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248 Cards in this Set
- Front
- Back
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describe the three layers of arteries and veins |
artieries: tunica intima (innermost endothelium, physical barrier between blood and the vessel)
turnica media (smooth muscle , separated from other layers by elastic tissue, stretches during systole and recoils during diastole. this is the thickest layer
turnica adventia (contains nourishing blood vessels, lymphatics, and nerves
veins: consist of endothelium covered by fibrous tissue
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what are the 6 functions of the endothelium? |
a barrier to trnasfer of large molecules into the intersitial space
produces heparin, thrombomodulin, and plasminogen activators to keep blood from clotting as it slows
releases NO and prostacyclin into circulatino to relax vessel
produces natriuetic hormone for volume control. does this by increasing urine sodium excretion
modulates size of vessel
releases chemockines for immune cells |
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what are the functions of the tunica media? (4) |
its the thickest layer
composed of smooth muscle
seperated from other layers by elastic fibers which stretch during systole and recoil during diasotle to propel blood forward
controls the diameter of the vessels by contracting or relaxing depending on the situation |
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the sum of the resistance of all the peripheral vaculature in teh systemic circulation |
peripheral vascular resistance |
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__, __, and __ all affect peripheral vacular resistance |
blood pressure, blood flow patterns, and blood volume |
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refers to low pressure reservoirs of blood in the venules |
capacitance |
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describes the sluggish flow of blood at the walls of the vessel but the smooth flow of blood in teh middle of teh vessel; the speed of blood going through the vessels is highest in teh middle (less resistance) |
laminar flow |
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describe how poiseullies law works |
Poiseulle’s Law postulates that resistance is inversely proportional to the radius of the vessel.
The smaller the diameter, the greater the resistance.
The larger the diameter, the less resistance.
In addition, vessels that are long have more resistance than several vessels in parallel (traffic flow on one highway versus several parallel highways) |
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how do baroreceptors regulate blood pressure through the sympathetic nervous system? |
Baroreceptors sense a change in tension in teh aortic arch
if tension is low epinephrine is released to increase HR and NE is released to constrict arterioles
if tension is high, the vagus nerve is stiumated through PNS to slow the HR and relax the blood vessels |
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explain how hormones regulates blood pressure |
ADH prevents the loss of fluid through the kidney (retains water)
aldosterone retains Na to retain water
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explain the renin-angiotensisn system |
low renal artery pressure, Na, or K stimulates renin to be secreted renin converts angiotensinogen to angiotensin I, ACE converts angiotensin I to angiotensin II which is used for fluid retention |
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explain how turbulence affects blood flow |
obrstuctions/digvergent paths create turbulence
causes an increase in resistance in teh vessels and an increased clotting risk |
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what is shock? |
an inadequate supply of O2 or nutrients to tissues |
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what are three of the main causes of shock? |
inadequate tissue perfusion
maldistribution of CO (cause of cardiogenic shock)
maldistribution through teh microcirculation (as blood flow ceases/slows in "communistic organs (all but heart and brain) blood clots aggregate in tissues), clotting leads to cellular ischemia along with lack of venous return) |
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hemorrhagic shock is a form of __ |
hypovolemic shock |
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___ is the most common form of shock and teh easiest to treat |
hypovolemic shock |
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__ shock can be caused by internal bleeding, external bleeding, GI tract losses through vomitting/diarrhea, obstretical loss (following delivery), loss of interstitail space after major surgery/trauma, loses of large volumes of urine (diabetes) |
hypovolemic shock |
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category of shock that is characterized by <15% blood/fluid loss o This occurs with blood donation o Generally well-tolerated o Treated with: oral rehydration (+ food) and occasional/judicious use of IV fluids (for those feeling faint after blood donations) |
class I |
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category of shock that is characterized by 15-30% volume loss o Signs and symptoms: tachycardia, anxiety, lowered urine output, thirst Increased HR is necessary to maintain CO (HRxSV) The kidneys retain water to maintain BP Increased thirst is signaling from the pituitary gland to maintain BP |
class II |
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how do you treat class II shock? |
IV cystalloids, control of hypotension to maintain MAP of 50-60 mmHg |
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category of shock that is characterized by 30-40% blood loss o Signs and symptoms: decreased BP, tachycardia, minimal urine output, confusion (due to reduced brain perfusion) o At this point, patient is unable to compensate for loss The compensation by the body (based on SNS - increased HR and decreased urine output) seen in class II help to maintain BP is failing at this point (in class III) Failure of compensation is indicated by a drop in BP o Treatment: control of bleeding, blood transfusion |
class III |
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category of shock that is characterized by >40% blood loss o Rapidly fatal condition o Signs and symptoms: profound hypotension, cool extremities (blood diverted), minimal to no urine output, minimally responsive to stimuli |
class IV |
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what are the three cases in which death occurs from class IV shock? |
