Nephrology Flashcards

1
Q

Main cause of cystitis

A

E. coli #1 cause

Enterobacteria

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2
Q

Typical signs of cystitis

A

dysuria, frequency, urgency, +/- hematuria

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3
Q

Antibiotic treatment for cystitis

A

Nitrofurantoin
Fluoroquinolones (Cipro)
TMP-SMX (Bactrim) becoming less effective due to resistant organisms

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4
Q

An ascending urinary tract infection

A

pyelonephritis

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5
Q

How does patient with pyelonephritis present differently than cystitis?

A

Fever, radiating flank pain, abd pain, nausea and vomiting

CV tenderness

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6
Q

UA results of pyelonephritis

A

Pyuria

WBC casts

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7
Q

Pyelonephritis treatment

A
  • Abx per urine culture: Cipro, Cephalosporins, gentamycin, Bactrim
  • Nephrectomy
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8
Q

Most common presenting symptom of bladder carcinoma

A

hematuria

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9
Q

Treatment of bladder carcinoma

A

Surgery: transurethral resection of bladder tumor (TURBT), partial or radical cystectomy

Adjuvant chemotherapy and radiation may be used

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10
Q

Hematuria + palpable abdominal mass + smoker

A

renal cell carcinoma

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11
Q

Child with hematuria and palpable abd mass or distended abd

A

Wilms tumor

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12
Q

1 risk factor of bladder cancer

A

smoking

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13
Q

I came in to see my physician assistant because of…

Nocturia
Hesitancy
Decreased urine flow
Incomplete bladder emptying
Frequency
Firm enlarged prostate on rectal exam
Negative urine culture
A

Benign Prostatic Hyperplasia (BPH)

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14
Q

How to treat BPH?

A

Behavior modification: decrease fluids before bed, decrease alcohol and caffeine, routine voiding schedule

Meds:
Alpha blockers - relax smooth muscle; Tamsulosin (Flomax), Prazosin, Terazosin
5 alpha reductase inhibitors - block DHT production which causes BPH; Finasteride, Dutasteride

Surgery:
Transurethral resection of the prostate (TURP)
Prostatectomy

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15
Q

3 types of urinary incontinence

A

Stress incontinence – Leaking of urine due to physical stress. Coughing, jumping, laughing etc. This is often due to urethral incompetence.

Urge incontinence – A sudden feeling of urgency and an associated loss of urine. Often associated with an overactive detrusor muscle. This may be due to neurologic disease

Overflow incontinence – Involuntary voiding without an urge to urinate typically secondary to urinary retention. This is often due to an outlet obstruction (think BPH) or an underactive detrusor muscle

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16
Q

I came in to see my physician assistant because of…

Sudden onset of severe flank pain
Nausea and vomiting
Hematuria

A

Nephro/urolithiasis (kidney stone)

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17
Q

Most kidney stones composed of what

A

calcium

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18
Q

Treatment of nephrolithiasis

A

Prevention: increased fluid intake

Meds: alpha blockers (Flomax, Prazosin), NSAID, corticosteroids

Ureteroscopic stone extraction
Extracorporeal shock wave lithotripsy

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19
Q

Normal GFR

A

100-130 mL/min/1.73 m^2

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20
Q

Symptoms of uremia may include…

A

Anorexia, Fatigue, Malaise, Dyspnea, Orthopnea, Change in mental status, restless legs, Weakness, Pruritis, Insomnia, Irritability, Cramping, etc

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21
Q

3 categories of AKI

A

Prerenal (decreased blood flow to kidney)
Intrinsic (kidney is having the problem)
Postrenal (urinary tract obstruction)

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22
Q

Prerenal causes of AKI

A
Renal artery stenosis
Renal artery thrombosis
Heart failure
Severe dehydration
NSAIDS
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23
Q

Intrinsic causes of AKI

A
Crush injury
Antibiotic reaction
Contrast dye
Glomerulonephritis
ATN
AIN
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24
Q

Postrenal causes of AKI

A

OBSTRUCTIONS!
BPH
Kidney stone

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25
Q

Most common types of AKI

A

prerenal and ATN

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26
Q

BUN/CR greater than 20:1 in ________.

A

acute GN, prerenal and postrenal AKI

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27
Q

BUN/CR less than 20:1 in ___________.

A

ATN, AIN

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28
Q

Lab findings of AKI

A

elevated BUN:Cr
hyperkalemia
anemia
decreased GFR

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29
Q

How is AKI treated?

A

Treat underlying cause

  • Correct CHF
  • Fluids if dehydrated
  • Avoid nephrotoxins
  • Treat post renal problem
  • Stenting of renal arteries

Dialysis

Transplant

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30
Q

How long until AKI becomes chronic?

