Physiology Flashcards
What % of potassium is intracellular? In what cells is it located?
What is considered hypokalemia?
Hyperkalemia?
What percentage is filtered then reabsorbed?
98% is ICF Muscle cells <3.5 mEq/L >5.0 mEq/L 86.1%
A histological slide shows shrunken cells. What can you infer about the K+ concentration?
There’s low levels of ICF plasma Potassium in the cells as well, what might this indicate?
Cell shrinkage = Loss of K+
Cell swelling = Gain of K+
Low plasma [K+] = Cell alkalosis
High plasma [K+] Cell acidosis
Calcium is mostly stored where? What percentage?
How much is bound to plasma proteins?
What effect does hypocalcemia have on muscle tissue?
What percentage is filtered then reabsorbed?
99% in bone
40% bound to plasma proteins
Hypocalcemia: increases excitability (decreased charge makes it easier for Na+ to get across membrane)
Hypercalcemia: decreases excitability
98.2%
Lab test shows elevated serum calcium, what are 2 differentials?
Now it’s low serum calcium. 3 differentials?
Elevated Serum Ca
Primary hyperparathyroidism
Malignancy
Low Serum
Hypoparathyroidism
Renal Disease
Vitamin D Deficiency
Where is phosphate stored? How much is bound to protein? HOw much of the unbound phosphate is filtered? Reabsorbed in PCT? Reabsorbed in PST?
85% in bone
14% ICM
31% is protein bound
90% filtered
70% reabsorbed PCT
15% reabsorbed PST
In phosphate metabolism, what is the dietary role?
Calcitriol?
PTH?
Renal Tubular?
Diet: Intake and absorption
Calcitriol: Increase phosphorus resorption from bone and absorption from intestine
PTH: Phosphorus resorption directly from bone. Sitmulates calcitriol
Renal Tube: Reabsorption of phosphorus. Stimulated by Tubular filtered load and inhibited by PTH.
A patient can present to the clinic with a variety of symptoms such as: Muscle cramps, epilepsy, SIDS, arrhtymia and migraines. What could cause these things?
Magensium deficiency
What is the MOA of pseudohypoparathyroidism?
Crappy GPCR complex
How much Mg is bound to plasma proteins? How much is filtered? Reabsorbed in PCT? Thich ascending LoH? DCT? Where is magnesium stored?
Bound: 20% Filtered: 80% PCT: 30% LoH: 60% DCT: 5%
50% bone, 49% ICF
What is the MOA of calcitonin?
What conditions may lead to stimulation of calcitonin?
- opposes PTH
Hypercalcemia –> Calcitionin –> promotes phosphate and calcium excretion
Osteoporosis
Paget’s disease
Hypercalcemia
What is the MOA of calcitriol?
Calcitriol = Vitamin D
binds to Vitam D receptor –> promotes phosphate and calcium reabsorption
A molecule must use the transcellular route to get through the endothelial cells of the tubules. What does this mean?
Goes straight through the cell, through the apical membrane –>
Diffusion through cytosol –> Transport across basolateral membrane –>
Through the interstitial space
Avoids tight junctions!
A molecule must use the paracellular route to get through the endothelial cells of the tubules. What does this mean?
Goes around the cells and through tight junctions. Mostly in the PCT
A cell needs a carrier to get through a membrane, but ATP is not needed. WHat type of transport is this?
Facilitated diffusion
You get to Wall Street and 26th and notice the one way doesn’t turn green unless there are 2 vehicles going the same direction. It seems the Jopper driver finds it harder to speed up than the California license plated driver. This reminds you of what type of transport? What molecule represents the California driver? What tissues is this found in?
Give 3 examples
Cotransport
ATP used indirectly
Na+ is going downhill, others are uphill.
Renal tubule and small intestine.
SGLT (Na, Glucose)
Na+, amino acid cotransport.
Na, K, 2Cl- cotransport.
What type of transporter is the NXC transporter?
What about hte Ca ATPase?
How do they work?
Countertransporter
Use energy from Na K ATPase. Solutes move opposite directions
3Na for every 1 Ca
Which transporter uses ATP directly?
Primary active transport
Carriers have to mediate 3 things. What 3 things affect carriers?
