Renal- Acute Renal Failure

Front 1

Likelihood of reversibility:
1) Chronic Renal Disease
2) ARF

Back 1

1) Low
2) High

Front 2

ARF symptoms
1) GFR
2) urine
3) nitrogenous
4) K+
5) lungs

Back 2

1) drop in GFR (increased cretinine)
2) oliguria and fluid retention
3) nitrogenous waste retention (increased BUN)
4) hyperkalemia
5) pulomary edema

Front 3

Definition of:
1) oliguria
2) anuria

3) what does urine output correlate with in terms of prognosis

Back 3

1) <500mL
2) <50 mL

Front 4

1) Mortality of ARF
2) most common setting for ARF
3) complicates __% of hospital admissions

Back 4

1) 50%
2) hospital
3)5%

Front 5

6 things that occur in ARF regardless of cause

Back 5

1) ECF increase
2) hyperkalemia
3) metabolic acidosis
4) hyperphosphatemia
5) anemia
6) uremic syndrome

Front 6

Three general classification of ARF origin.

Back 6

Pre-renal ARF
Intrinsic ARF
Post-renal ARF

Front 7

Pre-renal ARF definition

Back 7

hemodynamic phenomenon that reduce renal function

Front 8

1) Intrinsic ARF definition
2-4) 3 main subclasses

Back 8

1) all primary renal damage that causes rapid loss of kidney fxn.
2) Glomerular Vascular
3) Tubular Necrosis
4) Tubulointerstitial

Front 9

Post-Renal ARF

Back 9

urinary tract obstruction

Front 10

How do you evaluated ARF:
1) ASAP
2) 1-2 hrs
3) first 24 hours

Back 10

1) H&P and all previous labs
2) UA, FENa, cath placement to eval bladder dysfx. and calculate urine flow rate.
3)Renal sonogram to eval for obstruction

Front 11

Microscopic finding:
RBC, RBC cst

Give associated syndrome

Back 11

Glomerulonephritis

Front 12

Microscopic finding:
Granular casts

Give associated syndrome

Back 12

ATN

Front 13

Microscopic finding:
WBC

Give associated syndrome

Back 13

Infection/ Interstitial Nephritis

Front 14

Microscopic finding:
Eosinophils

Give associated syndrome

Back 14

Interstital Nephritis

Front 15

Microscopic finding:
Bland

Give associated syndrome

Back 15

Prerenal obstruction

Front 16

If a pt. presents with elevated creatinine of unknown duration. These things might suggest a chronic, rather than acute process

Back 16

HTN
DM
abnormal UA
Small kidneys on US (<9-10cm)

Front 17

1) in pre-renal ARF tubular fxn. and reabsorbtion are....
2) in intrinsic renal ARF tubular fxn. and reabsorbtion are....

Back 17

1) in tact
2) impaired

Front 18

Urine osmolality Value (uosm)
1) in Pre-renal ARF
2) In intrinsic ARF

Back 18

1) >600
2) <400

Front 19

Urine Sodium (UNa)
1) in Pre-renal ARF
2) In intrinsic ARF

Back 19

1) <20 mmol/L
2) >40 mmol/L

Front 20

Fraction of excreted sodium (FENa)
1) in Pre-renal ARF
2) In intrinsic ARF

Back 20

1) <1
2) >2

Front 21

If a pt. presents with elevated creatinine of unknown duration. These things might suggest a chronic, rather than acute process

Back 21

HTN
DM
abnormal UA
Small kidneys on US (<9-10cm)

Front 22

1) in pre-renal ARF tubular fxn. and reabsorbtion are....
2) in intrinsic renal ARF tubular fxn. and reabsorbtion are....

