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Pathophysiology 4 > Renal: AKI and CKD > Flashcards

Renal: AKI and CKD Flashcards

1
Q

renal autoregulation of GFR

incr in BP and its effect on aff and eff arteriole
-same with decr BP

A

INCR BP

  • constricts afferent arteriole
  • dilates efferent arteriole

DECR BR:

  • dilates afferent
  • constricts efferent
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2
Q

define renal insufficiency

A

decline of renal function to <60 ml/min

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3
Q

describe acute renal insuff

A

AKI= 50% increase in creatinine or incr in BUN or azotemia

-ABRUPT–within 48 hours–decr in kidney function–>retention of urea and other nitrogenous waste productions–>disregulation of ECF volume and electrolytes

AKI used instead of ARF bc theres a range of loss of renal function

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4
Q

describe chronic kid failure

  • characterized by?
  • major etiologies
A
  • kid damage or decr in GFR for >3 MO
  • characterized by any of the following
  • ->albuminuria
  • ->electrolute and acid base disturbs
  • ->anemia
  • ->urine casts
  • ->image finfings
  • ->abnm renal biopsy

two major causes=DM and HTN

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5
Q

define end stage renal failure

A

less than 10% of renal function remains

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6
Q

uremia

  • causes
  • cm
A

syndrome of renal failure
-elev urea and cr
CM=fatigue, anorexia, nausea, vom, pruritis, neuro changes

*causd by retention of toxic wastes, deficiency states, electryo imabalcne and proinflammatory states

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7
Q

Azotemia

  • what is it
  • causes
  • leads to?
A

***NITROGEN IN THE BLOOD
vs uremia= urea in te blood

INCR: serum urea + creatinine

renal insuff or renal failure cause it

both this and uremia lead to accumulation of nitrogenous waste prod in blood

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8
Q

criteria to classify AKI

A 
R-->risk 
I-->injury
F-->failure 
L-->loss
E-->end stage dz

**3 progressive levels of AKI

risk injury
failure–>with 2 outcomes determinants: loss and end stage renal dz

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9
Q

list three phases of AKI

A
  1. oliguria (maintenace phase)
  2. HyperK—met. acidosis
  3. diuretic phase (recovry)
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10
Q

Oliguria

  • define
  • how does it happen
A

<400 ml of UO/day

  • HOW DOES IT HAPPEN
    1. alterations in renal blood flow***
  • efferent arteriolar vasoconstriction
  • impaired autoregulation
  1. Tubular necrosis ***
    * necrosis of the tubules causes sloughing of cells—cast formation–ischemic edema— results in obstruction
  2. backlead
    * GFR normal—but tubular reabs leaks filtrate–accelerated by permeability
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11
Q

in hospital type of tubular obstruction?

A

ATN
acute tub necrosis

rhabdo

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12
Q

TYPES of AKI

A
  1. pre-renal (reversible)
  2. intra-renal (intrinsic)
  3. post-renal (reversible)—BPH or doble stone blcoking bilat ureters
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13
Q

MCC of pre-renal AKI

A

renal hypoperfusion

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14
Q

intra-renal AKI

  • define
  • MCC
A

-disorders involving renal parenchymal or insterstitial tissue

ATN caused by ischemiia is MCC

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15
Q

decrease in blood suppply to the kidneys aka decr renal perfusion

A

Pre renal AKI

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16
Q

patho for pre renal AKI

A

decr renal blood flow–>hypoprefusion–>decr GFR–>incr proximal tubule NA and H20 Abs–>incr aldosterone and ADH–>incr distal tutbule NA and H20 reabsoprtion –>OLIGURIA

17
Q

patho for intra trenal AKI

A

renal tubular injiry (necrosis, apoptosis)–>cast formation–>incr intratubular obstruction–>incr intratubular pressure–>tubular back leak–>decr GFR–>OLIGUIRA

18
Q

path for post renal AKI

A

bilateral obstruction to urine flow–>incr intraluminal pressure–>release of inflammatory mediators and vascular endothelial cell injiry–>renal vasoconstriction–>cellular/interstitial edema–>decr GF pressure–>OLGURIA

