreased calcium sensitivity and release
2) decreased ejection fraction (cardiac output)
3) shift in myosin isoform type
4) shift to a fetal gene program
5) use more glucose than fatty acids for metabolism |
|
Definition
| what are the changes associated with heart muscle that has undergone pathological hypertrophy |
|
|
Term
| infarction, pathological hypertrophy |
|
Definition
| typical causes of acute, moderate, heart failure |
|
|
Term
1)sympathetics strongly stimulated to increase cardiac output
2)fluid retention in the kidneys |
|
Definition
| compensated (acute) heart failure involves what 2 things? |
|
|
Term
digoxin to increase calcium, and contraction strength hopefully
(sympathomimetics may not help much because they are already active to increase CO) |
|
Definition
| what do you treat compesated heart failure with? |
|
|
Term
blood backs up in the circulation
excess fluid retention (overstretch heart, pulmonary edema, systemic edema) |
|
Definition
| what happens in chronic or severe (Decompensated) heart failure? |
|
|
Term
| diuretics to get rid of fluid to help the heart pump |
|
Definition
| what can you give a person with decompensated heart failure? |
|
|
Term
1)low contractility
2)reduced calcium transients during systole
3) decreased SERCA action (less Ca in SR)
4) increased Na/Ca exchanger (depolarizes cell easier, more Na+ in, but also more Ca++ out-bad) increased arrhythmias
5) decreased K+ channels (longer action potentials, cannot relax) |
|
Definition
| what happens to cardiac myocytes in heart failure? |
|
|
Term
|
Definition
generalized severe circulatory failure
-characterized by inadequate blood flow throughout the body, cant supply tissues with nutrients, O2, or remove waste |
|
|
Term
hyopvolemic
cardiogenic
septic shock
neurogenic
anaphylactic |
|
Definition
|
|
Term
|
Definition
| type of shock characterized by: decreased circulatory blood volume |
|
|
Term
|
Definition
| type of shock characterized by: failure to maintain cardiac output |
|
|
Term
|
Definition
| type of shock characterized by: bacterial toxins |
|
|
Term
|
Definition
| type of shock characterized by: loss of vasomotor tone |
|
|
Term
|
Definition
| type of shock characterized by: massive immune reactions |
|
|
Term
| it has a positive feedback loop which progressively decreases cardiac output |
|
Definition
| why is shock so bad if not treated immediately? |
|
|
Term
|
Definition
| type of shock characterized by: low blood volume, decreased venous return, and decreased cardiac output |
|
|
Term
1)increased sympathetic
2)baroceptor firing slows ->increase HR and increases SV
3)chemoreceptor reflex (if altered metabolism) -> increased HR, increased SV
4)increased sympathetics-especially in veins to maintain venous return and CO
5) increase in circulating hormones |
|
Definition
| what are the compensatory mechanisms for hypovolemic shock |
|
|
Term
| last ditch effort of the ishemic brain to increase CO |
|
Definition
| whats the bump at the end of the blood loss vs. cardiac output curve? |
|
|
Term
|
Definition
reduction in CO caused by inability of the heart to pump blood
-heart becomes weaker, or unable to properly beat
-CO falls, blood backs up in the system, pulmonary edema occurs |
|
|
Term
|
Definition
caused by spread of bacterial infection to many areas of the body (ruptures in the CO, strep/staph infection, gangrene)
causes vasodilation throughout the body, micro blood clots, and deterioration of capillaries due to release of cytokynes and immune factors (so capillaries leak blood and fluid) |
|
|
Term
|
Definition
CO and MABP drop drastically
antigen antibody reaction
release of histamines (inflammation)
vasodilation of arterioles and venules
increased capillary permeability |
|
|
Term
|
Definition
| what do all forms of shock do to blood pressure? |
|
|
Term
|
Definition
loss of vasomotor tone-> massive dilation
lose pressure, reduce venous return to the heart |
|
|
Term
deep general anesthesia (depress vasomotor center)
spinal anesthesia (block symp outflow)
brain damage (concussion/contusion in basal area of brain) |
|
Definition
| list the causes of neurogenic shock |
|
|
Term
blood, plasma, or electrolyte transfusion (increase volume and pressure)
Dextran
Epi
Head below feet (temporary raise venouse return)
O2
glucocorticoids |
|
Definition
| list the treatments of shock |
|
|
Term
| helps replace plasma proteins to maintain/increase plasma colloid oncotic pressure |
|
Definition
|
|
Term
| prevent inflammatory response in septic shock |
|
Definition
| how do glucocorticoids treat shock? |
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