Exsanguination: extensive blood loss; ongoing bleeding that leads to death (“bleeding out”). Occurs within minutes (usually depicted by person dying in a “pool” of blood) Progessive decompensation: occurs after a few hours (patients try to maintain BP, but it is at the expense of the heart, which can’t maintain very high BP for a long time, depriving the kidneys and other vital organs of blood, leading to organ damage) Sepsis and organ failure: occurs within a few days to a week (patient’s immune system is depressed, organs are damaged by ischemia and liquefactive and coagulative necrosis occur – involves bacterial invasion) |
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explain the pathophysiologic basis for tachycardia during shock |
cardiac output=stroke volume x heart rate
as stroke volume decreases HR must go up to maintian CO
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explain the pathophysiologic basis for low urine output during shock |
kidneys are a communist organ and divert blood to the capialist organs (brain and heart), try to increase their own bloodflow by incresing renin/aldosterone and ADH which reduces urine output |
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explain the pathophysiologic basis for anxiety and confusion during shock |
due to reduced cerebral blood flow |
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explain the pathophysiologic basis for thirst during shock |
reduced blood/fluid volume causes dehydration |
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describe how blood is diverted from or to organs of communist or capitalist nature |
when blood loss occurs organs deemed unnecessary for survival divert their blood to those deemed necessary for immediate survival (the heart and brain. this is done by increasing PVR by vasoconstirction by the ysmpthteitc nervous system, aldosterone, renin, and ADH |
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what are three sites that can be sites of blood loss which aren't easy to identify |
chest, pelvis, abdomen |
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how are the lungs affected by prolonged sympathetic stimulation |
first and most common organ to fail, is a communist organ meaning it vasconstircts its blood vessels making it different to get nourishment from blood |
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how are the kidneys affected by prolonged sympathetic stimulation |
decreased perfusion of nutrient blood to the kidney and decreased glomerluar filtration through the reanl artery. kidney faliure results |
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how are the GI tract affected by prolonged sympathetic stimulation |
early and common complication, GI tract is not well perfused in states of shock |
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how can organs be injured from clots and ischemia during shock? |
clotting causes obstruction leading to decreaesd tissue perfusion resulting in: metabolic acidosis, decreased myocardial contraction, cell hypoxia causing intracellular fluid loss causing venous return to decrease and decreases CO decreases CO decreases BP and tissue perfusion myarcardial function is reudced as a result of BP decreasing leading to reduced coronary perfusion |
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explain the pathogensis of atherosclerosis |
blood flow is normally laminar and smooth promoting NO release. NO vasodilates in a postive feedback loop to increase blood flow. laminar flow is interrupted when the blood flow has to change direction (like at a junction). when this happens the endolemium is dammaged and turbulent flow occurs
WBC's leak into the area of the damaged bloood vessels causing inflammatin of the tissue without antigoagulatnt and vasodilation properties leading to a clot forming.
lipoproteins combine with proteglycans which attracts monocytes which become foam cells after they eat them and promote inflammation.
foam cells accumulate in teh subendothelial layer to become fatty streaks. smooth muscle cells migrate the the intimal level
fibrotic plaques are formed restircting blood flow and laminar flow |
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explain the complications that arise from atheroscelerosis |
calcification of fibrotic plaques make the vessel rigid. this can increase chance of aneurism. plaque can rupture promoting an inflammatory response which can cause a clot. this can lead to and infarct. |
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what is the mian modifiable risk factor for athersclerosis? |
lipids/cholesterol |
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what are 11 modifable risk factors for atherosclerosis |
serum cholesterol: risk is 2x more likely if cholesterol is 240 mg/dl (200 is normal)
LDL: high LDL increases risk
HDL: low levels increase risk
cigarette smoking: after 3 years decreases risk to that of a nonsmoker
hypertension: causes injury to epithelium
diabetic contro: causes imparied endothelilal functions
obesity
inactivity: exercise produces NO
estorgen
elevated homocysteine: AA that promotes thrombisis
elevated c reactive protein: marker of inflammation |
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what three things decrease peripheral resistance? |
kinins, prostaglandins, NO |
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what two things increase peripheral resistance? |
angiotensin 2 and catecholamines |
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the innermost layer of blood vessels |
tunica intima |
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the middle layer of the blood vessels |
tunica media |
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the outermost layer of blood vessels |
tunica adventica |
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the part of the blood vessel that produces heparin |
tunica intima |
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part of the blood vessels that constrict or relax to change diameter |
tunica media |
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the part of the blood vessel that produces collagen |
tunica media |
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part of the blood vessel that releases NO |
tunica intima |
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how does resistance of teh blood vessel control blood pressure? |
precapillary sphincters reduce teh amount of blood reaching teh capillary
repeated distension with systole is followed by contraction to propel blood forward
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__ states that pressure is inveresly proportional to the diameter of a vessel |
poiseuilles law |
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what two ways to veins return blood to the right side of teh heart? |
1-way valves
muscle compression pumps |
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traffic flow in the middle lanes is a good explanation of __ |
laminar flow |
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massive vasodilation from an allergic reaction is an example of __ shock |
