• 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

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/90

Click to flip

90 Cards in this Set

  • Front
  • Back
organ that regulates Na balance
Kidney
controls long term BP
Kidney
effects short term BP
carotid sinus reflex
total circulatory fluid volume
amount of NaCl reabsorbed by the tubule largely determines the amount of water in the body and the total CFV
also regulates BP
constriction/dilation of arterioles
restricted arterioles
create increased total peripheral resistance (TPR) and higher BP
therapy directed towards individual with Essential hypertension
dilating vessels and/or slowing and relaxing the heart so it creates lower pressure
What happens when the kidneys reabsorb too much sodium and water?
stuffs the vasculature with more fluid and exacerbates hypertension... large problem in heart failure
Adrenal Cortex
secretes aldosterone in response to increased K+ levels, low systemic BP, and low pressure in the glomerular afferent arterioles
Low systemic BP
caused by failing left ventricle, or due to low circulatory fluid volume from dehydration, hemorrhage, or edematous states (CHF, cirrosis or nephrotic syndrome)
Low pressure in glomerular afferent arterioles
causes increased renin secretion
Renin
released by granular cells in respone to low BP, causes the production of Angiotensin II
Angiotensin II
causes vasoconstriction and aldosterone production
aldosterone
causes increased reabsorption of sodium and water by the distal tubules and collecting ducts: thereby, increasing total circulatory fluid volume: increasing BP
renin-angiotensin-aldosterone system
has significant effects on BP
principle cells
in distal tubules and collecting ducts; reabsorb Na from tubular fluid and secrete K+ and H+
hyperaldosteronism
causes hypertension due to excess sodium and water
alkalemic
caused by increased H+ excretion
hypokalemic
due to increased K+ excretion
How much filtered sodium is already reabsorbed by the time the tubular fluid has reached the collecting ducts?
90%
Maximal secretion of aldosterone can casue?
Extra reabsorption of 2% of total filtered Na
Minimal secretion of aldosterone can cause?
Extra 2% of total filtered Na is excreted
How can reabsorbing an extra 2% of Na make a difference?
equals 504 mEq Na retained each day, and kidneys reabsorb a proportional amount of water along with it
If normal Pna is 140 mEq/L, what new, extra, retained FLUID VOLUME would this newly retained Na occupy?
3.6 extra LITERS of saline in ONE DAY, which equals 7.9 lbs.
How much weight can a heart failure patient gain in one day (due to the kidneys secreting maximal amount of aldosterone?)
8 lbs in one day
Why should one weigh heart failure patients reguarly when they are being treated for an exacerbation of CHF (dyspnea and pulmonary edema)
because they could gain 8lbs in one day due to the kidneys releasing max amt of aldosterone (increasing Na and water reabsorption, which is the cause of the weight gain)
Essential hypertension
systemic arterioles are abnormally constricted, resulting in an increase in TOTAL PERIPHERAL RESISTANCE, increasing the total amount of fluid/blood pressure in the whole vascular system
Heart failure
total circulatory fluid volume and total peripheral resistance both increase.
What happens when the left ventricle fails and doesn't supply the pressure and flow that the kidney wants?
in order to increase BP: Granular cells release renin, which causes the production of Angiotensin II, which is a powerful vasoconstrictor--further increases systemic blood pressure
What do the kidneys do to increase blood flow?
the release of renin--> angiotensin II--> causes the release of ALDOSTERONE and ADH, both of which have effects that will increase the circulatory fluid volume.
sympathetic tone
stimulates granular cells to release renin, and other areas of the nephron to increase reabsorption of everything (increasing circulatory fluid volume)
how much filtered potassium gets reabsorbed by the time the tubular fluid reaches the collecting ducts?
90%
Does a low/high K+ diet effect the nephron from continuously reabsorbing K?
No (excpet the principle cells of the collecting duct, because they secrete K+)
Do intercalated cells in the collecting duct reabsorb K?
Yes
Do the principle cells of the collecting duct reabsorb K?
No, they secrete K+ into the tubular fluid for excretion
How is adjustment of K+ levels handed by the kidneys?
By the principle cells of the collecting duct--they secrete different levels of K+ based on high/low K diets
High K+ diet
principle cells of the collecting duct will secrete more K+ than the intercalated cells reabsorb, so excess K+ is excreted
Low K+ diet
the principle cells will secrete very little K+, so K+ is conserved
How much HCO3 do the proximal tubule cells reabsorb?
Almost 80%
What area makes the final adjustments by net secretion of either protons of bicarbonate?
The collecting ducts
Type B intercalated cells in the collecting duct
uses internal water and carbon dioxide to make H2CO3, and when this dissociates, the cell pumps the HCO3 into the tubular fluid for EXCRETION ad pumps H+ ion back out of the cell into the interstitium
divalent phosphate
urinary buffer that soaks up free H+ ions in the urine and permits the proton pump to continue excreting H+ into the urine
body pH
7.4
monovalent phosphate
H+ ions combine with filtered divalent phosphate and are excreted in the urine as this
urinary buffers
NH3, divalent phosphate, and glutamine
Ammonia (NH3)
binds secreted H+ ions in the tubular fluid and the product, the ammonium ion (NH4+) is excreted in the urine
Glutamine
compicated......but it is an important urinary buffer
What urinary buffers exist that permis us to excrete large quantities of H+ in the urine?
Divalent phosphate, glutamate, and ammonia
Kidney can (in regards to HCO3)
-reabsorb/reclain filted HCO3
-generate new HCO3 ions to be retained
-secrete excess HCO3 ions into the urine
-secrete excess H+ ions into the urine
Henderson-Hasselbalch (H&H) equation
quantifies the effects of hte bicarbonate buffer system on plasma/tissue pH. Physiologically powerful because the kidneys can control HCO3 and the lungs can retain/blow of CO2, both of which help to maintian body pH
How do the kidneys adjust CO2 levels?
The peripheral and central chemoreceptors detect what the respiratory rhythm center in the medulla tell them to do and either ventillate more or less
Fixed (dietary) acid production
metabolism of dietary protein generates 50-100 mMoles of H+ ions per day
How do the kidneys adjust pH?
excrete H+ ions generated from metabolism of dietary proteins. the body pH would be 2.62 (very acidic) if the kidneys couldnt adjust
What would the pH be if it wasnt possible to regulate fixed (dietary) acid production?
2.62 -- very acidic!
Plasma and extracellular sodium exist in how many mMoles per liter of fluid?
140 mMoles
How and why are our H+ concentrations kept extremely low?
Our bodies and enzymes are very sensitive to our H+ ion concentration; our lungs and kidneys both help to keep this H+ ion concentration at a low level
How is net water excretion/conservation controlled?
by ADH (antidiuretic hormone; aka vassopressin)
Where is ADH produced?
By two nuclei in the hypothalamus: the supraoptic nuclei and paraventricular nuclei
Where is ADH stored?
Posterior pituitary
Where does ADH work?
In the collecting ducts
How does ADH work?
By creating holes in the walls of the collecting ducts, allowing water to leave and enter the interstitium. Water moves by osmosis to the very high osmolarity of the interstitum near the loop of Henle. ...makes the collecting ducts leaky so osmosis can work for water conservation
What is the purpose for the very high osmolarity of the interstitial area near the loop of Henle?
It creates osmotic suction for the net conservation of water during times of personal drought.
less oral fluid intake
increased ADH production--> more pores-->increased water conservation
more oral fluid intake
decreased ADH production-->less pores-->less water conservation and more WATER EXCRETION
What stimulates the secretion of ADH?
-increased osmolarity of body fluids
-low BP
-angiotensin II
-nicotine
What inhibits ADH secretion>
Alcohol
Dietary vitaminD is either
D3 (cholecalciferol) or
D2 (ergocalciferol)
Where is D2 or D3 (inactive forms of Vit D) converted into the active form?
Renal Cortex
What is the active form of Vitamin D?
Calcitrol
Calcitrol
enable calcium absorption from food in the small intestine..regulates how much calcium comes into the body
What happens if there is no calcitrol?
very little calcium is absorbed
Parathyroid hormone (PTH)
regulates how much calcium is in the plasma
PTH
increases osteoclast activity-->increase release ofbone calcium --> increase Plasma calcium
PTH
increase calcium reabsorption in distal tubule--->increase Plasma Calclium
Chronic renal failure
causes decreased calcitrol production--> decreased calcium absorption from intestine -->chronically increased PTH secretion--> chronic bone reabsorption -------> RENAL OSTEODYSTROPHY (OSTEOPOROSIS)
inevitably, chronic renal failure leads to
Renal Osteodystrophy (osteoporosis caused by the kidneys)
Juxtaglomerular Apparatus (JGA)
senses low Na levels in Macula densa

