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71 Cards in this Set
- Front
- Back
Cardiac Output x peripheral resistance =
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blood pressure
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How do you get the mean BP and what is the normal mean
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DBP + 1/3 PP
70 |
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What is the normal BP
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120/80
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HTN is usually classified as BP > than what
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140/90
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what percent of the population has htn
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20%
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HTN is the leading cause for what diseases
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heart failure
coronary disease kidney failure CVA blindness |
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who is HTN more common in
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males 2:1 reduces close to menapause (65 years)
blacks 3:1 |
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what is more common diastolic or systolic HTN
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diastolic is usually first but systolic usually increases also
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What are the two classifications of HTN and which is more common
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primary (essential)- 90%
secondary- 10% |
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What causes secondary HTN
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some other pathalogical disease, if it is fixed then the HTN is fixed
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What controls the BP
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baroreceptors
Kidneys |
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explain blood flow through the kidneys
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renal artery
segmental arteries interlobar arteries arcuate arteries interlobular arteries afferent arterioles glomerular capillary efferent arterioles |
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what are the special cells around the afferent arteriole just before it enters the glomerulus
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Juxtaglomerular Cells (JG cells)
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What do the JG cells do
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stretch receptors - they are inhibited in high BP and activated in low BP to secrete renin
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What centers are tonically active to control Bp
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vasomotor center - constrict
cardiac accelatory- increase HR cardiac inhibitory- decrease HR |
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What are the three mechanisms of renin secretion
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activation of the JG cells by decreased stretch
direct sympathetic nerve stimulation Indirectly vial macula densa |
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How are the JG cells activated by sympathetic stimulation
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they have B 1 receptors that respond to Epi and NE in the blood to release renin
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How does the macula densa work
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senses decrease in Na in the distal conv. tubule which means GFR needs to increase. The macula densa activates the JG cells to secrete renin
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how does renin work
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converts angiotensinogen from the liver to angio I- ACE converts I to II in the lungs. II constricts the BV and increases PVR and stimulates the release of aldosterone
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What does aldosterone do and where does it come from
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comes from the adrenal cortex and increases salt absorption from the kidneys which then increases water reabsorption
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what are the causes of secondary HTN (10)
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renovascular disease
renal-parenchymal disease cushings syndrome primary aldosteronism pheochromocytoma oral contraceptives toxemia of pregnancy polycythemia volume loading hypertension hyperthyroidism |
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What is the disease of the ateries of the kidney that is involved with sclerosis that causes HTN
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renovascular disease- the decrease BP from sclerosis causes kidney to release renin
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how do you treat renovascular sclerosis and do they always have increased renin
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treat with beta blockers to block beta activity of the JG cells.
1/3 have normal renin levels prob JG cells have increased sensitivity |
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what causes renal parenchymal disease
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pyelonephritis
glomerulonephritis get decrease renal perfusion |
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how does renal parenchymal disease cause HTN
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prob because kidneys have decreased ability to produce vasodilator substances like histamine and prostaglandin (E2)
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what is cushings syndrome
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tumor of adrenal cortex - fasiculata or reticularium region that produce increased amounts fo glucocorticoids that increases the reabsorption of salt and water
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what is primary aldosteronism
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tumor of adrenal glomerulosa that produced increased amounts of aldosterone- increase salt and water
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what is pheochromocytoma
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tumor of adrenal medulla causing increased epi and NE released that increases PVR and BP
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how do oral contraceptives increase BP
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Increased estrogen stimulates increased angiotensinogen
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what causes abnormal thickening of the glomerular membrane that prevents filtration of proper amts of water salt and waste
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toxemia of pregnancy- this leads to increase BV and HTN
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when do you have volume loading HTN
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when there is 60-70% kidney mass damage and a person cannot excrete normal amounts of fluid leading to increase plasma volume
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how does hyperthyroidism cause HTN
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increased amount of thyroxin hormone that increases the metabolic rate and the workload on the heart- leads to HTN
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what stays abnormal in essential HTN- CO or PVR
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CO returns to normal but PR is always increased
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what happens to baroreceptors in essential HTN
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reset
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what is the cyclic process of HTN
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HTN causes atherosclerosis causes HTN
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does HTN have genetic tendancies
