Renal Control Of Electrolyte Balance

Front 1

organ that regulates Na balance

Back 1

Kidney

Front 2

controls long term BP

Back 2

Kidney

Front 3

effects short term BP

Back 3

carotid sinus reflex

Front 4

total circulatory fluid volume

Back 4

amount of NaCl reabsorbed by the tubule largely determines the amount of water in the body and the total CFV

Front 5

also regulates BP

Back 5

constriction/dilation of arterioles

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restricted arterioles

Back 6

create increased total peripheral resistance (TPR) and higher BP

Front 7

therapy directed towards individual with Essential hypertension

Back 7

dilating vessels and/or slowing and relaxing the heart so it creates lower pressure

Front 8

What happens when the kidneys reabsorb too much sodium and water?

Back 8

stuffs the vasculature with more fluid and exacerbates hypertension... large problem in heart failure

Front 9

Adrenal Cortex

Back 9

secretes aldosterone in response to increased K+ levels, low systemic BP, and low pressure in the glomerular afferent arterioles

Front 10

Low systemic BP

Back 10

caused by failing left ventricle, or due to low circulatory fluid volume from dehydration, hemorrhage, or edematous states (CHF, cirrosis or nephrotic syndrome)

Front 11

Low pressure in glomerular afferent arterioles

Back 11

causes increased renin secretion

Front 12

Renin

Back 12

released by granular cells in respone to low BP, causes the production of Angiotensin II

Front 13

Angiotensin II

Back 13

causes vasoconstriction and aldosterone production

Front 14

aldosterone

Back 14

causes increased reabsorption of sodium and water by the distal tubules and collecting ducts: thereby, increasing total circulatory fluid volume: increasing BP

Front 15

renin-angiotensin-aldosterone system

Back 15

has significant effects on BP

Front 16

principle cells

Back 16

in distal tubules and collecting ducts; reabsorb Na from tubular fluid and secrete K+ and H+

Front 17

hyperaldosteronism

Back 17

causes hypertension due to excess sodium and water

Front 18

alkalemic

Back 18

caused by increased H+ excretion

Front 19

hypokalemic

Back 19

due to increased K+ excretion

Front 20

How much filtered sodium is already reabsorbed by the time the tubular fluid has reached the collecting ducts?

Back 20

90%

Front 21

Maximal secretion of aldosterone can casue?

Back 21

Extra reabsorption of 2% of total filtered Na

Front 22

Minimal secretion of aldosterone can cause?

Back 22

Extra 2% of total filtered Na is excreted

Front 23

How can reabsorbing an extra 2% of Na make a difference?

Back 23

equals 504 mEq Na retained each day, and kidneys reabsorb a proportional amount of water along with it

Front 24

If normal Pna is 140 mEq/L, what new, extra, retained FLUID VOLUME would this newly retained Na occupy?

Back 24

3.6 extra LITERS of saline in ONE DAY, which equals 7.9 lbs.

Front 25

How much weight can a heart failure patient gain in one day (due to the kidneys secreting maximal amount of aldosterone?)

Back 25

8 lbs in one day

Front 26

Why should one weigh heart failure patients reguarly when they are being treated for an exacerbation of CHF (dyspnea and pulmonary edema)

Back 26

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)

Front 27

Essential hypertension

Back 27

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

Front 28

Heart failure

Back 28

total circulatory fluid volume and total peripheral resistance both increase.

Front 29

What happens when the left ventricle fails and doesn't supply the pressure and flow that the kidney wants?

Back 29

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

Front 30

What do the kidneys do to increase blood flow?

Back 30

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.

Front 31

sympathetic tone

Back 31

stimulates granular cells to release renin, and other areas of the nephron to increase reabsorption of everything (increasing circulatory fluid volume)

Front 32

how much filtered potassium gets reabsorbed by the time the tubular fluid reaches the collecting ducts?

Back 32

90%

Front 33

Does a low/high K+ diet effect the nephron from continuously reabsorbing K?

Back 33

No (excpet the principle cells of the collecting duct, because they secrete K+)

Front 34

Do intercalated cells in the collecting duct reabsorb K?

Back 34

Yes

Front 35

Do the principle cells of the collecting duct reabsorb K?

Back 35

No, they secrete K+ into the tubular fluid for excretion

Front 36

How is adjustment of K+ levels handed by the kidneys?

Back 36

By the principle cells of the collecting duct--they secrete different levels of K+ based on high/low K diets

Front 37

High K+ diet

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principle cells of the collecting duct will secrete more K+ than the intercalated cells reabsorb, so excess K+ is excreted

Front 38

Low K+ diet

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the principle cells will secrete very little K+, so K+ is conserved

Front 39

How much HCO3 do the proximal tubule cells reabsorb?

Back 39

Almost 80%

Front 40

What area makes the final adjustments by net secretion of either protons of bicarbonate?

Back 40

The collecting ducts

Front 41

Type B intercalated cells in the collecting duct

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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

Front 42

divalent phosphate

Back 42

urinary buffer that soaks up free H+ ions in the urine and permits the proton pump to continue excreting H+ into the urine

Front 43

body pH

Back 43

7.4

Front 44

monovalent phosphate

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H+ ions combine with filtered divalent phosphate and are excreted in the urine as this

Front 45

urinary buffers

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NH3, divalent phosphate, and glutamine

Front 46

Ammonia (NH3)

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binds secreted H+ ions in the tubular fluid and the product, the ammonium ion (NH4+) is excreted in the urine

Front 47

Glutamine

Back 47

compicated......but it is an important urinary buffer

Front 48

What urinary buffers exist that permis us to excrete large quantities of H+ in the urine?

