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Nep Flashcards

1
Q

_____ is defined as a rapid rise in blood urea nitrogen (BUN) or creatinine over a period of several hours to days

A

Acute renal failure (ARF), or better referred to as acute kidney injury (AKI),

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2
Q

_____ can be used interchangeably with the term renal insufficiency; literally,
azotemia means the buildup of azole groups or nitrogen in the blood.

A

Azotemia

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3
Q

____describes a syndrome of very severe renal failure in which there is the need for
dialysis to save life

A

Uremia

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4
Q

T or F

A

Uremia does not necessarily mean the same thing as chronic renal failure

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5
Q

AKI

____means decreased perfusion of the kidney.

_____ means decreased drainage from the kidney or decreased forward flow of urine.

____means there is a tubular or glomerular problem, and the kidney itself is defective.

A

Prerenal azotemia

Postrenal azotemia

Intrarenal

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6
Q

The BUN can be falsely low when there is ______

A

liver disease, malnutrition, or SIADH.

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7
Q

______ is our closest approximation of glomerular filtration rate (GFR) without the use of more cumbersome testing such as the clearance of inulin.

A

Creatinine clearance

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8
Q

Causes of pre-renal azotemia

A
  1. hypovolemia on any basis (dehydration, burns, poor oral intake, diuretic, vomiting, diarrhea, sweating, hemorrhage),
  2. hypotension on any basis (septic shock, cardiogenic shock, anaphylactic shock),
  3. third spacing of fluids such as peritonitis, osmotic diuresis,
  4. low aldosterone states such as Addison disease.
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9
Q

The first clue to the diagnosis of prerenal azotemia is a ______

A

BUN:creatinine ratio of 20:1.

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10
Q

Pre-renal azotemia

There is also a low _______

This results in a very high ______

A

urine sodium and low fractional excretion of sodium (FeNa <1%).

urine osmolality as well.

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11
Q

Pre-renal azotemia

Concentrated urine has a_____ and ______

A

high specific gravity (>1.010) and

a high urine osmolality (>500).

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12
Q

T or F

Low albumin states also lead to decreased renal perfusion

A

T

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13
Q

Pre-renal Azotemia

There is markedly diminished renal perfusion because of the obstruction in the renal artery.

A

Renal artery stenosis

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14
Q

Renal artery stenosis

This effect is greatly exaggerated with the use of ____which markedly diminish renal perfusio n

A

ACE inhibitors,

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15
Q

Pre-renal Azotemia

______ is renal failure based entirely on the presence of hepatic failure. The kidneys are normal. The etiology of the rise in BUN and creatinine is thought to be from
an intense vasoconstriction of the afferent arteriole, resulting in decreased renal perfusion

A

Hepatorenal syndrome

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16
Q

______is diagnostic of hepatorenal syndrome

A

No improvement in renal failure after 1.5 L of colloid,

like albumin,

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17
Q

HRS

____ and ____may be beneficial in hepatorenal syndrome. However, the best treatment is liver transplantation.

A

Midodrine,

an alpha agonist, and octreotide

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18
Q

ACE inhibitor–induced renal failure is from

A

vasodilation of the efferent arteriole

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19
Q

Despite the ability of ACE inhibitors to potentially worsen renal function, the overall effect on the kidney is _____

A

diminishing the rate of progression to uremia and renal failure

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20
Q

ACE inhibitors and angiotensin receptor blockers decrease ______

A

hypertension inside the glomerulus.

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21
Q

ACE inhibitors decrease proteinuria by_____

A

35–45%.

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22
Q

Creatinine will only begin to rise when you have lost at least_____

A

70–80% of renal function.

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23
Q

BUN Crea ration early and late post renal azotemia

A

Initially, the BUN and creatinine will elevate in a ratio of 20:1 as it does with prerenal azotemia.

then the BUN:creatinine ratio will lower to closer to
10:1, such as that seen in acute tubular necrosis (ATN).

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24
Q

About 85% of acute renal failure is secondary to _____

A

intrinsic renal disease such as ATN.

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25
Q

Three Phases of intrinsic renal failure (Not Seen in All Patients)
• ________—This is the time between the acute injury and the onset of renal failure.
• ________(<400 mL per 24 hours) or anuric (<100 mL per 24 hours)
•_____—This is a diuretic phase when all the water not previously excreted will now leave the body in a vigorous polyuria.

A

Prodromal

Oliguric

Postoliguric

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26
Q

Intrinsic renal failure

The initial clue is a BUN:creatinine ratio close to____

A

10:1.

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27
Q

Further clues to the diagnosis of ATN are a
1
2
3

A

high urine sodium (>40),
high fractional excretion of sodium (>1%),
and low urine osmolality (<350).