A

over 3 months

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31
Q

Most CKD is secondary to what?

A

HTN or DM

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32
Q

Lab findings of CKD that are not seen in AKI

A

Broad waxy casts
Proteinuria
HTN

  • both have elevated Cr/BUN, decreased GFR, hyperkalemia, anemia
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33
Q

CKD treatment

A

Aggressive treatment of HTN and DM

Treat hyperkalemia with calcium chlorid or bicarb

Diet: protein restriction, salt and water restriction, K+ restriction, Phos restriction

Hemodialysis if GFR below 15

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34
Q

I came in to see my physician assistant because of…

  • Edema (periorbital or scrotal area)
  • Dark (Tea Colored) urine
  • Red cell casts
A

glomerulonephritis

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35
Q

Causes of glomerulonephritis

A

Berger disease (IgA nephropathy)
Endocarditis
Lupus
Strep infection

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36
Q

Glomerulonephritis treatment

A

high dose corticosteroids

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37
Q

proteinuria > 3.5g/day, high cholesterol, edema

A

nephrotic syndrome

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38
Q

causes of nephrotic syndrome

A
Primary renal disease
SLE, rheumatoid etc
Post infectious causes
DM
NSAIDS
Lithium
Toxins
Pregnancy
Multiple myeloma
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39
Q

UA results of nephrotic syndrome

A

fatty casts, oval fat bodies

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40
Q

Nephrotic syndrome treatment

A

Diet - increase proteins to match loss of proteinuria, salt restriction

Diuretics - ACE or ARB

Steroids

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41
Q

How to differentiate nephrotic syndrome and nephritis?

A

proteinuria levels (3.5 nephrotic syndrome)

UA results (RBC casts in nephritis, fatty casts in nephrotic syndrome)

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42
Q

Causes of nephritic syndrome

A

Specific strains of Group A strep
Bacterial or viral infection
Lupus
Goodpasture’s syndrome

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43
Q

I came in to see my physician assistant because of…

Hematuria (coca cola urine)
Proteinuria
HTN
Oliguria
Edema
Pruritus
Loss of appetite
A

nephritic syndrome

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44
Q

Nephritic syndrome treatment

A

Treat HTN
ACEI or ARB
Corticosteroids

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45
Q

Causes of hydronephrosis

A

Abnormal anatomy leading to poor outflow (often congenital)

Obstruction of any kind

Compression of the bladder causing reverse urine flow

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46
Q

How is hydronephrosis detected?

A

Renal ultrasound during prenatal testing

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47
Q

I came in to see my physician assistant because of…

Flank pain
History of UTIs and kidney stones
Kidneys may be large and palpable

A

polycystic kidney disease

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48
Q

50% of patients with PCKD have ________ by 60 years old

A

end stage renal disease

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49
Q

PCKD treatment

A
Supportive care and pain meds
Cyst decompression
Antibiotics if cyst is infected
Decreased caffeine intake
Dialysis
Renal transplant
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50
Q

Granular or muddy brown casts on UA =

A

acute tubular necrosis

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51
Q

Broad waxy casts on UA =

A

Chronic kidney failure

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52
Q

Fatty casts on UA =

A

nephrotic syndrome

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53
Q

Red blood cell casts on UA =

A

glomerulonephritis/nephritic syndrome

54
Q

WBC casts on UA=

A

infection, pyelonephritis

55
Q

Epithelial casts on UA =

A

acute tubular necrosis

56
Q

Nephrotic syndrome consists of huge losses of ________.

A

protein

57
Q

Maltese crosses indicates _______.

A

nephrotic syndrome

58
Q

Tea colored urine indicates __________.

A

glomerulonephritis

59
Q

Causes of hypernatremia

A

Hypervolemic: iatrogenic (hypertonic saline), hyperaldosteronism

Hypovolemic: extrarenal loss (diarrhea, sweating, burns), urinary/renal loss (diuretics, renal disease)

Euvolemic: Diabetes Insipidus (ADH deficiency or insensitivity), hypodipsia

60
Q

Normal sodium levels

A

135-145

61
Q

Signs/sx’s of hypernatremia

A

Thirst, Lethargy, Irritability, Weakness, Change in mental status, dry mucous membranes, lack of tears (infants), hyperreflexia

62
Q

When should dialysis be done in hypernatremia?

A

Na > 200

63
Q

How should hypernatremia be treated based on circulating volume?

