Wk7 - secretion Flashcards
In terms of cellular mechanisms of secretion, what ion(s) is the following organ capable of secreting:
Kidney.
(note: answers are those relevant to this course).
- Hydrogen ions
2. Potassium ions
In terms of cellular mechanisms of secretion, what ion(s) is the following organ capable of secreting:
Stomach.
(note: answers are those relevant to this course).
Hydrogen ions from parietal cells only.
What is the main purpose of kidney tubule secretion? Is this an active or passive process?
Secretion of substances from peritubular capillaries/ ECF back into the filtrate is a way to rid the body of unwanted substances, as they will subsequently pass out of the body in the urine.
Transepithelial transport mechanisms for kidney tubule secretion involve BOTH passive and active mechanisms.
What is the main purpose of hydrogen ion secretion in the kidney? When would the kidney be secreting more hydrogen ions then usual?
The main purpose of hydrogen ion secretion is acid base balance. The kidney will be less hydrogen ions when the blood is too alkaline (not acidic enough), in order to conserve the blood H+.
What parts of the nephron undergo hydrogen ion secretion?
- PCT
- DCT
- CD
Where are potassium ions reabsorbed, and secreted in the nephron? Is this an active or passive process?
K+ ions are actively reabsorbed in the PCT, and actively secreted in the DCT + CD.
Normally, what percentage of K+ ions which enter the filtrate are excreted in the urine?
All of the potassium which is filtered in the glomerulus is actively reabsorbed. However, under normal conditions, 10-15% of that which was reabsorbed is then actively secreted back into the filtrate. The extent to which this occurs is based upon the bodies potassium balance at the time.
The secretion of K+ is coupled with the (secretion/ reabsorbtion) of what ion? Through what channel does this occur?
Na reabsorption. This occurs through a cation exchanger known as the NaK pump!
What factors alter the rate of potassium secretion?
- Acidosis: high [H+] causes decreased K+ secretion. This is because H+ and K+ compete in terms of secretion, and when a person is acidotic H+ secretion takes priority.
- Aldosterone: aldosterone stimulates K+ secretion.
Explain the relationship between the adrenal cortex and levels of K+.
High [K+] stimulates the adrenal cortex to release aldosterone.
High [aldosterone] stimulates the secretion of K+ into the tubules of the nephron.
Thus, a negative feedback cycle exists; where the end result (lowered K+) negates the stimulus (high K+).
List the 4 types of mucosal cells of the stomach.
- Chief (zymogenic) cells
- Parietal (oxyntic) cells
- Mucous neck cells
- Entero-endocrine cells
For the following mucosal cell of the stomach, state what it secretes:
Chief cell.
Chief cells release pepsinogen.
For the following mucosal cell of the stomach, state what it secretes:
Parietal cells.
Parietal cells release HCl and intrinsic factor.
For the following mucosal cell of the stomach, state what it secretes:
Mucous neck cells.
Mucous neck cells secrete mucous.
For the following mucosal cell of the stomach, state what it secretes:
Entero-endocrine cells.
Entero-endocrine cells release gastrin.
What is the name for the collective fluid released from the gastric glands.
Gastric juice.
Explain how chief and parietal cells functions are interdependent.
Chief cells secrete pepsinogen, whereas parietal cells secrete HCl (as well as intrinsic factor, although that is besides the point). Pepsinogen is inactive unless in an acidic environment, which is why the HCl from the parietal cells is imperative. The acidic environment converts pepsinogen into its active proteolytic form pepsin, so that it is able to break down proteins.
What occurs to parietal cells upon stimulation for them to secrete? (brief answer)
Parietal cells undergo a morphological change post stimulus to secrete.
What does the ionic composition of gastric secretion depends upon?
The ionic composition of gastric secretion depends upon the rate of secretion.
In times of high gastric secretion (ie. when lots of food is present), there is an increased secretion of H+, and thus high [H+] in the gastric juice.
In times of low gastric secretion, there is a decreased secretion of H+ and an increased secretion of Na+, resulting in a low [H+] but a high [Na+] within the gastric juice.
What are the 2 structural features of interest regarding parietal cells? What’re the functions of these features?
- Secretory canaliculi - region packed full of villi, and lined with microvilli. Occurs throughout the cytoplasm, connected by a common outlet to cells luminal surface. Function to increase the surface area of the parietal cell, increasing its efficiency of secretion.
- Tubulovesicular system (TV) - an extensive network of tubules and vesicles.
What occurs to parietal cells upon stimulation for them to secrete? (extended
- Increased SA - the tubulovesicular (TV) system fuses with the plasma membrane of the secretory canaliculi, bringing about a huge increase in surface area.
- Increased HCl pumping sites - within the TV system is the HCl secretory apparatus. By fusing with the secretory canaliculi, there is an increase in the amount of HCl pumping sites available.
At max rates of H+ secretion, parietal cells can pump out H+ against how steep of a gradient?
Express this in terms of the pH of the parietal cell, compared to the pH of the lumen.
