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Clin Med Exam 4 > Kidneys pt 1 > Flashcards

Kidneys pt 1 Flashcards

1
Q

Basic Renal function is to?

A
  • Filter the blood of
    • Removal of waste
    • Maintain proper concentrations of electrolytes
    • maintaining acid/base balance
  • Regulate blood volume and pressure
  • Produce EPO
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2
Q

What is the basic functional unit of the kidney?

A

Nephron - consists of glomerulus, renal tubule

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3
Q

Site of filtration in the kidney?

A

Glomerulus

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4
Q

Where does water and salt get reabsorbed in the kidney?

A

Renal tubule

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5
Q

The proximal convoluted tubule (PCT) reabsorbs what 65% of? 80% of? 100% of?

A
  • 65% of Sodium, potassium, calcium
  • 80% of phosphate, water, bicarbonate
  • 100% of glucose and amino acids
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6
Q

What else does the PCT do?

A

Reabsorbs 60% of the glomerular filtrate

Secretes drugs/toxins that are too big (or protein bound) to be filtered

Reasborbs water passively

Makes ammonia from gluatmine (acidifies urine)

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7
Q

What are the 4 segements of the loop of Henle?

A

4 segments -

thin descending limb (DLH)

Thin ascending limb (ALH)

Medullary thick ascending limb (mTALH)

Cortical thick ascending limb (cTALH)

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8
Q

Overall function of the loop of henle?

A

Create a concentration gradient and form concentrated urine.

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9
Q
A
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10
Q

What does the Collecting Tubule do?

A
  • Reabsorbs
    • NaCl
    • Bicarb
    • H20 - urine concentration
  • Excretes
    • H+
    • Urea
  • Regulates urine volume
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11
Q

AKI is?

A

Rapidly worsening of renal function

Clinically seen with quickly rising BUN/Cr

Accumulation of nitrogenous wastes in the blood

Caused by prerenal, postrenal, intrarenal

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12
Q

What is the definition of AKI?

A

Abrupt - within 48 hours - absolute increase in the serum creatinine of >0.3 mg/dl above baseline

OR

Serum creatinine increases 50% (known or presumed to have occured in the past 7 days)

OR

Oliguria of <0.5 ml/kg/hour for >6hours.

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13
Q

Clinical symptoms of AKI?

A

Weakness, lethargy, anorexia, N/V, General malaise, diarrhea, pruritis, drowsiness, hiccups, SOB, dizziness

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14
Q

Signs of AKI?

A

Usually point towards the underlying cause ie prerenal vs postrenal - Prerenal - tachycardic, hypotensive - Post renal - distended bladder, CVA tender, enlarged prostate

Anuria or Oliguria

Change in volume status/weight

Change in mental status

Edema

Weakness

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15
Q

What are the diagnostic tests you run for AKI?

A

BMP, Urinalysis & urine microscopy, - urine culture, measurement of urine output, renal ultrasound, may add urine spot for osmolaility, urine sodium, creatinine

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16
Q

What are possible life threatening complications of AKI?

A

Hyperkalemia

Fluid overload

Signs of uremia - pericarditis, altered mental status

Severe metabolic acidosis (pH <7.1)

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17
Q

Treatment for AKI? When should you dialyze?

A

Depends on the CAUSE

  • Dialyze if
    • serum creatinine is >5-10 mg/dl
    • Unresponsive acidosis
    • Fluid overload
    • Uremic complications
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18
Q

What is prerenal failure? This is the ________ of AKI.

A
  • Prerenal failure is reduced effective blood circulating to the kidney
    • Absolute reduction in fluid volume (hemorrhage, dehydration) or
    • Effective volume depletion - CHF, cirrhosis (hepatorenal syndrome)

this is the most common cause of AKI

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19
Q

Prerenal failiure is reversible? T/F

A

Yes, rapidly reversible if underlying cause is found and corrected - kidney themselves are okay

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20
Q

What are some examples of true intravascular depletion? What is this an example of?

A

Hemorrhage, burns, diuretics, dehydration, GI losses, vomiting, diarrhea, enteric fistula

This can lead to prerenal AKI

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21
Q

What are some examples of decreased circulating volume? This can lead to?

A

CHF, cardiac tamponade, aortic stenosis, cirrhosis with ascites, nephrotic syndrome

This can lead to prerenal AKI

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22
Q

What are some examples of impaired renal blood flow? What can this lead to?

A

ACEi - can decrease blood flow to kidneys

NSAIDs

Renal artery stenosis

Renal vein thrombosis

This can lead to prerenal AKI

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23
Q

What labs distinguish prerenal failure?

A

Serum BUN:Cr ratio > 20:1

Urine sodium <20 meg/L

Fractional excretion of sdoium (FENa) <1%

Urine specific gravity > 1.020

These occur because the kidney is responding to prerenal failure by increasing reabsorption.

24
Q

Serum BUN:Cr ratio in prerenal failure would be?

A

Greater than 20:1

25
Q

Urine sodium in prerenal failure would be?

A

<20 meg/L

26
Q

Fractional excretion of sodium (FENa) in prerenal failure would be?

A

<1%

Measures the percent of sodium filtered by the kidney that is excreted into the urine.