A

ISOTONIC IV FLUIDS

Hypovolemia: 0.9% NS, D5W

Normal volume: Drink water, D5W

Hypervolemia: Loop diuretic, D5W

64
Q

Causes of hyponatremia with hypervolemia

A

CHF, nephrotic syndrome, cirrhosis

65
Q

Causes of hyponatremia with euvolemia

A

SIADH (high ADH release)
Adrenal insufficiency
Hypothyroidism
Polydipsia

66
Q

Causes of hyponatremia with hypovolemia

A

Sodium loss (renal or extrarenal)

67
Q

Signs/Sx’s of hyponatremia

A

Nausea, Malaise, Headache, Lethargy, Mental status changes, Muscle cramps, Seizures

68
Q

Hyponatremia treatment

A
Fluid restriction
Hypertonic saline (D5 1/2 or D5 NS), but be very careful
69
Q

Normal serum pH

A

7.35-7.45

70
Q

Normal PCO2

A

35-45 mmHg

71
Q

Normal serum bicarb

A

22-26 mEq/L

72
Q

Acid-base imbalances of respiratory causes show up with changes in _______ and metabolic causes with changes in ________.

A

carbon dioxide

bicarb

73
Q

Metabolic acidosis treatment

A

Treat underlying cause

Give bicarbonate

74
Q

Metabolic alkalosis treatment

A

Stop diuretics or nasogastric suctioning

Give IV Normal saline

75
Q

Describe mneumonic “ROME” for acid-base disorders

A

Respiratory will be opposite (the RO in rome)
- so pCO2 will be opposite the pH (so in respiratory acidosis the pH is low but the pCO2 is high)

Metabolic always relate with Bicarb & if pH is alkalosis the bicarb will be the same (ME for metabolic equal)
- so for metabolic alkalosis pH is high and bicarb is also high

76
Q

Functions of the kidneys

A

Blood filtration
Regulation of blood volume and pressure
Activation of Vit D
Production of erythropoietin

77
Q

How does CHF contribute to renal failure?

A

inadequate heart pumping -> effective blood volume depletion -> decreased renal perfusion -> prerenal failure

78
Q

How does cirrhosis contribute to renal failure?

A

scarring of the live -> portal HTN -> blood pools in gut’s venous system -> effective blood volume depletion -> decreased renal perfusion -> prerenal failure

79
Q

How do the kidneys react to low blood volume?

A

kidneys reabsorb sodium and water in attempt to replenish intravascular volume

80
Q

What is elevated serum creatinine a sign of?

A

GFR is inadequate and renal function is impaired

81
Q

What is lab that distinguishes prerenal from intrinsic renal failure?

A

BUN/Cr >20:1 in prerenal and less than 20:1 in intrinsic AKI

82
Q

Why is BUN/Cr not as elevated in intrinsic AKI?

A

renal reabsorption is defective

83
Q

Urine changes in intrinsic AKI

A

reabsorption defective so wastes both water and sodium in urine -> urine dilute with high sodium

84
Q

Urine changes in prerenal AKI

A

reabsorbs Na and water to increase intravascular volume -> urine very concentrated with low sodium

85
Q

Function of ADH

A

increases water reabsorption from renal tubules to blood

86
Q

How can postrenal AKI be dx’d?

A

ultrasound of ureter, bladder, or urethra for possible obstruction

87
Q

Two categories of glomerulopathies

A

nephrotic and nephritic syndromes

88
Q

Signs of nephrotic syndrome

A

edema, proteinuria, hyperlipidemia

89
Q

Pathophysiology behind nephrotic and nephritic syndrome

A

damage or inflammation to filtering mechanism of glomerulus, allowing proteins through

90
Q

Signs of nephritic syndrome

A

HTN, hematuria, proteinuria

91
Q

Changes in the serum that occur with chronic kidney failure

A

increase: Na, K, H, Mg, Phos, ammonia, PTH
decrease: Vit D, calcium, erythropoietin

92
Q

Why does calcium concentration decrease in CKD?

A

In renal failure, Vit D activation decreases. Without Vit D, calcium cannot be absorbed from the diet and calcium in serum decreases

93
Q

What hormone increases serum calcium by releasing it from bone?

A

PTH

94
Q

Why does renal failure cause anemia?

A

kidneys are responsible for erythropoietin production

95
Q

Urethritis most often caused by what?

A

Gonorrhea and Chlamydia

96
Q

What is the significance of cells vs casts on UA?

A

cells with normal morphology -> lower GU tract disease
cells with abnormal morphology -> renal disease
casts are conglomerates of protein and cells -> glomerular or tubular disease

97
Q

White cells from kidney =

White cells from lower UG =

A

AIN

infection - cystitis or urethritis

98
Q

Red cells from kidney =

Red cells from lower UG =

A

glomerulonephritis

nephrolithiasis, hemorrhagic cystitis, or bladder cancer

99
Q

What kind of casts occur in ATN and pyelonephritis?

