Case studies Flashcards
What is hyperkalemia?
- Heightened levels of potassium
- Potassium level > 5.5 mEq/L
What happens to equilibrium potential if you increase the concentration of extracellular potassium?
- It changes the EP for potassium in every cell in the body
- Excitable cells change their excitability
What does the secondary in secondary hyperparathyroidism mean?
That there’s some secondary problem that’s triggering the thyroid gland to over-secrete its chemical messenger
Effects of increased extracellular potassium (think about this to understand the symptoms)
- A shift in the equilibrium potential of potassium from a very negative value to a less negative value (e.g. -80 -> -60)
- The membrane potential of other cells drifts up as well
- For excitable cells (muscles and nerves), this causes a change in firing properties
Hyperkalemia symptoms
- General fatigue
- Muscle weakness
- Arrhythmias (QRS widening)
- Bradycardia
- Paresthesias (abnormal somatic sensory signals) (neurons misfiring)
Where is most of the potassium in the body found?
- Sequestered inside of cells, in a high concentration
- In the extracellular fluid, there’s very little potassium (this maintains the steep gradient that gives you a very negative equilibrium potential for potassium)
Does it take a lot of potassium ions being added to the extracellular fluid to significantly shift the concentration?
No, a small change has a significant impact
What causes QRS widening?
- The spread of the depolarization through the ventricles is broadened, not as synchronized
- It takes longer for the wave of depolarization to travel through
Parasthesias
A feeling that’s alongside normal (e.g. tingling sensations with no stimulus present)
Increased extracellular potassium
(and how it decreases excitabilty of heart muscle cells, which slows the conduction of depolarization through the ventricels)
- Myocytes are unique. They typically have a very negative resting membrane potential and the depolarizing inward current through gap junctions is very large, which yields a rapid depolarization that spreads to the next myocyte very quickly.
- Slowing down depolarization of each myocyte in the ‘daisy chain’ of myocytes significantly increases conduction time through the whole ventricle
- Depolarized Vm rest (Ek less negative)
- At rest, there is a smaller percentage of VG Na+ channels in a closed state –> higher threshold and slower depolarizatoin –> slower, less synchronized conduction
- Decreased Vmax and faster repolarization
Normal EKG (after correction) and in hyperkalemia
20 mins
Causes of hyperkalemia
- Diabetic ketoacidosis (DKA)
- Other causes
How can diabetic ketoacidosis cause hyperkalemia?
- Decreased insulin = decreased Na+/K+/ATPase activity in many cells of the body
- Potassium shifts from inside cells to outside cells
Other causes of hyperkalemia
- Renal failure
- Crush trauma (rhabdomyolysis)
- ACE inhibitors
- Potassium supplements, potassium-sparing diuretics
Hyperkalemia treatments
- Calcium (to stabilize Vm in excitable cells)
- Insulin for those with diabetic ketoacidosis (DKA)
- Insulin and glucose for non-diabetics (immediate, shift K+ from extracellular to intracellular)
- Dialysis
- Dietary restrictions
Diuretics (for treatment of CHF and hypertension)
K+ sparing (keep in body) and K+ wasting (eliminate in urine)
Aldosterone effects on H+ excretion & effects of extra Na+ in lumen of collecting duct
Aldosterone stimulates A-type cells in the collecting duct (new wrinkle to the aldosterone story)
- More HCO3- and K+ reabsorbed, water follows, isoosmotic reabsorption of volume
- More H+ excreted
How does more Na+ in collecting duct lumen cause K+ wasting and acidosis?
- More Na+ in lumen of collecting duct = more Na+/K+ exchange in cells responding to aldosterone
- More Na+ in lumen of collecting duct = more H+ excreted from Type A cells. More Na+ moving into cell from lumen causes decreased Vm along the apical membrane and less electric barrier to H+ pumps
Carbonic anhydrase inhibitors
- If you inhibit carbonic anhydrase, the mechanism of reabsorption of sodium, exchange for protons, will be diminished
- So more sodium stays in the lumen and more protons stay in the body
Loop diuretics (affect the thick ascending limb)
- If you block the reabsorption of sodium, chloride, and potassium, the direct obvious effect is that more of them will end up in the lumen and escape into the bladder, along with water
- Secondary effect: more sodium ions come down the collecting duct
Thiazide diuretics (distal tubule)
- Affects the distal tubule
- Blocks sodium and chloride reabsorption
- More NaCl in the lumen and being lost in urine
- More potassium lost and more protons excreted (alkalosis)
Summary of diuretics
Vitamin D, Ca++, and phosphate absorption in the gut (don’t need to know)
Parathyroid hormone stimulates the activity of an enzyme in the kidney that plays upon the vitamin D pathway
PTH (parathyroid hormone) (don’t need to know)
Parathyroid gland and plasma calcium regulation
