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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
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USMLE Step 2 CK
l Internal Medicine
or calcium. They are used when the calcium level is abnormally high because of vitamin D
replacement. Cinacalcet is a substance that simulates the effect of calcium on the parathyroid.
Cinacalcet is used in severe, refractory cases. Cinacalcet will tell the parathyroid to shut off
parathyroid hormone production and helps decrease phosphate in this way.
Aluminum-containing phosphate binders should not be used. Aluminum is associated both
with CNS accumulation and dementia as well as bone abnormalities.
Osteodystrophy. 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. The low
calcium leads to secondary hyperparathyroidism, which removes calcium from the bones. In
addition, bones buffer acidosis by removing calcium from bone. When you want to demineralize a piece of bone in a lab, you soak it in acid; this is what is happening in the body. Renal
osteodystrophy is controlled with improving calcium and phosphorous levels and treating the
secondary hyperparathyroidism.
Hypermagnesemia. Magnesium accumulates because of decreased renal excretion. Treatment
is by restricting magnesium intake.
Hypertension and Accelerated Atherosclerosis. Renal disease results in a rapidly progressive
coronary artery disease. The reason for this is not precisely clear, however, this is the most
common cause of death for those on dialysis. This is why the goal of blood pressure management is lower at <130/80 for those with renal impairment.
Infection. ESRD patients are at increased risk of infection because neutrophils and other
white cells do not work normally in a uremic environment. This is the second most common
cause of death in dialysis patients. 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.
Bleeding. Although nephrotic syndrome gives thrombophilia because of the urinary loss of
protein C, protein S, and antithrombin, the most common coagulation problem with ESRD is
bleeding. This is because of uremia-induced platelet dysfunction. It gives an increased bleeding time. Uremia-induced bleeding is treated with desmopressin, which releases subendothelial stores of von Willebrand factor and factor VIII, which increase platelet aggregation and
adherence. Rarely, estrogen or cryoprecipitate are used.
Dietary Treatment. Patients with severe renal disease should be on a diet restricted in potassium, sodium, protein, magnesium, and phosphate.
Other abnormalities associated with ESRD are pruritus, hyperuricemia, decreased libido from
low testosterone levels, weakness, fatigue, and glucose intolerance. Although not life threatening, they do have a significant impact on function. The only way to improve them is with
dialysis, although, by themselves, they are not indications for dialysis (the indications for
dialysis are hyperkalemia, acidosis, fluid overload, encephalopathy, and pericarditis).
RENAL TRANSPLANTATION
The duration of survival is by far superior with transplantation when compared with maintenance on dialysis.
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Table 8-4. Duration of Survival
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Live related donor 95% at 1 year, 72% at 5 years
Cadaver donor 88% at 1 year, 58% at 5 years
Dialysis alone 30–40% at 5 years
Diabetics on dialysis 20% at 5 years
The average wait to obtain a kidney for transplantation is 2–4 years and becoming longer
because of an insufficient donor supply.
Post-transplantation renal graft rejection is prevented by using cyclosporine, tacrolimus, and
mycophenolate. These are all medications that inhibit T-cell function.
FLUID AND ELECTROLYTE DISORDERS
Hyponatremia
Hyponatremia is defined as a low serum sodium concentration with a level <135 mEq. This
generally occurs from either increased free water retention or urinary sodium loss. About
85–90% of sodium is extracellular. Serum osmolality is largely a function of the serum
sodium level.
Chapter 8
l Nephrology
Serum osmolality = (2 × sodium) + BUN/2.8 + glucose/18
When the glucose and BUN are normal, this roughly comes out to be 2 × sodium + 10.
Presentation. The symptoms of hyponatremia are predominantly neurologic. They range
from mild confusion and forgetfulness to disorientation and obtundation to seizure or coma,
depending on the severity of the hyponatremia. The symptoms do not correspond to a specific level of sodium because the symptoms largely depend on how fast the level dropped.
