Treatment Options For Hyperkalaemia

If hyperkalaemia is indeed real and not caused by haemolysis or a bad sample, treatment can be appropriate. It’s urgent if there are ECG changes.

  • Calcium gluconate
    • Stops membrane depolarisation
    • Does not reduce the serum potassium level
  • Sodium bicarbonate IV
    • To treat metabolic acidosis, which can be a potential underlying cause
      • Potassium moves out of cells because it exchanges with hydrogen ions
  • Insulin and glucose IV
    • Use short-acting insulin
    • To promote uptake of potassium into cells
    • Effective in kidney failure
  • Polystyrene resin orally
    • Removes potassium from bowel lumen by exchanging it for sodium or calcium
    • Comes in sodium or calcium varieties, called Resonium
      • Sodium type adds to sodium load in body
      • Calcium type avoids this but is unsuitable in hypercalcaemia
  • Dialysis
    • Last resort if extreme hyperkalaemia and nothing else works

Of course, the underlying cause should be treated; if it’s hypoaldosteronism, such as from adrenal insufficiency, corticosteroids should be given. If it’s volume depletion, that should be corrected. If the hyperkalaemia is caused by a medication, that medication should be ceased.

References

  1. Electrolyte abnormalities. In: eTG complete [Internet]. Melbourne: Therapeutic Guidelines Limited (eTG November 2017 edition); 2017 Nov.
  2. acutecaretesting.org. (2013). On the relationship between potassium and acid-base balance. [online] Available at: https://acutecaretesting.org/en/journal-scans/on-the-relationship-between-potassium-and-acid-base-balance [Accessed 17 Feb. 2018].
Advertisements

Urinary Tract Infections

The urinary tract is divided into two parts:

  • Upper
    • Kidneys
    • Ureters
  • Lower
    • Bladder
    • Urethra

Uncomplicated UTIs occur when there isn’t a functional or anatomical abnormality. Females are the main target.

Complicated UTIs occur when there’s a functional or anatomical abnormality, such as bladder issues, kidney stones or diabetes mellitus.

In both forms, the most common bacterial cause of UTIs is Pee coli. That is, E. coli. Multidrug-resistant strains are emerging.

Acute pyelonephritis

Pyelonephritis means inflammation of the renal pelvis. Causes include:

  • Ascending UTI, where bacteria march up the urinary tract
  • Vesicoureteral reflux, which is where urine goes the wrong way up the urinary tract, due to an anatomical abnormality or blockage

Symptoms include:

  • Fever and chills
  • Flank pain
  • Nausea and vomiting

Investigations can show leukocytes in the urine and blood, plus other generic markers of infection.

For treatment, collect urine samples before administering antibiotics. For mild cases, oral antibiotics are sufficient. For severe cases, IV antibiotics are warranted.

Acute cystitis

Cystitis means inflammation of the bladder.

Empirical treatment can be started in non-pregnant females with uncomplicated cystitis. In other cases, collect urine samples before administering antibiotics.

References

  1. Urinary tract infections [revised 2015 Oct]. In: eTG complete [Internet]. Melbourne: Therapeutic Guidelines Limited (eTG November 2017 edition); 2017 Nov.
  2. Manski, D. (2017). Acute Pyelonephritis: Definition and Causes. [online] Urology Textbook. Available at: http://www.urology-textbook.com/acute-pyelonephritis.html [Accessed 29 Dec. 2017].
  3. Shah, V. and Gaillard, F. (2017). Acute pyelonephritis. [online] Radiopaedia. Available at: https://radiopaedia.org/articles/acute-pyelonephritis-1 [Accessed 29 Dec. 2017].
  4. Better Health Channel. (2017). Cystitis. [online] Available at: https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/cystitis [Accessed 29 Dec. 2017].
  5. Mayo Clinic. (2017). Vesicoureteral reflux. [online] Available at: https://www.mayoclinic.org/diseases-conditions/vesicoureteral-reflux/symptoms-causes/syc-20378819 [Accessed 29 Dec. 2017].
  6. Healthline. (2017). Pyelonephritis | Definition & Patient Education. [online] Available at: https://www.healthline.com/health/pyelonephritis#risk-factors [Accessed 29 Dec. 2017].
  7. Colgan, R., Williams, M. and Johnson, J. R. (2011). Diagnosis and Treatment of Acute Pyelonephritis in Women. [online] American Family Physician. Available at: https://www.aafp.org/afp/2011/0901/p519.html [Accessed 29 Dec. 2017].
  8. Harding, M. (2016). Pyelonephritis. [online] Patient. Available at: https://patient.info/doctor/pyelonephritis [Accessed 29 Dec. 2017].

