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Heart Lung and Kidney > HLK Week 5 > Flashcards

HLK Week 5 Flashcards

1
Q

What % of renal plasma flow filters into Bowman’s capsule? How much of that flows back into the peritubular capillaries?

A
  • About 20%

- 99%

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2
Q

What is the composition of the filtrate in Bowman’s capsule?

A

Basically just like plasma, except virtually no protein.

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3
Q

In addition to the foot process and slit membrane, what ultimately prevents protein from being filtered in Bowman’s capsule?

A

There’s an electrical barrier of negative charge in Bowman’s space that prevents proteins from filtering.

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4
Q

How is inulin used to measure GFR?

A
  • Freely filterable across glomerular capillaries
  • Not reabsorbed in tubules
  • Not secreted
  • Therefore, amount excreted is equal to amount filtered.
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5
Q

Does creatinine over- or underestimate the true GFR?

A

Overestimates it because a little is secreted by tubules.

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6
Q

When the clearance of a substance is less than the GFR, it is…?

A

Reabsorbed.

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7
Q

2 things that are needed to make a concentrated urine:

A
  • Loop of Henle

- Vasopressin

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8
Q

What 2 mechanisms downregulate the release of vasopressin? Which is more sensitive?

A
  • Low osmolality
  • High ECF volume
  • Osmolality is more sensitive
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9
Q

True or false: measuring plasma sodium is the best way to measure sodium balance.

A

False: plasma sodium is an indicator of water balance, not sodium balance. So, measuring plasma Na is not a good way to test for hyponatremia.

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10
Q

Explain how the macula densa affects renin secretion:

A

Osmoreceptors in the macula densa sense salt in the ascending limb of the loop of henle and downregulate renin secretion.

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11
Q

What is the most common INTRINSIC cause of acute kidney injury?

A

Acute tubular necrosis

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12
Q

True or false: BUN rises out of proportion with creatinine in pre-renal states.

A

True

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13
Q

How do acidosis/alkalosis affect movement of potassium into/out of cells?

What’s the easy way to remember this?

A
  • Acidosis = movement out of cells = hyperkalemia
  • Alkalosis = movement into cells = hypokalemia
  • If “ka” is in the word, Ka is in the cell. Al-ka-losis = Ka moves in
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14
Q

What type of imaging is needed to diagnose minimal change disease?

A

Electron microscopy

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15
Q

What is the preferred treatment for minimal change disease?

A

Prednisone + ACE inhibitor

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16
Q

Lab finding that is very specific for glomerular disease:

A

Acanthocytes or RBC casts

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17
Q

Describe the pathophysiology of minimal change disease:

A

Destruction of podocytes leads to proteinuria, which changes the oncotic pressure in systemic capillaries, causing edema.

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18
Q

Nephritic vs. Nephrotic

A 
Nephritic: inflammatory infiltrate
- Hematuria
- Decreased GFR leads to oliguria, HTN
Nephrotic: massive proteinuria
- Hypoalbuminemia
- Loss of oncotic pressure leads to edema
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19
Q

Is it necessary to do a biopsy in kids with proteinuria?

A

Not unless they don’t respond to steroids. 90% of proteinuria in kids is due to minimal change disease, so it’s assumed to be this unless they don’t respond to Tx.

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20
Q

Very common cause of glomerulonephropathy, especially in Asia:

A

IgA Nephropathy (aka Berger’s disease, or Henoch-Schonlein purpura if systemic)

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21
Q

How do adrenergic agonists lead to hypokalemia?

A
  • (Nor)epinephrine and other adrenergic agonists increase activity of Na-Ka-ATPase, which moves Ka into cells.
  • The corollary is that B-blockers cause hyperkalemia.
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22
Q

How does insulin lead to Ka uptake by cells?

A
  • Also stimulates activity of Na-Ka-ATPase.

- The corollary is that diabetes can cause hyperkalemia.

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23
Q

Explain how aldosterone regulates Ka levels:

A

Acts on the distal tubule to excrete Ka in exchange for reabsorption of Na into the body.

24
Q

How does urine flow rate contribute to hyper/hypokalemia?

A
  • Increased urine flow rate = increased Ka excretion, leading to hypokalemia.
  • Decreased rate = decreased Ka excretion, leading to hyperkalemia.
25
Q

Why is it bad to use NSAIDS with ACE’s/ARB’s

A

ACE’s/ARB’s dilate efferent arteriole and NSAID’s constrict afferent arterioles. Together, this dramatically reduces GFR.

26
Q

Treatment of acute hyperkalemia:

A
  • Get ECG if Ka greater than 5.9
  • Stabilize myocardium if ECG is abnormal
  • Increase cellular uptake of Ka: insulin
  • Increase excretion of Ka: kayexalate (GI), loop diuretic, dialysis.
27
Q

How can you tell if hypokalemia is due to kidney dysfunction or GI dysfunction?

A
  • If GI, urine Ka will be appropriately conserved (i.e., low).
  • If kidney, urine Ka will be high
28
Q

What is the hallmark sign of hypokalemia on ECG?

