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Renal, Urinary Systems & Electrolytes Flashcards

1
Q

Patients with chronic diabetes mellitus > 10 years can develop:

  2. 3.
A
  1. Microangiopathy
  2. Nephropathy
  3. Glomerulosclerosis
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2
Q

What are the risk factors for the development of diabetic nephropathy?

A
  1. Poor glycemic control
  2. Elevated blood pressure
  3. Smoking
  4. Increasing age
  5. Race (Black, Mexican American)
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3
Q

Clinical findings for:

Diabetic nephropathy

A
  1. Mild-Moderate proteinuria

2. Chronic kidney disease (elevated creatinine)

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4
Q

Diagnosis:

  1. Flank pain
  2. Low-volume voids with or without occasional high-volume voids
A

Obstructive uropathy

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5
Q

Define post-obstructive diuresis?

A

Post-obstructive diuresis is when a high-volume urination occurs due to a large volume of retained urine overcoming an obstruction.

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6
Q

What are the consequences of obstructive uropathy in a patient with:

  1. One kidney
  2. Two kidneys
A
  1. Acute renal failure

2. Post-obstructive diuresis

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7
Q

What are the consequences of recurrent vomiting?

A
  1. Depletion of fluid acid
  2. Depletion of sodium chloride
  3. Metabolic acidosis
  4. Activation of RAAS
  5. Increased urinary potassium loss
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8
Q

Treatment:

Initial treatment for recurrent vomiting in a patient with hypokalemia

A

Normal Saline + Potassium

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9
Q

Hypokalemic, hypochloremic metabolic alkalosis

A

Recurrent vomiting

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10
Q

Signs and Symptoms:

Nephritic glomerulonephritis

A
  1. Urinary sediment with: RBCs, occasional WBCs, Red cell casts or mixed cellular casts
  2. Edema
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11
Q

What is the cause of edema in nephritic glomerulonephritis?

A

Decreased GFR and retention of sodium and water by the kidneys

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12
Q

Why is infusion rate important for chronic kidney disease patients receiving sodium nitroprusside?

A

Prolonged infusion of sodium nitroprusside at high rates can lead to cyanide toxicity, especially in patients with chronic kidney disease.

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13
Q

What medication leads to cyanide toxicity if infused for too long and too fast?

A

Sodium nitroprusside; DO NOT infused for long than 24 hours or at rates >2ug/kg/min.

Potent arterial and venous dilator used to treat hypertensive emergencies.

Patients with chronic kidney disease are at a high risk for this infusion associated toxicity.*

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14
Q

Clinical Presentation:

  1. Headache
  2. Confusion
  3. Arrhythmia
  4. Flushing
  5. Respiratory depression
A

Cyanide toxicity

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15
Q

Treatment:

Hyperkalemia with ECG changes

A

Calcium gluconate OR calcium chloride followed by

IV insulin + Definitive treatment (cation exchange resin, dialysis)

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16
Q

Treatment:

Temporary treatment for hyperkalemia

A

IV insulin+glucose –> works the fastest
Beta-agonists (eg, albuterol)

First give calcium gluconate to stabilize the cardiac membrane.

**These agents shift K intracellularly and lower serum K+. **

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17
Q

Treatment:

Definitive treatment for hyperkalemia

A
  1. Cation exchange resin (eg, sodium polystyrene sulfonate)
  2. Dialysis
  • First give calcium gluconate to stabilize the cardiac membrane.*
  • *These agents decrease the total body K+ content. **
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18
Q

What ECG findings are associated with hyperkalemia of the following levels:

K+= 6-7 mEq/L
K+= 7-8 mEq/L
K+= >8 mEq/L
A

K+= 6-7 mEq/L

  1. Prolonged PR interval
  2. Tall peaked T wave

K+= 7-8 mEq/L

  1. Loss of P wave
  2. ST elevation
  3. Tall peaked T wave

K+= >8 mEq/L

  1. Widened QRS (sine wave pattern)
  2. AV node block
  3. Fascicle and BB blocks
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19
Q

Adverse effect:

Associated with using aminoglycosides (eg, amikacin) to treat multi-drug resistant pyelonephritis in the elderly

A

Nephrotoxicity (i.e. acute renal failure)

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20
Q

Diagnosis:

  1. Bladder pain worsened by filling and relieved by voiding
  2. Dyspareunia
  3. Urinary frequency
  4. Urinary urgency
A

Interstitial cystitis

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21
Q

Treatment:

Interstitial cystitis

A
  1. Behavioral modification & trigger avoidance
  2. Amitriptyline
  3. Analgesics for exacerbations
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22
Q

What is the most common cause interstitial nephritis?