- Saturation: Limited number of binding sites, so once saturated, you’ve hit Tm and rate levels off.
- Stereospecificity: Only transports certain conformations of a molecule (simple diffusion takes glucose, stereospecificty says only L-type glucose)
- Competition: Chemically related solutes compete for the spot.
What specific transporter is located on every cell’s membrane?
What is it’s MOA? include shapes and ratios.
Na K ATPase
3Na –> ECF
2K –> ICF
alpha subunit is where things bind.
- E1: Let go of K+
- E1 –P : grabs onto 3 IC Na
- E2-P: Lets go of Na+
- E2: grabs onto EC K+
What specific transporter is found on gastric parietal cells and alpha intercalated (dark cells) in the renal collecting duct?
What is it’s MOA?
H/K+ ATPase
Pumps H+ from ICF to lumen of stomach.
What specific transporter is located on Sarcoplasmic reticulum and Endoplasmic reticulum?include shapes and ratios
Ca++ ATPase
AKA PMCA
1 Ca++ = 1 ATP
E1 binds IC Ca++
E2 releases Ca to EC
A pt presents with frequent urination and elevated glucose levels in blood and glucosuria. What causes glucosuria?
Diabetes Mellitus, Pregnancy, Congenital abnormality of Na- glucose cotransporter.
What is MOA of glucosuria and diabetes mellitis?
Pregnancy?
Crappy Na Glucose cotransporter?
DM: no insulin to uptake glucose –> glucose overwhelms the cotransporter –> not as much reabsorbed
Pregnancy:
GFR increased -> increased filtration –> So much filtered that Cotransporter is overwhelmed.
Crappy Na glucose cotransporter:
Decreased Tm, glucose excreted at lower than normal plasma concentrations.
Why does splay happen?
Reabsorption is aproaching saturation but hasn’t gotten tehre yet, glucose is still excreted. Why?
Low affinity of Na- glucose cotransporter -if glucose falls off, it’s not getting back onto another one because they’re full.
All nephrons do not have the same Tm
Why is the TF:P ratio valuable?
If you have high TF to P, what can you assume?
WHat 4 molecules will have a TF greater than a P?
Helps distinguish how much is being filtered into urine/ultrafiltrate and how much remains in plasma.
Substance is reabsorbed less avidly than water (more excreted)
Inulin, PAH, urea, Cl-
In the Early Proximal COnvoluted Tubule, what is absorbed at 100% 70% 50% 30%
100: glucose and amino acids
70: H2O, PO4, K+, Ca+, Na+
50% urea
30% Mg++
How does water diffuse through the glomerular complex?
Aquaporins
In the late proximal tubule what is absorbed?
Na+ and Cl-
Absorbed via Na - H antiporter and Cl- base antiporter
How is glucose reabsorbed?
In the early PCT
Apical = SGLT
Basolateral = GLUT1
(SGLT = Na/Glucose symporter; secondary active transporter)
What is the apical membrane?
What is the basolateral membrane?
Apical = tubular lumen –> Endothelial cell
Basolateral membrane = Endothelial cell –> Interstitial/blood
If GFR is increased and plasma glucose concentration remained constant, how would this affect the filtered load?
Would the threshold of glucose saturation value change?
Increase filtered load
Theshold would not change, but due to the increased filtration, you may have too much glucose in blood to be reabsorbed.
You administer a drug that inhibits Na K ATPase. What happens to reabsorption of glucose?
Na/K ATPase maintains the low Na+ content inside the cell so the SGLT transporter can use Na/glucose cotransporter to go inside.
So if you messed up the Na/K, you would mess up all SGLT transporters, lowering the glucose reabsorption
You administer a drug that inhibits OATs.
What builds up on the tubule lumen side?
MOA of OAT?
aKG
Organic anions out of the cell for aKG into the cell
What other transporters does Na/K ATPase power?
Na+ /HCO3 /AA /Pi /H+ SGLT anything using Na+ to get in
In what ways does aKG get into an endothelial cell?
OAT4 (1,2,3)
NaDC3
How does an organic anion cross the basolateral membrane, and the apical membrane?
Basolateral: OAT 1,2,3,
Apical Membrane: OAT4
How does an organic cation cross the basolateral membrane, and the apical membrane?