anaphylactic |
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postpartum hemmorhage is an exampl eof __ shock |
hemorrhagic shock |
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the loss of a large quantity of diarrhea cuases __ shock |
hypvolemic |
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bleeding into the intestines from a ruptured peptic ulcer causes __ shock |
hemorrhagic |
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heart failure with ejection fractin of 10% causes __ shock |
cardiogenic |
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how does the structure of the heart muscle different from skeletal? |
design is branched, not long, has intracellular communication, and lots of mitochondria |
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coronary arteries fill during __ |
diastole |
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why do some older people who have heart attacks not even know it? |
collaterals have develop |
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how does frank stalkings law affect cardiac performance? |
stretch (to a point) improves contraction |
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the initial stretch prior to contraction from passive atrial filling |
preload |
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the force that the heart must work against to open the aortic semilunar valve. measured as BP |
afterload |
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__ law states that the amount of tension generated in teh wall of teh ventricle is inversely related to wall thickness |
laplaces law |
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what is the normal mean electrical axis? |
0-90 |
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severe obesity, and a mean electircal axis of less than 0 degrees causes a __ shift in the mean electrical axis |
left axis deviation |
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a MEA of greater than 90 degrees, COPD, and being a child or a tall person can lead to __ |
right axis deviation |
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explain the 4 stages of an EKG |
phase 4: resting, Ca enters cells, baseline of EKG
Phase 0: rapid deplarization, fast Na channels open, QRS wave
phase 1: closer of fast Na channels
Phase 2: movement of K outward, ST segment
Phase 3: K leaves, T wave |
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class __ agents interfere with the Na channels |
class 1 |
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class __ agens are anti-sympathetics agents. all agents in this class are beta blockers |
class 2 |
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class __ agents affect K+ influx |
class 3 |
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class __ agents affect the AV node |
IV |
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class __ agents work by other or unknown mechansims |
V |
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describe normal conduction |
begins in sinus node, speads to atria (AV node), passes down purkinje system, wraps back up to ventricles |
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what is the normal rate of teh sinus node? |
50-100 |
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on an EKG, what does each small box and large box count for |
.04 s and .2 sec |
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the part of the EKG, marks the atrial contraction, due to small muscle mass of the atria and is wide due to the time it takes for teh impulse to move from right to left |
P wave |
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the part of the EKG that represents the time to collect message from the atria |
P-R interval |
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part of the EKG representing ventricular contraction. its large due to the size of ventricle. its narrow due to the speed of contraction |
QRS wave |
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the part of the EKG that should be flat between teh S and T wave. |
ST segement |
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part of teh EKG that represents repolarization, must occur in order for teh next wave to occur |
T wave |
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what are the characteristics of a sinus rhytherm? |
rate 60-100
PR interval 3-5 small boxses |
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the normal PR interval should be less than __ |
.2 seconds |
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the normal QRS interval should be less than __ s |
.12 |
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the normal QT interval should be less than __ s |
.4 |
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what are the charactersitics of sinus bradycardia |
rate less than 60 bpm
each has a P wave and each P wave looks the same |
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what is the charactersistics of sinus tachycardia? |
rate over 100 bpm |
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with atrial dysfunctions you see a change in teh __ |
p wave |
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this kind of dysrhythmia shows uneven, someimte missed p waves |
atrial fibrillation |
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dysrthmia that gives you a "saw toothed" appearnce on an EKG |
atrial flutter |
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caused by the sinus node not firing and teh junction taking over teh role as pace maker. it has an intrinsic rate of 40-60, there is no p wave evident propr to QRS. CO is impaired due to loss of atria kick |
junctional rhythms |
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caused by diorderes of the atria (changes in p waves), most time atrial rhythm is fast and blocked by the junction
due to abnormal flow of blood in atria there is a risk of clots forming on teh atrial walls |
atrial dysrhythmias |
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dysryhtmia where there is no P wave |
idojunctional ryhtem |
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dyrythemia where the PR interval is greater than .2 seconds |
1st degree AV block |
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dysrythmia where there is a longer delay in teh AV node where teh QRS is dropped. this requires a pacemaker. |
second degree heart block |
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where the rhythem begins in teh ventricles due to failure of teh atira and junction to fire. this has a rate of <40 bpm. this has poor cardiac output due to slow rate and no ventricular filling if beat originates high int eh ventricle. often life treatenting |
ventricular rhythems |
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when the EKG seems to go backwards and the rate is incredibly slow |
