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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
.pdf
USMLE Step 2 CK
l Internal Medicine
Diagnosis. Patients are unable to absorb bicarbonate loading (sodium bicarb IV) and have
a basic urine in the presence of acidemia. Normal individuals do not excrete bicarbonate in
their urine until serum bicarbonate is >24.
Treatment. 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. Bicarbonate is generally ineffective and that is why they must be used in such
high amounts. Bicarbonate administration increases renal potassium loss.
Hyporeninemic/Hypoaldosteronism (Type IV)
Etiology
• 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
Presentation
• Usually asymptomatic hyperkalemia
• Mild to moderate renal insufficiency
• Hyperchloremic metabolic acidosis (nonanion gap)
Diagnosis. Presence of high urine sodium with oral salt restriction establishes the diagnosis.
Treatment. Administration of fludrocortisone. Fludrocortisone has a high degree of mineralo-
corticoid effect and is similar to administering aldosterone. Further, loop diuretics will lower
potassium.
NEPHROLITHIASIS
Etiology. Occurs in 1–5% of the population.
• Composition of stones
• Calcium oxalate 70%
• Calcium phosphate 10%
• Mg/aluminum/phosphate (Struvite) 5–10%
• Uric acid 5%
• Cysteine 1%
• Indinavir
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Hypercalciuria
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• Increased absorption
– Vitamin D intoxication
– Increased vitamin D with sarcoid and other granulomatous disease
– Familial
• Idiopathic renal hypercalciuria
• Resorptive
– Hyperparathyroidism (10–30% of patients present with stones)
– Multiple myeloma, metastatic disease to bone, hypercalcemia of malignancy
Hyperoxaluria
• Primary familial
• Enteric
With fat malabsorption, the fat binds to calcium, leaving oxalate to be reabsorbed in increased
amounts.
Chapter 8
l Nephrology
Hypocitraturia
Citrate usually binds with calcium and prevents calcium absorption. Low citrate leads to an
increase in calcium absorption. Causes of hypocitraturia include any acidotic condition.
Uric acid stones
They form in an acid environment and are associated with diseases like gout, hematologic
malignancies, and Crohn’s disease. Radiolucent on x-rays.
Cystinuria
Only associated with the genetic disorder.
Infection
Urinary infection with urease-producing organisms such as Proteus, Staphylococcus,
Pseudomonas, and Klebsiella give a highly alkaline urine that produces struvite stones.
Presentation
• Constant flank pain (not colicky), hematuria, and pain radiating to groin
• Stones <5 mm should pass spontaneously
Diagnosis
• Plain x-ray (80% yield)—x-ray is rarely used
• U/S—high-yield test and most cost-effective
• Strain the urine
• Check serum and urine calcium
• IV pyelogram—always wrong
• Helical (spiral) CT scan—no contrast needed for stones; contrast is to identify masses,
abscesses, and tumors; high-yield test
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Treatment. Analgesia, hydration, and bed rest are the mainstays of treatment.
• Shockwave lithotripsy for stones <2 cm. Unfortunately, the fragments may cause
obstruction themselves.
• Ureteroscopy
• Percutaneous removal (requires more anesthesia and hospital stay)
• Borderline-sized stones 5–7 mm can be expelled by using nifedipine and tamsulosin.
HEREDITARY CYSTIC DISEASE
Adult Polycystic Kidney Disease
Etiology
• Genetic—prevalence of 1:200 to 1:1,000
• Pathogenesis is uncertain
Presentation
• Flank pain, hematuria (micro and gross), infections, and calculi
• May also present as asymptomatic on screening of family members
• Extra-renal manifestations
– Hepatic cysts (40–60%)
– Colonic diverticula
– Hypertension (50%)
– Intracranial aneurysm (10–20%)—other vascular aneurysms may be seen
– Mitral valve prolapse (25%)
Diagnosis. U/S and CT scan.
Treatment. Nonspecific; management of complications (UTI, calculi, and hypertension).
Simple Cysts
They are very common, and if they are smooth-walled with no debris in the cyst, they can be
managed without any further treatment or need for diagnostic tests. Cysts with irregular walls
or debris inside should be closely followed to exclude malignancy. Dialysis causes cysts.
