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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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CCS NOTE
This patient has severe hypertension and symptoms (headache). Therapy to lower BP
should be ordered before the results of all specific diagnostic tests are obtained.
Phenoxybenzamine is a good choice for pheochromocytoma.
Initial Managment
Setting: outpatient or (rarely) emergency department
Diagnostic/Therapeutic Plan
Test Results
Assessment
The clinical presentation of paroxysms of headache, sweating, palpitations, and anxiety attacks
in association with labile hypertension is classic for pheochromocytoma. Patients most
commonly seek attention in the setting of a hypertensive crisis.
Patients with pheochromocytoma also present with paroxysmal hypertension or sustained
hypertension. Signs and symptoms of an increased metabolic rate may include profuse
24-hour urine collection for catecholamines
Plasma free metanephrines
Increased urine catecholamines
Increased plasma metanephrines
451
sweating, tachycardia, and weight loss. Supraventricular arrhythmias are commonly seen.
Measurement of 24-hour urine vanillylmandelic acid levels is diagnostic in 95% of cases of
pheochromocytoma. CT scan is used to try to identify the exact location of the tumor.
Further Management Plan/Results
Left adrenal mass present
No evidence of metastatic
disease
CLINICAL PEARL
Treatment Plan
Abdominal CT scan
Metaiodobenzylguanidine (MIBG) scan to identify extra-adrenal
tumors
10% of pheochromocytomas are extra-adrenal
10% are malignant
10% are seen in children
10% are bilateral
10% are multiple
10% are familial
Pheochromocytoma also occurs in MEN2
Alpha-adrenergic antagonist (phentolamine or phenoxybenzamine) until the BP is well
controlled. Remember: Besides alpha-blockers, no other antihypertensives should be
1.
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Discussion
Fewer than 0.1% of patients with hypertension have an underlying pheochromocytoma.
However, in the appropriate clinical setting, this diagnosis should be aggressively pursued
because it is a potentially reversible cause of hypertension. Approximately:
Once the diagnosis is established, surgical excision is the treatment of choice. Preoperative
management focuses on establishing alpha-adrenergic blockade. Beta-blockers should be given
only once alpha-blockade is achieved. Beta-blockers are used in patients with tachycardia only
after alpha-blockers are used. Once the pheochromocytoma is removed, flow cytometry is done
to detect abnormal DNA in order to predict malignant tumors.
Ambulatory BP monitoring to detect paroxysm of hypertension is necessary only when its
diagnosis is not obvious. It is not necessary in this particular case.
Final Diagnosis
Pheochromocytoma
used initially in the management to control symptoms (tachycardia, etc.) Beta-blockers
are used only after alpha-blockers are used and BP is stable.
Fluid replacement2.
Surgical consultation for resection of the tumor3.
90% of lesions are unilateral and localized to the adrenals
10% are bilateral
10% occur extra-adrenally
5% are associated with the familial multiple endocrine neoplasia (MEN) 2 and 3 syndromes
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Case 8
Chief Complaint
Follow-up of uncontrolled diabetes
History and Physical Examination
A 52-year-old man with an 8-year history of type 2 diabetes mellitus is evaluated in your
office for poorly controlled diabetes. He has taken glipizide 10 mg daily for the past few
years, and reports fasting home glucose measurements >180 mg/dL and postprandial
measurements 220–260 mg/dL. He reports no hypoglycemic events. His Hb A1C level
increased from 7.2% to 8.7%. A recent ophthalmic evaluation showed no retinopathy.
He is obese (BMI 30 kg/m
2
). His BP is 152/90 mm Hg, pulse 72/min and regular, and
respirations 12/min. Physical exam shows a normal cardiac and lung exam. Abdominal
exam is benign without evidence of hepatosplenomegaly. Foot exam shows normal
sensation (assessed by monofilament), normal skin, and normal pulses. The patient asks
about his risk of microvascular disease and for ways to better improve glycemic control.
Differential Diagnosis
There is no specific differential diagnosis here, since we know the patient has diabetes (given
the age group and use of oral agents, this is type 2 diabetes). The issue surrounding a diabetic
with worsening glycemic control is the following: Is the patient adherent to the medication or is
this a failure of our treatment plan?
455
Initial Management
Setting: outpatient
Diagnostic/Therapeutic Plan
Test Results
Assessment
Outpatient management of diabetic patients is one of the most common problems faced by
primary care and family practice physicians.