Diuretics

Types

Carbonic Anhydrase Inhibitor

  • Acts on proximal convoluted tubule
  • Inhibits the enzyme carbonic anhydrase, which is normally involved in the breakdown of carbonic acid into carbon dioxide and water
    • Inhibition of carbonic anhydrase leads to a build-up of bicarbonate instead, as the alternate pathway for carbonic acid metabolism
    • Because there is now too much of it, more bicarbonate is set free into the urine
    • But hydrogen ions are used as currency to exchange for the resorption of sodium ions, so a diuretic effect ensues
  • Examples: acetazolamide
    • The name has “c” and “a” in it

Loop

  • Acts on thick ascending limb of Loop Of Henle
  • Blocks Na+-K+-2Cl- transporter
    • This has four ions in it, just as “loop” has four letters in it, as does the word “four
  • Examples: frusemide/furosemide

Thiazide

  • Acts on distal convoluted tubule
  • Blocks Na+-Cl- channel, affectionately called NKCC pump
    • This has two ions in it and “thiazide” starts with “ttoo
  • Examples: hydrochlorothiazide

Potassium-Sparing

  • Acts on collecting duct
  • Does not evict potassium into urine for an ungracious hypokalaemia like the others
  • Examples: amiloride, spironolactone

Others

Diuresis refers to the increased production of urine. Thus, further substances exist that can exact a diuretic effect but do not work on kidneys in the ways listed above. For example, coffee can have a weak diuretic effect, while that of alcohol is stronger.

Diuretic Actions On Calcium

Loop –> Hypocalcaemia

Thiazide –> Hypercalcaemia

Triple Whammy

References

  1. Chaudhry, S. (2017). DIURETICS AND RENAL HORMONES. [online] McMaster Pathophysiology Review. Available at: http://www.pathophys.org/diuretics/ [Accessed 12 Sep. 2017].

ACE Inhibitors

Let’s learn about a good friend: ACE inhibitors!

Pertinent Facts

  • class of medication
  • used to treat hypertension
  • end in -pril
  • stop ACE from working its magic on the angiotensin I –> angiotensin II conversion
  • side effects: dry cough (due to bradykinin), hyperkalaemia (because of less aldosterone), angioedema (rare and life-threatening)
  • ARBs are an alternative

Further Details

Renin-Angiotensin-Aldosterone System

Renin (from those pesky organs called kidneys) turns angiotensinogen (also known as renin substrate) into angiotensin I.

ACE (whose full title is angiotensin-converting enzyme) turns angiotensin I into angiotensin II.

Angiotensin II has numerous magical properties: vasoconstriction, stimulating aldosterone release and more…so magical!

Dry Cough, Courtesy Of Bradykinin

Angiotensin II normally clears bradykinin. When ACE inhibitors block that, bradykinin builds up and makes the person cough.

Hyperkalaemia, Due To Vicious Subjugation Of Aldosterone

Aldosterone retains sodium and kicks out potassium. Take that, distal kidney parts! That’s where it acts.

Spironolactone, a medication well-known for its alluring gynaecomastia properties, is an aldosterone antagonist. It’s a potassium-sparing diuretic, which means it helps pass more urine without destroying the person’s blood potassium level to low, low amounts.

Let’s return to aldosterone itself, however. Aldosterone is like a vindictive, electrolyte-discriminating landlord that takes in sodium but evicts potassium from the rental property. It’s the excessively muscly security guard who stops that drunken, disorderly potassium from trying to enter the blood club.

Given the above, inhibition of aldosterone causes the opposite of its normal effects: not ejecting as much potassium from the system. Too much potassium is in the nightclub of your blood! That means hyperkalaemia!

Therefore, anything that stops the triggering of aldosterone creates a risk of hyperkalaemia.

But an ACE inhibitor stops angiotensin II from being formed! And that indirectly reduces the triggering of aldosterone that otherwise would have occurred! Hyperkalaemia might ensue! Chaos everywhere!

That explains one of the potential side effects of ACE inhibitors.

Angioedema Is Serious And Bad

If an ACE inhibitor triggers this, the patient can be switched to an ARB, which is an angiotensin II receptor blocker. It achieves a similar effect without as much risk of the side effects of ACE inhibitors.

Well, well, well, ACE inhibitors. We’ve figured you out now!

References

  1. CV Pharmacology. (2017). CV Pharmacology | Angiotensin Converting Enzyme (ACE) Inhibitors. [online] Available at: http://cvpharmacology.com/vasodilator/ACE [Accessed 30 Jul. 2017].
  2. Howarth, D. A. (2017). RACGP – ACE inhibitor angioedema: a very late presentation. [online] racgp.org.au. Available at: http://www.racgp.org.au/afp/2013/december/ace-inhibitor-angioedema/ [Accessed 30 Jul. 2017].
  3. Uptodate.com. (2017). Medline ® Abstract for Reference 63 of ‘ACE inhibitor-induced angioedema’. [online] Available at: https://www.uptodate.com/contents/ace-inhibitor-induced-angioedema/abstract/63?utdPopup=true [Accessed 30 Jul. 2017].