A

Drug-induced

  1. Cephalosporins
  2. Penicillins
  3. Sulfonamides
  4. Sulfonamide containing diuretics
  5. NSAIDs
  6. Rifampin
  7. Phenytoin
  8. Allopurinol
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23
Q

Treatment:

Drug-induced interstitial nephritis

A

Discontinue the offending drug.

  1. Cephalosporins
  2. Penicillins
  3. Sulfonamides
  4. Sulfonamide containing diuretics
  5. NSAIDs
  6. Rifampin
  7. Phenytoin
  8. Allopurinol
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24
Q

Define:

Nephrotic Syndrome

A
  1. Heavy proteinuria (>3.5g/24hr)
  2. Hypoalbuminemia
  3. Edema
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25
Q

What are the two most common causes of nephrotic syndrome in the absence of systemic disease?

A
  1. Focal segmental glomerulosclerosis (FSGS)

2. Membranous nephropathy

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26
Q

What are the clinical associations for focal segmental glomerulosclerosis (FSGS) as the etiology of nephrotic syndrome without systemic disease?

A

African-American and Hispanic ethnicity, obesity, HIV and heroin use

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27
Q

What are the clinical associations for membranous nephropathy as the etiology of nephrotic syndrome without systemic disease?

A

Adenocarcinoma (eg, breast, lung); NSAIDs; hepatitis B; systemic lupus erythmatosus

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28
Q

What are the primary renal causes of nephrotic syndrome?

A
  1. Focal segmental glomeruloscerlosis
  2. Membranous nephropathy
  3. Membranoproliferative glomerulonephritis
  4. Minimal change disease
  5. IgA nephropathy
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29
Q

How does the body respond to hypovolemia?

A
  1. JGA of the kidney releases renin
  2. Renin converts angiotensinogen to angiotensin I
  3. ACE, from the lungs, converts angiotensin I into angiotensin II
  4. Angiotensin II
    A. Directly increases proximal tubule Na reabsorption
    B. Leads to the secretion of Aldosterone to further increase Na and water reabsorption in the distal tubule
    C. Causes Vasoconstriction which improves GFR and BP
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30
Q

How does the kidney respond to respiratory alkalosis?

A

Alkalinization of the urine (increased urine pH), by excreting bicarbonate in the urine.

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31
Q

Treatment:

Refractory hypokalemia in a chronic alcoholic

A

Correct hypomagnesia as well.

Chronic alcoholics typically present with multiple electrolyte abnormalities.

**Magnesium functions to inhibit renal potassium excretion. In its absence you have unopposed loss of potassium. **

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32
Q

Diagnosis:

  1. Midline abdominal pain
  2. No urination or bowel movement in 2 days
  3. Hx of BPH
  4. Chronic neck pain treated with amitriptyline
A

Amitriptyline-induced urinary retention

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33
Q

Treatment:

Amitriptyline-induced urinary retention

A
  1. Urinary catheterization

2. Discontinue any anticholinergic medications (eg, amitriptyline)

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34
Q

Mechanism of Action:

Amitriptyline-induced urinary retention

A

Anticholinergic drugs prevent:

  1. Detrusor muscle contraction
  2. Urinary sphincter relaxation
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35
Q

What medications cause hyperkalemia?

A
  1. Nonselective beta-adrenergic blockers
  2. ACE inhibitors, ARBs and K+ sparing diuretics
  3. Digitalis
  4. Cyclosporine
  5. Heparin
  6. NSAIDs
  7. Succinylcholine
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36
Q

Mechanism of Action:

Trimethoprim induced hyperkalemia

A

TMP blocks epithelial Na channel in the collecting tubule

This effect occurs most commonly in HIV patients.

