Kidney Disease Patho Flashcards
1
Q
Kidneys
A
- Paired, retroperitoneal organs just above the lower edge of ribs bilaterally
- Received 20-25% of cardiac output
- Functional units = nephrons
- Born with ~1 million/kidney, do NOT regenerate
2
Q
AKI
A
- Acute Kidney Injury
- Abrupt/rapid decrease in kidney functional
- Possibly reversible if correct early
3
Q
CKD
A
- Chronic Kidney Disease
- Progressive decrease in kidney function
- Often irreversible
4
Q
Types of AKI
A
- Prerenal
- Intrinsic - focus on drug-induced causes
- Postrenal
5
Q
Prerenal AKI
A
- Volume depletion - hemorrhage, GI losses, renal losses, skin loss, etc.
- Decrease in BV - decreased CO, pulmonary hypertension, valvular disease, liver failure, sepsis, etc.
- Functional - NSAIDs, ACEIs, ARBs, etc.
6
Q
Intrinsic AKI
A
- Vascular damage
- Glomerular damage
- Acute tubular necrosis
- Acute interstitial nephritis
7
Q
AKI Patho
A
- Common denominator: decreased renal blood flow
- Prerenal: compromised kidney perfusion leads to decreased GFR
- Intrinsic: glomerular/tubular injury causing release of renal afferent arteriole vasoconstrictors
- Postrenal: obstruction of urinary tract increases tubular pressure and decreases the filtration driving force
- Decreased renal blood flow leads to cell ischemia and death
8
Q
Glomerularnephritis
A
Causes by immune diseases, infections, and drugs
-Immune diseases: lupus, IgA nephropathy
-Infections: Stept, bacterial endocarditis
-Drugs: chronic heroin abuse
Symptoms: proteinuria, hematuria, edema, increased blood pressure, RBCs = mickey mouse
9
Q
Polycystic Kidney Disease
A
- Hereditary
- Form noncancerous fluid-filled sacs
- Disrupts kidney function
- Presentation: enlarged abdomen, flank pain, hematuria, frequent UTI, increased BP
10
Q
Other Diseases Causing AKI
A
- Urinary tract obstruction: BPH
- Anatomic urinary tract abnormalities - reflux
- Recurrent UTI
- Kidney stones
- Unrecovered AKI
- Drug-induced kidney disease
11
Q
CKD Hypothesis
A
- Initial kidney injury via decreased nephron mass or increased metabolic demand
- Increased workload for remaining nephrons to maintain similar level of solute excretion
- Residual nephrons compensate (renal reserve) => hypertrophy and hyperfiltration
- Typically signs/symptoms are absent early on
12
Q
Adaptions = Maladaptive
A
- Residual nephron hyperfilter and hypertrophy to maintain GFR but also progress CKD
- Increases glomerular capillary pressure, damages capillaries, leads to glomerulosclerosis
- Signs/symptoms may not be apparent until 75% of nephrons or more are lost
13
Q
Functions of Kidney (6)
A
- Waste Product Excretion: removal of urea, creatinine, drugs, etc.
- Bone Structure: vitamin D activation, calcium/phosphorous balance
- Blood Formation: EPO synthesis
- Blood Pressure: renin synthesis, sodium removal, water balance
- Acid-Base Regulation: H+/NH4+/HCO3- balance
- Cardiac Activity: potassium balance
14
Q
AKI Definition
A
- Increased SCr >= 0.3 mg/dL within 48 hours
- Increased SCr >= 1.5 from baseline within 7 days
- Decreased urine volume <0.5 mL/kg/hour for 6 hours
15
Q
CKD Definition
A
-Abnormalities in kidney structure/function preset for 3 or more months
AND
-Implications for health
-Could also be defined by structural abnormalities AND/OR eGFR decreases
16
Q
Uremia
A
- Accumulation of nitrogenous waste products
- Tons of symptoms associated with ESRD
- Slide 18
17
Q
AKI/CKD Relationships
A
AKI
- Increased risk of CKD/ESRD
- Possible AKI outcomes: GFR returning to baseline, decreased GFR, ESRD
CKD
- Increased risk of AKI
- *Go hand in hand**