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28
Q

Diagnosis:

Urine osmolarity: >500

Urine Na+: <20

FeNa+: <1%

Urine sediment: Scant

A

Pre-renal azotemia

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29
Q

Diagnosis:

Urine osmolarity: <350

Urine Na+: >40

FeNa+:>1%

Urine sediment: Full (brownish pigmented
granular casts, epithelial casts)

A

ATN

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30
Q

T or F

Diuretics such as furosemide or mannitol do not reverse the ATN

A

T

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31
Q

T or F

Hydration can prevent contrast-induced renal failure, but it does not reverse it once it occurs

A

T

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32
Q

ATN

Another form of ineffective therapy is ____ at low dose to increase renal perfusion

A

dopamine

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33
Q

_____ accounts for 10–15% of intrinsic renal failure. It can be distinguished from other causes of renal failure by the presence of fever and rash on physical
examination and many WBCs, occasionally eosinophils.

A

Allergic interstitial nephritis (AIN)

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34
Q

Meds causing AIN

A

can be from penicillins, cephalosporins,

sulfa drugs, allopurinol, rifampin, and quinolones

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35
Q

It is important to remember that any sulfa drug can cause allergic reactions. Besides antibiotics, other examples of sulfa drugs are diuretics such as ________

A

thiazides, furosemide, or acetazolamide.

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36
Q

The most common infections to result in AIN are ______

A

leptospirosis, legionella, CMV, rickettsia, and streptococci.

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37
Q

____ is present in 80% of those with AIN.

_____ is present in 25–50% of patients

A

Fever

Rash

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38
Q

The best initial test for AIN is a ______

A

urinalysis (UA) looking for white cells.

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39
Q

The most accurate test for urine eosinophils is a ______

A

Hansel stain or Wright stain of the urine

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40
Q

Massive hemoglobinuria severe enough to cause renal failure is generally only caused by an ______

A

ABO

incompatibility

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41
Q

The most important test when there has been a severe crush injury or seizure and the rhabdomyolysis is potentially life threatening is an ______

A

EKG or potassium level

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42
Q

The best initial test that is specific for rhabdomyolysis is a _____

A

UA in which you find a dipstick that is positive for blood but in which no red cells are seen

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43
Q

Rhabdomyolysis is confirmed with a markedly elevated _____

A

serum CPK level

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44
Q

CPK

In order for nephrotoxicity to occur, the level must be enormously elevated into the _____ range with a normal value generally <500 or less.

A

10,000 to 100,000

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45
Q

Rhabdomyolysis

If there are EKG abnormalities from the hyperkalemia the best initial therapy is ______

A

calcium chloride or gluconate

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46
Q

Rhabdomyolysis

_____ may help prevent the precipitation of the pigment in the tubule

A

Alkalinizing the urine with bicarbonate

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47
Q

_____ proteins, such as in myeloma, also cause tubular damage.

A

Bence-Jones

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48
Q

____ is most prominently a cause of nephritic syndrome, however, not tubular damage

A

Myeloma

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49
Q

The most common cause of hyperoxaluria resulting in acute renal failure is from_____ in a suicidal person who ingests antifreeze

A

ethylene glycol overdose

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50
Q

ethylene glycol overdose

The diagnosis is confirmed by finding _____

A

oxalate crystals on a UA. Oxalate crystals are shaped like envelopes

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51
Q

Acute ethylene glycol overdose is treated with _____ to prevent the formation of the toxic metabolite of ethylene glycol, which is oxalic acid.

A

fomepizole infusion

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52
Q

Chronic hyperoxaluria and kidney stones can be caused by _____

A

Crohn’s disease because of fat and

calcium malabsorption.

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53
Q

What is given to prevent uric acid nephropathy. in pts with tumor lysis syndrome

A

Allopurinol treatment with alkalinization of urine markedly reduces the risk of uric acid nephropathy

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54
Q

Calcium precipitates in the kidney tubule, forming stones. In addition, hypercalcemia can lead ________ and ____

A

to distal RTA and nephrogenic diabetes insipidus

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55
Q

The most common cause of hypercalcemia is_____

A

primary hyperparathyroidism.

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56
Q

The most common toxins to be associated with renal insufficiency and ATN are_____

A

NSAIDs, aminoglycosides, cephalosporins, contrast agents, amphotericin, chemotherapy such as cisplatin,
radiation effect, heavy metals such as lead, mercury, or gold, and cyclosporine

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57
Q

The difference between the basis of allergic interstitial nephritis and direct toxins is that allergic nephritis
_______

A

occurs with the first dose and is associated with fever, rash, joint pain, and eosinophils in both
blood and urine.

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58
Q

______is the least nephrotoxic compared with gentamicin and amikacin.

A

Tobramycin

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59
Q

_____ generally takes 5–10 days of administration to result in toxicity

A

Aminoglycoside toxicity

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60
Q

Renal failure due to aminoglycosides is

frequently _______

A

non-oliguric (K+ levels not elevated)

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61
Q

The ability of antibiotics to kill bacteria is associated with
the peak level, but the likelihood of toxicity is associated with the _______

A

trough level

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62
Q

Aminoglycoside-related nephrotoxicity is estimated to

be between _____ of all drug-induced nephrotoxicity and is usually reversible.

