Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Human Physiology > Renal phys 2 > Flashcards

Renal phys 2 Flashcards

1
Q

Describe the effect that occurs when there is no anti-diuretic hormone

A

Without anti-diuretic hormone the aquaporin 2 channels are all endocytosed. This means there are no channels for water to pass out of the collecting duct, and it the walls are impermeable to water. Thus the osmolarity doesn’t change.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the effect when anti-diuretic hormone is present

A

The aquaporin 2 channels are present in the walls, and thus the collecting duct is permeable to water. Thus, the osmolarity will increase as the fluid moves down the collecting duct. - lower volume, concentrated urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the sensors for ADH release?

A

Osmoreceptors, baroreceptors, and volume receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do osmoreceptors act in order to cause ADH release?

A

Increase in plasma osmolarity (hyperosmolarity) causes osmoreceptors to decrease in volume, sending more action potentials to the hypothalamus (specialized neurons detect osmolarity - more AP signalling). Results in ADH release.
- the opposite can also happen, where the osmoreceptors swell in hypo-osmotic solution)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do baroreceptors act in order to cause ADH release?

A

When blood pressure is decreased, less action potentials are sent to the NTS (nucleus tractus solitarius), relieves inhibition of stimulatory connection to these hypothalamic neurons. This all leads to ADH release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do volume receptors act in order to cause ADH release?

A

When blood volume decreased, less action potentials sent to the NTS, relieves inhibition of stimulatory connection to these hypothalamic neurons. This all leads to ADH release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is diuresis?

A
  • increased production of urine
  • osmotic diuresis caused by excess solutes being excreted and water following solutes
  • very hydrated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is natriuresis?

A
  • increased excretion of sodium
  • results in higher urine volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some common diuretics?

A
  1. Ethanol: inhibits release of ADH (alcohol) - increases urine volume, produce more urine
  2. AVP receptor antagonist: blocks binding of ADH
  3. NKCC2 antagonist: reduces ion reabsorption - NKCC2 is a major ion reabsorber. Often diagnosed to people with high blood pressure - loop diuretics (water pills). More ions excreted, water follows by osmosis.
  4. Coffee - acts on smooth muscle causing to contract - affects on heart rate (increase), causes bladder to be hyperactive, have urge to pee sooner than needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Diabetes Insipidus?

A

Failure to release ADH (neurogenic) or failure of collecting duct cells to response to ADH (nephrogenic) - mutation to receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe potassium handling - increase and decrease in ECF?

A
  • if potassium in the ECF increases too much: Hyperkalaemia. Particularly bad for the heart/ heart rate (SA node*)
  • if potassium in the ECF decreases too low: Hypokalaemia. Particularly bad for control on insulin secretion.
    Aldosterone released due to angiotensin II, or high levels of plasma K+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do you treat Hyperkalaemia or Hypokalaemia?

A
  • in the situation of hypokalaemia, treatment involves
    providing more K+
    through oral ingestion.
  • More dangerous is the situation of hyperkalaemia, where
    the extra K+ would need to be removed quickly.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does aldosterone affect K+ secretion?

A
  • Aldosterone sometimes causes ROMK channels to move to the apical membrane, which then allows secretion of potassium (K+). Not all the time.
  • BK channels (big capacitance) are gated potassium channels always found at apical membrane - they are gated though and require a trigger to be opened. When opened, they open quickly and frequently, get lots of K+ secreted.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the different situations of K+ secretion within the body?

A
  1. Low K+ secretion: ROMK sequestered, and BK closed (may flicker open briefly)
  2. Normal K+ secretion: ROMK open, and BK closed or ROMK sequestered and BK open more frequently
  3. High K+ secretion: ROMK open, and BK open
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the triggers for ROMK?

A
  • Aldosterone
  • Angiotensin II inhibits ROMK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the triggers for BK?

