AKI, CKD, Tubulointerstitial and Cystic Pathology (incomplete) Flashcards

1
Q

what causes elevated urea and creatinine (uremia) due to toxic waste accumulating

A

AKI

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2
Q

what is the presentation of AKI

A

Fatigue
nausea/vomitting
pruritis
anorexia
neurologic dysfunction

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3
Q

what is the pathophysiology of pre-renal AKI

A

hypovolemia - dehydration
hypotension
shock
cardiac failure
massive PE
stenosis of renal artery
increased intraabdominal pressure
medications - NSAIDS

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4
Q

what are the pathophysiology of intrarenal AKI

A

acute tubular necrosis
glomerulopathies
interstitial necrosis
vascular damage or embolism
malignant HTN
Bilateral acute pyelonephritis

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5
Q

what are the pathophysiologies of post-renal AKI

A

obstructive disorders
ureteral destruction
enlarged prostate
neurogenic bladder

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6
Q

What are intarenal AKI

A

acute tubular necrosis
nephrotoxic ATN (contrast, ABX)
glumerulonephritis
Vascular issue (HTN, DIC, vasculitis)

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7
Q

what is the process of intra-renal AKI

A

decreased blood flow - ischemia - necrosis - dead, sad nephrons

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8
Q

how do you differentiate between pre-renal and intra-renal

A

fluid responsiveness

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9
Q

what is acute on chronic kidney injury

A

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

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10
Q

what is CKD

A

disruption of GRF - reduced GFR value
lasts > 3 months

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11
Q

what will urine contain with CKD

A

increased protein, RBC, WBC, casts
*brown casts with kidney tubule injuury

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12
Q

What are causes of CKD

A

DM **
HTN**
SLE
chronic glomerulonephritis
obstructive pathology
vascular disorders

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13
Q

What is Azotemia

A

increased urea, creatinine, nitrogenous compounds

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14
Q

what is uremia

A

pro-inflammatory state - uremic syndrome

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15
Q

what is the presentation of CKD

A

results from decreased excretion of waste products that are produced during protein metabolism

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16
Q

What are systemic changes of CKD

A

fractures
pulmonary edema, Kussmaul respiration
LVH, cardiomyopathy, ischemic heart disease, HTN, accelerated atherosclerosis (increase work load)
encephalopathy
anemia
abnormal skin pigmentation, pruritus
decreased immunity

17
Q

What are the elecrolyte changes with CKD

A

Hyperkalemia
hypocalcemia
hper/onatremia
hypoalbuminemia
K+ super important (determines emergency dialysis needs)

18
Q

What are hyperglycemic osmotic pressures

A

osmotic diuresis (poyluria) - electrolyte shifts
dehydration will trigger osmoreceptors - increased third (Polydipsia)

19
Q

what does the metabolism of fats release

A

keto acids

20
Q

what is acute tubular necrosis/injury associated with most commonly

A

ischemic injury, toxins, sepsis

21
Q

what is the most common cause of intrarenal AKI

A

acute tubular necrosis/injury

22
Q

what are the factors leading to ischemic induced ATN

A

hypovolemia
systemic vasodilation
coagulopathy

23
Q

what are factors leading to nephrotoxic induced ATN

A

abx
contast
others

24
Q

what occurs with ATN

A

decrease in GFR - activation of RAAS - continued hypoxia- increased inflammatory response - further damage to cells

25
Q

what is a simple cyst

A

acquired, thin walled cyst within the surface of the kidney
- serous fluid
common often incidental finding

26
Q

What is a autosomal dominant pathology leading to renal cysts (ADPKD)

A

polycystic kidney disease (thousands of cysts)

27
Q

What does PKD effect

A

decreases signaling between cells