A

10–20%

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63
Q

This medication is associated with renal insufficiency as well as distal renal tubular acidosis.

A

Amphotericin B.

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64
Q

Labs of Amphotericin B toxicity

A

It is expected that after several days or weeks of amphotericin use, the patient will develop a high creatinine as well as a decreased magnesium, bicarbonate, and potassiumlevel.

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65
Q

What is the possible etiology?

patient who undergoes a vascular catheter procedure such as angioplasty who develops renal failure several days later

A

Atheroembolic Disease

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66
Q

The BUN and creatinine may be up in a 20:1 ratio, such as in prerenal azotemia, because the
hypertonicity of the agent provokes an intense vasospasm of the afferent arteriol

A

Radiocontrast material for CT scanning

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67
Q

____ is associated with renal failure in addition to its toxicity on the pancreas

A

Pentamidine

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68
Q

____is a protease inhibitor that results in renal failure usually from the drug precipitating out in the kidney tubules

A

Indinavir

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69
Q

NSAIDs are a frequent cause of renal failure. NSAIDS cause renal failure by several mechanisms:

A
  • Interstitial nephritis
  • Direct toxic effect on the tubules
  • Papillary necrosis
  • Inhibition of vasodilatory prostaglandins in the afferent arteriole
  • Membranous glomerulonephritis
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70
Q

_____occurs in patients with a history of sickle cell disease, diabetes, urinary obstruction, or chronic pyelonephritis

A

Acute papillary necrosis

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71
Q

Acute papillary necrosis SSx

A

The presentation is with the sudden onset of flank pain, hematuria, pyuria, and fever.

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72
Q

The most accurate diagnostic test for papillary necrosis

is a_____

A

CT scan. The CT scan will show “bumpy” contours in the renal pelvis where the papillae have sloughed off.

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73
Q

In those patients with significant underlying renal disease who have an unavoidable radiologic procedure requiring contrast, you must ____

A

hydrate with 1–2 liters of normal saline over 12

hours before the procedure

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74
Q

______have also been shown to decrease the risk of renal failure in CIN

A

Bicarbonate and N-acetyl cysteine

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75
Q

___ and ______ cause glomerular disease and are certainly the most common causes of nephrotic syndrome and end stage renal disease

A

Diabetes and hypertension

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76
Q

All forms of GN can be characterized by _____

A

edema, hematuria, red cell casts, and hypertension

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77
Q

The edema of GN is found first in areas of low tissue tension, such as the______

A

periorbital area or the scrotum

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78
Q

The most important distinction between GN and nephrotic syndrome is_____

A

the degree of proteinuria.

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79
Q

GN is also characterized by modest amounts of protein in the urine with the daily total being _____ per 24 hours, although by definition nephrotic syndrome does not begin until there are ____ grams per 24 hours

A

<2 grams

> 3.5

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80
Q

However, the single most important test

to diagnose GN is the______

A

renal biopsy

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81
Q

Causes of Glomerulonephritis Disease Spectrum

Vascular disease

A 
Wegener granulomatosis
Churg-Strauss syndrome
Henoch-Schönlein purpura
Polyarteritis nodosa
Thrombotic thrombocytopenic purpura (TTP)
Hemolytic uremic syndrome (HUS)
Cryoglobulinemia
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82
Q

Causes of Glomerulonephritis Disease Spectrum

Glomerular Disease

A 
Goodpasture syndrome
Postinfectious glomerulonephritis
Henoch-Schönlein purpura 
SLE
Idiopathic rapidly progressive glomerulonephritis
 Alport syndrome
 Diabetes and hypertension (most common causes)
Amyloid
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83
Q

______ is characterized by systemic vasculitis that most often involves the kidney, lung, and upper respiratory tract such as the sinuses or middle ear

A

Wegener granulomatosis (WG)

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84
Q

Laboratory abnormalities in WG are _____

A

elevated ESR, anemia, and leukocytosis. Rheumatoid factor is positive in 50%.

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85
Q

The best initial test that is specific for WG is the ____

A

anti-proteinase-3 antibody, which is also known as cytoplasmic antineutrophil cytoplasmic antibody, or C-ANCA.

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86
Q

The most accurate test for WG is a_____

A

biopsy of the kidney, nasal septum, or lung looking for

granulomas

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87
Q

______ characterized by a history of asthma, eosinophilia, and other atopic diseases. The characteristic diagnostic tests are the elevated eosinophil count and positive P-ANCA or antimyeloperoxidase

A

Churg-Strauss Syndrome

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88
Q

Churg-Strauss Syndrome

The most accurate test is a______ showing the granulomas and eosinophils.

Treatment is with _______

A

lung biopsy

glucocorticoids and cyclophosphamide.

