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69 Cards in this Set
- Front
- Back
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How does the sympathetic nervous system affect short-term control of arterial pressure |
effects on peripheral vascular resistance and capacitance and on cardiac pumping ability
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an increase of arterial pressure of only a few mililiters has what affect on renal output of water
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doubles renal output of water (pressure diuresis) and salt (pressure natriuresis)
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Two ways in which pressure at the equilibrium point can change
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1) shifting pressure level of renal output curve for salt and water 2) changing level of salt and water intake
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basic equation for arterial pressure
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equals CO times total peripheral resistance
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when does increased arterial pressure affect action of kidneys
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when increases of the intrarenal vascular resistance occurs at the same time
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What causes increased arterial pressure, but will return to normal if the kidney is not affected
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Beriberi, AV shunts, hyperthyroidism, pulmonary disease, paget's disease
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What causes decreased arterial pressure, but will return to normal if the kidney is not affected
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removal of 4 limbs, hypothyroidism
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steps of increased arterial pressure with increased fluid volume (6)
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1) increased ECF volume 2) increased blood V 3) increased mean circulatory filling P 4) increased venous return of blood to heart 5) increased CO 6) increased arterial P
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2 ways CO can increase arterial P
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1) direct effect 2) indirect by raising total peripheral resistance through autoregulation
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autoregulation definition
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regulation of blood flow by the tissues itself
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an increase of 5-10 percent of CO can cause mean arterial pressure to rise from…
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100 mmHg to 150 mmHg
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why can increased salt intake affect arterial P more than increased water intake
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salt is not excreted as easily
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why does salt increase ECF volume?
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1) osmolarity (can cause thirst) 2) increased ADH casused kidneys to increase reabsorption of water
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what mean arterial pressure is considered hypertensive
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greater than 110 mmHg (90 is normal)
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lethal effects of hypertension (3)
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1) excess workload on heart 2) high P often damages major vessels in brain 3) high P damages kidneys
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what does excess workload on the heart cause/lead to
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early heart failure, coronary heart disease, heart attack
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volume loading hypertension definition
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hypertension caused by excess accumulation of extracellular fluid in the body
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long term cause of hypertension in volume-loading
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initially due to CO, but then is due to peripheral resistance
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what causes increased total peripheral resistane in volume loading
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increased CO caused excess blood flow through tissues which causes progressive constriction of the local arterioles
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what hormones can cause a volume-loading type of hypertension
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aldosterone or occasionally by excess of other steroids
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primary aldosteronism
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aldosterone secreting tumor in an adrenal gland
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what is aldosterone's affect on the kidneys
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increases rate of reabsorption of salt and water in kidney tubules
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what additionally causes hypertension in someone with excess aldosterone in the long term (months/years)
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pathologic changes in kideys causing even more salt/water retention
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what is a big concern when using artificial kidney
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causing volume-loading hypertension if incorrect fluids added/removed
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where is renin synthesized and stored
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in inactive form called prorenin in JG cells of kidney
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what are JG cells
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modified smooth muscle cells in walls of afferent arterioles immediatedly proximal to the glomeruli
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what is renin
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protein enzyme, NOT vasoactive; acts on angiotensinogen in plasma
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what is angiotensin I
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10 aa peptide with mild vasoconstrictor properties
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how long does renin persist in the blood
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30 mins to 1 hour
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angiotensin II
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formed mostly in lungs by cleaving 2 aas from angiotensin I
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what converts angiotensin I to II
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converting enzyme in the endothelium of lung vessels
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angiotensin II action
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powerful vasoconstrictor (especially in arterioles) and decreases excretion of salt and water in kidneys; persists only for 1-2 minutes
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why does angiotensin only last 1-2 minutes
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rapidly inactivated by multiple blood and tissue enzymes called angiotensinases
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how long does it take for the renin-angiotensin system to become fully active
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~20 minutes
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2 ways angiotnsin causes kidneys to retain salt and water
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1) directly 2) causes adrenal glands to secrete aldosterone