idoventricular rhythm |
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what three things does mycardial demand depend on? |
ventricular wall stress, heart rate, contractility |
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what two things does myocardial supply depend on? |
O2 carrying capacity of blood, rate of coronary blood flow |
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a mismatch between myocardial supply and demand. possibly also caused by decreased perfusion to the coronoaires, severe loss of blood, too much demand of the heart |
myocardial ischemia |
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caused when plaque obstructs 70 5 of lumen flow, may be able to meet resting needs but not active needs. lack of functional endothelium leads to contracted vessels, during teh physical exertion, increased demand cannot be met |
stable angina |
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caused by a partially occlusive thrombus. the EKG shows no ST segment elevation. there are no elevations of troponin. it presents with a crescendo pattern of chest pain, angina at rest, and a new onset of severe angina |
unstable angina |
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caused by a spasm of epicardial artery. due to stressors like inflammation and infection. commonly seen with chronic stable angina |
prinzmetals angina |
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>90% are due to disruption of a plaque with aggregation of platelets and formation of a thrombus. rupture caused by inflammatory cytokinds and stress from pressures. leads to necrosis of myocardium. the ST segment is elevated on the EKG. damaged endothelium starts clotting mechanisms. severe imbalance between supply and demand of the myocardium |
acute coronary syndrome |
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resembles angina but more sever, lasts longer and may radiate. you may feel impending doom, does not improve with rest, has diaphoresis, cool skin, and clammy skin. |
acute coronary syndrome |
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the __ is the innermost layer of myocardium that is particularly susceptible to ischemia (few collateral vessles) |
subendocardial |
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a level of injury that encompasses the entire thickness of myocardium |
transmural |
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what happens during myocardial ischemia? |
O2 levels fall cuasing anaerobic metabolism to occur (2 min)
ATP pump fails causing Na and Ca to accumulate in the cell (20 min)
edema of myocardium (4-12 hours)
coagulative necrosis (18-24 hours) myoglobin rises 1-4 hours after troponin rises 3-4 hours after CK-MB rises 3-8 hours after |
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what are 4 complicatoins of an MI? |
decreased contractility, electrical instability, tissue necrosis, and pericardial inflammation |
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what are three treatments for MI? |
stop clotting
stop ischemia
improve myocardial O2 |
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the __ is a two layered sac that encircles the heart |
pericardium |
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viruses like coxsackie, influenza, measales, mumps, mononucleuosis, TB, and pyrogenic bacteria are all __ causes of pericarditis |
infectious |
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post MI, uremia, cancer, radiation side effections, autoimmune diseases, and drug side effects are all causes of __ pericarditis |
noninfectious |
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what is the pathophysiology of pericarditis? |
collection of fluid in teh percaridal space (vasodilation)
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chest pain that worsens in a supine position, fever, sinus tachycardia, and friction rub over the cardiac apex and sternal border is indicitive of what? |
pericarditis |
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a collection of fluid or blood in the pericardium |
pericardial effusion/tamponade |
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the pericardium can stretch with __ |
slow accumulations |
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the pericardiumc annot stretch with __ of over __ |
rapid accumulations, 50-100 ml |
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if pressure in the pericardium equals __, the heart will not be able to pump |
diastolic pressure |
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pulsus paradoxus (BP of 10 mmHG lower during inspiration indicating impaired diastolic filling), distant or muffled heart sounds, poorly palpable apical pulse, dyspnea on exertion, and dull chest pain is indicitive of what? |
pericardial effusion/tamponade |
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a group of diseases due to toxic or structural problems in the myocardium |
cardiomyopathy |
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ischemia, hypertension, infections, toxins, connective tissue disease, inflitrative diseases, and nutritional diseases are all common causes of __ |
cardiomyopathy |
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what are teh three kinds of cardiomyopahty? |
dilated (heart dilates with heart failure)
hypertrophic
restrictive |
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kind of cardiomyopathy where ventricualr dilation and grossly reduced systolic function are seen. caueses are alcohol abuse (most common), post infections response, geneitc cuases, and toxic reposne to chemo. |
dilated cardiomyopathy |
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what is the most common cause of cardiomyopathy? |
alcohol abuse |
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the clinical signs of __ are dyspnea and fatigue, lung congestion, systemic and pulmonary emboli, elevated BP, and cardiac murmurs |
dilated cardiomyopathy |
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what is the hallmark of hypertorphic cardiomyopthay? |
a wide septum |
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hypertorphic cardiomyopahty is a __ disease. it has variable penetrance and expression and is caused by abnormal genes for sarcomere proteins |
autosomal dominant |
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what does the wide septum in hypertorpic cardiomyopahty cause? |
hyperdynamic state (increased myocardial contractility and EF) |
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what happens to people with hypertrophic cardiomyopathy as their septum continues to enlarge? |
outflow from teh LV is impaired causing sudden cardiac death in preadolescent and adolescent kids |
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a person presenting with angina, dysrthmia (due to an impaired pathway running through teh septum), syncope, palpitations, and left sided heart failrue has teh clinical signs of __ |