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89
Q

______ is an idiopathic disorder of renal and lung disease characterized by a unique antibasement membrane antibody

A

Goodpasture syndrome (GP)

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90
Q

Unlike Wegener or Churg-Strauss, GP does not affect multiple organs or sites in the body besides the____

A

lung and the kidney

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91
Q

Goodpasture syndrome (GP)

The best initial test to confirm the diagnosis is the____

A

level of

antibasement membrane antibodies to type IV collagen

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92
Q

Goodpasture syndrome (GP)

The single most accurate test is a

A

lung or kidney biopsy.

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93
Q

Goodpasture syndrome (GP)

The biopsy shows _____

A

linear deposits on immunofluorescence

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94
Q

______is a systemic vasculitis of small- and medium-sized arteries that affects virtually every organ in the body with the exception of the lung

A

Polyarteritis nodosa (PAN)

95
Q

PAN

The most accurate diagnostic test is a____, and treatment is with _____

A

biopsy

cyclophosphamide
and steroids.

96
Q

_____ presents with mild hematuria that resolves spontaneously in 30% of patients. About 40–50% of patients progress to end stage renal disease

A

IgA nephropathy

97
Q

How to distinguish psgn from IgA nephropathy

A

This is to distinguish it from poststreptococcal

glomerulonephritis, in which the renal involvement occurs 1–2 weeks later or longer

98
Q

The treatment of IgA nephropathy is difficult. There is no proven effective therapy. Anyone with proteinuria should receive______

A

ACE inhibitors or angiotensin receptor blockers (ARB).

99
Q

In addition to group ______ numerous other

infections can be associated with postinfectious glomerulonephritis.

A

A beta hemolytic streptococci (Streptococcus pyogenes),

100
Q

The best initial test for PSGN is

A 
the antistreptolysin (ASO) test and the antihyaluronic acid
(AHT) test.
101
Q

The most accurate test for PSGN is the _____

A

renal

biopsy showing “humps” on electron microscopy.

102
Q

Renal disease from _____ is associated with chronic hepatitis C or less commonly B.

A

cryoglobulinemia

103
Q

Besides the renal disease, cryoglobulinemia is associated with ________

A

joint pain, neuropathy, and purpuric skin lesions

104
Q

Cryoglobulinemia is associated with an elevated

_____and low levels of ____ and is confirmed with a test for the cryoglobulins

A

ESR

complement

105
Q

The incidence of glomerular involvement in diabetes is directly proportional to the ____

A

duration of the diabetes

106
Q

What dse?

Double-stranded DNA levels go up and complement levels go down as a marker of severity in flare-ups of the disease.

A

SLE

107
Q

Tx of SLE with Proliferative disease:

A

Use steroids combined with mycophenolate. Mycophenolate is superior to cyclophosphamide.

108
Q

_____ is the combination of glomerular disease with congenital eye and ear abnormalities. There is sensorineural hearing loss

A

Alport syndrome

109
Q

What type of amyloidosis

A

Plasma cell dyscrasia causing deposition of protein derived from immunoglobulin
light chains. This may be associated with multiple myeloma

110
Q

Amyloidosis

Other unique methods of diagnosis are_____

A

aspirating the abdominal fat pad or taking a sample of

the rectum

111
Q

AMyloidosis

___ and _____can control protein
production.

A

Melphalan and prednisone

112
Q

Nephrotic syndrome is defined as the presence of renal disease sufficient to produce

A

a level of proteinuria >3.5 grams per 24 hours, hyperlipidemia,
edema, and a
low serum albumin level

113
Q

Why is there hyperlipidemia in NS

A

Hyperlipidemia is of unclear etiology but is most
likely from the loss of the lipoprotein markers or signals on the surface of chylomicrons and LDL that lead to the clearance of these lipids from the bloodstream

114
Q

NS

Hypercoagulable states or thrombophilia develops from the _____

A

urinary loss of natural anticoagulant

proteins such as antithrombin, protein C, and protein S

115
Q

NS

If steroids do not work, the next best step in therapy is to add______

A

cyclophosphamide

or mycophenolate

116
Q

______is the most common cause of nephrotic syndrome in adults.

A

FSGS

117
Q

____ Associated with the use of heroin as well as

HIV. Limited response (only 20–40%) to steroids

A

Focal-Segmental Glomerulosclerosis (FSGS).

118
Q

FSGS May progress to end stage renal disease

(ESRD) over_____

A

5–10 years.

119
Q

What kind of NS

______Associated with cancer such as lymphoma or breast cancer, and infections such
as endocarditis or chronic hepatitis B or C. Other etiologies are lupus, penicillamine, gold
salts, and NSAIDs

A

Membranous.

120
Q

What kind of NS

Most common form in children, although it may
account for 15% of adult disease. NSAIDs have also been associated with nil lesion disease

A

Nil Lesion (Minimal Change Disease).