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what happens to long-term renal-body fluid mechanism for arterial P when excess angiotensin is circulating
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automaticcaly becomes set to a higher arterial P level than normal
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direct effects of angiotensin on kidney
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1) constrict renal arterioles 2) causes rapis absoption of fluid from tubules 3) acts on tubular cells to increase Na/water reabsorption
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What is the total result of the direct angiotensin effects on the kidneys
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reduce urine output less than 1/5 normal
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fxn of aldosterone on kidneys
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increase in sodium reabsoption by kidney tubules
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what seems to be the most potent effect on the kidneys via angiotensin
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direct effect may be 3 or more times as potent
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action of captopril
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block conversion of angiotensin I to II
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what occurs when salt intake increased as much as 50 fold when fxnal renin-angiotenson system in place
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arterial P rises no more than 4-6 mmHg
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what occurs when salt intake increased as much as 50 fold when renin-angiotenson system not fxnal
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arterial P increase as much as 50-60 mmHg
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what occurs within seconds of infusion of angiotensin
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constricting arterioles increasing peripheral resistance
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what happens to renin secretion in 'one kidney' Glodblatt hypertension
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increased dramatically, but then returns to normal once system is 'reset' to higher P
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one of most common causes of renal hypertension, especially in older persons |
patchy ischemic kidney disease
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why is arterial P in upper and lower body about equal in coarctation of the aorta
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long-term autoregulation develops so nearly completely that local blood control mechanisms have compensated almost 100% for differences in P
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what percent of expectant mothers delevop preclampsia
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5-10%
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potential causes of preclampsia
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ischemia of placenta, thickening of kidney glomerular membranes (autoimmune?)
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what does ischemia of the placenta cause
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toxins released thatcause dysfunction of vascular endothelial cells throughout body; decreases NO release causing vasoconstriction
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acute hypertension can be caused by…
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neurogenic hypertension via strong stimulation of sympathetic nervous system
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where do nerve from the carotid and aortic baroreceptors connect in the brain stem
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tractus solitaris on each side of the medulla oblongata
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what occurs when these nerves are severed
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same as dramatic decrease in BP, causes rapid increase in BP that returns to normal in about 2 days
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2 structural changes observed in late stages of hypertension |
1) increased preglomerular renal artery resistance 2) decreased permeability of glomerular membranes
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primary hypertension aka essential hypertension
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unknown origin; 90-95% of all people with hypertension
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65-70 % of risk for developing primary hypertension
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excess weight gain/obesity
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characteristics of primary hypertension caused by excess weight gain/obesity
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1) CO increased 2) sympathetic nerve activity increased 3) angiotensin II and aldosterone levels increased 2-3 fold 4) renal-pressure natriuresis mechanism impaired
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What is suspected cause of sympathetic nerve activity increase
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hormones like leptin released from fat cells directly stimulate multiple regions of hypothalamus which have excitatory influence on vasomotor centers of brain medulla
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what ocurs if arterial P is artificially reduced to 100 mmHg from 150 mmHg
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causes almost total anuria and person will retain salt and water until BP is back at elevated level
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what must occur for artificail reduction of BP to be effective
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must improve renal=pressure natriuresis
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2 types of essential hypertension
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1) nonsalt-sensitive 2) salt-sensitive
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what occurs to salt sensitivity as people age
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gradually becomes more salt sensitive, especially after 50 or 60
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what can cause salt sensitivity
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aging, chronic renal diseases, abnormal renin-angiotensin fxn
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2 general types of drugs used in hypertension treatment
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1) vasodilator 2) natriretic/diuretic drugs
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different modes of action in vasodilator drugs
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1) inhibit sympathetic nervous signals to kidneys (or transmitter substance) 2) directly relaxing smooth muscle 3) block action of renin-angiotensin system
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rapidly acting pressure control mechanisms
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1) baroreceptor feedback mechanism 2) CNS ischemic control mechanism 3) chemoreceptor mechanism
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what affects do the rapidly acting mechanisms have
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1) constriction of veins 2) increased heart rate and contractility 3) constriction of most peripheral arterioles
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P control mechanisms that act after many minutes
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1) renin-angiotensin 2) stress relaxation of vasculature 3) shift of fluid btwn blood and ECF
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long-term mechanisms for P regulation
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1)renal-blood volume pressure control 2) aldosterone
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