Renal Disorders Flashcards
(21 cards)
Define Glomerulonephritis
inflammatory damage to glomeruli (tiny network of blood vessels that are the “cleaning unit” of the kidney)
caused by: immune responses, toxins/medications, vascular disorders, system diseases
Damage to the filtration membrane makes it more permeable– leads to proteinuria and hematuria
Glomerular scarring leads to decreased GFR
Polycystic kidney disease
an autosomal dominant genetic disorder that causes the nephron epithelial tubular cells to proliferate, form outpouchings filled with filtrate
this leads to mechanical compression of other nephron structures-> chronic kidney damage-> chronic renal failure->death
Describe acute kidney injury
-a sudden reduction in blood flow to the kidneys or exposure to nephrotoxic agents
-manifestations are caused by decreased GFR and accumulated nitrogenous waste products (Azotemia) in the blood
-symptoms include decreased urine output (Oliguria), fluid overload, electrolyte imbalance and metabolic acidosis
-if untreated, can lead to kidney failure, cardiovascular disease and death
Describe chronic kidney disease
-manifestations are caused by decreased GFR and accumulated nitrogenous waste products (Azotemia) in the blood
-progressive and irreversible renal disorder that develops over a long period of time
-CKD can be caused by diabetes, hypertension or damaged kidneys
-manifestations include fatigue, nausea, vomiting, edema, anemia, and Oliguria
Define Glomerular filtration rate (GFR)
is a measure of how effectively the kidneys are filtering waste products from the blood. A reduced GFR may indicate the kidney dysfunction or disease
What are the 3 phases of AKI pathogenesis? Describe each phase
- Initiation
–> injury triggers the cascade events that lead to kidney dysfunction (ex. Ischemia, toxins, infection, dehydration, urinary obstruction, autoimmune disorders) - Maintenance (oliguric phase)
–> Ongoing kidney dysfunction – Inflammatory response, tubular dysfunction (can lead to electrolyte imbalances, fluid retention, and metabolic acidosis), renal ischemia and hypoxia, activation of RAAS - Recovery
–> kidneys start to regain their normal function, injury heals, regeneration of nephrons, restoration of renal blood flow, normalization of urine output and electrolytes – this phase features polyuria (yay)
What are the clinical features of the Maintenance Phase (AKI)
-decreased glomerular filtration rate (GFR)
-oliguria
- azotemia
-uremia
-fluid and electrolyte imbalance
-hypertension
What is an example of a prerenal acute kidney injury?
renal hypoperfusion (reduced blood flow to the kidneys)
any condition that reduces renal blood flow can cause prerenal AKI, including: hypovolemia, inadequate cardiac output, restricted renal blood flow
What are the three main types of Intrarenal acute kidney injuries?
- acute tubular necrosis
- acute interstitial nephritis
- glomerulonephritis
clinical features may include:
-proteinuria
-hematuria
Define acute tubular necrosis (ATN)
ischemic or nephrotoxic damage to renal tubules
Define acute interstitial nephritis
the spaces between the kidney tubules (interstitial tissue) become swollen (inflamed)
Describe Nephrotic Syndrome
a condition characterized by the excessive loss of protein in the urine due to damage to the glomeruli
manifestations: hyperproteinuria, hypoalbuminea, hyperlipidemia, and edema
exact cause is unknown but key factors include: immune dysfunction, genetic predisposition, and environmental factors
Nephritic Syndrome
manifestations: hematuria, RBC casts, azotemia/uremia, and HTN
occurs primarily with the infection-related glomerulonephritis
Describe the CKD etiology
-gradual decline in renal function (+3 months)
-decreased GFR
-oliguria
-azotemia–> uremia
-irreversible and potentially life-threatening
Describe the pathogenesis of CKD
Early stage– normal urine output, very little signs if any due to the healthy nephrons increasing their filtration rates to compensate (glomerular hyperfiltration)
Late stage– decreased GFR and urine output, uremia, systemic clinical manifestations
Define glomerular hyperfiltration
the compensatory mechanism in which healthy nephrons increase their filtration rate to make up for the damaged nephrons
Define glomerular sclerosis
damage done to the healthy nephrons during extended glomerular hyperfiltration– they harden and die– which only furthers the cycle of nephron loss
leads to late-stage CKD
Describe the progression from HTN to CKD
HTN causes blood vessels to thicken
Thickened blood vessels are narrower
Narrow renal blood vessels cause ischemia and glomerulosclerosis
Irreversible nephron loss
<GF
CKD
Describe the progression from diabetic nephropathy to CKD
Blood vessel wall glycation which makes them thicker and narrows the arterioles
Glomerular HTN
Hyperfiltration
Glomerulosclerosis
Irreversible nephron loss
<GFR
CKD
Define nonezymatic glycation
excess glucose in the blood that sticks to proteins in the blood vessel walls– leads to thicker walls and narrower blood vessels
What are the clinical manifestations of CKD?
azotemia/uremia
Fluid and electrolyte imbalances
seizures and coma
HTN and cardiac dysrhythmia
renal osteodystrophy
bleeding