Back 22

1) in tact
2) impaired

Front 23

Urine osmolality Value (uosm)
1) in Pre-renal ARF
2) In intrinsic ARF

Back 23

1) >600
2) <400

Front 24

Urine Sodium (UNa)
1) in Pre-renal ARF
2) In intrinsic ARF

Back 24

1) <20 mmol/L
2) >40 mmol/L

Front 25

Fraction of excreted sodium (FENa)
1) in Pre-renal ARF
2) In intrinsic ARF

Back 25

1) <1
2) >2

Front 26

Calculate FENa from blood and urine labs

Back 26

FENa= (UNa/PNa)/(UCr/PCr)

Front 27

Oliguric ARF with FENa > 2% is almost always

Back 27

ATN

Front 28

Oliguric ARF with FENa <1%
can be caused by three main things

Back 28

1) Volume depletion
2) Ineffective circulating volume
3) Intra-renal vasoconstriction

Front 29

4 things which cause Ineffective circulating volume

Back 29

Hepatorenal sydrome
Congestive HF
Severe Nephrotic Syndrome
Sepsis

Front 30

4 things that cause Intra-renal vasoconstriction

Back 30

Acute glomerulonephritis
Radiocontrast ARF
NSAID-associated ARF
Cyclosporine toxicity

Front 31

1)Prerenal ARF occurs when the patient has
2) Physical exam
3) UNa?
4) Uosm?
5) BUN and Creatinine

Back 31

1)low volume or low effective IVV
2) Anything you would see in hypovolemia
3) Low urine sodium <20
4)high >600
5) Both high but BUN proportionally higher because kidney is retaining NH3 to use as gradient. This makes BUN/Creatinine >20

Front 32

THese things can all cause....
MI
CHF
Low fluid intake
Renal or GI fluid loss
Blood loss
Peripheral vasodialtion
sepsis
Anti-HTN Rx
PG inhibitors
ACE inhibitors
ACE-I, AII-Inhibitors
Vasconstrictors (NE)

Back 32

Pre- Renal ARF

Think how all of these things can be causes.

Front 33

1) GFR begins to fall when MAP falls below...
2) this causes

Back 33

1) 80 mmHg
2) pre-renal ARF

Front 34

1) How does AII play a role in Autoregulation
2) PGE2?

Back 34

1) preferentially constricts afferetn over efferent to maintain GFR
2) dilates afferent to counteract vasoconstriction of AII and NE

Front 35

1) how do COXII inhibitors cause pre-renal ARF?

Back 35

block PGE2 which disaalows Afferent vasodilation

Front 36

Endocrine response to pre-renal ARF

Back 36

secrete ADH and Aldo to reabsorb salt and water to increase volume

Front 37

1) Management of pre-renal ARF
2) If not managed quickly, what can happen?

Back 37

correct underlying problem, i.e. replete IVV or increase effective IVV.

2) can develop ischemic kidney, causing intrinsic ARF.

Front 38

Hepatorenal syndrome:
1) Mechanism?
2) DIffusible inducers of the state that causes this syndrome?

Back 38

1) Liver failure induces systemic vasodilation which shunts blood away from kidney. This reduces effective IVV and causes release of vasoconstricitors like AII, renin, vasopressin, and endothelin. These effect renal vasculature.
2) NO and endotoxins

Front 39

Hepatorenal Clinical presentation
1) UNa?
2)Urine output
3) treatment?

Back 39

1) very low (<10)
2) decreased
3) correct liver failure or TRANSPLANT!!! Some respond to fluid, albumin, and vasoconstrictors.

Front 40

Post renal- ARF (obstruction)
1) acute obstruction uf the upper tract is so painful why?
2) chronic obstruction of upper tract is not painful and presents with?
3) chronic obstruction of the loer tract presents with

Back 40

1) stretching of the kidney capsule
2) hematuria, infection, or symptoms of renal failure
3) decresed force of the urinary stream

Front 41

Post renal- ARF (obstruction):
main lab findings

Back 41

increased creatinine and BUN

Front 42

These are all causes of?
urethral stricture
urethral valves
BPH
prostatic and baldder cancer
neurogenic bladder (antcholinergics)
stones
clots
papillary necrosis
cervical cancer
accidental surgical ligation
retroperitoneal fibrosis

Back 42

post-renal ARF

Front 43

Three most common places that urinary tract obstruction occur

Back 43

ureteropelvic junction (at renal pelvis)
ureterovesicular junction
urethra

Front 44

1)Resolution of urinary tract obstruction can result in:
2) why?

Back 44

1) polyuria, enuresis
2) volume expansion, osmotic diuresis from retained salts, residual tubular dysfucntion.