121
Q

EM findings of MCD

A

Light microscopy is normal and electron microscopy is needed to see fusion of foot processes

122
Q

Associations of MCD

A

Hodgkin’s lymphoma has an association with nil

lesion disease.

123
Q

What NS

Mostly idiopathic, steroid-resistant type of nephrotic syndrome. Immunofluorescent
staining shows IgM deposits in an expanded mesangium

A

Mesangial.

124
Q

What NS

____Associated with chronic hepatitis and low serum complement levels

A

Membranoproliferative.

125
Q

____ and ____ are also useful therapeutically. for Membranoproliferative NS

A

Dipyridamole and aspirin

126
Q

Proteinuria suggestive of problems in?

A

This can be from either glomerular or tubular diseases, although glomerular diseases can give greater amounts

127
Q

Proteinuria is also caused by prolonged standing,

which is known as ______

A

orthostatic proteinuria.

128
Q

Nitrites. _________educe nitrate to nitrite, which is a marker of infection

A

Gram-negative bacteria r

129
Q

By itself, the isolated finding of bacteria in the urine is of very limited significance. The most important exception is in ______ whom you should screen for bacteria
and treat.

A

pregnant women,

130
Q

What kind of cast?

Asstd with Dehydration. These casts develop as an accumulation of the normal amount of tubular protein. They do not necessarily mean disease.

A

Hyaline

131
Q

What kind of cast?

Asstd with Glomerulonephritis

A

Red cell

132
Q

What kind of cast?

Asstd with Chronic renal failure

A

Broad, waxy

133
Q

What kind of cast?

Also called “dirty” or “muddy.” They are associated with acute tubular necrosis and represent accumulated epithelial cells

A

Granular

134
Q

What kind of cast?

Asstd with Pyelonephritis, interstitial nephritis

A

White cell

135
Q

The most common causes of end stage renal disease (ESRD) that require dialysis are __ and ____

A

diabetes

and hypertension

136
Q

The anemia of ESRD is ____ and _____

A

normochromic and normocytic

137
Q

Cause of Hypocalcemia/Hyperphosphatemia in ESRD

A

This is from the loss of 1,25-dihydroxyvitamin D production

138
Q

IN ESRD

High phosphate levels contribute to low
calcium levels by _____

A

precipitating out in tissues in combination with the calcium.

139
Q

Tx of High phosphate levels in ESRD

A

treated with phosphate binders, such as calcium carbonate or calcium acetate

140
Q

_____ is a substance that simulates the effect of calcium on the parathyroid. It is used in severe, refractory cases

A

Cinacalcet

141
Q

MOA of Cinacalcet

A

Cinacalcet will tell the parathyroid to shut off

parathyroid hormone production and helps decrease phosphate in this way

142
Q

In ESRD

_____containing phosphate binders should not be used. It is associated both with CNS accumulation and dementia as well as bone abnormalities.

A

Aluminum-

143
Q

This is also known as osteitis fibrosa cystica. Bone abnormalities occur because dead kidneys don’t make 1,25 vitamin D. This leads to a low calcium level

A

Osteodystrophy

144
Q

The reason for this is not precisely clear, however, this is the most common cause of death for those on dialysis.

A

Hypertension and Accelerated Atherosclerosis

145
Q

This is the second most common cause of death in dialysis patients.

A

Infection.

146
Q

MCC of infxn in ERSD

A

The most common organism is Staphylococcus because of
the constant need to penetrate the skin to place someone on dialysis for 4–6 hours 3–4 times
a week.

147
Q

Although nephrotic syndrome gives thrombophilia because of the urinary loss of ______ the most common coagulation problem with ESRD is
bleeding

A

protein C, protein S, and antithrombin,

148
Q

Reason of inc bleeding in ESRD

A

This is because of uremia-induced platelet dysfunction

149
Q

Uremia-induced bleeding is treated with ____which releases subendothelial stores of von Willebrand factor and factor VIII, which increase platelet aggregation and
adherence.

A

desmopressin,

150
Q

Duration of Survival

Live related donor _______

Cadaver donor _______

Dialysis alone _____

Diabetics on dialysis ____

A

95% at 1 year, 72% at 5 years

88% at 1 year, 58% at 5 years

30–40% at 5 years

20% at 5 years

151
Q

Cause iof hyponatremia from ESRD

A

This generally occurs from either increased free water retention or urinary sodium loss. About
85–90% of sodium is extracellular

152
Q

An acute 15–20 point drop in sodium level can result in a ____

A

seizure or coma

153
Q

Moderate hyponatremia can be managed with ____

A

normal saline administration combined with a

loop diuretic such as furosemide

154
Q

Severe and chronic hyponatremia such as that resulting in seizure or coma should be managed with ____

A

3% hypertonic saline or the V2 receptor-antagonists conivaptan and tolvaptan

155
Q

These are conditions in which the total body sodium level is truly normal and the sodium blood level is artificially low. Treatment is directed at etiology of the lab
artifact, not specifically the sodium level

A

Pseudohyponatremia.