27
Q

Urine specific gravity in prerenal failure would be?

A

Greater than 1.020

28
Q

What is the treatment for prerenal AKI? CHF, Dehydration, Hemorrhage

A

Correct the underlying cause

CHF - Diurese the patient

Dehydration - IVF

Hemorrhage: Blood and fluids.

29
Q

What is postrenal failure? What are some of the causes?

A

This is damage to the kidneys, AKI, due to something after the kidneys - in the ureters, bladder, urethra. Blockage at those spots cause renal failure

Nephrolithiasis, BPH, obstructring tumor in the GU stystem, bladder outlet obstruction, blood clots within the urinary tract, medications, neurogenic bladder

30
Q

What are clinical symptoms of postrenal failure?

A

May have abdominal or groin pain, bladder discomfort

Mass at flank, suprapubic area, or abdomen

Rectal exam

Pelvic exam

Anuria

31
Q

What is the diagnostic testing you should do with postrenal failure?

A

Post void residual - >100 ml –> Bladder outlet obstruction.

Ultrasound or IVP (intravenous pyelogram) - dilated ureters or renal pelvis

Abdominal CT - to evaluate for mass.

32
Q

What is the treatment for postrenal failure?

A

Relieve the obstruction

May - catheterize patient, nephrostomy tube, stenting, lithotripsy, perform surgery to remove a mass

33
Q

What is intrinsic renal failure?

A

One or both kidneys have been damaged and don’t work properly

some causes happen quickly, others develop over time.

34
Q

What are causes of Intrinsic renal failure?

A

Acute tubular necrosis (ATN) - most common cause of intrinsic AKI

Nephrotoxins - NSAIDS, contrast agents, aminoglycosides, cyclosporine A, cisplatin, heme pigments

Interstitial diseases - acute interstitial nephritis, SLE, infectino

Glomerulonephritis

Vascular disease - polyarteritis nodosa, vasculitis

35
Q

What labs define intrinsic renal failure?

A

Serum BUN:Cr ratio of 10-15:1

Urine sodium: >40 meq/l

FENa: >2%

Urine specific gravity of 1.010-1.020

36
Q

Serum BUN:Cr ratio in intrinsic renal failure would be?

A

10-15:1

37
Q

Urine sodium in intrinsic renal failure would be?

A

>40 meq/l

38
Q

FENa in intrinsic renal failure would be?

A

>2%

39
Q

Urine specific gravity in intrinsic renal failure would be?

A

1.010-1.020

40
Q

What is the most common cause of intrinsic AKI?

A

Acute tubular necrosis

41
Q

What are the three major causes of acute tubular necrosis?

A

Renal ischemia - all causes of severe prerenal disease can cause postischemic ATN

Nephrotoxins - aminoglycosides, heme pigments, cisplatin, radiocontrast media, pentamide, mannitol, synthetic cannabinoides

Sepsis

42
Q

How do you diagnose acute tubular necrosis?

A

Classic UA description - Muddy brown granular epithelial cell casts and free renal tubular epithelial cells

FENa, BUN:Cr ratio, urine specific gravity, urine osmolality consistent with intrinsic AKI

May also have hyperkalemia and have metabolic acidosis

43
Q

How do you treat acute tubular necrosis?

A

Hold nephrotoxins

Treat underlying cause - supportive management

Some will give diuretics for fluid overload - don’t use if oliguric

Most patients spontaneously recover renal function - better if non oliguric

44
Q

Prognosis of ATN?

A

May not return to baseline renal function - worse with each episode

ATN during hospitalization associated with higher in hospital and long term mortality.

45
Q

What is Acute interstitial nephritis?

A

Immune mediated process of tubulointerstitial injury - inflammatory infiltrate in the interstitium

46
Q

What medications most commonly cause acute interstitial nephritis (AIN)

A

Cephalosporins, penicllins, allopurinol, diuretics, NSAIDs, sulfonamides

47
Q

What triad (classic) is associated with AIN.

A

Fever, maculopapular rash, eosinophilia

48
Q

What are the UA findings of AIN?

A

WBCs, white cell casts, may have eosinophils, protein

49
Q

What is the treatment for AIN?

A

Stop offending med/treat underlying cause - Glucocorticoids

Usually good prognosis after treatment

50
Q

What is glomerulonephritis?

A

Renal glomeruli are damgaed by deposition of inflammatory proteins in the glomerular membrane

51
Q

What causes glomerulonephritis?

A

Focal: Henoch-Schonleinpurpura, postinfectious, IgA nephropathy, Hereditary nephritis, SLE

Diffuse: Postinfectious, membranoproliferative, SLE, vasculitis, rapidly progressive GN

52
Q

What are the clinical features of glomerulonephritis?

A

Hematuria, edema of face/eyes in the morning, feet/ankles in the evening, HTN common

53
Q

How do you diagnose Glomerulonephritis?

A

HEmaturia, urine might be tea or cola colored.

RBCs, and RBC casts on UA, misshapen RBCs, proteinuria

Renal biopsy

54
Q

What’s the treatment for Glomerulonephritis?

A

Steroids, immunosuprressants/chemo medications.

55
Q
A

Clin Med Exam 4 (15 decks)

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