Physiology-Control and Composition of Body Fluids Flashcards Preview

CPR II > Physiology-Control and Composition of Body Fluids > Flashcards

Flashcards in Physiology-Control and Composition of Body Fluids Deck (47)
Loading flashcards...
1
Q

What things does the kidney try to control?

A

Water, Na, K, Ca, P, Mg and Acid-Base

2
Q

A storm hits your city really hard and you get snowed in. All you have to eat is potato chips and water storage. Why might you see a weight gain after eating your emergency food supply for a couple of days?

A

As you increase sodium intake, your body tries to maintain a constant plasma osmolarity. With increased salt intake, you must retain more water to maintain the same osmolarity and will gain water weight.

3
Q

How does the body assess its water content?

A

Plasma osmolarity and the Effective Circulating Volume (fullness of vascular system)

4
Q

Where are plasma osmolarity receptors and baroreceptors found in the body?

A

Osmoreceptors = Hypothalamus. Baroreceptors = Aortic arch and carotid sinus.

5
Q

You’re hungry for your morning snack and grab a bag of chips. While pounding the chips you ingest 9g of NaCl. How does your body respond to this?

A

This will increase plasma osmolarity by about 3%. The hypothalamus will sense this and send a signal to the pituitary gland to release more ADH (10x) in response to the increase in plasma osmolarity. Osmoreceptor stimulation also increases the thirst reflex. These two consequences = increased H2O intake & decreased H2O excretion

6
Q

What kind of change do you need in the effective circulating volume in order to get the same increase in ADH seen in changes with osmolarity?

A

Baroreceptors are not as sensitive as osmoreceptors. You need about 15% decrease in ECV to get a 10-fold increase in ADH.

7
Q

What drives passive reabsorption of H2O in the proximal convoluted tubule?

A

Reabsorption of Na+ and glucose causes a change in osmolarity that makes H2O follow them

8
Q

Where in the nephron does H2O reabsorption not occur?

A

Ascending loop of Henle.

9
Q

Where does ADH have its greatest effect on reabsorption of H2O?

A

Collecting duct (can vary from 8-17%). Everywhere else in the nephron stays constant (PCT:67%, Descending Loop of Henle: 15%)

10
Q

What signaling cascade happens as a result of ADH biding to the V1 receptor on a light cell in the collecting duct?

A

G-protein activation of adenylyl cyclase -> increased cAMP levels -> activation of PKA -> phosphorylation of aquaporin II -> aquaporin II moves to the lumenal membrane of the light cell -> H2O can pass into aquaporin II, go through the cell and leave through aquaporin IV.

11
Q

How does the body know when to get rid of sodium?

A

It knows to get rid of sodium when the effective circulatory volume is high. This is sensed by the baroreceptors in the aortic arch and carotid sinus, the right atrium and juxtaglomerular apparatus in the kidney.

12
Q

How does sodium reabsorption progress as you move along the nephron?

A

*

13
Q

How is sodium reabsorbed in the proximal tubule?

A

Na-K ATPase pump maintains a low intracellular Na gradient. This allows for Na to flow down its gradient from the PCT lumen, through exchangers, into the cells and out the basement membrane.

14
Q

How is sodium reabsorbed in the thick ascending limb?

A

Na-K-2Cl Cotransport, K+ channel and Na/K ATPase.

15
Q

How is sodium reabsorbed in the distal convoluted tubule?

A

NaCl Cotransport and Na/K ATPase.

16
Q

How is sodium reabsorbed in the principal cell of the collecting duct?

A

Epithelial Na channel and Na/K ATPase.

17
Q

What four signal systems are responsible for control of sodium reabsorption in the kidney?

A

Direct hemodynamics, RAAS, Sympathetics, Natriuretics

18
Q

What mechanisms are responsible for the constant perfusion pressure in the glomerulus and thus constant GFR?

A

Myogenic and tubulo-glomerular.

19
Q

An isolated kidney is tested in an experiment on high blood pressure and urine production. The results are shown in the graph below. What accounts for this?

A

Increased BP increases the peritubular hydrostatic pressure. It also decreases the filtration fraction. This results in a decrease in oncotic pressure. With these two factors combined, you get “back leaking” of Na+ and water into the collecting duct and sent out as urine.

20
Q

How do cells in the kidney work to increase Na filtration in response to a decreased effective circulating volume?

A

Macula densa cells sense a decrease in filtered Na+. They signal to juxtaglomerular cells to secrete more renin. Renin is secreted. Angiotensin II is formed and stimulates the zona granulosa in the adrenal cortex to secrete aldosterone.

21
Q

How does aldosterone increase reabsorption of sodium in the kidney?

A

Aldosterone activates genes in the principal cells of the collecting ducts. Short term, these genes code for more Na+ channels. Long term they code of more Na/K ATPase pumps.

22
Q

How does the sympathetic nervous system play a role in Na+ reabsorption?

A

Decreased effective circulating volume causes baroreceptor-mediated signaling to the brain. The brain activates the sympathetic nervous system (the renal nerve specifically) to release renin from juxtaglomerular cells, vasoconstrict the afferent arteriole and increase PCT Na+ reabsorption.

23
Q

A patient comes to see you from the heart failure clinic. Blood tests reveal an elevated ANP. What does ANP do?

A

*

24
Q

What are the main controllers of short-term and long-term blood pressure values?

A

Short-term = Sympathetic Nervous System. Long-term = homeostatic control of Na and H2O by the kidney

25
Q

A 49 year old male comes to your clinic with essential hypertension. You prescribe him lisinopril and hydrochlorothiazide. Why this combination of drugs for this patient?