HYPERTENSION
Essential Hypertension
Definition. The most recent guidelines recommend that hypertension be diagnosed when a
person’s systolic blood pressure is 140 mm Hg or diastolic blood pressure ≥90 mm Hg (or
both) on repeated examination.
Systolic blood pressure is particularly important, and is the basis for diagnosis in most patients.
These numbers apply to all adults age >18 years, although for patients age ≥80 a systolic blood
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pressure up to 150 mm Hg is now regarded as acceptable. The goal for treatment of hyperten-
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sion is to reduce blood pressure to levels below the numbers used for making the diagnosis.
Some recent guidelines have recommended diagnostic values of 130/80 mm Hg for patients
with diabetes or chronic kidney disease. However, the clinical benefits of this lower target
have not been established, so these patients should be treated to <140/90 mm Hg.
Patients with very severe hypertension, such as those with a blood pressure >160/100 mm Hg,
should receive initial therapy with 2 medications, this is because patients with a blood pressure
>160 mm Hg will not be successfully controlled with just one medication.
Table 8-6. Guidelines
Normal BP 120/80 mm Hg
Hypertension
Chapter 8
l Nephrology
Stage 1
Stage 2
Etiology/Epidemiology. An estimated 50 million Americans have high blood pressure.
Essential hypertension accounts for >95% of all cases of hypertension. Despite multiple theories on the mechanism, there is no clear understanding of what causes essential hypertension.
It is more common with increasing age and is found in half the population over age 60. It is
more common in men than women until after menopause. It is more common in the black
population at all ages, and the incidence of end organ damage is more common in blacks as
well. Onset is usually between ages 25–55.
Presentation. The most common presentation of essential hypertension is an asymptomatic
patient on whom the elevation of blood pressure is found during a routine examination or
during evaluation for other medical problems.
When symptoms are associated with hypertension, it is more correct to think of them as:
• Acute symptoms associated with a hypertensive emergency, or
• Complications from end-organ damage
With hypertensive emergency, signs and symptoms of cardiac, neurologic, renal, and retinal
involvement are the most common. These include evidence of stroke, subarachnoid hemorrhage,
encephalopathy, myocardial ischemia, and abnormalities on fundoscopic examination. Requires
substantial reduction of blood pressure within one hour to avoid serious morbidity or death.
These can acutely and most commonly result in headache, dizziness, chest pain, dyspnea, blurred
vision, and palpitations. Malignant HTN is defined as encephalopathy or nephropathy with
accompanying papilledema as seen on funduscopic examination.
Systolic 140–159
Diastolic 90–99
Systolic ≥160
Diastolic ≥100
Long-Term Complications
• Cardiac—myocardial ischemia or infarction, CHF, left ventricular hypertrophy, aortic
aneurysm, and dissection, on physical exam an S4 gallop, accentuated A2 heart sound,
and prominent left ventricular impulse can be present
• Cerebrovascular—transient ischemic attack (TIA) or stroke
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• Renal proteinuria—microscopic hematuria, and elevation of BUN/creatinine, which
may lead to the necessity of dialysis
• Retinopathy—hemorrhages, exudates, arteriolar narrowing, and papilledema; they
result in blurred vision, scotomata, and sometimes blindness
Secondary Hypertension. Less than 5% of patients have secondary hypertension. The presentation depends upon the individual cause. For example: renovascular disease gives an abdominal
bruit; Cushing disease gives weight gain, moon-like facies, striae, and ecchymoses; pheochromocytoma gives episodic hypertension associated with headache, palpitations, and sweating; primary aldosteronism (Conn syndrome) gives muscular weakness and polyuria/polydipsia from
hypokalemia. These are discussed more fully later in the notes.
Diagnosis. As much as 20–25% of mild office hypertension is artifactual in nature. These
initial elevated readings merely represent a manifestation of anxiety on the part of the patient
to the doctor and medical environment. This is known as “white coat hypertension.” In this
case, we are talking about patients who have no evidence of end-organ damage. When these
patients are given time to adjust to the environment by being allowed to sit quietly before
the reading is taken, their pressure will lower. When these patients are given an ambulatory
pressure-monitoring device to measure their own pressure at home or work, many of them
will normalize their pressure. In addition, with each subsequent visit to the physician’s office,
the patient’s pressure will often lower toward its true value.