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37
Q

How is the GFR affected in Trimethoprim-induced hyperkalemia?

A

It isn’t. TMP inhibits renal tubular creatinine secretion and artificially raises the creatinine, but GFR is unaffected.

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38
Q

What are the potential causes of normal anion gap metabolic acidosis?

A
  1. Hyperalimentation (IV nutrition)
  2. Addison disease
  3. Renal tubular acidosis
  4. Diarrhea
  5. Acetazolamine (Carbonic anhydrase inhibitors)
  6. Spironolactone
  7. Saline infusion
  8. Fistulas (eg, pancreatic ileocutaneous, etc)
  9. Urethral diversion (eg, ileal loop)

Think ‘HARD ASS’ + FU.

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39
Q

What group of diagnoses should you consider if you have normal anion gap metabolic acidosis and hyperkalemia that occur out of proportion to the renal dysfunction?

(i.e. potassium is high, bicarb is low, anion gap is normal, and creatinine is only moderately elevated)

A

Renal tubular acidosis (RTA)

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40
Q

What alterations would you see in Type 4 renal tubular acidosis:

  1. Anion gap
  2. Potassium level
  3. Renal function
A
  1. Anion gap would be normal, 8-12
  2. Hyperkalemic
  3. Mild to moderate renal insufficiency
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41
Q

Mechanism of Action:

Type 4 renal tubular acidosis in an elderly patient with poorly controlled diabetes

A
  1. Diabetes damages the JGA
  2. Patient enters a state of hyporeninemic and hypoaldosteronism (low renin; low aldosterone)
  3. Aldosterone deficiency leads to cortical collecting tubule dysfunction and retention of H+ and K+
  4. Remaining nephrons secrete acid as NH4+ in the urine until so metabolic acidosis is not seen until late in disease
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42
Q

What patients are at risk for Type 4 Renal Tubular Acidosis?

A

Poorly controlled diabetics

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43
Q

What type of acid-base disorder would you expect in aspirin toxicity?

A

Mixed respiratory alkalosis and anion gap metabolic acidosis

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44
Q

Symptoms:

Aspirin toxicity

A
  1. Fever
  2. Tinnitus
  3. Tachypnea
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45
Q

What would the pH be in mixed respiratory alkalosis and anion gap metabolic acidosis?

A

Normal

46
Q

What is the equation for Winter’s formula?

A

[(1.5xHCO3-)+8 ]+/-2= the PaCO2 obtained from the ABG

This is used to determine if respiratory compensation is adequate in metabolic acidosis.

If you have a respiratory acidosis and you want to know if metabolic compensation is adequate:

expected HCO3- change= 0.1xPaCO2 change

If you have metabolic alkalosis and you want to know if there is concomitant respiratory alkalosis

expected PaCO2 change= 0.7xHCO3- change

47
Q

Why might a patient with post-obstructive uropathy present with weakness?

A

Excessive diuresis may lead to potassium wasting and dehydration, both of which cause weakness.

48
Q

Diagnose:

Interstitial nephritis

A
  1. Fever
  2. Rash
  3. Acute kidney injury
  4. Eosinophilia (UA)
  5. WBC cast
49
Q

Which glomerulopathy is caused by persistent activation of the alternative complement pathway?

A

Membranoproliferative glomerulonephritis type 2 (Dense Deposit Disease)

50
Q

How do diabetics in DKA compensate for metabolic acidosis?

A

Kussmaul breathing (deep, rapid breathing)

51
Q

What is a normal acid base status?

pH
HCO3-
PaCO2

A
  1. pH= 7.35-7.45
  2. HCO3-=22-28
  3. PaCO2=33-45
52
Q

How can you classify metabolic alkalosis?

A

Saline-responsive
1. Urine Cl-<20

Saline-unresponsive
1. Urine Cl- >20

53
Q

In which patients should metformin administration be avoided?