156
Q

The sodium level is decreased by ____for every 100 mg/dL increase in glucose above normal

A

1.6 mEq/L

157
Q

How does hyperglycemia cause Pseudohyponatremia

A

The high glucose load causes a transcellular shift of
water out of the cell into the vascular space unaccompanied by sodium. This drops the
serum sodium level. Mannitol and sorbitol can do the same

158
Q

Hypervolemic States (Increased ECF). These are all conditions in which there is a decrease in intravascular volume resulting in an increase in ADH secretion from the posterior pituitary. This is a form of appropriate increased ADH syndrome

A
  • CHF
  • Nephrotic syndrome and low albumin states
  • Cirrhosis
  • Renal insufficiency:
159
Q

Hypovolemic States (Decreased ECF). For most of these, the hyponatremia develops because_____

A

of the loss of sodium through body fluids and replacement with free water

160
Q

Urine Na <20 causes

A

Dehydration
Vomiting
Diarrhea
Sweating

161
Q

Urine Na >20

A 
Diuretics
ACE inhibitors
Renal salt wasting
Addison disease
Cerebral sodium wasting
162
Q

Causes of hyponatremia with euvolumic states

A
  • Psychogenic polydipsia
  • Hypothyroidism: mechanism unknown
  • Diuretics: can be both hypovolemic and euvolemic
  • ACE inhibitors: probably through an increase in ADH
  • Endurance exercise
  • Syndrome of inappropriate secretion of ADH (SIADH)
163
Q

Meds causing SIADH

A
  • SSRIs
  • Tricyclic antidepressants
  • Haloperidol
  • Cyclophosphamide
  • Vincristine
  • Carbamazepine
  • Thiazide diuretics
164
Q

If urine osmolality is >100 in the presence of hyponatremia, the person most likely has_____

A

SIADH

165
Q

Treatment of SIADH is to _____for mild disease and give _____ for severe disease as was previously described.

A

restrict fluids

hypertonic saline

166
Q

For chronic disease in which the underlying cause of the SIADH cannot be corrected, therapy with ______.

These medications inhibit the effect of ADH on the kidney tubule and lead to water diuresis.

A

conivaptan, tolvaptan, or demeclocycline is used

167
Q

Conivaptan and tolvaptan are ______-antagonists

A

V2 receptor

168
Q

Demeclocycline and lithium treat SIADH by inducing _____

A

nephrogenic diabetes insipidus.

169
Q

Presentation of hypernatremia

A

Insensible losses
GI loss:
Transcellular shift:
Renal

170
Q

Acute hypernatremia is treated with ______

A

isotonic fluids intravenously

171
Q

Watching for a decrease in urine volume after administering_______ distinguishes CDI from NDI.

A

ADH

172
Q

Mx of CDI.

  1. Correct the underlying cause, if possible.
  2. ______
A

Vasopressin (ADH). It can be given subcutaneously, intravenously, intramuscularly, or by nasal spray (all routes except oral).

173
Q

Mechanism of trancellular shift causing hypo K

A

Increased entry into cells (transcellular shift) can be from alkalosis, increased levels of insulin, beta adrenergic activity, and the replacement of vitamin B12 in B12-deficient patients.

Trauma patients have increased beta adrenergic activity, that may lead to hypokalemia

174
Q

effect of Mg on K levels

A

Low magnesium levels. Magnesium decreases urinary loss of potassium. When you are deficient in magnesium, you start to spill potassium into the urine.

175
Q

Most impt dxtic in hypoK

A

In emergency cases, the most important diagnostic test is the EKG.

176
Q

EKG findings for Hypo K

A

EKG abnormalities include T-wave flattening and U-waves.

177
Q

____ is an extra wave after the T-wave that is indicative of Purkinje fiber repolarization.

A

U-wave

178
Q

Why not to use dextrose containing fluids in K correction

A

Dextrose will provide the shift of potassium into the cells and will further lower potassium levels.

179
Q

Mechanisms of transcellular shift causing hyperK

_______—secondary hemolysis, mechanical trauma during venipuncture, platelet count >1,000,000 (106), WBC count >100,000 (105)

_______—secondary cellular buffering (H+ moves into cells, K+ moves out)

A

–– Pseudohyperkalemia

–– Acidosis

180
Q

Hyper K from decreased urinary excretion

–– Renal failure
––\_\_\_\_\_\_: ACE inhibitors, type IV RTA, adrenal enzyme deficiency; heparin inhibits production of aldosterone
–– \_\_\_\_\_\_\_\_\_ or adrenalectomy
–– Potassium-sparing diuretics—\_\_\_\_\_
–– NSAIDs
A