An acute 15–20 point drop in sodium level can result in a seizure or coma. If the level drops
gradually, the patient can sustain an extremely low sodium level with no symptoms at all.
Generally, there should be no symptoms at all unless the level drops below 125.
Treatment. Mild hyponatremia should resolve with fluid restriction. “Mild” refers to the
absence of symptoms, not a specific level.
Moderate hyponatremia can be managed with normal saline administration combined with a
loop diuretic such as furosemide. The saline gives sodium, and the loop diuretic causes a net
free water loss.
Severe and chronic hyponatremia such as that resulting in seizure or coma should be managed with 3% hypertonic saline or the V2 receptor-antagonists conivaptan and tolvaptan. It
would be unusual to see severe symptoms with a sodium level >120.
The rate of rise of the sodium level should be monitored so as not to cause central pontine
myelinolysis. This is what occurs if the sodium level is corrected too rapidly. Generally, the
rate of rise should not exceed 0.5–1 mEq per hour. This means no more than a 12-point
rise in a 12–24-hour period. Hyponatremia can be corrected as rapidly as 2 mEq per hour
if the patient is seizing and it is extremely urgent. Fludrocortisone is used for cerebral salt
wasting disease.
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USMLE Step 2 CK
l Internal Medicine
Specific etiologies
Pseudohyponatremia. 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.
• Hyperglycemia: The sodium level is decreased by 1.6 mEq/L for every 100 mg/dL
increase in glucose above normal. 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.
• Hyperlipidemia: In this case, there is a normal sodium level and this is simply a lab
artifact.
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.
• CHF
• Nephrotic syndrome and low albumin states
• Cirrhosis
• Renal insufficiency: When renal failure becomes advanced, the impaired free water
excretion will drop the sodium level.
Hypovolemic States (Decreased ECF). For most of these, the hyponatremia develops because
of the loss of sodium through body fluids and replacement with free water. For example,
sweating is a cause of hypernatremia because sweat is mostly free water and only has a little
sodium. However, when you sweat and replace only with free water, the sodium level drops
over time.
• GI loss: vomiting, diarrhea, gastric suction
• Skin loss: burns, sweating, cystic fibrosis
• Diuretics: you urinate out a little salt but replace with only free water
• Renal sodium loss: The kidney can lose the ability to reabsorb sodium in the proximal convoluted tubule as the kidney is damaged. Damaged tubules cannot reabsorb
sodium.
• Adrenal insufficiency (Addison disease): Aldosterone reabsorbs sodium from the kidney.
Without aldosterone, you lose sodium.
• ACE inhibitors: unclear etiology
Table 8-5. Causes of Hypovolemic Hyponatremia
Urine Na <20 Urine Na >20
Dehydration Diuretics
Vomiting ACE inhibitors
Diarrhea Renal salt wasting
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Sweating Addison disease
Cerebral sodium wasting
Euvolemic States. These patients are neither dehydrated nor volume overloaded. There is no
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edema, neither is there orthostasis or decreased skin turgor.
• Psychogenic polydipsia: patients must drink at least 15–20 liters a day of fluid to overwhelm the diluting capacity of the kidney
• 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)
SIADH
Etiology
• CNS diseases: infections, stroke, tumor, trauma, vasculitis, pain
• Pulmonary diseases: pneumonia, TB, PE, asthma
• Neoplastic disease: lung cancer, as well as cancer of the pancreas, duodenum, or thymus
Medications
• SSRIs
• Tricyclic antidepressants
• Haloperidol
• Cyclophosphamide
• Vincristine
• Carbamazepine
• Thiazide diuretics
Chapter 8
l Nephrology
The presentation of SIADH is similar to all forms of hyponatremia in terms of neurologic
symptoms in proportion to the degree of hyponatremia. The diagnosis is based on finding
an elevated urine osmolality and urine sodium level. This is inappropriate to find in a patient
with hyponatremia. The range on urine osmolality is 50–1,200 mOsm/L. If urine osmolality
is >100 in the presence of hyponatremia, the person most likely has SIADH. The single most
accurate test is an elevated ADH level, though it is rarely done and is inferred from the urine
osmolarity.