hypertorphic cardiomyopahty |
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happens when the myocardium is inflitrated with materials that stiffen the muscle. the heart is unable to stretch and has reduced filling pressures and output. |
restrictive cardiomyopathy |
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what are three causes of restrictive cardiomyopathy? |
amyloidosis (proteins build up in the heart, making it stiff)
hemochromatosis (build up of iron)
sarcodiosis (glycogen storage disesase) |
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Patients with this disease often present at an advanced stage of disease with pronounced cardiopulmonary symptoms. • The patient's history may reveal the following: – Angina – Dyspnea, orthopnea, or dyspnea on exertion – Paroxysmal nocturnal dyspnea – Peripheral edema – Abdominal discomfort, liver tenderness – Increased abdominal girth, ascites • Physical Findings – Elevated jugular venous pulse, Kussmaul sign – y descent blunted relative to x – S3 and/or S4 – Occasional mitral or tricuspid regurgitation murmur – Distant heart sounds – Pulmonary rales – Peripheral edema – Pulsus paradoxus • Disappears as the restrictive process progresses |
restrictive cardiomyopathy |
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an infecition of the endocardium, commonly from strep or staph |
infectious endocarditis |
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valvular heart disease, prostetic valves, conential proglems that create turbulent flow, and IV durg use/long term catheters all are risk factors for __ |
infective endocarditis |
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what is the pathogenesis of infective endocarditsi? |
endothelial damage exposes endocardium tissues, create injury response and attracts WBC's to form thrombus
microorganisms attach to thrombus and enters injured endocardium
bacteria prolifersate in thrombus |
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what are the valves on the R side of the heart? |
tricuspoid and pulmonary |
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what are teh valves on teh L side of the heart? |
mitral and aortic |
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what happens to valves during diastole? |
tricuspid and mitral valves open to fill venticles |
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what happens to vales during systole? |
pulmonary and aortic valves open to send blood forward |
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a valular disease where the valve does not completely open. forward flow is impeded, the chamber behind dilates, fails, and hypertorphys |
stenosis |
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valvular disease also known as insufficiency or icomeptence. the vale fails to close. teh chamber behind hypertorphies due to increase workload |
regurgitation |
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valvular disease caused when the cusps of a vlave billow during sysotle. some are normal and asymptomatic |
prolapse |
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__ valve prolaspe may be autosomal dominant |
mitral valve |
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what are three causes of valve disease? |
bacterial endocarditis (produce vegetations on the heart)
acute rheumatic fever (caused by strep infecition)
heart failure (stretches space between valves |
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the mortality rate of congentical heart deffects is __ in teh first year of life |
35% |
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what are four classifications of congentical heart defects? |
increased pulmonary blood flow (L-R shunt)
obstruction of blood flow from ventricles
decreased pulmonary blood flow (R-L shunt)
mixed blood flow |
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what are thee important chagnes in teh embryonic heart that are different from the adult heart? |
ductus venosus allows blood to bipass liver
foramen ovale allows blood to be shunted from the R atrium to the L atrium
ductus arteriosus allows blood to bipass the lungs |
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what are the 4 problesm in tetrology of fallot? |
large ventricular septal defect
pulmonary stensosis
overrriding aorta
hypertrophic R ventricle |
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difficultly feeding, faliure to gain weight, and cyanosis are signs of __ |
tetrology of fallot |
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what is a common manifestion of the tetrology of fallot when infants are agitated and have very severe cyanosis? |
TET spell |
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a kind of mixed bloodflow congenital heart deffect characterized by an underdeveloped L heart. there is a hypoplastic ascending aorta and a hypoplastic L ventricle |
hypoplastic L heart |
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a congential heart defect characerized by L-R shunting of blood in the heart. this enlagrges the R atrium and ventricle. |
atrial septal defect |
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a congential heart defect where there is a narrowing at, before, or after the ductus arteriosos. it is more serious if the coarctation is before the ductus arteriosus. |
coartaction of the aorta |
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what are 5 common effects of congenital heart disease? |
murmurs
dysfunction of "normal" cardiac vacularture
hematologic problems
increased risk of CHF
failure to thrive |
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the ability of the heart to sponstaneously depolarize iteslf to a threshold voltage |
automaticity |
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what are the specialeized pacemaker cells of the heart? |
SA node
AV node
ventricular conduction system |
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explain teh path of conduction in the heart |
begins at SA node with rate of 60-100 bpm, causes atria to depolarize
pauses at junction to gather impulses from atria
rapidly spreads through the ventricle down bundle branchs and up purkinje fibers in teh ventricles rapidly depolarizing the ventricles |
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what is the pacemakers of the heart? |
the SA node |
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what doe the AV node and bundle of his beat at intrinsically? |
50-60 |
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what does the purkinje system in the ventricles beat at intrisnically? |
30-40 |
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the ion leak for the SA node cells peaks at phae __ |
4 |
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explain ion changes in SA node cells during phase 4 |