A

Patients who are acutely ill presenting with:

  1. Acute renal failure
  2. Liver failure
  3. Sepsis
  • You are concerned about lactic acidosis.*
54
Q

Diagnosis:

Patient with severe liver cirrhosis with acute renal failure unresponsive to intravenous fluid resuscitation.

A

Hepatorenal syndrome

    1. Cr <1.5 mg/dL
      1. Urine Na <10 mEq/L
      2. Urine without blood, cast and protein
      3. No improvement of renal function with IV fluid resuscitation.*
55
Q

Diagnosis:

Liver cirrhosis patient with:

  1. Cr <1.5 mg/dL
  2. Urine Na <10 mEq/L
  3. Urine without blood, cast and protein
  4. No improvement of renal function with IV fluid resuscitation and diuretic withdrawal
A

Hepatorenal syndrome

56
Q

Diagnosis:

Non-anion gap metabolic acidosis with hyponatremia and hyperkalemia in a patient with TB

A

Addison’s disease

  • Tuberculosis is a common cause of primary adrenal insufficiency (Addison’s disease).*
57
Q

List the two main causes of hyponatremia.

A
  1. Inappropriate antidiuretic hormone secretion

2. Primary polydipsia

58
Q

What population is at risk for primary polydipsia?

A

Patients with psychiatric conditions.

MA: Central defect in thirst regulation

59
Q

Signs and Symptoms:

Primary polydipsia

A
  1. Hyponatremia
  2. Dilute urine w/ urine osmolality <100 mOsm/kg
  3. Confusion
  4. Lethargy
  5. Psychosis
  6. Seizures
60
Q

Signs and Symptoms:

Diuretic abuse

A
  1. Dehydration
  2. Weight loss (this is why people abuse diuretics)
  3. Orthostatic hypotension
  4. Hyponatremia
  5. Hypokalemia
  6. Elevated urinary Na+ and K+
61
Q

What should you suspect if urine analysis shows a large amount of blood, but urine microscopy shows no RBCs?

A

Myoglobinuria

This is generally caused by rhabdomyolysis and frequently leads to renal failure.

62
Q

Treatment:

Inappropriate antidiuretic hormone secretion

A

Asymptomatic/Mild Symptoms –> fluid restriction

Severe symptoms –> hypertonic (3%) saline

Mild: nausea, forgetfulness
Severe: seizures, coma

63
Q

Signs and Symptoms:

recurrent vomiting

A

Depletion of:

  1. Fluid
  2. Acid
  3. NaCl
  4. K+
64
Q

Metabolic alkalosis vs. Metabolic acidosis

Recurrent vomiting

A

Hypochloremic metabolic alkalosis

65
Q

Treatment:

Recurrent vomiting

A
  1. Volume resuscitation (Normal Saline)

2. Potassium repletion

66
Q

What are the clinical features of prerenal acute kidney injury?

A
  1. Increased serum creatinine (>50% from baseline)
  2. Decreased urine output
  3. BUN/Cr ratio >20:1
  4. FeNa <1%
  5. Unremarkable urine sediment

The elderly are especially susceptible to intravascular volume depletion leading to prerenal AKI due to poor oral intake and excessive volume loss.

67
Q

Acid-Base change:

Aspirin intoxication

A

Mixed respiratory alkalosis and metabolic acidosis

Respiratory alkalosis: increased respiratory drive

Metabolic acidosis: increased production and decreased renal elimination of organic acid (eg, lactic acid, ketoacids)

68
Q

Acid-Base change:

Allergic reaction with stridor

A

Respiratory acidosis

MA: impaired ventilation and CO2 retention.

69
Q

Acid-Base change:

Asthma exacerbation

A

Respiratory alkalosis

MA: tachypnea

70
Q

Acid-Base change:

Excessive diuresis

A

Metabolic alkalosis

71
Q

What are the most common pathologies associated with drug-induced chronic renal failure?

A
  1. Papillary necrosis

2. Chronic tubulointerstitial nephritis

72
Q

What are the risk factors associated with chronic analgesic abuse?