A
  • Depolarization of principal cells (can be caused by sodium entrance into cells)
  • Increase in intracellular Ca ion levels
  • bending of cilia on principal cells with fluid flow
17
Q

Describe the following sodium & potassium scenarios:
1. Low Na+, normal K+
2. Normal Na+, high K+

A
  1. low Na, normal K
    - Angiotensin II is released which increase Na reabsorption in the proximal tubule because of renin in blood
    - Aldosterone released, increases Na reabsorption in the principal cells
    - Angiotensin II inhibits ROMK channels from moving to the apical membrane
    - BK channels remain mostly closed = not much potassium secretion
  2. normal Na, high K
18
Q

Describe the following sodium & potassium scenarios:
1. Low Na+, normal K+
2. Normal Na+, high K+

A
  1. low Na, normal K
    - Angiotensin II is released which increase Na reabsorption in the proximal tubule because of renin in blood
    - Aldosterone released, increases Na reabsorption in the principal cells
    - Angiotensin II inhibits ROMK channels from moving to the apical membrane
    - BK channels remain mostly closed = not much potassium secretion
  2. normal Na, high K
    - Angiotensin II not released - no stimulus for renin
    - Aldosterone released - due to high levels or K - increases Na reabsorption in collecting duct
    - ROMK move to apical membrane to secrete K
    - principal cells depolarize due to Na
    - BK channels open and secrete K
19
Q

Describe the acid/ base balance

A
  • if the body becomes too acidic then the kidneys will excrete H+ and conserve HCO3
  • Mechanisms to perform acid/base balance:
    1. Reabsorb HCO3 (major buffer)
    2. Excrete H+
    3. Create new HCO3
    *really want to conserve HCO3 - helps to buffer blood and assist with pH
  • the proximal tubule is important for the conservation of filtered bicarbonate
  • intercalated cells of the collecting duct fine-tune proton or bicarbonate secretion
20
Q

Acid/ base reaction formula:

A

CO2 + H2O -> H2CO3 -> H ion + HCO -
carbon dioxide and water -> carbonic acid -> hydrogen ions and bicarbonate buffer
This reaction can move in either direction, and is catalyzed by carbonic anhydrase (CA) - shift to left or right depend on concentrations in the body

21
Q

Describe the process (steps) of bicarbonate reabsorption

A
  1. NHE3 secretes H+
  2. HCO3- combines with secreted H+ to form CO2
  3. CO2 diffuses into the cells
  4. CO2 combines with H2O cells to form H+ and HCO3-
  5. H+ is secreted again (recycled back across apical membrane in order for reaction to occur again)
  6. HCO3- is reabsorbed with Na+ (symporter)- basolateral membrane, bicarbonate drives symporter
    * proximal tubule does not have channel/ permeability for bicarbonate
    * bicarbonate conservation
22
Q

Describe type A intercalated cells: response to acidosis

A
  • type A cells = acid secreting (when pH in blood or interstitial space is low - high concentration of protons
  • these cells put two types of channels into the apical membrane that assist with proton secretion
  • these cells contain water and CO2 and also contain as carbonic anhydrase within them, converts to bicarbonate
  • will secrete the proton in 2 ways: hydrogen potassium ATPase and a simple proton ATPase, *both protons and potassium moving against gradient
  • bicarbonate - chloride exchanger keeps things neutral, bicarbonate used as a buffer
  • acidosis (too many protons, low blood pH) - because of response, serum potassium levels will increase - hyperkalaemic (antiporter)
23
Q

Describe type B intercalated cells: response to alkalosis

A
  • type B cells basically do the opposite of type A, the membrane is flipped
  • activated when your blood is too alkaline, too few protons
  • these cells have CO2 and water
  • when activated they produce bicarbonate and proton, bicarbonate is exchanged along apical membrane in a bicarbonate - chloride antiporter/ exchanger
  • excrete bicarbonate in urine (brings pH down)
  • have hydrogen - potassium ATPase (exchanger) and hydrogen symporter (requires ATP) - both pump protons across basolateral membrane
  • all to lower the blood pH
  • consequence is an increased secretion of potassium - lower potassium levels (hypokaleemic)
24
Q

What are the different causes of acid/base imbalance?