A

Appearance of U wave

29
Q

How does alkalosis affect plasma CA?

A
  • Alkalosis = increased CA binding to albumin

- Total CA levels unchanged

30
Q

What is the first step in a patient with hyponatremia?

A

Measure plasma osmolality to determine whether the hyponatremia is hyposmolar, isosmolar of hyperosmolar.

31
Q

When do you have to worry about the risk of Central Pontine Myelinolysis?

A

Hyposmotic hyponatremia

32
Q

SIADH:

A
  • ADH is made without appropriate stimulus
  • Plasma osmolality is low
  • Euvolemic
  • Enhanced ADH action in kidney (UOsm > POsm)
33
Q

What are the challenges to measuring CrCl with 24 hour urine collection?

A
  • Incomplete collection
  • Day to day variation
  • Must be in a steady state
34
Q

Indications for dialysis:

A 
A- Acidosis
E- Electrolyte imbalance
I- Ingestions
O- Volume overload
U- Uremia
35
Q

Which aminoglycoside is the least nephrotoxic?

A

Streptomycin

36
Q

Drugs that can cause acute tubular necrosis (ATN):

A
  • Antibiotics: aminoglycosides, amphotericin B, vancomycin, cephalosporins
  • Acyclovir
  • Cyclosporine
  • Antineoplastics such as cisplatin
37
Q

Interpret the finding of a red/brown supernatant that’s positive for heme:

A

Probably myoglobinuria due to rhabdomyolysis, which can lead to acute tubular necrosis.

38
Q

Drugs that can cause interstitial nephritis:

A
  • PCN’s/cephalosporins/sulfonamides
  • Sulfonamide-containing diuretics
  • NSAIDS
  • Rifampin, phenytoin, allopurinol
  • PPI’s
39
Q

Mnemonic for drugs that can cause acute tubular necrosis (ATN):

A

ATN:

  • Antibiotics/antivirals/ACE’s (aminoglycosides, amphotericin B, vancomycin, cephalosporins, acyclovir)
  • Transplant drugs (cyclosporine)
  • Neoplastic drugs (cisplatin)
40
Q

Treatment for interstitial nephritis:

A
  • Removal of offending agent (drug, if drug induced)

- Steroids sometimes helpful

41
Q

Essentials of Dx of acute interstitial nephritis:

A
  • Fever
  • Arthralgia
  • Rash
  • White cell casts, hematuria, sterile pyuria
42
Q

Common lab findings in acute tubular necrosis:

A
  • Hyperkalemia
  • Hyperphosphatemia
  • Muddy brown casts in urinalysis
  • BUN/creatinine ratio less than 20:1
43
Q

Essentials of Dx of acute tubular necrosis:

A
  • Acute kidney injury
  • Ischemic or toxic insult or sepsis
  • Nephrotoxins (drugs and dyes)
  • Urine sediment with muddy brown casts and tubular epithelial cells
44
Q

Essentials of Dx of acute glomerulonephritis:

A
  • Acute kidney injury
  • Hematuria, proteinuria, dysmorphic red cells and red cell casts
  • Dependent edema (esp periorbital, scrotal) and HTN
45
Q

Anti-GBM antibodies are associated with which disease?

A

Goodpasture syndrome

46
Q

What causes injury in Goodpasture syndrome?

A

Autoantibodies against basement membrane type IV collagen.

47
Q

Some common causes of acute glomerulonephritis due to immune complex deposition:

A
  • Lupus
  • IgA nephropathy (Berger’s disease)
  • Endocarditis
  • Post-infectious glomerulonephritis
  • Cryoglobulinemic glomerulonephritis (seen with Hep C)
48
Q

True or false: acute glomerulonephritis is a common cause of acute kidney injury.

A

False: only about 5% of acute kidney injuries are due to glomerulonephritis.

49
Q

Pauci-immune acute glomerulonephritis:

A
  • Includes granulomatosis with polyangitis (Wegener’s dz) and microscopic polyangitis.
  • Immune-cell mediated tissue damage
  • Can evolve to crescentic glomerulonephritis with poor prognosis unless treatment is started early.
50
Q

True or false: elevated BUN and creatinine cannot be used to distinguish acute kidney injury from CKD.

A

True

51
Q

Common etiology for rapidly progressing glomerulonephritis (RPGM):

A

Any of the immunologic conditions:

  • Anti-GBM
  • ANCA diseases
  • Immune complex deposition diseases
52
Q

SSx of uremia:

A
  • Asterixis
  • Pericardial rub
  • Altered mental status
  • Seizures
53
Q

Urine pattern seen in post-renal disease:

A

Bland sediment

54
Q

Urine pattern seen in pre-renal disease:

A
  • Concentrated urine

- Hyaline casts

55
Q

Urine pattern seen in ATN:

A
  • Renal tubular epithelial cells
  • granular casts
  • “muddy brown casts”
56
Q

Essentials of renal artery stenosis:

A
  • Can be caused by atherosclerosis or fibromuscular dysplasia (less common)
  • HTN
  • ACE’s cause acute kidney injury

Heart Lung and Kidney (6 decks)

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