A
  1. Premature aging
  2. Atherosclerotic vascular disease
  3. Urinary tract cancer
73
Q

Diagnosis:

  1. Decreased GFR in the absence of other causes of renal dysfunction.
  2. Minimal hematuria
  3. No improvement with volume resuscitation
A

Hepatorenal syndrome

74
Q

Mechanism of Action:

Nephrolithiasis in a patient with Crohn’s disease

A

Increased oxalate absorption –> hyperoxaluria –> oxalate stone formation

Increased oxalate absorption occurs in any intestinal disease that causes fat malabsorption.

75
Q

Diagnosis:

Urine Analysis: needle-shaped crystals

A

Uric acid stones

76
Q

What is the appropriate work-up for uric acid stones?

A

Evaluation with:

CT
US OR
IV pyelography

77
Q

Treatment:

Uric acid stones

A

<1 cm: hydration and analgesia, most pass on their own

> 1cm: Surgical intervention required

78
Q

What side effect must you be aware of when using diuretics to treat cor pulmonale symptoms in a patient with COPD?

A

Prerenal azotemia/AKI

Diuretics will decrease cardiac output and thus decrease renal perfusion.

Patients may develop elevated BUN and creatinine.

79
Q

What acid base disturbance is associated with COPD?

A

primary respiratory acidosis with compensatory metabolic alkalosis due to CO2 retention

80
Q

How do glucocorticoids affect the BMP?

A

Elevated BUN; no change in creatinine

MA: Glucocorticoids catabolize the body proteins and cause hyperglycemia.

81
Q

What glucose level should you expect in a patient presenting with diabetic ketoacidosis?

A

> 400 mg/dL

82
Q

Laboratory values:

Prerenal azotemia/AKI

Cr:
BUN:
BUN:Cr
Anion gap/No anion gap?

A
  1. Elevated Cr (doubled from admission)
  2. Elevated BUN
  3. BUN:Cr >20
  4. Anion gap metabolic acidosis
83
Q

Management:

AKI in a patient with BPH

A

Renal US to assess for hydronephrosis

84
Q

What are the most common causes of anionic gap metabolic acidosis?

A
  1. Lactic acidosis (lactate)
  2. Ketoacidosis (beta-hydroxy butyrate, acetoacetic acid)
  3. Methanol/formaldehyde ingestion (formic acid)
  4. Ethylene glycol ingestion (glycol acid, oxalic acid)
  5. Salicylate poisoning (salicylic, lactic, sulfuric and phosphoric acids)
  6. Uremia (impaired excretion one H+ in ESRD)
85
Q

Diagnosis:

colicky flank pain with radiation to the goin

A

renal colic

86
Q

What is the most common composition of a kidney stone?

A

75-90% are calcium oxalate

87
Q

What predisposes a person to the formation of calcium oxalate stones?

A
  1. Small bowel disease
  2. Surgical section
  3. Chronic diarrhea

These things lead to malabsorption of fatty acids and bile salts. Unabsorbed fatty acid chelate calcium. Ultimately oxalic acid becomes free for absorption.

88
Q

What type of renal stones are associated with:

  1. Primary hyperparathyroidism
  2. Renal tubular acidosis
A

Calcium phosphate stones

89
Q

When might you expect a patient to have a uric acid stone?

A
  1. Acidic urine
  2. Increased cell turnover
  3. Dehydration
90
Q

When might you expect a patient to produce a strait stone?

A

When urine is alkaline due to urease producing bacteria (eg, Proteus).

Expect a history of recurrent UTI.

91
Q

Which lab values provide the best picture of acid-base status?

A
  1. pH
  2. PaCO2

You can calculate HCO3- from these two values using the Henderson-Hasselbalch equation.

92
Q

Treatment:

Urge incontinence in patients who fail to respond to bladder training and pelvic floor exercises

A

Antimuscarinic agents (eg oxybutynin)

93
Q

Diagnosis:

  1. Fever
  2. Maculopapular rash
  3. Renal failure
  4. Urine analysis with WBC casts

In a patient recently treated with Bactrim.

A

Drug-induced interstitial nephritis

Urine analysis may also have eosinophils.

94
Q

What are the diagnostic tests of choice to diagnose ureteral calculi?