Treatment of SIADH is to restrict fluids for mild disease and give hypertonic saline for
severe disease as was previously described. Normal saline with a loop diuretic is also useful
to raise the sodium level. For chronic disease in which the underlying cause of the SIADH
cannot be corrected, therapy with conivaptan, tolvaptan, or demeclocycline is used. These
medications inhibit the effect of ADH on the kidney tubule and lead to water diuresis.
Conivaptan and tolvaptan are V2 receptor-antagonists. Demeclocycline and lithium treat
SIADH by inducing nephrogenic diabetes insipidus. Lithium, due to toxicity, is rarely used.
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l Internal Medicine
Hypernatremia
Etiology
• Insensible losses: extrarenal loss without intake of hypotonic fluids; increased skin loss
(sweating, burns, fever, exercise) or respiratory infections
• GI loss: osmotic diarrhea (e.g., lactulose, malabsorption), some infectious diarrhea
• Transcellular shift: rhabdomyolysis or seizures causing muscles to avidly take up water
and ↑Na
• Renal
– Nephrogenic diabetes insipidus (NDI), secondary to renal disease, increased cal-
cium, decreased potassium, lithium, demeclocycline, sickle cell disease, and others
– Central DI (CDI)
– Idiopathic, trauma, infectious, tumor, granulomatous, hypoxic brain damage or
from neurosurgery. Idiopathic most common.
– Osmotic diuresis: diabetic ketoacidosis (DKA), nonketotic hyperosmolar coma,
mannitol, diuretics
Presentation
• Primarily neurologic
• Lethargy, weakness, irritability, seizures, and coma are present with severe hypernatremia of any cause. Diabetes insipidus gives a dilute diuresis of 3–20 L per day.
Diagnosis. Watching for a decrease in urine volume after administering ADH distinguishes
CDI from NDI.
Treatment. Acute hypernatremia is treated with isotonic fluids intravenously. Correction of
sodium should not be >1 mEq every 2 hours or 12 mEq per day. Complications of overly
rapid correction include cerebral edema, permanent neurologic damage, or seizures. A rate of
correction as fast as 1 mEq per hour is also acceptable if the patient is seizing.
CDI. Correct the underlying cause, if possible.
• Vasopressin (ADH). It can be given subcutaneously, intravenously, intramuscularly,
or by nasal spray (all routes except oral).
NDI. Correct underlying cause, if possible.
• Diuretic or NSAIDs. NSAIDs work by inhibiting prostaglandins, which impair concentrating ability. NSAIDs will increase the action of ADH at the kidney.
Hypokalemia
Potassium levels are maintained by transcellular shift and rates of renal excretion. About 95%
of potassium is intracellular.
Etiology
• GI losses. This can be from any form of GI loss, such as vomiting, diarrhea, or tube
drainage.
• 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.
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• Urinary losses:
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– Diuretics
– Increased aldosterone states, such as Conn syndrome, excessive licorice ingestion,
Bartter syndrome, or Cushing disease. Aldosterone is the most important regulator
of potassium levels in the body. Renal artery stenosis results in a high renin/aldosterone state.
– Low magnesium levels. Magnesium decreases urinary loss of potassium. When you
are deficient in magnesium, you start to spill potassium into the urine.
Presentation. The symptoms of hypokalemia predominantly affect muscles and the heart.
Patients have weakness, paralysis when it is severe, arrhythmias that can be fatal, and even
rhabdomyolysis. Potassium is necessary for ADH effect on the kidney, and hypokalemic
patients present with nephrogenic diabetes insipidus.
Diagnostic testing. In emergency cases, the most important diagnostic test is the EKG. EKG
abnormalities include T-wave flattening and U-waves. A U-wave is an extra wave after the
T-wave that is indicative of Purkinje fiber repolarization.