A

white and epithelial casts

100
Q

Which IV solution increases sodium in blood to increase intravascular volume?

A

hypertonic saline (D10W, 3% NS)

101
Q

Which IV solution dilutes sodium in blood vessels and causes water to leave bloodstream and enter cells?

A

hypotonic saline (1/2 NS)

102
Q

Which saline causes intravascular volume increase without any fluid shifts?

A

isotonic saline

103
Q

Which IV saline should be used in hypovolemic patient?

A

isotonic (0.9% NS, D5W, LR)

104
Q

What can occur if electrolyte imbalances are corrected too quickly with IV fluids?

A

central pontine myelinolysis; brain does not have time to re-equilibrate

105
Q

Function of aldosterone

A

reabsorption of sodium and secretion of potassium

106
Q

______ is the main extracellular cation and _____ is the main intracellular cation.

A

sodium

potassium

107
Q

How are “-volemias” (hyper, hypo, euvolemia) determined?

A

based on perceived clinical exam (edema, dryness, skin tenting, etc.)

108
Q

Hypervolemic hypernatremia most commonly caused by what?

A

iatrogenic - administration of sodium bicarb or dialysis solutions

109
Q

How can renal and extrarenal losses of water and/or sodium be distinguished in hypovolemic hypernatremia?

A

renal - higher concentration of sodium in urine

extrarenal - kidneys hold on to as much sodium as possible, so lower concentration in urine

110
Q

Central vs Nephrogenic diabetes insipidus

A

central - decreased production of ADH from posterior pituitary

nephrogenic - decreased sensitivity of kidneys to ADH

111
Q

Well known med that causes renal toxicity

A

lithium

112
Q

Main signs of diabetes insipidus?

A

excess and dilute urine (ADH is not absorbing water)

113
Q

How do diabetes insidious and polydipsia present similarly in clinic? How can they be differentiated?

A

both have polyuriaserum [Na]

will be low in polydipsia and high in DI

114
Q

What is SIADH and what does it cause to happen in body?

A

inappropriate and excessive secretion of ADH, which dilutes serum and causes hyponatremia

115
Q

What would you expect on UA of SIADH?

A

concentrated urine, elevated urine [Na]

116
Q

Pathophysiology behind pseudohyponatremia?

A
  • increase in glucose, lipids, proteins, or urea in blood causes increased water reabsorption
  • dilutes intravascular space and causes hyponatremia even though there is actually no change in serum sodium
117
Q

_________ is a net gain in sodium or a net loss in water.

A

hypernatremia

118
Q

3 basic mechanisms that cause hyperkalemia:

A

increased intake
decreased urinary excretion
increased movement of K+ from cells into bloodstream

119
Q

Hyperkalemia on ECG

A

peaked T waves

120
Q

Shifts of K+ and H+ in acidosis and alkalosis

A

acidosis: H+ into cell, K+ out of cell = hyperkalemia
alkalosis: H+ out of cell, K+ into cell = hypokalemia

121
Q

Which drugs cause H+ to rush into cell and cause hyperkalemia?

A

beta blockers

122
Q

How does insulin affect H+ shift into and out of cells?

A

low insulin = H+ into cellhigh insulin = H+ out of cell* opposite for K+

123
Q

______ and ______ are main players in acid-base balance.

A

kidney and lungs

124
Q

Respiratory acidosis is caused by elevated _____.

A

CO2

125
Q

How does body compensate for respiratory acidosis?

A

kidney reabsorbs more HCO3- to buffer

126
Q

How does body compensate for metabolic alkalosis?

A

lung retains more CO2 to buffer

127
Q

What causes respiratory acidosis?

A

decreased expiration of CO2: obstruction, damage to lungs or chest wall, problem with respiratory muscles

128
Q

What causes respiratory alkalosis?

A

hyperventilation

129
Q

What causes metabolic alkalosis?

A

hyperaldosterone
vomiting
diuretics

130
Q

Causes of acid gain in metabolic acidosis

A
"MUD-PILES"
Methanol
Uremia
DKA
Paraldehyde
Isoniazid or Iron
Lactic acid
Ethylene glycol
Salicylates
131
Q

How to determine the cause of metabolic acidosis?

A

Calculate serum anion gap: Na - (Cl + HCO3)

  • Over 10-12 (another acid present) -> MUD-PILERS
  • Normal -> diarrhea or renal

Calculate urine anion gap: Na + K - Cl = -NH4

  • Negative -> diarrhea
  • Positive or zero -> renal tubular acidosis