Hypoaldosteronism

Primary adrenal insufficiency (Addison disease)

amiloride, spironolactone

181
Q

Tx of HyperK

  • ______—membrane stabilization (most emergent treatment in presence of EKG abnormalities). Effect is immediate and short lived.
  • _______—alkalosis drives K+ into cells. Do not give in same IV line as calcium. Forms CaCO3 precipitates.
  • _______—drives K+ intracellular, takes 30–60 minutes to work
A

Calcium chloride

Sodium bicarbonate

Glucose and insulin

182
Q

Tx of hyper K

1
2
3

A
  • Diuretics, beta agonists
  • Cation exchange resin (Kayexalate)
  • Dialysis
183
Q

For every ____ increase in the level of serum bicarbonate, there is a______point increase in the
pCO2

A

1-point

0.7-

184
Q

Volume contraction of dehydration results in an increased level of _____, which leads to ______

A

aldosterone

metabolic alkalosis

185
Q

Increased levels of aldosterone in volume contraction lead to increased levels of ______) excretion.

A

hydrogen ion (H+

186
Q

Causes of alkalosis from H loss

A
  • Exogenous steroids
  • GI loss (vomiting, nasogastric suction)
  • Renal loss (Conn syndrome, Cushing, ACTH overproduction, licorice, Bartter syndrome)
  • Decreased chloride intake
  • Diuretics
187
Q

Causes of alkalosis from HCO3 retention

A

Bicarbonate administration
• Contraction alkalosis
• Milk-alkali syndrome

188
Q

How to compute anion gap

A

Anion gap = (Na+) – (HCO3 –) + Cl–)

normal: 8–12

189
Q

Causes of low anion gap Metabolic Acidosis (MAC)

A
  • Myeloma
  • Low albumin level
  • Lithium
190
Q

The anion gap is a gauge of the ______ in the bloodstream

A

unmeasured anions

191
Q

The majority of the unmeasured anions are usually ____which has a significant amount of negative charge

A

albumin,

192
Q

In addition to albumin, which is normal, the other anionic substances are______

A

lactate, ketoacids, and the metabolic end products of toxic alcohols

193
Q

Na+ and cations = ______

A

HCO3 – and Cl– and anions

194
Q

Causes of NAGMA

A
  • Diarrhea
  • Renal tubular acidosis
  • Ureterosigmoidostomy
195
Q

Causes of HAGMA

A

LA MUD PIE (Mnemonic)
Lactate (sepsis, ischemia, etc.)
Aspirin
Methanol
Uremia
Diabetic ketoacidosis (DKA)—Beta hydroxybutyric acid (BHB) and acetoacetate, which are
formed from fatty acids, are an alternate fuel source because the cells cannot absorb glucose
because there is a deficiency of insulin
Paraldehyde, Propylene glycol
Isopropyl alcohol, INH
Ethylene glycol (antifreeze, low calcium)

196
Q

Causes of distal RTA (type 1)

A
  • Usually sporadic
  • Also secondary to autoimmune disease (e.g., Sjögren syndrome, SLE)
  • Drugs—
  • Nephrocalcinosis, sickle cell, chronic infection
  • Familial
  • Chronic hepatitis
197
Q

Drugs causing distal RTA

A

amphotericin, lithium, analgesics, iphosphamide

198
Q

SSx of distal RTA

A
  • Inability to develop a high H+ concentration in urine. Urine pH is >5.3.
  • Secondary hyperaldosteronism and hypokalemia
  • Nephrocalcinosis and nephrolithiasis
199
Q

Acid load test; give ammonium chloride, which should lower urine pH secondary to increased H+ formation. With type I RTA, ________

A

the urine pH remains elevated. Serum bicarbonate

= 10.

200
Q

MOA of hypoK in pts with distal RTA

A

Patients with distal RTA develop hypokalemia because patients lose the ability to secrete
hydrogen ions or H+. Instead of excreting H+, the kidney will excrete K+.

201
Q

TX of distal RTA

A

Oral bicarbonate is the treatment because bicarbonate reabsorption in the proximal tubule still works.

Also, potassium replacement; potassium citrate will replace both bicarbonate as well as potassium in distal RTA.

Further, citrate is an effective calcium stone antagonist

202
Q

Etiology of Proximal RTA

A

Fanconi syndrome, Wilson disease, amyloidosis, myeloma, acetazolamide, vitamin D deficiency, secondary hyperparathyroidism, chronic hypocalcemia, heavy metals, chronic hepatitis, autoimmune diseases such as SLE and Sjögren syndrome

203
Q

Etiology of Proximal RTA

A

Inability to absorb bicarbonate. The initial urine pH is basic (until the body loses enough bicarbonate that it is within the range of absorption of the distal tubule), then
the urine will become acidic (pH <5.4).

204
Q

Patients with type II get_____ whereas type I get

_______ Both get hypokalemia

A

bone lesions (osteomalacia and rickets),

kidney stones.

205
Q

Dx of Prox RTA

A

Patients are unable to absorb bicarbonate loading (sodium bicarb IV) and have a basic urine in the presence of acidemia.