Na leaks in by slow channels
fast Na, Ca and K channels open. |
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the wave of teh EKG where teh Na/K pump is replacing ions, must have this to be able to fire again |
T wave |
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what kind of dysrhythmias are caused by altered impulse formation? |
escape rhythms
ectopic beats |
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what kind of dysryhthmias are caused by altered impulse conduction? |
blocks
re-entry |
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what can cause altered impuse formation and a change in SA node firing? |
neurohormone factors from SNS or PNS |
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a kind of altered impulse formation where the characteristics of a sinus rhythm are the same but the rate is slower. this can lead to syncope due to low outputs but can be normal in athletes |
sinus bradycarida |
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a kind of altered impulse formation where it has the characteristics of a normal sinus rhythem but the rate is greater than 100 bpm. this can lead to myocardial ischemia due to O2 demands |
sinus tachycardia |
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a kind of altered impulse formation where the SA node is suppressed from vagal stimulation. the pacemaker cell shifts to other atrial cells to prevent bradycardia. after teh 2n beat of sinus orgin, the T wave is dormored by an atrial escape beat. |
escape rhythems |
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a dysrhythmia caused by the atrial cells firing early where depolarization is the same but the P wave has a different configuration. the SA node resumes the pacer function after a compensatory pause |
premature atrial contraction |
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a dysrhythmia that occurs when latent pacer cells develop and intrinsic rate that is faster than the SA node. the SNS stimulation increases automaticity of latent pacer cells. |
an ectopic beat |
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how does cardiac tissue injury lead to increased automacticity in cells outside of teh conduction system? |
ischemia of cells makes their membrane more leaky and prone to firing. |
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when an impulse is blocked when it reaches an area that cannot depolarize b/c its either still not repolarized from its last beat, ischemic, or fibrotic/scarred from prior injury. it may lead to escape beats when an area beyond teh block has to assume pacer funciton |
conduction blocks |
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a conduction block characterized by a slowed conduction through the AV node (greater than .2 s) |
1st degree heart block |
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__ degree heart block is caused by digitalis and other antidyrhthmetics, infectous diseases like lyme disease, or in well trained athleres with lots of vagal tone) |
1st |
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conduction block caused by a progressive lengthening of PR interval until a QRS is dropped. |
2nd degree (mobitz 1 or wenckeback) |
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kind of conduction block where conduction fails intermittently in teh bundle of his-pukinje. the impulse arrives during the absolue refractory period resulting in teh absence of conduction and no QRS. caused by actue inferior wall myocardial infarction, myocarditis, rheumatic fever, digitalis, beta blockers, Ca channel blockers, or excessive vagal tone |
second degree heart block (mobitz II) |
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conduction block where there is atrial ventricular dissociation. atiral depolarization is completely blocked at teh AV node, normal atrial conraction is present but not coordinated with venticles. it presents as severe fatigue due to very limited cardiac output |
3rd degree heart block |
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a rhythm that becomes self sustaining and repeatedly depolarizes the same tissue. these are very dangerous b/c of decreased cardiac output, risk of clotting. |
reentry |
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what are four kinds of reentry dysrhtmias? |
atrial fibrillation, atiral flutter, ventricular tachycardia, venticular fibrillation |
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is a chaotic atrial contraction (300-600 bpm) from reentry of impulses. it is blocked by the junction b/c it hasn't repolarized. there are little discernable P waves, the rhythm is irregularly irregular. common in patients with enlarged atria. blood clots are a high risk b/c of quickering atria leads to stagnent blood |
atrial fibrillation |
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a rapid atrial contraction from the same pacer cell (but not the SA node) with a rate of 300-600 bpm. wave look saw toothed. atrial contraction is blocked by the AV node. ventricular contraction is failry regular. |
atrial flutter |
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a rapid rhythm form teh ventricular pacer cells. there is not cardiac output. can quickly detriorate into V fib |
ventricular tachycardia |
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a disordered rhythm of ventricular pacers. there is no cardiac output. will deteriorate into a fine fibrillation and asysotle. more difficult to shock |
ventricular fibrillation |
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patients with CHF usually have a __ year mortality |
5 |
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coronary artery disease, hypertension, valvualr heart disease, congential heart disease, cardiomyopathy, and infectious endocarditis are all causes of __ |
heart failure |
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all changes in heart failure are due to __ |
decreased cardiac output |
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how does the heart change during heart failure? |
decreased SV due to:
decreased systolic function (loss of contractility)
decreased diasolic function (L ventricle becomes stiffer)
high ventriculr end-diastolic volumes in attempt to use frank starling law to increase SV. myocardium hypertorphies and needs more fuel |
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what neurohumoral changes occur due to heart failures? |
activation of SNS by baroreceptors
activation of renin angiotensin system due to low pressure in renal A
these produce arteriolar vasocontriction to maintain BP and venous vassocontriction to increase return. increases preload and edema |
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describe teh pathogenesis of heart failure |
ventricular failure leads to decreased CO and decreased arterial pressure.
