• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/85

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

85 Cards in this Set

  • Front
  • Back
WHAT IS DIURESIS
increased H2O excretion
what is Naturiuresis
increased Na excretion
what happens when the ECF increases
increase in ECF > increase Blood Volume > Increase Venous return > Increase Cardiac Output > increase BP > Kidney reduces retention and increases excretions (natureisis/diuresis)
what is oliguria and when does it occurs
it is less urine output and occurs when there is a drop in ECF
what happens when the BP is bellow 50mmHg
the kidney stops making urine (anuria) because it can't afford to lose fluids
what causes an increase in ECF
increase Salt intake or increased H2O intake
how does increased Salt intake effect ECF
increase in salt intake > become more thirsty/drink more water > increase in ECF > increase in Blood Volume
what determines long term arterial pressure
salt/h2o intake
salt/h2o excretion

a problem arises when there is an imbalance between these two causing increase in BP
why is it not detrimental if we consume a lot of salt in one day
kidney makes sure that our body has an optimum amount of sodium and will secrete the excess
what are the two classes of hormones that effect BP
natriuretic (na excretion)
antinatruretic (na retention)
what does Blood lose do to Bp
causes a drop in BP
when are antinaturetics needed
when there is a decrease in BP or blood loss
what does longterm regulation of arterial BP involve
kidneys and hormones (SNS is for short term)
what is RAS
renin angiotensin system
what does RAS do
when there is a decrease in BP or Blood volume

kidneys release the enzyme renin

renin converts angiotensinogen to ANGIOTENSIN I

Angiotensin I gets converted to Angiotensin II by ACE (comes from lungs)
what is ACE
angiotensin converting enzyme
what does Angiotensin II do
vasoconstrictor (constricts BV therefore Increase in BP)

acts directly on the kidney or inderectly (via aldosterone) causing Na/H2O retention (increases blood volume)
what comes into action when someone loses a lot of blood
RAS and SNS
what does SNS effect
CO and TPR
what does the Kidney effect
CO by altering blood volume
what do Hormones/Peptides effect
TPR and CO
what does an Increase in SNS do to the kidneys
causes kidney to retain more water
what is the most potent substance in the body for Na/H2O retention
Angiotensin II
what causes the activation of the RAS
blood loss
decrease in BP
low salt intake
what are the renin levels if you intake a lot of salt
low/0 because the body doesn't want to retain fluid
what does an increase in Blood Volume do to renin levels
makes it 0 because body doesn't want to retain fluid
what does an increase in BP do to renin levels
makes it 0 because body doesn't want to retain fluid which causes an increase in BP
what is the process that occurs w/ renin/angiotensin when INCREASE NA INTAKE
increase Na intake

increase ECF

increase in BP

decrease in renin/angiotensin II levels

decreases Na/H2O retention

normalization of ECF and BP
when is angiotensin II released
when BP is low
what does Angiotensin do to arterioles
causes constriction
what does Angiotensin 2 do to the heart
causes ventricular hypertrophy
what does Angiotensin 2 do to the brain
causes an increase in SNS activity and release of antiduiretic hormone (ADH)
what does Angiotensin 2 DIRECTLY do to the kidneys
causes them to retain Na/H2O
what does Angiotensin 2 INDIRECTLY do to the kidneys
causes the kidneys to release aldosterone which causes Na/H2O retention
why are ACE inhibitors and Angiotensin II antagonist given to people with high BP
because people w/ high BP are hypersensitive to angiotensin 2

ace inhibitors inhibit the enzyme ACE from converting Angiotensin I to Angiotensin II

Angiotensin II antagonist block the receptor that Angiotensin II binds to
what factors increase BP and retention of Na/H2O
SNS and Angiotensin II increase BP

Angiotensin II increases fluid reteniton as well

Aldosterone acts on kidney increasing fluid retention and therefore increasing BP

Endothelin - hormone secreted by endothelial cells that line cardiovascular system and acts as a vasoconstrictor
what is endotholin
a hormone secreted by endothelial cells that line the cardiovascular system. endothelins act as a vasoconstrictor
what factors increase renal secretion and decrease BP
atrial natriuretic peptide
Nitric Oxide
Dopamine
Bradykinin
what does atrial natriuretic peptide do
released when the atria is stretched too much (occurs when there is a high volume)

CAUSES NA/H2O EXCRETION TEHREFORE DECREASES BP AND RETENTION
what does nitric oxide do
made by endothelial cells

acts as a vasodilator and therefore decreases BP
what does Dopamine do
acts on kidneys causing Na/H2O excretion

CAUSES NATURYESIS/DIURESIS
what hormone causes naturiesis/diuresis
dopamine
what does bradykinin do
causes vasodilation
what has increased in chronic hypertension
afterload in the ventricles
what can hypertension lead to
stroke

uncontrolled hypertension leads to kidney failure
what is the BP of someone with hypertension
140/90 or higher
what are the two main forms of hypertension
primary (essential) hypertension - no known cause

secondary hypertension - high bp is secondary because it is caused by something else
where is aldosterone relesed
cortex of adrenal gland
where is epinephrin and norepinephrin released
medulla of adrenal gland
what is Phetochromocytoma
tumor in adrenal medula causing increased production of epi/norepi leading to an increase in BP
what is Primary Aldosteronism
occurs when adrenal cortex is making an excess amount of aldosterone which causes Na/H2O retention and increases BP
what is Preeclempsia
high BP due to pregnancy

theory is placenta is ischemic and releases toxic compounds causing decrease in NO levels therefore constriction occurs
what is Renal hypertension
occurs b/c narrowing/occlusion of arterioles that supply kidney with blood.

this causes the kidney to think that there is low BP and it responds by retaining Na/H2O and INCREASES RENIN SECRETION CAUSING INCREASE BP
what is primary hypertension
majority of people with hypertension have this

unknown cause

theory is it may be due to excess Na intake or stress

40-50% OF PEOPLE WITH PRIMARY ARE SALT SENSITIVE
how does BMI effect BP
the higher the BMI the greater the chance of high BP
what occurs in stage one of hypertension
stage 1 = early hypertension

increase CO b/c kidney retaining more water, ECF, Blood Volume all of which increase BP
what happens in stage two of hypertension
stage 2 = well established hypertension
ECF/CO/Blood Volume are normal but TPR and Arterial pressure has increased

vascular hypertrophy occurs
increase in vascular reactivity
what do diuretics do
lower blood volume by promoting na/h2o excretion
what is the SNS activity in early stages of hypertension (stage 1)
increased activity therefore increased water retention of kidney
what is the SNS activity in established hypertension (stage 2)
variable SNS activity
why is there an increase in TPR in established hypertension (stage 2)
this is due to the organs throughout the body getting more blood than they need and as a result they constrict their blood vessels (this is a response to the increased CO) (AUTOREGULATION)
what kind of dysfunction do people with hypertension have
endothelial and they are hypersensitive to angiotensin 2
what happens when endothelial cells are dysfunctional
decrease NO release
increase Endotholin release

THIS CAUSES INCREASE IN BP
what drugs inhibit Na absorption
diuretics
what happens when you stand up
venous pooling occurs in the leg causing a decrease in venous return/CO therefore decrease in BP this leads to REFLEX TACHYCARDIA which increases your HR
what is reabsorbed in the proximal tubule
65% water
65% salt
what transporters are in the proximal tubule
Na/H
Na/Glucose
Na/AA
what is being pumped in the proximal tubule
glucose
amino acids
H pumped out

NA IS PUMPED IN
what is the fluid that leaves the proximal tubule
isotonic
what is the purpose of the Na/Glucose pump and Na/AA pump
insures that 100% glucose is reabsorbed and tries to absorb 100% AA
what is the absorption in the thin descending loop of henle
reabsorbs 10% of water
what areas of the tubule are permeable to water
thin descending loop of henle

late distal tubule/collecting tubule water permeability depends on whether ADH is there
is the thin descending loop of henle permeable to water
yes
what is the absorption in the thick ascending loop of henle
25% sodium absorption
what areas of the tubule are not permeable to water
thick ascending loop of henle
early distal tubule
fluid leaving the descending loop of henle is
hyperosmotic
fluid leaving the ascending loop of henle is
hypoosmotic
what transporters are in the thick ascending loop of henle
NK2CL
Na/H
what does the NK2CL pump do
2ndary diffusion of CL
fascilitated diffusion of Na
what do loop diuretics do and where do they act on
they effect the NK2CL pump in the thick ascending loop of henle and cause Na not to be reabsorbed therefore Na/K will be excreted more

this means that 25% of Na will not be reabsorbed
what is the absorption in the early distal tube
5-7% Na
what is the early distal tube not permeable to
water
what pump does the early distal tube have
Na/Cl pump

Na transported via fascilitated diffusion
Cl transported via cotransporter/2ndary diffusion
what do thiozide diuretics do and where do they work
they inhibit the Na/Cl pump in the early distal tubule meaning decrease in Na reabsorption
what are the diluting segments in the tubule
thick ascending loop
early distal tubule