206
Q

Normal response to bicarbonate loading

A

Normal individuals do not excrete bicarbonate in

their urine until serum bicarbonate is >24

207
Q

Tx of Prox RTA

A

Give potassium; mild volume depletion will enhance proximal bicarbonate reabsorption (a type of contraction alkalosis).

Thiazide diuretics and very large amounts of bicarbonates
are used.

208
Q

Hyporeninemic/Hypoaldosteronism (Type IV) causes

A 
• An aldosterone deficiency of any cause or adrenal insensitivity to angiotensin II, which
normally stimulates aldosterone release
• Diabetes (50%)
• Addison disease
• Sickle cell disease
• Renal insufficiency
209
Q

SSx of Hyporeninemic/Hypoaldosteronism (Type IV) causes

A

Presence of high urine sodium with oral salt restriction establishes the diagnosis.

210
Q

TX of Hyporeninemic/Hypoaldosteronism (Type IV)

A

Treatment. Administration of fludrocortisone

211
Q

MOA of fludrocortisone

A

Fludrocortisone has a high degree of mineralocorticoid

effect and is similar to administering aldosterone.

212
Q

Etiology of hypercalcuria

A

Increased absorption
Idiopathic renal hypercalciuria
Resorptive

213
Q

hypercalcuria from Increased absorption causes

A

–– Vitamin D intoxication
–– Increased vitamin D with sarcoid and other granulomatous disease
–– Familial

214
Q

hypercalcuria from inc Resorptive causes

A

–– Hyperparathyroidism (10–30% of patients present with stones)
–– Multiple myeloma, metastatic disease to bone, hypercalcemia of malignancy

215
Q

Causes of Hyperoxaluria

A
  • Primary familial

* Enteric

216
Q

UTI causing stones

A

Urinary infection with urease-producing organisms such as Proteus, Staphylococcus, Pseudomonas, and Klebsiella give a highly alkaline urine that produces struvite stones

217
Q

Dx of stones

  • __________—high-yield test and most cost-effective
  • ________—no contrast needed for stones; contrast is to identify masses, abscesses, and tumors; high-yield test
A

U/S

Helical (spiral) CT scan

218
Q

TX of nephrolithias

A

• Shockwave lithotripsy for stones <2 cm. Unfortunately, the fragments may cause
obstruction themselves.
• Ureteroscopy
• Percutaneous removal (requires more anesthesia and hospital stay)

219
Q

Adult Polycystic Kidney Disease

Extra-renal manifestations

A 
–– Hepatic cysts (40–60%)
–– Colonic diverticula
–– Hypertension (50%)
–– Intracranial aneurysm (10–20%)—other vascular aneurysms may be seen
–– Mitral valve prolapse (25%)
220
Q

This is due to atherosclerotic disease in elderly persons and fibromuscular dysplasia in young women.

A

Renal Artery Stenosis

221
Q

Renal Artery Stenosis SSx

A

The key feature is an upper abdominal bruit radiating laterally, which is present
in 50–70% of patients

222
Q

RAS

The best initial screening test is the _____

A

abdominal U/S.

223
Q

The______ is a test that measures the uptake of a radioisotope before and after the administration of captopril. A positive test is when there is decreased uptake of the isotope (i.e., decreased GFR) after giving the
captopril

A

captopril renogram

224
Q

RAS

The ______ is still the best method of confirming the diagnosis

A

arteriogram

225
Q

Best initial Tx of RAS

A

The best initial treatment is percutaneous transluminal angioplasty. If stenosis recurs, then the procedure should be repeated. If angioplasty fails, surgical resection is
attempted

226
Q

This is most commonly due to a unilateral adenoma. Adenomas can also be bilateral. The rest of the cases are from bilateral hyperplasia

A

Primary Hyperaldosteronism (Conn Syndrome

227
Q

SSx of Conn syndrome

A

Hypertension in association with hypokalemia found on routine screening tests or
• Symptoms of hypokalemia such as muscular weakness and polyuria and/or polydipsia from a nephrogenic diabetes insipidus

228
Q

Dx of Conn

A

Elevated aldosterone levels in urine and blood.

229
Q

Tx of Conn

A

Surgical resection in those with an adenoma. Potassium-sparing diuretics such as spironolactone in those with hyperplasia

230
Q

The key feature is episodic hypertension in association with headaches, sweating, palpitations, and tachycardia. Pallor or flushing may also occur.

A

Pheochromocytoma

231
Q

The best initial tests are

A

urinary vanillylmandelic acid (VMA), metanephines, and

free urinary catecholamines

232
Q

The key feature is hypertension in association with characteristic cushingoid manifestations such as truncal obesity, buffalo hump, menstrual abnormalities, striae and
impaired healing, etc.

A

Cushing Disease

233
Q

Dx of Cushings

A

Dexamethasone suppression testing and 24-hour urine cortisol are the best initial tests.

CK IM (9 decks)

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