increased SNS, angiotensin II, aldosterone, and vasopressin all increased systemic resistance and decreasing CO.
aldosterone and sngiotensin 2 increases blood volume and venous tone causing pulmonary edema and increasing venous return |
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early remodeling leads to early adaptation in heart failure due to __ and __ |
increased stroke volume, decreased wall stress |
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later remoddling leadys to problems in heart failure due to __, __, __, and __ |
increased O2 demands, myocardial ischemia, impaired contraction, dysrhthmias |
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caused by a decreased in endogenous vasodilators (NO, prostaglandins, and ANP), an increased in vasocontrictors which produces increased preload and afterload, more remodeling, and fluid accumulation |
decompensated heart failure |
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a heart failure caused by elevated systemic aterial pressure leading to hypertophy of teh LV and pulmonary edema
increased pulmonary pressures increase workload on teh right sid eof teh heart
elevated systemic venous pressure leads to edema in teh periphery and elevated R sided pressures. |
backward failure |
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kind of heart fialure where there is a dilated LV with impaired contractility |
systolic heart failrure |
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kind of heart failure with a normal LV with impaired ability to relax adn recieve blood and eject blood |
diastolic |
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both systolic and diastolic heart filaure result in __ |
decreased SV, activation of baroreflexes and chemoreflexes which promotes LV hypertrophy |
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desceibe teh 4 classifications of heart failure |
class I: no limitations, ordinary physical activity doesn't cause undue fatigue, dysnpea, or palpitations
class II: slight limitations of physical activity, comfortable at rest. ordinary Pa results in fatigue, palpitaions, dysnpea, or angina
class III: marked limitation of pa, pts comfortable at rest but less than ordinary activity leads to fatigue, dysnpea, palpitations, or angina
class IV: symptomatic at rest. discomfort increases with any pa |
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__ is more common in CHF pts which increases risk of death by 30-60% |
anemia |
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atrial fib, ventricualr fib/tachycardia, acute prerenal renal failure, mitral regurgitation, cardiac cachexia, venous stasis and ulcers, and pulmonary edema are all compications of __ |
heart failure |
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what are 5 common causes of pulmonary edema |
altered capillary permeability, increaed pulmonary capillary pressure, decreased oncotic pressure, lymphatic insufficiency, and a large negative pleural pressure iwth increased end expriatory volume |
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an unintentional nonedematous severe weight loss. a 7.5% loss of premorbid weight over >6 months. caused by portal hypertension. |
cardiac cachexia |
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where are the stem cells for blood cells found? |
bone marrow |
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what hormone inlfuiences RBC formation? |
erythopoietin |
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how much time is required for erythropoietin to produec RBCs? |
5 days |
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__ signals produce WBC's |
inflammatory |
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__ signals produce platelets |
bleeding |
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what 3 things does blood consist of? |
RBC, WBC, platelets |
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what are the two kinds of WBC? |
granular (netrophils, basophils, eosinophils)
agranular (lymphocytes, monocytes) |
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what does plasma consist of? |
plasma proteins and serum |
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what are the three plasma proteins? |
albumin, globulins, fibrinogen (clotting proetins) |
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what is the general pathway fo cell development for blood cells? |
stem cells, progenitor cells (blast cells), differentiate in hematopoietc organs, become mature cells |
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RBC's have a __ production and a __ life span |
continuous, 120 day |
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where is bone marrow in adults, children, and neonates? |
adults: vetebrae, ribs, sternum, skull, proximal epiphyses
children : all bones
neonates: all bones, spleen, liver, lymph nodes |
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where is most iron used in the body? |
Hgb |
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where is most iron absorbed in teh body? |
duodenum and proximal jejunum |
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iron from __ is easier to absorb than __ |
meat, veggies |
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what are the three categoreis of anemia? |
macrocytic (megaloblastic)
microcytic
normocytic |
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kind of anemia where RBC are large and contain a lot of HgB, usually due to impaired synthesis |
macrocytic anemia |
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kind of anemia where RBC's are small and have low volume. usually due to lack of building materials (iron, folate, vitamin B12) |
microcytic |
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kind of anemia where RBC's look normal, usually from loss of volume |
normocytic |