Front 45

1) After 24 hours of total obstrution, ___ % of nephrons will recover function.
2) After 2 weeks of total obstrution, ___ % of nephrons will recover function.
3) After 1 month of total obstrution, ___ % of nephrons will recover function.

Back 45

1) 75-80%
2) 10%
3) 1%

Front 46

1) ATN is really a shorthand for this process
2) why is it a bit of a misnomer?

Back 46

1)Ischemic ARF
2) not much necrosis is seen

Front 47

3 Main contributors to decreased GFR in generalized intrinsic ARF

Back 47

reduced blood flow
tubular obstruction
backleak of ultrafiltrate across tubular basement membrane

Front 48

At the intact organ level, describe how these two things play a role in intrinsic ATN
1) renal hemodynamics
2) Tubular dysfunction

Back 48

1) reduced renal blood flow, high endothelin, and low NO, may also involve TGF due to increased presentation of NaCl to MAcula Densa
2) tubular obstruction by cell debris, ultrafiltrate backleak

Front 49

Changes in tubular endothelium during intrinsic ARF. Give the direction and the rationale.
1) ATP production
2) Cellular Ca++ levels
3) ROS
4) Phospholipase and protease action
5) actin cytoskeleton and adhesion molecules.

Back 49

1) Decrease in ATP production due to ischemia which can inhibit the Na+/K+ ATPase. If prolonged, AMP can be broken down into adenosine and lost from cell.
2) increased because Ca++ export is reliant upon ATPases. Leads ot Phospholipase activation and cytoskeleton disruption
3) ROS generation during reperfusion due tometabolism of hypoxanthine by xanthine oxidase and superoxide dismutase
4) Increased activation due to Ca++ influx
5) Disruption leads to Loss of cell polarity, loosening of cellular juntions, redistribution of Na/K ATase to apical membrane.

Front 50

How do people recover after ischemic Intrinsic ARF?

Back 50

recovery of injured cells
removal of necrotic cells and casts
regeneration from de-differentiated forms to re-establish tubule

Front 51

Three mechanisms by which drugs can cause ARF

Back 51

1) tubular toxixity
2) vasoconstriction
3) tubular precipitation

Front 52

Aminoglycosides (gentamycin, tobramycin, amikacin, streptomycin)
1) Risk of ARF increases with?
2) how do we monitor this
3) causes oliguira?
4) When can the renal defect present?
5) can cause ___hypokalemia ____magnesiemia

Back 52

1) duration of dose (10% in first week, >40% with over 2 weeks treatment)
2) serial Creatinines
3) non-oliguric ARF
4) during or AFTER the drug administration
5) hypokalemia, hypomagnesemia

Front 53

1)how do aminoglycosides cause ARF?

2) treatment?

3) recovery may take how long?

Back 53

1) stongly cationic and bind to anionic phospholipid in membrane and alter phospholipid activites.
2) stop drug and discontinue all other nephrotoxic agents
3) 4-6 weeks

Front 54

Amphotericin B
1) used for?
2) Risk of ARF increased by?
3) oliguric
4) Mechanism of injury (twofold)
5) can cause ___hypokalemia ____magnesiemia
6) treatment?
7) prevention?

Back 54

1) life threatening fungal infections
2) dose, duration, hypovolemia,
3) oliguric or non-oliguric
4) binds to membrane sterols and forms pores, AND vasoconstriction
5) hypokalemia, hypomagnesemia
6) Na+ loading to expand volume
7) Liposomal preparations of Amphotericin B

Front 55

Cyclosporine
1) use
2) mechanism of ARF
3) anatomic manifestations
4) what causes these anatomic change
5) treatment

Back 55

1) prevent solid organ transplant rejection and GVHD
2) reversible afferent and efferent arteriolar vasoconstriction. This is due to increase intracellular Ca++, endothelin release, and inhibition of PGs.
3) arteriolopathy, interstitial fibrosis
4) chronic AII and inhibiton of NO
5) stop drug

Front 56

Acyclovir
1) manifestations
2) mechanism of injury
3) Treatment?

