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71 Cards in this Set

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