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is necessary for all cellular DNA synthesis including RBC's. can cause microcytic anemia |
vitamin B 12 |
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what is the bodies response to anemia? |
etiology, decrease in RBC's and hemoglobin, decreased in O2 carrying capcity, tissue hypoxia, compensatory mechanicsms (increase in erythropoietin, stroke volume, renin/aldosterone, DPG) |
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normal digestion of cobalamin (B 12) needs __ to be absorbed or metabolized |
IF |
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an anemia caused by inpaied absorptin of vitamin B 12. could be due to a lack of intrinsic factor by partietal cells in teh stomach. |
pernicious |
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dietary lack of B12, stomach, small bowel, and pancrease disorders, bacterial overgrowth in interstine, strict vegetarian diets, breast fed children of vegetarians, and classic prenicous snemia due to failure of intrenic factor production are all cuases of __ |
cobalamin deficinecy ( B 12) |
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pernicious anemia is probably an __ disease |
autoimmune |
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very similar to pernicous anemia, absorpiton is impared inteh jejunum. |
folate deficiency anemia |
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folate is needed for __ |
RBC production |
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pernicious anemia may be present in individuals with __ infections |
H pylori |
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pts with weigh tloss of 10-15 lbs, lab value changes of Hct>20% well tolerated but <20% HR increases and angina, smoth tongue wihout papillae, changes in BM/urine and CNS chagnes may have __ |
pernicous anemia |
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inadequate intake of folate (green vegetables), pregancy, drugs that impair folate absorption (anticonvulsants, sulfadiazine), drugs that impair metabolism (ehtanol, triamterene), and diseases of teh jejunum are causes of __ |
folate deficiencs |
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anemia caused by lack of substrate (esepcailly Fe for Hgb). common forms are iron deficiency, thalassemia (improper Hgb formation), and anemia of chronic illness |
microcytic anemias |
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caused by decreased iron intake, decreased iron abosrbtion, and increased iron loss |
iron deficiency anemia |
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what is teh pathogensis of anemia of chonic disease? |
there is a distrubance in iron metaboism, RBC survival is shortened, ther eis impaired production on bone marrow |
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a failure to make RBC's. can be caused by exposure to toxic substances to bone marrow, side effecst of meds, or from viral infectiosn or pregnancy |
aplastic anemia |
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inherited disorder caused by a mutant sickle cell hemoglobin. highest risk groups are western affricans |
sickle cell disease |
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how does sickle cell disease work? |
Hemoglobin becomes sickle shapped and inflexibly and deoxygenated. |
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sickle cell anemia is an __ disease |
autosomal recessive |
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what are teh outcomes of sickle cell disease? |
sickled cells beocme sticky and lead to clots. thy obstruct microcirculation leading to hypoxia and can damage RBCs |
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the premature destruction fo RBC's. can be aquired or hereditary |
hemolytic anemia |
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__'s clinical presentation is 5-15 min after a transfusion. you see anaphlaxis, bleeding at teh surgical site, falling BP, golden urine |
hemolytic anemia |
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what is the normal reaction to hemorrhage? |
vasconstiction, platelet adhsion/aggregation, fibrin formation and stabilization, clot dissolving |
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a loss of balance between teh clot promoting and lysing systems. mild forms have markes of thrombin formation but no clots/bleeding. more serious forms have depostion of fibrin and bleeding with inappropriate accelerated systemic activation of coagulation. |
disseminated intravascular coagulation |
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low platelet counts caused by decreased production due to bone marrow disease or lack of vitamin B12 |
thrombocytopenia |
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how does DIC happen? |
teh clot starts (small clots form impairing perfusion, tissue ischemia occurs, intravascular thrombin is reduced, fibrigogen is converted to fibrin, there is capillary clotting). bleeding ends (fibrin split products increase, inability of blood to cot, hemorrhage, hypovolemia, shock, and death) |
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an autoimmune bleeding disorder caused by antibodies being produced to a bodies own plateltes. causes sepsis and damgage to heart valves |
idiopathic thrombocytopenia purpura |
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what is taking place in DIC? |
much thrombin tips the Too much thrombin tips the balance toward the balance toward the prothrombic state, and the patient presents state, and the patient presents with thrombosis. Alternatively, with thrombosis. Alternatively, too much clot too much clot lysis (fibrinolysis) results from ) results from plasmin formation, and the formation, and the patient presents with a patient presents with a hemorrhagic state. hemorrhagic state. |