A
  1. Metabolic acidosis - excessive breakdown of fats/ amino acids, ingestion of aspirin, methanol and antifreeze (e.g. on a keto diet - only eat fats and proteins, produce too many ketones, may cause keto acidoses)
  2. Respiratory acidosis - hypoventilation, drug induced respiratory depression - airway resistance due to asthma, fibrosis, muscle weakness - muscular dystrophy (e.g. with hypoventilation - not breathing enough, have a CO2 accumulation, increases protons = acidosis)
  3. Metabolic Alkalosis - excessive loss of H+ due to vomiting (throwing up the acid from stomach) - excessive ingestion of antacids
  4. Respiratory Alkalosis - excessive amounts of CO2 exhaled (hyperventilation) - losing protons -> alkalosis
25
Q

Describe the hypothalamic integration of ADH release

A
  • activating both osmoreceptors and baroreceptors leads to maximal ADH secretion.
26
Q

What happens when the inputs to the osmoreceptors and baroreceptors oppose each other? ie. decrease in plasma osmolarity and decrease in blood volume/pressure

A
  • the osmoreceptor signal matters more (osmolarity is more important - valued more in the body)
  • if there is a decrease in plasma osmolarity and decrease in blood volume, there will still be some aldosterone released but not as much as if the plasma osmolarity increased
  • exception: if hemorrhaging and losing lots of blood volume, the body will release max amount of ADH (recognizes the importance of blood volume at this time)
  • ADH also called vasopressin - vasoconstricts blood vessels
27
Q

Describe the behavioural response for having the proper sodium and water levels?

A
  • although conservation of sodium and water is good, the renal response to RAAS and ADH are not always sufficient
  • behavioural changes are usually necessary to achieve balance of either sodium or water
  • Angiotensin II stimulates salt desire
    ADH stimulates thirst
28
Q

Describe an example of when you have a decrease in volume and an increase in osmolarity

A
  • dehydration
  • sweat loss
  • diarrhea
29
Q

Describe an example of when you have an increase in volume and a decrease in osmolarity

A

Drinking large amounts of water
- probably won’t get ADH release

30
Q

Describe an example of when you have an increase in volume and an increase in osmolarity

A

Ingestion of a hypertonic saline (V8)
- probably will get a moderate release of ADH

31
Q

Describe the response to sweating

A

Sweat is a hypo-osmotic solution) - removal
- causes increased plasma osmolarity + decreased ECF volume
- both of these cause ADH release, which increases water reabsorption
- because of decreased ECF volume there will also be RAAS activation which leads to release of Angiotensin II and Aldosterone - which leads to sodium reabsorption
- this whole process will lead to even more water reabsorption
- once you get normal blood volume, RAAS pathway is turned off - will still get ADH and water reabsorption until the osmolarity is normal again

32
Q

Describe the response to eating salt without consuming fluids

A
  • increased Na+ absorption -> increase plasma osmolarity -> causes ADH release and more water reabsorption (leads to higher blood volume)
  • increased plasma osmolarity also causes water to move from the cells to the ECF which causes increased blood volume
  • increased blood volume is a trigger which inhibits ADH release (because there is a separate trigger causing release of ADH, will still get some, but much less)
  • increased blood volume also causes ANP release which allows more Na+ excreted and this decreases the plasma osmolarity
33
Q

What are the actions of an ACE inhibitor (drug)?

A
  • inhibits RAAS which reduces the production of Angiotensin II
  • ANG II is a vasoconstrictor, so blocking reduces blood pressure
  • acts on proximal tubule - less Na+ reabsorbed
34
Q

What are the actions of a loop diuretic (ex. Furosemide)?

A
  • inhibits NKCC2 (blocks function) which reduces ion/ solute reabsorption in the ascending limb
  • causes osmotic diuresis (water unable to be reabsorbed because of solutes present - thus excreted) - water follows by osmosis
  • decreased medulla concentration and decreased ability to concentrate urine (large volume of dilute urine excreted)
35
Q

What are the actions of Spironolactone (drug)?

A
  • inhibits activity of mineralocorticoid receptor (MR) - usually aldosterone acts on this receptor to increase sodium reabsorption (Na+/K+ ATPase = antiporter)
  • causes osmotic diuresis
  • potassium sparing (increased reabsorption of potassium)
36
Q

What may be the consequence of Spironolactone overtime? How could we solve this? Why is it also important?

A

May lead to hyperkalaemia.
Can be solved by:
1. Stopping Spironolactone
2. Modify dose
3. Reduce K+ in diet (spinach, bananas, etc.)
Potassium is very important for diabetes due to the fact beta cells in the pancreas are dependent on potassium to release insulin.

Human Physiology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions