Acute Kidney Injury Flashcards
(10 cards)
What does AKI mean?
Acute renal injury
What is the pathophysiology of the pre-renal AKI stage?
this stage is primarily caused by reduced blood flow to the kideys leading to a decrese in glomerular filtration rate (GFR). This can result from various factors like hypovolemia, hypotension, or decreased cardiac output. The body attempts to compensate by conserving fluids and activating the renin-angiotensin-aldosterone system (RAAS) and antidiuetic hormone (ADH).
Explain the relation of AKI with opioids
the presence of renal impairment not only alters the clearance of the parent compound but also affects accumulation of its metabolites.
What is RAAS?
renin-angiotensin-aldosterone system
Explain the RAAS
When BP falls, kidneys releases the enzyme renin into the bloodstream. Renin converts into angiotensin, a protein that liver makes and releases into a form known as angiotensin I. Angiotensin I is an inactive hormone which flows through bloodstream and converts into angiotensin-converting enzyme (ACE) in the lungs and kidneys. This will then be converted into angiotensin II which is an active hormone that causes muscular walls of small arteries (arterioles) to constrict (narrow) which increases blood pressure. Angiotensin II also trigger the adrenal glands to release aldosterone and the pituitary gland to release antidiuretic hormone (ADH/vasopressin). Aldosterone and ADH cause the kidneys to retain sodium. Moreover, aldosterone also causes the kidney to excrete potassium through urine. The increase of sodium in the bloodstream causes water retention which increases blood volume and blood pressure. This completed the renin-angiotensin aldosterone system.
Explain the pharmacodynamics of AKI and NSAIDs
By blocking COX-1 and COX-2, NSAIDs reduce synthesis of prostaglandins which plays a critical role in maintaining renal blood flow, particularly under account of stress (e.g., dehydration, reduced blood volume). It impacts on renal function by afferent arteriole vasoconstriction, reduced glomerular filtration rate (GFR), and impaired sodium balance. Prostaglandins produced by COX-1 causes vasodilation of the afferent arteriole which increases blood flow into the glomerulus. By inhibiting prostaglandin production, NSAIDs lead to vasoconstriction of the afferent arteriole which reduces renal blood flow. It also decreases blood flow through the afferent arteriole which lowers the hydrostatic pressure in the glomerulus, reducing GFR. Prostaglandins also influences sodium and water excretion. Therefore, the inhibition of prostaglandin synthesis can lead to sodium retention and reduced excretion of water which causes fluid retention and hypertension.
Explain the pharmacokinetics of drugs during AKI in terms of excretion
excretion of drugs eliminate by glomerular filtration and tubular secretion. It has potential to accumulate during an episode of AKI. Increased drug concentrations means higher risk of adverse effects which may lead to further deterioration of kidney function or central nervous system (CNS) toxicity.
What is the pharmacokinetics of codeine in terms of metabolism and excretion?
Metabolism - a pro-drug, which means it metabolises into active metabolites where approximately 10% of it metabolises to morphine which counts for its analgesic properties
Excretion - excreted via kidneys where a reduction in clearance of codeine and its metabolites results in accumulation.
What is the pharmacokinetics of morphine in terms of metabolism and excretion?
It is metabolised in the liver in to active metabolites where its half-life increases from 2.1 hours in normal renal function to 27 hours in end stage of renal failure.
E - renally.
What is the urine output calculation formula?
0.5mL/kg/hr