19
Q

causes of pre-renal AKI

A
  • hypovolemia–>diuretic use, GI loss (V/D), blood loss
  • impaired pericardial tamponade
  • decr vasc resistance –>hypotension–> CHF with decr pump function
  • renal vasoconstriction—> afferent arteriole vasconstriction—>NSAIDs or IV contrast OR efferent arteriole constriction (ACEI, ARBs)
20
Q

causes of intra renal AKI

A
  1. Glomerular dz
    * Acute glomerulonephritis
    * thombotic events
    * atheroembolic dz
  2. Tubular damage
    * ATN—ischemic or nephrotoxic
  3. Vascular damange
    * malignant HTN
    * atheroembolic dz
    * preeclampsia/eclampsia
    * HUS
  4. Intersitital damage
    * allergic rxn to meds
21
Q

causes of post renal AKI

A
  • bph
  • prostate CA
  • gynecologic CA–cervical
  • retroperitoneal fibrosis
  • ureteral stones BILAT
  • papillary necrosis
  • neurogenic bladder
  • intratubular obstruction
22
Q 
intrinsic AKI 
-
-whats imp? 
-whats most susceptible 
-mcc (in hosp pt? ) 
-other causes 
-decrisbe what happens with ATN 
-based off the patho--what lab findings woudl you see
A

site of injury is imp bc it determines the dz causing AKI—vascular, glomerular, tubular or interstitial (sepsis, infection)

SEGMENTS=most susceptible to ischemia and nephrotoxins

  • ->PCT
  • ->medullary thick ascenidng limp of LOH

MCC in hosp pt=ischemic—-ATN
**decr blood flow–>tubular necrosis (ie hypotension, sepsis, contrinued pre-renal state)

OTHER CAUSE= nephrotoxic

  • contrast dyes
  • aminoglycosides
  • amphotericin
  • heme pigments (rhabdo)

ATN= sloughing of tubular lumen—leads to occlusion from debris and cast
Acute Interstitial Nephritis—inflammatory and allergic response in the interstitium—spares glomeruli and BVs
Acute GN

LABS

  • serum BUN: Cr <20:1
  • hyperK
  • high phosphate
  • urine FENA >1
  • urinary Na >20 (MC >40)
  • low urine osmo–>cant concentrate urine
  • SEDEMENT:
  • MUDDY BROWN CASTS
  • renal tubular ethilial cells
  • granular cells
23
Q

list the three phases of injury for intrinsic AKI

  • what happens in each
  • timing of each
A
  1. Initiation phase
    * the initial insult
    - reduced perfusion or toxicity –early fall in GFR
    - RENAL INJURY IS EVOLING
    - lasts 24-36 hours
    - prevention of futher injury is possible
  2. Maintenance or Oliguric phase
    - established renal injury
    - weeks to months
    - urine output is LOWST
    - cr, BUN, and serum K+ increase
    - NA and water overload
  3. Recovery phase or post-oliguric phase
    - injury is REPAIRED
    - renal function reestablished
    - RISK OF HYPOK, potentially fatal complication due to polyuria via incr in diuresis
24
Q

explain the relationship of CA, PTH in CKD

A

in CKD–kidneys cannot make vit d—- therefore CA cannot be absorbed from the diet– causing hyPOCALEMIA–>this triggers parathyroid glands to secrete more and more PTH in attempt to incr blood CA–>this leads to SECONDARY PARATHYROIDISM
—>HOW does PTH release more CA into the blood? by breaking down bone—- so also in CKD—> CONSTANT BONE BREAK DOWN–>leading to RENAL OSTEODYSTOPHY

25
Q

why is there decr RBC in CKD

A

kidneys also make EPO— so if they cannot do this due to CKD—- then theres decr RBC count aka ANEMIA

26
Q

define CKD

A

GFR <60 for 3 MO or more regardless of cause

27
Q

when do CM of CKD start to show

A

until renal functino is <25%

Pathophysiology 4 (8 decks)

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