Lust 1 Flashcards
1
Q
What are common sources of Potassium in our diet?
A
- Orange Juice, Bananas
2
Q
Review the Potassium Balance in our body
A
- Insulin, epinephrine, and aldosterone moves K into ICF
- reduces risk of hyperkalemia
- Good balance occurs when intake and output is balanced
- Loss of K is not from ICF, it is from ECF generally
- Acidosis and cell damage=loss of K from ICF
3
Q
Characterize Aldosterone:
A
- adrenal cortex secretion
- steroids-> intracellular target-> acts in nucleus
- adrenal gland is related to pituitary via cortisol and ACTH (minor role)
- aldosterone for responsive to plasma K and angiotensin II
- comes from 1 place- adrenal cortex secretion, acts on 1 place- kidneys
- aldosterone has a K wasting effect
- diuretics that act on natural K wasting is a sparring diuretic
- feedback is directly by K and indirectly by angiotensin
4
Q
Where is Potassium Reabsorbed in the Nephron?
A
- 100% of the K+ filtered load is reabsorbed before the distal tubule
- Proximal Tubule-60-70%
- TAL-20%
- Potassium is secreted in the late distal tubule and collecting tube in the presence of aldosterone
5
Q
Illustrate, recall: Potassium Excretion
A
- more Na brought in, more K is excreted
- ions move with pathway and electrochemical gradient
(dictates if it goes to blood or lumen) - extra:
Both aldosterone and an increase in plasma potassium act to increase potassium secretion by the principal cells of the distal tubule. - Aldosterone causes an increase in the expression of the apical sodium channels and an increase in the expression and activity of the basolateral sodium potassium ATPase. The transepithelial reabsorption of sodium creates a lumen negative transepithelial potential, and this transepithelial electrical gradient promotes the secretion of potassium into the lumen.
- Because identical potassium channels are on both the apical and basolateral surfaces of the principal cell, an increase in plasma potassium will reduce potassium movement across the basolateral surface. The net effect is to promote potassium secretion into the lumen, and enhance the renal excretion of potassium.
6
Q
What is the effect of Aldosterone intake on Potassium Excretion
A
- function of potassium levels and aldosterone levels
- the effectiveness of aldosterone inc with higher potassium levels
extra:
- This graph illustrates the synergism between the aldosterone regulation of potassium excretion and the potassium filtrate load regulation of potassium excretion.
- At a low level of aldosterone infusion, potassium excretion is low, but increases as plasma potassium levels increase.
In an individual with abnormally low plasma potassium levels (3.2 mEq/l, the light circles on the graph), an increase in aldosterone causes only a small increase in potassium excretion. - In individuals with normal potassium levels (4.2 mEq/l, dark triangles on the graph), an increase in aldosterone greatly increases aldosterone secretion.
- In an individual with high normal plasma potassium levels, aldosterone infusion causes a marked increase in potassium excretion.
7
Q
What is Hyperkalemia?
A
- K+> 5.5 mEq/L
- High potassium destabillizes membrane potentials
8
Q
What are signs of hyperkalemia?
A
- K+> 5.5 mEq/L
- Reduced Urinary K+ excretion
- Kidney disease
- Increased K+ release from cells
- Metabolic acidosis, tissue damage, exercise [high exercise in inexperiences individual], crush injury, tumor lysis syndrome
- results in loss of K from ICF
- Decreased Na+/K+ ATPase activity (digitalis)
- Endocrine disorders
- Hypoaldosteronism
- Insulin deficiency [more likely explanation]
- Treatment
- Insulin infusion (with glucose, to prevent hypogylcemia)
9
Q
What is the consequence of Hypokalemia?
A
- typically occurs when we cannot move K from ECF to ICF
- Increased K+ movement into cells
- alkalosis
- Decreased K+ intake
- Increased K+ loss (diarrhea, diuretics)
- Endocrine disorders
- Hyperinsulinemia
- Hyperaldosteronism (Conn’s syndrome)
- [also too much sodium and water reabsorption, worried about hypertension and intracranial pressure]
- Increased epinephrine (β2 activity) w/o exercise
10
Q
Where is calcium?
A
- Strength of bone
- contraction of muscle
- paired with Vitamin A & D
11
Q
Where is calcium in our diets?