Hence, prior to labeling a patient with a mild elevation as truly hypertensive and initiating
therapy, the following steps are necessary:
• Allow the patient to sit quietly for 5 minutes before the pressure is measured
• Never label a patient as hypertensive after only a single reading
• Repeat the reading 3–6 times over several months before confirming the diagnosis and
initiating therapy
Laboratory Investigation. Most routine lab testing will generally be normal. Testing is usually kept within the bounds of those done during a routine medical evaluation. The purpose
is to evaluate the extent of end-organ damage as well as to exclude some forms of secondary
hypertension. The reasons listed are the most common ones, not the only ones.
Basic studies include:
• Urinalysis for protein, glucose, and RBCs
• Hematocrit
• Serum potassium to exclude hyperaldosteronism
• Serum creatinine and BUN
• Electrocardiogram to evaluate for left ventricular hypertrophy
• Glucose and plasma lipid analysis as an indicator of atherosclerotic risk
Treatment. Patients with confirmed mild and moderate hypertension should initially be
treated with nonpharmacologic modifications in lifestyle. These include weight reduction in
the obese, dietary sodium restriction, aerobic exercise, and avoiding excessive alcohol intake.
Dietary modifications such as a low-fat diet with increased dietary fiber can also be effective.
Relaxation methods have inconsistent effects. DASH eating plan: increase fruits, vegetables,
low-fat dairy, and low-fat diet.
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Patients with severe hypertension (diastolic >100 mm Hg) should generally be started imme-
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diately on drug therapy. Patients with a blood pressure of >160/100 mm Hg should be started
on two medications as part of initial therapy. There is a linear correlation of increasing weight
with increasing blood pressure. Obesity further increases cardiovascular risk by increasing LDL
cholesterol, decreasing HDL, and decreasing glucose tolerance. There is generally a 0.5–1.0 mm
Hg drop in systolic and diastolic blood pressure for every kilogram of weight lost.
Drug Treatment
• Who to treat?
Patients who continue to have a diastolic BP >90 mm Hg despite a 3- to 6-month trial
of nonpharmacologic therapy should generally be started on antihypertensive drugs.
The decrease in end-organ damage, such as myocardial infarction and stroke with
drug treatment, is generally greater in those who have a higher baseline BP. In other
words, someone who has a diastolic pressure >100 will show a much greater reduction
in risk of stroke with drug therapy compared with someone whose diastolic pressure is
only 90–95 mm Hg.
• What to use?
There are almost 50 different medications approved for the initial treatment of hyper-
tension, not including combination medications. The major medications with their
individual characteristics are listed at the end of this section.
• General principles:
In the absence of a specific indication or contraindication, diuretics are still recom-
mended as initial treatment. For stage III HTN, BP >160/100, a two-drug combination should be used—diuretic with an ACE/ARB/CCB or beta blocker.
The mortality benefit of diuretics has been unsurpassed when compared with other
medications. If diuretics do not control the blood pressure, then a second medication should be added. The second medication can be a beta-blocker, calcium-channel blocker, ACE inhibitor, or angiotensin-receptor blocker. Beta blockers should be
avoided in those with a history of asthma, COPD, heart block, or depression.
Every attempt should be made to individualize therapy based on the characteristics
of each patient. To do this, you must be familiar with the characteristics of each
class of drugs.
• What are the indications for specific hypertensive groups?
Diabetics: Should be treated with ACE inhibitors or ARBs, which prevent the devel-
opment of nephropathy. The blood pressure goal in a diabetic is lower, at <130/80
mm Hg; this is also true in those with renal insufficiency, CHF, retinopathy, or stroke.
Patients with microalbuminuria should receive an ACE inhibitor.
Postmyocardial infarction (ischemic heart disease): Should be treated with beta blockers.
Diminished left-ventricular systolic function (such as with CHF or postmyocardial
infarction): Should receive ACE inhibitors and/or beta blockers.
African-American patients are least effectively treated with ACE inhibitors.