10^6:1.
pH parietal cell = 7.0
pH gastric lumen = 1.0
The following question regards parietal cells:
How does chloride secretion occur?
a. ) Energy is used to pump H+ into the gastric lumen against its concentration gradient, and this sets up the electrical gradient for Cl- anions to follow. Thus, Cl- passively moves down an electrical gradient due to the large amount of H+ in the gastric lumen.
b. ) Chloride molecule influx occurs in parallel with carbonic acid efflux. As so much Cl- is within the cell (due to so much HCO3- having to leave, which is a product of how much H+ secretion there is), there is an elecrochemical gradient for Cl- to flow out of the cell and into the gastric lumen. It does so through an electrogenic channel.
(note: A & B are both likely to be true, but primarily reason is A)
From where is H+ derived, for secretion from parietal cells? Explain the path taken by molecules subsequently. (extended answer)
H+ is derived from the dissociation of water, into OH- and H+. H+ is then secreted from the parietal cell with a cation exchanger (active, bringing K+ into the cell, H, K-activated ATPase or primary protein pump).
The OH- then combines with CO2, with aid of carbonic anhydrase, to form carbonic acid. Carbonic acid then exits the parietal cell into the interstitial fluid, in exchange for a Cl- molecule (anion exchanger). Carbonic acid moves down its electrochemical gradient and so this is a passive process.
From where can CO2 be sourced in any general cell?
- CO2 derived from metabolic reactions occurring within the cell.
- CO2 from blood/ plasma.
What is the protein responsible for the secretion of H+ in parietal cells called?
The primary proton pump.
H+, K+ activated ATPase.
What is an essential condition required for the primary proton pump to work?
The stomach must have a ready supply of K+.
Explain what is meant by the following general term(s):
Alkaline tide.
In times of high levels of digestion, the stomach produces H+ in excess. This means there is an equally large increase in the amount of HCO3- which leaves the parietal cell in the blood. This wave of alkaline substance is thus referred to as an ‘alkaline tide’.
Briefly detail the 3 phases for gastric secretion & motility.
- Cephalic phase (excitatory) - sight/ smell/ thought of food stimulates CC and hypothalamus, parasympathetic stimulation.
- Gastric phase (excitatory & continuing) - stretch receptors pick up distention of stomach & chemoreceptors pick up increased pH of gastric juice.
- Intestinal phase (inhibitory) - duodenum stretch receptors pick up distention and regulate how much chyme can pass into rest of small intestine. This is done in effort to regulate the work load of the main “business end” of the GIT; the small intestine.
The following question regards control of gastric secretion at the cellular level:
What hormones are responsible for binding to receptors on parietal cells, inducing an increase of HCl secretion?
Do these hormones bind on the same, or different receptors?
ACh, gastrin and histamine all bind to separate receptors on the parietal cell, to bring about an increase of HCl secretion.
The following question regards control of gastric secretion at the cellular level:
From where does ACh arise?
ACh comes from the parasympathetic nerves innervating the gut.
The following question regards control of gastric secretion at the cellular level:
From where does gastrin arise?
Gastrin comes from the G cells in the mucosa of the duodenum and the gastric antrum. Gastrin then reaches parietal cells through the bloodstream.
The following question regards control of gastric secretion at the cellular level:
From where does histamine arise?
Histamine originates from mast cells within the gastric mucosa, and diffuses to the parietal cells.
The following question regards control of gastric secretion at the cellular level:
How is it that gastrin, ACh and histamine cause an increase in the level of HCl secretion? (basic answer)
Histamine, ACh and gastrin all induce the fusion of the TV system with the apical membrane, which increases the amount of H+ pumping sites available.
The following question regards control of gastric secretion at the cellular level:
How do ACh and gastrin bring about an increase in the level of HCl secretion? (detailed answer)
- ACh and gastrin bind to their respective receptors.
- This opens calcium channels, increasing intracellular [Ca+2].
- Increased Ca+2 increased HCl secretion.
(note: exact mechanism by which increased Ca+2 or increased cAMP enchances HCl secretion unknown)
The following question regards control of gastric secretion at the cellular level:
How does histamine bring about an increase in the level of HCl secretion? (detailed answer)
- Histamine binds to H2 receptors.
- This activates adenyl cyclase.
- Adenyl cyclase increases [cAMP].
- Increased cAMP increases HCl secretion.
(note: exact mechanism by which increased Ca+2 or increased cAMP enchances HCl secretion unknown)
The following question regards control of gastric secretion at the cellular level:
What drugs are able to block the effect of gastrin/ histamine/ ACh?
- Cimetidine
2. Ranitidine.
What are histamine H1 receptors involved with (as oppose to H2 receptors, which activate adenyl cyclase)?
Histamine H1 receptors are involved in the immune response.
The following question regards control of gastric secretion at the cellular level:
Compare the potency of the 3 chemicals which control gastric secretion, at the cellular level.
Histamine - most potent.
ACh - potent.
Gastrin - less potent.