-senses low perfussion pressure in afferent arterioles...increases sympathetic tone by ANS
sympathetic tone of ANS
stimulates granular cells of JGA to release renin into the plasma
renin
causes production of Angiotensin I----->Angiotensin II (by ACE from epithelial cells)
Angiotensin I
converted into Angiotensin II by ACE (angiotensin converting enzyme by epithelial cells, esp. in teh lungs)
Angiotensin II
Increases release of ADH from posterior pituitary

-secretion of aldosteron by adrenal cortex

-IS A POWERFUL VASOCONSTRICTOR OF SYSTEMIC ARTERIOLES: INCREASING SYSTEMIC BP
ADH release from anterior pituitary
increases water reabsorption from collecting ducts--->increases total circulatory flow volume--->increasing systemic BP
Aldosterone secretion from Adrenal cortex
Increases Na and water reabsorption by the distal tubules and collecting ducts-->increasing total circulatory fluid volume-->increasing systemic BP
Na reabsorption
aldosterone-- principle cells of distal tubule & collecting duct
K+ secretion
principle cells of the collecting duct
HCO3- reabsorption
Proximal tubule cells "reconstitue" filtered HCO3
HCO3- secretion
Type B intercalated cells of collecting duct (B for Bicarbonate)
H+ secretion
Type A intercalated cells of collecting duct (type A is for Acid)
H20 reabsorption
increased reabsorption in the collecting duct if Increase of ADH

decreased absorption in collecting duct if decrease ADH
Calcium
PTH: increases calcium reabsorption in distal tubule, increasing the plasma calcium levels

and increases bone osteoclast activity