Basolateral: OCT2 (uniporter)
Apical: MDRI ( ATP), MATE (H+)
PAH is filtered, secreted and excreted. Why is so much excreted?
Very low Tm
As the plasma concentration of PAH goes up, what happens to its clearance?
What about inulin?
And glucose?
Which clearance represents GFR?
PAH: Clearance decreases to 125
Glucose increases to 125
Inulin stays at 125
Inulin.
As the plasma concentration increases, what happens to the urinary concentration of PAH, inulin and glucose?
PAH goes up incredibly fast,
Inulin increases at a steadfast rate
glucose increases slowly at first, then faster.
When can acids and bases cross the membrane?
Once they have been neutralized.
You neutralize a weak acid with acid environment.
You charge a weak acid with basic environment.
An acidic environment favors reabsorption of what? What gets trapped in the tubule?
organic weak acids
Organic weak bases
(Vice versa for bases)
Your pt has an acidic environment in his urine. What is your goal and how do you treat this pt?
Keep HCO3- from being reabsorbed or take more H+ out of tubule.
Tx: actiated charcoal and Sodium bicarbonate IV
What are 4 factors that shift K+ into ICF?
What factors shift K+ Out of cells?
In: Insulin Aldosterone beta adrenergic stimulation Alkalosis
Out: Diabetes mellitus Addison's disease (low adlosterone) B adrenergic blockade Cell lysis Strenuous exercise Increased ECF osmolarity
Arrhythmias can result from [K+] variations. What appears on an EKG if you have 1.5 mM of [K+]?? (Normal is 4.5)
What about during hyperkalemia?
Hypokalemia: U waves
Hyperkalemia: High T waves and eventually death via Vfib
The body Potassium is important to regulate. What cells do the regulating? Where are these cells?
What transporters are used?
beta intercalated cells secrete K+ into the collecting tubule and DCT.
Alpha intercalated cells reabsorb K+
Epothelial –> Tubular lumen (Apical) K+ Out
BK, ROMK
Na+ in
Why might K+ be reabsorbed?
K+ deficiency, low K+ diet, hypokalemia, severe diarrhea
What cells secrete K+, HCO3- and Reabsorb H+ Cl-
Beta intercalated cells
What cells secrete H+ and reabsorb K+ HCO3-
a Intercalated cells
What cells secrete K+ and reabsorb Na+, H2O
Principal cells
What is the normal K+ Serum level?
What 4 ways can that level be changed?
4.2 mEq/L
- Na/K ATPase pump messes up
- Reduced leakage of K+ from ICF to renal interstitium
- increased synthesis of K channels and insertion into luminal membrane
- increased Aldosterone secretion
If you eat a high potassium diet, you may see an increase in what kidney function?
Tubular flow rate
What 3 things stimulate potassium secretion?
Increased ECF [K+]
Aldosterone
Increased Tubular Flow Rate
A pt presents in acute alkalosis. What is the body doing to compensate?
Hypokalemia via increased activity of Na/K ATPase and K+ Secretion
A pt presents in acute acidosis. What is the body doing to compensate?
Send the body into hyperkalemia via decreased activity of Na/K ATPase pump and decreaed K secetion
In order to stabilize K+ secretion, there are opposing factors as to not get extreme. In acidosis, what increases K+ Secretion? What decreases it?
Acidosis
Increase: decrease intracellular [K+] content
Decrease: decrease proximal reabsorption and increase distal flow
In order to stabilize K+ secretion, there are opposing factors as to not get extreme. In volume expansion, what increases K+ Secretion? What decreases it?
increase:
decrease proximal reabsorption
Increase distal flow
Decrease:
Decrease aldosterone
In order to stabilize K+ secretion, there are opposing factors as to not get extreme. In volume contraction, what increases K+ Secretion? What decreases it?
increase:
increase renin, AGII and Aldosterone
Decrease:
Lower GFR and distal flow
In order to stabilize K+ secretion, there are opposing factors as to not get extreme. In high water intake, what increases K+ Secretion? What decreases it?
Increases: Decreased ADH decreases distal water reabsorption while increasing distal flow
Decreased:
Decreased ADH decreases K+ Secretion.