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yes
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what are the theories for essential HTN
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neurogenic theory
arterial pressure- Urinary Output theory regulatory imbalance theory |
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explain the neurogenic theory
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increased SNS outflow over a period of years causing smooth muscle hypertrophy - decrease lumen size- increased resistance- HTN
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what happens in arterial pressure -urinary output theory
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something happens to the kidney to prevent normal salt and water excretion at normal BP levels, so the BP must stay increased to maintain normal salt and water excretion
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what clinical evidence supports arterial pressure -urinary output theory
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pts put on vasodilators to decrease PVR and increase blood flow to the kidneys but they still cant excrete enough salt and water- need a diuretic also
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what is the regulatory balance theory
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just that there are a lot of factors that contribute to CO and PR and if any are out of balance it can lead to HTN
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What is the problem with HTN
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extra work to left ventricle and the heart muscle hypertrophies and fails- blood backs up can have pulmonary edema and eventually peripheral edema and righ heart failure
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treatment for secondary htn
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treat the cause
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treatment of primary htn
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remove stress
restrict calories- low choles. low fat, low Na exercise vasodilators- ACE inhib., BB, CCB diuretics |
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what is the inadequacy of blood flow to the extent tissue damage occurs
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hypotension (shock syndrome)
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what BP and mean = shock
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< 90/60
mean 70 |
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what are the three stages of shock
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Compensated (non-progressive)
Progressive Irreversible |
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what stage of hypotension does tissue damage begin to occur
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Progressive
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how do you differentiate between progressive and irreversible shock
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you can't
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What are the types of shock (6)
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hypovolemic
cardiogenic neurogenic anaphylactic septic obstructive |
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what can cause hypovolemic shock
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trauma
severe vomiting and diarrhea severe dehydration burns decrease blood volume- hemorrhagic shock |
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what is the normal blood volume
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12-14 pints
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what does a10% volume loss cause
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no effect on CO or arterial pressure
baroreceptors compensate |
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what does a 15-20% volume loss cause (2 pints)
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small decrease in CO but arterial pressure is maintained by baroreceptors causing vasoconstriction
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at what volume loss can baroreceptors no longer compensate
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more than 20-25 % (2-3 pints) this is when progressive shock begins and tissue perfusion begins to suffer
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what happens at 35% volume loss (3-4 pints)
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arterial pressure will stabalize and plateau at about half of normal perfusion pressure but CO will continue to drop
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what happens at 45-50% volume loss
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everything fails and becomes irreversible shock
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what is responsible for the pressure stabalization at 35-45% volume loss
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CNS ischemic response (sympathetic response)
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what is the CNS ischemic response
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last attempt by the brain to preserve its function
causes vasoconstriction of every vessel in the body except those supplying the brain and heart will see blancing of the periphery - will cause tissue gangrene |
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what is the failure of the heart to provide adequate CO and tissue perfusion
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cardiogenic shock
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causes of cardiogenic shock
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MI
chf or just compromised heart |
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what causes neurogenic shock
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inhibition of the vasomotor center in the brainstem causing peripheral resistance to fall, tone is lost in the bv and blood pools in the peripheral capillaries
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what is the most common form of neurogenic shock
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fainting
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what can inhibit the vasomotor center
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anesthetics
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what causes anaphylactic shock
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antigen antibody type reaction producing an inflammatory response in the wall of the blood vessels releasing large amounts of histamine- vasodilates and decreases BP
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what causes septic shock
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foreign toxin that causes large amounts of histamine and other vasodilator substances
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type of shock caused by viral or bacterial toxins
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septicemia
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what causes obstructive shock
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any obstruction of the normal vascular pathway that causes no or reduced blood flow - reduces venous return to heart
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most common cause of obstructive shock
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embolus- decreases CO
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symptoms of shock
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decrease bp
increase pulse rate, decrease pulse volume pallor, cold, wet skin dilated pupils peripheral cyanosis anxiety air hunger decrease capillary refill lactic acidosis hypercapnia |
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treatment of shock
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reestablishment of circulating volume- fluids
cardiotonic agent- stimulate the heart steroid therapy- for anti-inflammatory response |