Treatment. Correction of underlying cause when possible. Replete as follows:
• IV maximum 10–20 mEq/h; do not use dextrose containing fluids, as they increase
insulin release and lower potassium.
• Oral: Gut regulates absorption; there is no maximum rate of oral potassium replacement.
• GI tract slows absorption; no dextrose-containing fluids; dextrose brings
increased extracellular potassium entry into cells.
• Potential complication of too-rapid repletion is fatal arrhythmia.
Chapter 8
l Nephrology
Very large amounts of potassium may be necessary to raise the body potassium level by even
1 or 2 points. The total body requirement is to give 4–5 mEq per kg per point. It is important
not to use IV fluids that contain dextrose. Dextrose will provide the shift of potassium into
the cells and will further lower potassium levels.
Hyperkalemia
Etiology
• Increased intake (orally or by IV)—usually in presence of impaired excretion
•
Movement from cells to extracellular fluid (ECF)
– Pseudohyperkalemia—secondary hemolysis, mechanical trauma during venipunc-
ture, platelet count >1,000,000 (106), WBC count >100,000 (105)
– Acidosis—secondary cellular buffering (H+ moves into cells, K+ moves out)
– For every 0.1-point decrease in the pH, the potassium level will increase by
0.7 points because of the transcellular shift
– Insulin deficiency
– Tissue breakdown—rhabdomyolysis, tumor lysis after seizures or severe exercise
– Periodic paralysis—mild, brief episodes of muscle weakness with mild increase in
K+; diagnosis with recurrent attacks and family history
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l Internal Medicine
• Decreased urinary excretion
– Renal failure
– Hypoaldosteronism: ACE inhibitors, type IV RTA, adrenal enzyme deficiency; hep-
arin inhibits production of aldosterone
– Primary adrenal insufficiency (Addison disease) or adrenalectomy
– Potassium-sparing diuretics—amiloride, spironolactone
– NSAIDs
Presentation
• Muscular weakness can begin usually with K+ levels >6.5.
• Abnormal cardiac conduction is the most common cause of death, hypoventilation.
Diagnosis. EKG findings: peaked T waves, widened QRS, short QT, or prolonged PR
Treatment
• Calcium chloride—membrane stabilization (most emergent treatment in presence of
EKG abnormalities). Effect is immediate and short lived.
• Sodium bicarbonate—alkalosis drives K+ into cells. Do not give in same IV line as calcium. Forms CaCO3 precipitates.
• Glucose and insulin—drives K+ intracellular, takes 30–60 minutes to work
• Diuretics, beta agonists
• Cation exchange resin (Kayexalate)—resin absorbs 1 mEq K+ per g and releases
1 mEq Na+. Given with sorbitol to prevent constipation. Kayexalate must be given with
the above treatments because they only cause cellular redistribution of K+ and do not
remove it from the body. It can also be given as a retention enema for those who cannot take it orally.
• Dialysis
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ACID/BASE DISTURBANCES
Alkalosis (High pH)
Metabolic
For every 1-point increase in the level of serum bicarbonate, there is a 0.7-point increase in the
pCO2. Volume contraction of dehydration results in an increased level of aldosterone, which
leads to metabolic alkalosis. Increased levels of aldosterone in volume contraction lead to
increased levels of hydrogen ion (H+) excretion. Increased sodium delivery to the distal tubule
leads to increased sodium reabsorption in a segment of the tubule that excretes H+ and K+.
H+ Ion Loss
• Exogenous steroids
• GI loss (vomiting, nasogastric suction)
• Renal loss (Conn syndrome, Cushing, ACTH overproduction, licorice, Bartter syndrome)
• Decreased chloride intake
• Diuretics
HCO3 Retention
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• Bicarbonate administration
• Contraction alkalosis
• Milk-alkali syndrome
H+ Movement into Cells
• Hypokalemia
Respiratory
Hyperventilation of Any Cause
• Anemia
• Pulmonary embolus
• Sarcoid
• Anxiety
• Pain
Progesterone, catecholamines, hypoxia, cirrhosis, pregnancy, and salicylates are all events or
substances that increase the respiratory rate and minute ventilation and lead to respiratory
alkalosis.