Back 56

1) flank pain, hematuria, oliguria
2) crystallization and obstruction
3)IV fluids to increase urine volume, and discontinuation of drug

Front 57

2 other drugs not discussed also associated with ARF (actually three, but 2 are very similar)

Back 57

cisplatin and carboplatin
pentamidine

Front 58

Radio-contrast Media induced ARF-
1) risk factors
2) oliguria?
3) urine Osm?
4) FENa low
5) Mechanism of ARF?
6) Tx? (and Rx)

Back 58

1) increased creatinine, age, diabetes, low volume
2) either/or
3) low (unexplained)
4) low (unexplained)
5) vasoconstriction
6) Volume maintenance and NAc

Front 59

1)This protein mops up hemoglobin when it is spilled into the plasma so it doesnt hurt the kidneys when in reasonable amounts
2) is there an analogous protein for myoglobin?

Back 59

1)Haptoglobin
2) no

Front 60

1) what causes massive hemoglobin release induced ARF?
2) what causes myoglobin release induced ARF?
3) other than myoglobin, what other 3 substances found in the blood indicate muscle injury
4) which of thee 4 (myoglobin +3 otheres) is the best blood test for muscle damage?

Back 60

1) Hemolysis, esecially in transfusion rxns.
2) rhabdomyolysis, from trauma, drugs, toxins
3) creatine phosphokinase, K+, Phosphorus
4) creatinine kinase

Front 61

Describe how hemoglobin and myoglobin cause renal damage

Back 61

hypovolemia/renal ischemia i the case of muscle damage--> bleeding
can cause obstruction
direct tubular toxicity
Under acidic concentrations can liberate ferrohemate which can go to Fe which promotes free radical formation.

Front 62

Tx. for pigment ARF (More specifically rhabdomyolysis)

Back 62

Fluids to restore ECF
Alkalinize urine to protect kidney

Front 63

Multiple myeloma ARF
1) what is MM?
2) Classic symptoms
3) Classic bone marrow finding
4) protein electrophoresis finding?

Back 63

1) overproduction of monoclonal immunoglobulin light chains
2) bone pain, hypercalcemia, anemia
3) plasma cells
4) gamma spike

Front 64

Multiple Myeloma Associated ARF
1) what part of the kidney are the light chains toxic to?
2) Can Cause a _______-like syndrome
3-4) Can cause casts made of light chains in association with ____3____ which is made in ___4______
5) Treatment is:

Back 64

1) Proximal tubule
2) Fanconi
3) Tamm-Horsfall protein
4) TALH
5) Volume repletion and Chemotherapy for the underlying multiple myeloma

Front 65

Treatment of ARF
1) most pressing issue
2) volume contraction is treated with
3) procedures
4) Drug dose should be adjusted based upon _____ NOT _______

Back 65

1) hyperkalemia
2) fluid, blood, and pressors
3 catheter placement
4) estimated renal funtion, NOT Creatinine

Front 66

ARF management
Two main indications for dialysis

(either/or, both need not be present)

Back 66

1) Hyperkalemia > 6.0 unresponsive to non-dialytic mangement
2) Life-threatening volume overload unresponsive to diuretics

Front 67

Major risk factors for in-hospital ARF

Back 67

major surgery
contrast
heart failure
Cirrhosis

Front 68

Experimental Tx for ARF
1) Low dose dopamine- What is it supposed to do
2) does it work?
3) ANP what is it supposed to do?
4) Does it work?
5) IGF-1- what does it accomplish?
6) why dont we care?
7)Ca++ channel blockers- theory

Back 68

1) Increase RBF
2) NO
3) reduce Na+ transport and O2 demand
4) NO
5) Improves creatinine clearance
6) no change in outcomes
7) may reduce vasoconstriction before an ischemic insul

Front 69

1) Earliest sight of recovery from ARF
2) followed by

Back 69

1) increased urine output
2) reduction in creatinine and BUN

Front 70

Three phases of sickness and recovery from ARF and what characterizes them

Back 70

1) oliguria- ARF
2) recovery- rising urine output and
3) diuretic- from volume overload, osmotic diuresis, and iregular reabsorptive capacity

Front 71

If a pt. is going to recover from ARF it will probably be within _______ after the onset of the episode

Back 71

6 weeks