A
- Dairy
- Green vegetables
12
Q
Describe Calcium Balance
A
- ICF is largely bone (reservoir)
- ParaThyroid Hormone moves calcium from bone toward the blood (ECF) because of hypocalcemia
13
Q
How does the Kidney impact the Calcium Levels
A
- Filters 50-60 % of total plasma Calcium
- The Rest bound to albumin, other plasma proteins
- 60-70% reabsorbed in Proximal Tubule
- paracellular
- proportional to water reabsorption
- 20% reabsorbed in TAL
- paracellular [tighter gap junctions, less]
- paracellin
- Distal tubule reabsorption is regulated by PTH [hormones change percentage uptake in ions in distal tubule]
- Acutely and chronically increases Ca reabsorption
- Ca ATPase on basolateral surface
- Na/Ca exchange on basolateral surface
- Decreases PO4 reabsorption [this can bind to Ca and prevent reabsorption]
- Acutely and chronically increases Ca reabsorption
*note the functions of PTH with calcium
14
Q
Where do most hormones act in the nephron
A
Distal Tubule
15
Q
How does parathyroid hormone act in the nephron
A
- increases renal conversion of inactive VIT to active VIT D
- increases Ca uptake from GI tract
- increases osteoclast activity in bone, causing release of Ca from bone
- increase urinary excretion of Phosphate, increasing free calcium levels
- increases Ca reabosorption in distal tubule/cortical collecting duct
- inc activity of the basolateral side:
- Na-Ca Exchanger (NCX)
- Ca ATPase
- inc calcium channel on apical side
- TRPV5/6
- inc activity of the basolateral side:
- PTH stimulates klotho gene transcription
- drives TRP receptors
- increases number of Ca2+ ATPases
16
Q
Where is parathyroid hormone made
A
Parathyroid cells embedded in the thyroid gland
17
Q
What is the negative feedback with parathyroid and calcium
A
- with calcium, there is a counterregulatory hormone- calcitonin
- abnormalities of calcitonin has no manifestation of disease
- classic negative feedback
18
Q
How does PTH act on bone?
A
- inhibits Osteoblast Activity
- Release Cytokines to stimulate osteoclasts
- net: Bone Resorption
19
Q
What vitamin do we need for calicum reabsorption?
A
Vitamin D
20
Q
Vitamin D
A
- fat-soluble vitamin
- ingested or produced in precursor form in skin
- cofactor for calcium absorption in the gut
- Must undergo two hydroxylation steps to be in active form:
1,25 dihydroxy vitamin D
* Liver and kidney participate in hydroxylation steps * PTH converts change from inactive to active form
21
Q
Where is calcitonin secreted from?
A
- C cells in thyroid gland
22
Q
What is the target of calcitonin and what is its function?
A
- Primary target is bone
- inhibits osteoclast activity= net bone deposition
- Does not regulate serum Ca2++
- Preserves bone structure during pregnancy and lactation, or postmenopause (if other treatments fail)
- No diseases of oversecretion or undersecretion of calcitonin
23
Q
Characterize hypercalcemia
A
- Ca2+ >10.2 mg/dL
- Primary hyperparathyroidism (Ca++ <12 mg/dl
- Malignancy (Ca++ > 13 mg/dl)
- 45% bound to albumin.
- Distinguish between total Ca++ and free Ca++ when albumin abnormal
- Albumin is secreted in the liver, so liver function impacts this
24
Q
Characterize hypocalcemia and its caues
A
- Ca2+ <8.4mg/dL
- Hypoparathyroidism (decreased PTH as a cause)
- Genetic, thyroidectomy
- Hyperparathyroidism (elevated PTH as an ineffective response)
- Secondary to hypocalcemia
- 45% bound to albumin. Distinguish between total Ca++ and free Ca++ when albumin abnormal
25
recall: What is the intake and outtake of calcium?
* bone serves as the resevoir when intake doesn't match outtake
26
What is the intake and outtake of phosphate?
27
What is the intake and outtake of Magnesium?
28
does calcium, phosphate or magnesium absorption or excretion not respond to PTH
Magnesium
29
Where is calcium reabsorption in the kidney?
30
where is phosphorus reabsorption in the kidney
31
Where is magnesium in the kidney?
32
What are the transporters in the proximal tubule?
33
What are the transporters in the thick ascending limb?
34
What are the transporters in the distal convoluted tubule?