Pregnant patients are best treated with alpha-methyldopa, labetalol, hydralazine, or cal-
cium-channel blockers. ACE inhibitors and angiotensin-receptor blockers are absolutely
contraindicated in pregnant patients. Diuretics are relatively contraindicated.
Chapter 8
l Nephrology
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Note
Malignant HTN
Encephalopathy or
nephropathy with
accompanying papilledema
as seen on funduscopic
examination.
Note
Resistant HTN
Failure to reach blood
pressure control in those who
are adherent to full doses
of a 3-drug regimen, which
includes a diuretic.
Hypertensive Emergencies
Definition. The acute onset of severe hypertension in association with severe and rapidly
worsening symptoms of end-organ damage. This usually happens with diastolic pressure
>120–130 mm Hg. The terms “malignant” and “accelerated” hypertension are difficult to distinguish clinically, with “malignant” usually referring to the more severe syndrome.
Etiology/Epidemiology. The cause is unknown. Hypertensive emergencies occur in about 1%
of hypertensive patients.
Presentation
Neurologic: Encephalopathy, headache, confusion, seizures, and subarachnoid or intracere-
bral hemorrhage.
Cardiac: Chest pain, myocardial infarction, palpitations, dyspnea, pulmonary edema, jugular
venous distension, and gallops.
Nephropathy: Acutely progressive hematuria, proteinuria, and renal dysfunction.
Retinopathy: Papilledema, hemorrhages, and blurred vision.
Diagnosis. The laboratory evaluation is the same as with essential hypertension except that
there is no concern of artifactual “white coat hypertension” given the clear symptoms. CT
scan of the head may be necessary to exclude hemorrhage. EKG is more important as an initial test to exclude infarction.
Treatment. IV therapy is indicated. Nitroprusside and labetalol are the two best agents.
Nitroglycerin is preferable in those who have evidence of myocardial ischemia. Enalaprilat is
an IV ACE inhibitor that is now being used as well. Other less commonly used agents include
esmolol, diazoxide, and trimethaphan.
The most important point in management is not to lower the pressure too far (e.g., not <95–
100 mm Hg diastolic) so as not to compromise myocardial or cerebral perfusion. The initial
goal is to reduce BP by no more than 25% within the first 1 to 2 hours.
Secondary Hypertension
Definition. Hypertension in the presence of an identifiable underlying cause.
Etiology/Epidemiology. <5% of cases of hypertension are secondary to an identifiable under-
lying cause. Renal artery stenosis is the most common of these causes.
The following groups should be screened for secondary hypertension:
• Those who become hypertensive either very young or very old (age <25 or >55)
• Those with a key feature of history, physical examination, or laboratory abnormality
consistent with a particular form as described below
• Patients who remain hypertensive despite increasing dosages and numbers of antihypertensive medications, i.e., those refractory to what should normally be effective therapy
Renal Artery Stenosis. This is due to atherosclerotic disease in elderly persons and fibromuscular dysplasia in young women.
Presentation: The key feature is an upper abdominal bruit radiating laterally, which is present
in 50–70% of patients.
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Diagnosis: The best initial screening test is the abdominal U/S. The captopril renogram is a test
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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. The captopril renogram is a noninvasive method of confirming the diagnosis of renal
artery stenosis. The accuracy is diminished with renal insufficiency. The arteriogram is still the
best method of confirming the diagnosis. Duplex Doppler ultrasonography and magnetic resonance angiography are also used to noninvasively detect stenosis. The accuracy of duplex U/S is
operator-dependent.
Treatment: The best initial treatment is percutaneous transluminal angioplasty. If stenosis recurs, then the procedure should be repeated. If angioplasty fails, surgical resection is
attempted. Medical therapy with ACE inhibitors should be reserved only for those in whom
angioplasty or surgery either fails or is not possible. For unilateral disease it is not clear that
angioplasty is superior to ACE inhibitors.
Primary Hyperaldosteronism (Conn Syndrome). This is most commonly due to a unilateral
adenoma. Adenomas can also be bilateral. The rest of the cases are from bilateral hyperplasia.
Cancer is rare as a cause of hyperaldosteronism.
Presentation: The key features are either:
• 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
Chapter 8
l Nephrology
Diagnosis: Elevated aldosterone levels in urine and blood.