A

ACE-I prevents aldosterone-induced increased reabsorption of Na at the collecting ducts. HCTZ blocks Na reabsorption at the distal tubule. Both of these result in increased Na excretion, increased H2O excretion, reduced effective circulating volume and reduced BP.

26
Q

Where do the different diuretics act in the nephron?

A

Carbonic anhydrase inhibitors (inhibits Na-H exchanger in PCT), Loop diuretics (inhibits Na/K/2Cl exchanger in thick ascending loop of Henle), Thiazides (inhibits Na-Cl transport at distal tubule) and Amiloride (inhibits Na reabsorption at collecting duct principal cells)

27
Q

Why are heart failure patients so prone to developing edema?

A

Despite back up of blood, the body still senses a decreases effective circulating volume. Consequently RAAS and sympathetic tone are unregulated. Na and H2O are increasingly absorbed and you get fluid overload leading to edema.

28
Q

How does your body immediately respond when you eat three bananas in one sitting? How does it regain normal homeostasis?

A

If all of the K+ in the banana went into the blood you would become hyperkalemic and at risk for arrhythmias. Typically the body will secrete insulin and epinephrine (within minutes) to stimulated skeletal muscle uptake of K+ in the blood to keep levels consistent. For long-term regaining of homeostasis, aldosterone is secreted (within hours) and K+ is secreted into the collecting duct from the blood.

29
Q

How does K+ secretion occur?

A

Na/K ATPase pump is bringing K+ into the cell. The secretory K+ channel lets it pass into the collecting duct.

30
Q

What signal systems control K+ levels?

A

Serum [K+], aldosterone, tubular flow rate, ADH and acid-base.

31
Q

How does an increase in serum K+ alone cause increased secretion of K+ into the collecting duct?

A

Increased extracellular K+ levels stimulates the Na/K ATPase pump. More K+ is taken into the cell and more K+ goes out the secretory K+ channel into the collecting duct.

32
Q

How does aldosterone adjust the cell’s ability to secrete K+?

A

Gene activation to increase # of K+ secretory channels and Na/K ATPase pumps.

33
Q

How does an increase in tubular flow rate cause increased K+ secretion?

A

As more K+ comes out, it is quickly whisked away into the urine, maintaining a high diffusion gradient from the cells to the collecting duct.

34
Q

How does the body separate the effects of aldosterone on Na+ and K+ in response to increased ECV?

A

Tubular flow rate & aldosterone balance each other out. An increased ECV causes decreased PCT reabsorption of K+, increased distal tubular flow and increased K+ secretion. At the same time, the increased ECV stimulates decreased aldosterone secretion and decreases the K+ secretory stimulation.

35
Q

How does the body separate the effects of aldsoterone on Na+ and K+ in response to decreased ECV?

A

Decreased ECV causes increased K+ reabsorption at the PCT. This causes a decrease in distal flow rate which will decrease K+ secretion. However, the decreased ECV will stimulate aldosterone release to secrete more sodium and potassium and the K+ effects will balance out.

36
Q

Why are patients with hyperaldosteronism at high risk for hypokalemia?

A

Increased aldosterone increases K+ secretory channels and K+ secretion. It also causes an increase in ECV, decreased PCT reabsorption, increased distal tubular flow and further increased K+ secretion.

37
Q

Why are patients on loop diuretics at risk for hypokalemia?

A

Blocking the Na/K/2Cl uptake channel in the thick ascending limb decreases Na reabsorption. This will increase the distal flow rate and increase K+ excretion. It will also cause a decrease in ECV which will cause an increase in aldosterone & an increase in K+ excretion. Finally, it will cause a decrease in loop K+ reabsorption, increased distal [K+] and increased K+ excretion.

38
Q

How does ADH promote K+ secretion and how do the effects of ADH help to maintain a constant K+ balance?

A

ADH stimulates increased K+ secretory channels and thus increased excretion. However, ADH also stimulates water reuptake via the aquaporin channels which decreases urinary flow rate and distal K+ secretion.

39
Q

How does the body increase or decrease K+ secretion in response alkalosis or acidosis?

A

Acidosis inhibits the Na/K ATPase pump and K+ secretory channel, increasing K+ retention. Alkalosis stimulates the Na/K ATPase pump and K+ secretory channel.

40
Q

How does the body recover from hypokalemia?

A

It shuts off all K+ secretory mechanisms. Max reabsorption of K+ is carried out in the collecting ducts by the intercalated (dark) cell’s K+/H+ exchange channel.

41
Q

How does the parathyroid hormone reduce Ca excretion in response to low plasma Ca levels?

A

*

42
Q

How much serum Ca2+ usually gets filtered by the glomerulus?

A

40%. The other 60% is bound to serum proteins.

43
Q

Where and how does most Ca2+ reabsorption take place in the nephron?

A

60% occurs at the PCT via passive paracellular transport

44
Q

How does PTH increase Ca2+ reabsorption?

A

Stimulation of active transcellular transport channels, ATPase pumps and Na/Ca2+ exchangers.

45
Q

How does PTH increase excretion of PO4-?

A

PO4- reabsorption is limited by its transport maximum. PTH blocks the Na/PO4 exchangers, lowering the transport maximum and increasing the amount of PO4 excreted in the urine.

46
Q

What percentage of serum magnesium is filtered by the glomerulus?

A

40%. The other 60% is bound to serum protein.

47
Q

Where is most magnesium reabsorbed?

A

70% is reabsorbed in the Loop of Henle and 25% in the PCT.