AKI, CKD, Tubulointerstitial and Cystic Pathology (incomplete) Flashcards
what causes elevated urea and creatinine (uremia) due to toxic waste accumulating
AKI
what is the presentation of AKI
Fatigue
nausea/vomitting
pruritis
anorexia
neurologic dysfunction
what is the pathophysiology of pre-renal AKI
hypovolemia - dehydration
hypotension
shock
cardiac failure
massive PE
stenosis of renal artery
increased intraabdominal pressure
medications - NSAIDS
what are the pathophysiology of intrarenal AKI
acute tubular necrosis
glomerulopathies
interstitial necrosis
vascular damage or embolism
malignant HTN
Bilateral acute pyelonephritis
what are the pathophysiologies of post-renal AKI
obstructive disorders
ureteral destruction
enlarged prostate
neurogenic bladder
What are intarenal AKI
acute tubular necrosis
nephrotoxic ATN (contrast, ABX)
glumerulonephritis
Vascular issue (HTN, DIC, vasculitis)
what is the process of intra-renal AKI
decreased blood flow - ischemia - necrosis - dead, sad nephrons
how do you differentiate between pre-renal and intra-renal
fluid responsiveness
what is acute on chronic kidney injury
chronic lower GRF has sudden change in setting of increased physiologic stress
prolonged AKI-> CKD
cellular damage from previous AKI increase risk of developing CKD
what is CKD
disruption of GRF - reduced GFR value
lasts > 3 months
what will urine contain with CKD
increased protein, RBC, WBC, casts
*brown casts with kidney tubule injuury
What are causes of CKD
DM **
HTN**
SLE
chronic glomerulonephritis
obstructive pathology
vascular disorders
What is Azotemia
increased urea, creatinine, nitrogenous compounds
what is uremia
pro-inflammatory state - uremic syndrome
what is the presentation of CKD
results from decreased excretion of waste products that are produced during protein metabolism
What are systemic changes of CKD
fractures
pulmonary edema, Kussmaul respiration
LVH, cardiomyopathy, ischemic heart disease, HTN, accelerated atherosclerosis (increase work load)
encephalopathy
anemia
abnormal skin pigmentation, pruritus
decreased immunity
What are the elecrolyte changes with CKD
Hyperkalemia
hypocalcemia
hper/onatremia
hypoalbuminemia
K+ super important (determines emergency dialysis needs)
What are hyperglycemic osmotic pressures
osmotic diuresis (poyluria) - electrolyte shifts
dehydration will trigger osmoreceptors - increased third (Polydipsia)
what does the metabolism of fats release
keto acids
what is acute tubular necrosis/injury associated with most commonly
ischemic injury, toxins, sepsis
what is the most common cause of intrarenal AKI
acute tubular necrosis/injury
what are the factors leading to ischemic induced ATN
hypovolemia
systemic vasodilation
coagulopathy
what are factors leading to nephrotoxic induced ATN
abx
contast
others
what occurs with ATN
decrease in GFR - activation of RAAS - continued hypoxia- increased inflammatory response - further damage to cells
what is a simple cyst
acquired, thin walled cyst within the surface of the kidney
- serous fluid
common often incidental finding
What is a autosomal dominant pathology leading to renal cysts (ADPKD)
polycystic kidney disease (thousands of cysts)
What does PKD effect
decreases signaling between cells