Treatment: Surgical resection in those with an adenoma. Potassium-sparing diuretics such as
spironolactone in those with hyperplasia.
Pheochromocytoma. Most often due to a benign tumor of the adrenal gland; 10% are bilateral, 10% are malignant, and 10% are extra-adrenal.
Presentation: The key feature is episodic hypertension in association with headaches, sweating, palpitations, and tachycardia. Pallor or flushing may also occur.
Diagnosis: The best initial tests are urinary vanillylmandelic acid (VMA), metanephines, and
free urinary catecholamines. Plasma catecholamine evaluation is helpful as well. CT and MRI
scanning is used to localize the site of the tumor.
Treatment: Alpha-adrenergic blockade followed by surgical removal.
Cushing Disease. Most often due to ACTH hypersecretion by a pituitary adenoma.
Presentation: The key feature is hypertension in association with characteristic cushingoid
manifestations such as truncal obesity, buffalo hump, menstrual abnormalities, striae and
impaired healing, etc.
Diagnosis: Dexamethasone suppression testing and 24-hour urine cortisol are the best initial
tests.
Treatment: Surgical resection is best when possible.
Coarctation of the Aorta. The key feature is hypertension markedly greater in the upper
extremities compared with the lower extremities.
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Miscellaneous. Other causes of secondary hypertension are the use of oral contraceptives, acromegaly, congenital adrenal enzyme deficiencies, and virtually any cause of chronic renal disease
such as glomerulonephritis, polycystic disease, diabetic nephropathy, or chronic pyelonephritis.
Antihypertensive Medications
Table 8-7. Antihypertensive Medications
Thiazides Loop Diuretics Potassium Sparing
Hydrochlorothiazide Furosemide Spironolactone
Chlorthalidone Bumetanide Amiloride
Metolazone Torsemide Triamterene
Indapamide
Diuretics
Specific Indications. CHF, edematous states, African-American patients; least expensive.
Major Side Effects. Decreases in potassium and magnesium; increases in calcium, uric acid,
glucose, LDL-cholesterol; gynecomastia.
Relative Contraindications. Diabetes, gout, hyperlipidemia.
Angiotensin converting enzyme (ACE) inhibitors
Benazepril Enalaprilat (only IV form) Moexipril
Captopril Fosinopril Quinapril
Enalapril Lisinopril Ramipril
Specific Indications
• Diabetics with hypertension to prevent neuropathy; the blood pressure goal in a diabetic patient is <130/80 mm Hg
• CHF as afterload reduction
• Postmyocardial infarction with left ventricular impairment
Major Side Effects. Cough, angioneurotic edema, neutropenia, hyperkalemia, taste disturbances, anaphylactoid reactions.
Relative Contraindications. Less effective in African-American patients.
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Absolute Contraindications. Bilateral renal artery stenosis, pregnancy.
Calcium channel blockers
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Amlodipine Nicardipine
Diltiazem Nifedipine
Felodipine Verapamil
Isradipine
Specific Indications. Angina pectoris, supraventricular arrhythmia, migraine, Raynaud phenomenon, esophageal spasm.
Major Side Effects. Peripheral edema, constipation, heart block, reflex tachycardia.
Relative Contraindications. Atrioventricular conduction defects, CHF from systolic dysfunction.
Angiotensin receptor antagonists
Chapter 8
l Nephrology
Losartan Valsartan Irbesartan
Candesartan Telmisartan
Specific Indications. Those intolerant to ACE inhibitors (especially because of cough).
Major Side Effects. Few. This is the newest class of antihypertensives.
Absolute Contraindications. Pregnancy.
The remainder of these medications should be considered second- or third-line agents.
Beta blockers
Acebutolol Bisoprolol Metoprolol Pindolol
Atenolol Labetalol (combined
alpha/beta)
Betaxolol Penbutolol Timolol
Metoprolol and atenolol are the most commonly used.
Specific Indications
• Myocardial infarction or ischemic heart disease
• Supraventricular arrhythmias
• Migraine headaches, glaucoma, anxiety (resting tachycardia)
• Congestive failure from diastolic dysfunction
Nadolol Propranolol
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