Potassium pathology Flashcards
Describe the distribution of potassium in the body
140 mmol/l - IC
4mmol/l-EC
Total= 3976mmol
What are the 3 steps that potassium is regulated by?
Intake, Cellular distribution and Renal Excretion
How much of potassium is filtered a day in a kidney?
576mmol
What are the components that cellular distribution depends on?
-insulin- this is the IN hormone, moves K+, glucose INSIDE the cell
-catecholamines
-ph- decrease in PH -> increase in K+
-osmolarity- hypertonicity causes water out of cell and brings K+ with it
-cell turnover(construction/destruction) K+ leaves the cell if there is trauma, lysis, haemolysis and hypothermia of the cell
treating megaloblastic anemia K+ in
Where is the filtered potassium reabsorbed in the kidney?
Loop of Henle and proximal tubule
Where is the potassium in excreted urine secreted from in the kidney?
cortical collecting ducts
What cells are present in the cortical collecting duct?And which cell is a/w K+ excretion
Principal cells a/w K+ excretion
and also intercalated cells ( H+ excretion)
Explain how K+ is excreted
Sodium passes down cortical collecting duct to which it enters the principal cell via ENAC flowing down a chemical gradient and also causes negative charge on interior of collecting duct lumen. This is followed by potassium secretion where increased NAK+ATPase decreases intracellular sodium
What is the principal determinant for potassium secretion by the kidney ?
How is it affected?
negative charge on interior of cortical collecting duct
disrupted by chloride resorption
What two processes regulate potassium handling
tubular flow
aldosterone - which increases number and activity of NaKATPase, ENaC, K channel
When do potassium disorders occur?
When both aldosterone and distal tubular flow are affected
hypokalaemia: aldosterone and tubular flow increased
hyperkalaemia: decreased aldosterone and tubular flow
Define hypokalemia
normal, moderate, severe
<3.0mmol/L
moderate hypokalemia is a serum level of <3.0mmol/L
severe hypokalemia <2.5mmol/L
List the causes of hypokalemia
decreased intake
intracellular shift
increased excretion -> primary and sec hyperaldosteronism and potassium wasting nephropathies
What are some potassium wasting nephropathies?
hypomagnesemia, drug toxicity, RTA, polyuria ,unresorbable anions
What is a/w secondary hyperaldosteronism
diuretics, salt wasting nephropathies and vomiting
What are causes of intracellular shift?
Beta agonist for asthma and COPD, refeeding syndrome, cell growth, periodic paralysis, tocolytics for preterm labor
Consequences of hypokalemia
hypertension and stroke (due to high aldosterone)
ECG changes and arrythmia
muscle weakness/paralysis
urinary concentrating deficits
Treatment of hypokalemia
give preferably oral potassium
Why shouldnt IV potassium be given?
conc IV potassium can cause phlebitis
IV potassium in dextrose can cause a release of insulin lowering plasma potassium
IV potassium in saline- volume overload
Define HYPERkalaemia
K+ >5.4mmol/L
Causes of hyperkaleamia
increased intake, extracellular shift and decreased renal excretion
What are the components of increased potassium intake?
salt substitutes, TPN, enteral supplements, penicillin, high potassium foods , blood transfusions, dialysate
What causes extracellular shift?
hyperosmolality -DKA and hypergylcaemia Cell destruction -rhabdomyolysis -tumor lysis syndrome Drugs -Beta blockers -Digoxin -Succinylcholine Acidemia
Aaron Has Da Cell(phone)
What causes decreased renal K+ excretion?
Renal failure, hypoaldosteronism, Drugs- ARBS ACEI, NSAIDS, spironolactone, trimethoprim , triamterene, amiloride, RTA1 and 4, Gordon’s syndrome
What causes a loss of GFR by decreasing delivery of NA to distal nephron thus preventing potassium excretion
kidney failure, NSAIDs, Gordon’s syndrome
What drugs block eNAc channel
amiloride, triamterene, trimethoprim
What diseases cause blockade of eNaC channel
Type 1 RTA
Pseudohypoaldosteronism type 1
What does hypoaldosteronism do?
Reduce number and activity of eNAC, K channel and NAKATPAse
Explain causes of hypoaldosteronism
congenital, adrenal insufficiency (Addisons disease) , diabetes (hyporenin-hypoaldosterone)
Drugs : ACEi/ARB/Renin inhibitors, heparin, ketoconazole, spironolacotone
Consequences of hyperkaelmia
muscle weakness
ECG changes and arrythmia
Treatment for hyperkalemia
reduce intake(stop K+ products i.e PTN, enteral , blood transfusion, products high in K+) , induce intracellular shift (IV insulin, inhaled beta agonists) and increase renal excretion - diuretics, fludrocortisone, dialysis, bolysterene resins
What is the goal of tx for hyperkalaemia
prevent arrythmias
What can be given to stabilize cardiac membranes
calcium