A
  1. Abdominal US (preferred in pregnant patients)

2. Spiral CT Abdomen/Pelvis without contrast

95
Q

Why aren’t X-rays the diagnostic test of choice for identifying ureteral calculi?

A
  1. Non-radiopauque (non-calcium) stone (~15% of all stones) are not visible on Xray.
  2. X-ray does not provide information about obstruction of the ureter or kidney
96
Q

Treatment:

  1. Mild hypernatremia
  2. Severe hypernatremia
A
  1. %5 dextrose in 0.45% saline
  2. 0.9% saline

The most common cause of hypernatremia is hypovolemia.

97
Q

What is the most common malignancy associated with painless hematuria?

A

Bladder tumor

98
Q

Workup:

Painless, gross hematuria in a patient >35

A
  1. CT urogram
  2. cystoscopy

You need to rule out urological neoplasm.

99
Q

How do you screen patients for microalbuminuria?

A
  1. Random urine collection for microalbumin/creatinine ratio

* 24-hour urine collection is more accurate, but is inconvenient to the patient.*

100
Q

Diagnosis:

  1. Left flank pain that radiates to the groin
  2. Hx of recurrent kidney stones from childhood
  3. Positive FHx
  4. UA with hexagonal crystals
  5. Hard, radiopaque stones
  6. Positive urinary cyanide nitroprusside test
A

Cystinuria

101
Q

Mechanism of Action:

cystinuria

A
  1. Brush border of renal tubular and intestinal epithelial cells have defective transport of dibasic amino acids (cystine, lysine, arginine and ornithine)
  2. Cystine is poorly soluble in water
  3. Hard radiopaque stones form
102
Q

What is the screening test used to detect possible cystinuria?

A

Urinary cyanide nitroprusside test

F: detects elevated cystine levels.

Especially useful in detected homozygotes.

103
Q

How can you differentiate IgA nephropathy from post infectious glomerulonephritis?

A
  1. Early onset of URI-related glomerulonephritis (IgA=5 days; post-infection=2-3 weeks)
  2. Normal serum complement levels
  3. Kidney biopsy showing, mesangial IgA deposits
104
Q

Post-pharyngitic vs. Synpharyngitic

Post-infection glomerulonephritis

A

post-pharyngitic

Typically occurs 10-21 days after URI.

105
Q

Post-pharyngitic vs. Synpharyngitic

IgA nephropathy

A

Synpharyngitic

Occurs within 5 days of URI.

106
Q

What did the ALLHAT show?

A

Chlorthalidone was associated with an overall decrease in cardiovascular mortality comparable to that seen with novel antihypertensive agents.

Thus, chlorthalidone became the preferred thiazide agent for HTN.

107
Q

How do thiazides effect glucose tolerance?

A

Thiazides (especially chlorthalidone) impair insulin release from the pancreas and glucose utilization in the peripheral tissues.

This leads to glucose intolerance.

108
Q

Which patients are most susceptible to Thiazide-induced glucose intolerance?

A

Patients with:

  1. DM
  2. Metabolic syndrome (HTN, dyslipidemia, abdominal obesity)
109
Q

Side effects:

Thiazide diuretics

A
  1. Hyperglycemia
  2. Increased LDL cholesterol
  3. Increased TG
  4. HypERuricemia
  5. HypOnatremia
  6. HypOkalemia
  7. HypOmagnesemia
  8. HypERcalcemia
110
Q

Which type of nephrotic syndrome is most commonly associated with renal vein thrombosis?

A

Membranous glomerulopathy

Although, renal vein thrombosis is a possible complication of all types of nephrotic syndrome.

111
Q

Treatment:

Postictal lactic acidosis

A

Observe and repeat labs in 90 minutes

The anion gap is usually transient.

Tonic-clonic seizures lead to skeletal muscle hypoxia and impaired hepatic lactic acid uptake.

112
Q

How do you differentiate between acute-on-chronic hypercarbia and chronic CO2 retention?

A

Acute-on-chronic hypercarbia: acidosis, low serum bicarbonate

Chronic CO2 retention: normal pH high serum bicarbonate

Step 2CK (10 decks)

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