HYPERKALEMIA Flashcards

1
Q

What cells within the kidneys produce renin ?

A

Juxtaglomerular cells (JG cells)

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2
Q

Causes of Hyperkalemia.

A

1 - AKI/ CKD. If a patient has one of these conditions, the DCT will be damaged, reducing the secretion of K+ into the renal tubule. Equally, there will be a reduced GFR; therefore, the K+ will not easily get into the tubule. Therefore, be absorbed as both of these can cause hyperkalemia due to kidney damage.

2- Issue with the adrenal cortex. The adrenal cortex produces aldosterone, and aldosterone works on the DCT to increase sodium reabsorption (into the blood) and increase K+ secretion (into the nephron).

3- NSAIDS. Renin is produced by the juxta glomerulus cells. NSAIDs inhibit the JG cells and prevent renin from turning angiotensinogen into angiotensin 1; therefore, angiotensin two is not produced to stimulate aldosterone. ALDOSTERONE production, affecting the DCT.

4 - ACE INHIBITORS - ACE INHIBITORS inhibit angiotensin 1, getting converted into angiotensin two and, therefore, less ALDOSTERONE. This affects the DCT.

5- K-sparing diuretics (Spiranoloctone) prevent aldosterone binding to receptors and stop NA from being reabsorbed and K being excreted.

6- Transcellular shift - Insulin stimulates the NA/K ATPASE. Therefore a decrease in insulin eg DIABETES MELLITUS, has an increased risk of hyperkalemia.

7 - Beta- blocker - B2 receptors stimulate NA/K ATPASE. Therefore beta blockers can reduce this and cause hyperkalemia.

8 - Digoxin - Inhibits NA/K ATPASE. Doesnt allow potassium to be pushed into cells so it stays outside, resulting in hyperkalemia.

9- Severe acidosis. An increase in H+ leads to an acidic environment, and therefore the protons are pumped into the cell; however, as it is positive, and so is k+, the H+ enters the cell and pushes the K+ out of the cell. THEREFORE ACIDOSIS IS LIKLEY TO CAUSE HYPERKALEMIA.

10 - hyperosmolar hyperglycaemic state (HHS). This pulls water out of our cells and into the blood. This affects the potassium gradient compared to outside the cell yanking the potassium outside of the cell and into the blood.

11 - For the same reason as 10, severe dehydration of diuretics can result in hyperkalemia.

12 - Rhabdomyolysis - It’s due to damage of the skeletal muscle cells, allowing them to pop open and the intracellular k+ to escape into the blood leading to hyperkalemia.

13 - Tumour lysis syndrome - occurs when tumour cells release their contents into the bloodstream, either spontaneously or in response to therapy, leading to hyperkalemia.

14 - increased potassium intake e.g. IV replacement, bananas ect

15- Psuedohyperkalemia - during venepuncture due to torque, red blood cells can rupture and release k+.

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3
Q

Is potassium intracellular or extracellular

A

95% intracellular.

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4
Q

What is the function of NA/K ATPASE.

A

Pump 3 NA out of the cell and 2 K into the cell

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5
Q

What stimulates NA/K ATPASE?

A

Insulin
B2 recptors

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6
Q

What is Rhabomyocysis

A

Causes because of things such as seizures, crush injuries, or severe exertion.

It’s due to damage to the skeletal muscle cells, allowing them to pop open and the intracellular k+ to escape into the blood, leading to hyperkalemia.

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7
Q

How does tumour lysis syndrome result in hyperkalemia?

A

Occurs when tumor cells release their contents into the bloodstream, either spontaneously or in response to therapy leading to hyperkalemia.

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8
Q

What are excitable cells?

A

cardiac, smooth, skeleton and neutron

They have potassium leakage channels to let potassium leak out of the cell.

Which is why cell is usually -70

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