Warning! DNA! Deoxyribonucleic acid? No!
Do not administer!
The triple whammy can lead to bad effects on the kidneys.
There are three major ones, plus more!
The way to remember this is that, in line with the subpar nature of hypokalaemia, everything is weak and low!
ST depression is a depression, so it is low.
The T waves have low amplitude, so they too are low.
The dip of the letter U, as in U waves, looks like the minimum point of a parabola, so it’s also low.
Conveniently, it all follows an alphabetical pattern: ST, T, U.
The heart isn’t actually heart-shaped, but kidneys really are kidney-shaped!
In this episode, Dr Lucy talks about renal medicine, how to make it into physician specialty training and finding a job in the modern medical climate.
About the guest speaker
Dr Lucy Wynter did her nephrology training at Royal Prince Alfred Hospital and Concord Hospital and maintains close ties with both centres. She completed a Bachelor of Science, Bachelor of Medicine, Bachelor of Surgery with honours and a Masters of Bioethics, at Sydney University.
Dr Lucy lectures at the University of Sydney Medical School and is currently employed part time as a Senior Lecturer and Clinical Studies Advisor to the Office of Medical Education.
Dr Lucy’s particular interests include: Hypertension, Chronic Kidney Disease, Diabetic Nephropathy, Kidney Stones, Cardio-renal Syndrome and Renal Supportive Care.
Opening and closing themes by Lily Chen.
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.
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.
The urinary tract is divided into two parts:
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.
Pyelonephritis means inflammation of the renal pelvis. Causes include:
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.
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.
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.
Loop –> Hypocalcaemia
Thiazide –> Hypercalcaemia
Let’s learn about a good friend: ACE inhibitors!
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!
Angiotensin II normally clears bradykinin. When ACE inhibitors block that, bradykinin builds up and makes the person cough.
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.
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!