Back 48

Divalent phosphate, glutamate, and ammonia

Front 49

Kidney can (in regards to HCO3)

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-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

Front 50

Henderson-Hasselbalch (H&H) equation

Back 50

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

Front 51

How do the kidneys adjust CO2 levels?

Back 51

The peripheral and central chemoreceptors detect what the respiratory rhythm center in the medulla tell them to do and either ventillate more or less

Front 52

Fixed (dietary) acid production

Back 52

metabolism of dietary protein generates 50-100 mMoles of H+ ions per day

Front 53

How do the kidneys adjust pH?

Back 53

excrete H+ ions generated from metabolism of dietary proteins. the body pH would be 2.62 (very acidic) if the kidneys couldnt adjust

Front 54

What would the pH be if it wasnt possible to regulate fixed (dietary) acid production?

Back 54

2.62 -- very acidic!

Front 55

Plasma and extracellular sodium exist in how many mMoles per liter of fluid?

Back 55

140 mMoles

Front 56

How and why are our H+ concentrations kept extremely low?

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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

Front 57

How is net water excretion/conservation controlled?

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by ADH (antidiuretic hormone; aka vassopressin)

Front 58

Where is ADH produced?

Back 58

By two nuclei in the hypothalamus: the supraoptic nuclei and paraventricular nuclei

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Where is ADH stored?

Back 59

Posterior pituitary

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Where does ADH work?

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In the collecting ducts

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How does ADH work?

Back 61

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

Front 62

What is the purpose for the very high osmolarity of the interstitial area near the loop of Henle?

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It creates osmotic suction for the net conservation of water during times of personal drought.

Front 63

less oral fluid intake

Back 63

increased ADH production--> more pores-->increased water conservation

Front 64

more oral fluid intake

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decreased ADH production-->less pores-->less water conservation and more WATER EXCRETION

Front 65

What stimulates the secretion of ADH?

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-increased osmolarity of body fluids
-low BP
-angiotensin II
-nicotine

Front 66

What inhibits ADH secretion>

Back 66

Alcohol

Front 67

Dietary vitaminD is either

Back 67

D3 (cholecalciferol) or
D2 (ergocalciferol)

Front 68

Where is D2 or D3 (inactive forms of Vit D) converted into the active form?

Back 68

Renal Cortex

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What is the active form of Vitamin D?

Back 69

Calcitrol

Front 70

Calcitrol

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enable calcium absorption from food in the small intestine..regulates how much calcium comes into the body

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What happens if there is no calcitrol?

Back 71

very little calcium is absorbed

Front 72

Parathyroid hormone (PTH)

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regulates how much calcium is in the plasma

Front 73

PTH

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increases osteoclast activity-->increase release ofbone calcium --> increase Plasma calcium

Front 74

PTH

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increase calcium reabsorption in distal tubule--->increase Plasma Calclium

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Chronic renal failure

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causes decreased calcitrol production--> decreased calcium absorption from intestine -->chronically increased PTH secretion--> chronic bone reabsorption -------> RENAL OSTEODYSTROPHY (OSTEOPOROSIS)

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inevitably, chronic renal failure leads to

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Renal Osteodystrophy (osteoporosis caused by the kidneys)

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Juxtaglomerular Apparatus (JGA)

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senses low Na levels in Macula densa

-senses low perfussion pressure in afferent arterioles...increases sympathetic tone by ANS

Front 78

sympathetic tone of ANS

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stimulates granular cells of JGA to release renin into the plasma

Front 79

renin

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causes production of Angiotensin I----->Angiotensin II (by ACE from epithelial cells)

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Angiotensin I

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converted into Angiotensin II by ACE (angiotensin converting enzyme by epithelial cells, esp. in teh lungs)

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Angiotensin II

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Increases release of ADH from posterior pituitary

-secretion of aldosteron by adrenal cortex

-IS A POWERFUL VASOCONSTRICTOR OF SYSTEMIC ARTERIOLES: INCREASING SYSTEMIC BP

Front 82

ADH release from anterior pituitary

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increases water reabsorption from collecting ducts--->increases total circulatory flow volume--->increasing systemic BP

Front 83

Aldosterone secretion from Adrenal cortex

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Increases Na and water reabsorption by the distal tubules and collecting ducts-->increasing total circulatory fluid volume-->increasing systemic BP

Front 84

Na reabsorption

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aldosterone-- principle cells of distal tubule & collecting duct

Front 85

K+ secretion

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principle cells of the collecting duct

Front 86

HCO3- reabsorption

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Proximal tubule cells "reconstitue" filtered HCO3

Front 87

HCO3- secretion

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Type B intercalated cells of collecting duct (B for Bicarbonate)

Front 88

H+ secretion

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Type A intercalated cells of collecting duct (type A is for Acid)

Front 89

H20 reabsorption

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increased reabsorption in the collecting duct if Increase of ADH

decreased absorption in collecting duct if decrease ADH

Front 90

Calcium

Back 90

PTH: increases calcium reabsorption in distal tubule, increasing the plasma calcium levels

and increases bone osteoclast activity