Chapter 8
l Nephrology
Anion gap = (Na+) – (HCO
–
+ Cl–)
3
(normal: 8–12)
Acidosis (Low pH)
Metabolic
Low Anion Gap
• Myeloma
Low albumin level
•
• Lithium
The anion gap is a gauge of the unmeasured anions in the bloodstream. The majority of the
unmeasured anions are usually albumin, which has a significant amount of negative charge.
In addition to albumin, which is normal, the other anionic substances are lactate, ketoacids,
and the metabolic end products of toxic alcohols.
Na+ and cations = HCO
Hence, if the sodium and cations remain the same and the anions go up, then HCO
go down. On the other hand, if the amount of cations goes up, this leads to an increase in the
amount of HCO
–
and Cl–. This is why there is a decreased anion gap in myeloma. Myeloma
3
proteins are cationic. This leads to an increase in the chloride and bicarbonate levels and
therefore a decreased anion gap.
–
and Cl– and anions
3
–
must
3
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USMLE Step 2 CK
l Internal Medicine
A low albumin level does the same thing. For every 1-point decrease in albumin, there is a
2-point decrease in the anion gap. If albumin, the main unmeasured anion, goes down, then
the levels of chloride and bicarbonate increase to assure electrical neutrality.
Lithium, magnesium, and calcium are all divalent cations that decrease the sodium level.
If the sodium level drops and everything else remains the same, there will be a decreased
anion gap. If sodium is lower, but bicarbonate and chloride stay the same, then the anion
gap must decrease.
Normal Anion Gap
• Diarrhea
• Renal tubular acidosis
• Ureterosigmoidostomy
Increased Anion Gap
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)
Respiratory
Hypoventilation of any cause
• Chronic obstructive pulmonary disease (COPD)
• Pickwickian
• Obesity
• Suffocation
• Opiates
• Sleep apnea
• Kyphoscoliosis
• Myopathies
• Neuropathy
• Effusion
• Aspiration
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RENAL TUBULAR ACIDOSIS
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Distal (Type I)
Etiology
• Usually sporadic
• Also secondary to autoimmune disease (e.g., Sjögren syndrome, SLE)
• Drugs—amphotericin, lithium, analgesics, iphosphamide
• Nephrocalcinosis, sickle cell, chronic infection
• Familial
• Chronic hepatitis
Presentation
• Inability to develop a high H+ concentration in urine. Urine pH is >5.3.
Secondary hyperaldosteronism and hypokalemia
•
• Nephrocalcinosis and nephrolithiasis
Diagnosis. Acid load test; give ammonium chloride, which should lower urine pH secondary
to increased H+ formation. With type I RTA, the urine pH remains elevated. Serum bicarbonate = 10.
Chapter 8
l Nephrology
Patients with distal RTA develop hypokalemia because patients lose the ability to secrete
hydrogen ions or H
Diarrhea: Metabolic acidosis with intact ability to excrete acid. The NH4Cl level will be high
in urine. The urinary anion gap will be negative.
RTA : Kidneys cannot excrete acid in the urine. The urine NH4Cl level will be low. The urinary
anion gap will be positive.
Basically, urine anion gap is a way of distinguishing whether a patient with a normal anion
gap metabolic acidosis has diarrhea or distal RTA as the etiology.
Treatment. 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.
+
. Instead of excreting H+, the kidney will excrete K+.
Proximal (Type II)
Etiology. 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.
Presentation
• 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).
• Also with hypokalemia and a serum bicarbonate of 18–20, as well as proximal tubule
leak of glucose, phosphate, urate, amino acids
• Patients with type II get bone lesions (osteomalacia and rickets), whereas type I get
kidney stones. Both get hypokalemia.
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