In type 2 diabetes, studies have documented that response to monotherapy is limited (in this
case, the patient is taking only sulfonylurea) with rates of failure to sulfonylureas of up to 10%
per year. So it is expected that this patient will eventually fail sulfonylurea treatment. Some
studies have shown that almost 80–90% of patients who have had diabetes for 10 yrs will
benefit from insulin (either as monotherapy or added to oral hypoglycemic agents).
Add metformin and determine effectiveness of regimen by monitoring A1C (Hb A1C should
fall to ≤7.5% over the next 3 months if treatment is effective; eventually the goal of therapy
should be an ideal Hb A1C level <6.5–7%) and home glucose monitoring (fasting glucose
should be <126 mg/dL).
If A1C levels do not fall, the patient should be encouraged to start insulin or add a glitazone
to metformin and sulfonylureas (this last option is less effective and predisposes the patient
to side effects). Adequate glycemic control reduces the risk for microvascular complication
(neuropathy, nephropathy, retinopathy).
Home-glucose monitoring of fasting glucose 100–120 mg/dL; patient reports no
hypoglycemic events
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In this case, we have a few options:
Metformin works by inhibiting hepatic neoglucogenesis and provides an effective addition to
sulfonylureas. Metformin does not cause weight gain and hypoglycemia is uncommon. It is
contraindicated in patients with renal failure since it may cause lactic acidosis.
Insulin (NPH or glargine) is a good option and can be used alone or in combination with oral
hypoglycemic agents. Some studies have shown that insulin may be the most effective
treatment, in terms of glycemic control, though it causes significant weight gain.
Thiazolidinediones or glitazones (pioglitazone) have also been shown to be effective as
combination therapy with other oral hypoglycemic agents. They are less effective as single
agents since they are less powerful hypoglycemic agents. They cause edema and weight gain
(though not as much as insulin and sulfonylureas). Glitazones lower glucose by sensitizing cells
to insulin. Glitazones lower triglycerides in the serum but increase LDL and HDL cholesterol
by 10%. Liver toxicity was reported only with troglitazone and was pulled off the market in
2000. Increased cardiovascular events have been reported with rosiglitazone, which has also
been removed from the market.
There is no ‘single best answer,’ but given the patient’s obesity, metformin may be a better
option since insulin will cause weight gain and predispose the patient to hypoglycemic events.
Further Diagnostic Plan/Results
Add metformin
Add insulin
Add glitazone
Check A1C at 2 mos after adjustment of medication: 7.0%
457
Treatment Plan
Continue metformin and sulfonylureas, and monitor A1C and fasting glucose at home.
Discussion
This patient has a systolic BP 152 mm Hg and is considered to be ‘hypertensive’ since he has
diabetes. An ACE inhibitor should be initiated to reduce the risk of nephropathy and renal
failure.
Also, increased urinary protein is the earliest marker for diabetic nephropathy and thus, a
specific test for microalbuminuria should be done frequently to assess for early nephropathy
(the urine dipstick is insensitive since it becomes positive with proteinuria >300 mg/day).
Consistent microalbuminuria >30 mg/d usually indicates early nephropathy, which should be a
consideration for an ACE I; ACE inhibitors have been shown to slow the progression to overt
proteinuria as well as slow the increase in creatinine levels.
When should an ACE inhibitor be started in patients with diabetes? With either
hypertension or microalbuminuria, or both.
Diabetic patients who develop proliferative retinopathy are at increased risk for blindness.
Proliferative retinopathy is characterized by the development of new blood vessels on the
retinal surface. These new vessels cause traction as they form and may lead to vitreous
hemorrhages and retinal detachment. Diabetic retinopathy may be prevented with adequate
glycemic control, but once proliferative changes occur, laser photocoagulation is the only way
to stabilize the vessels and prevent blindness. Diabetics are also at risk for cataracts and
glaucoma, which are also causes of blindness. Screen type 2 diabetic patients for retinopathy
once a year from the onset of diabetes!
When should we refer new onset type 2 diabetic to the ophthalmologist? Immediately and
then (at least) 1× a year.
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Peripheral neuropathy is the most common form of neuropathy seen in diabetics
(mononeuropathy and autonomic neuropathy are the other forms). It sometimes manifests as
‘pins and needles’ and ‘numbness’ in a stocking and glove distribution. Early neuropathy may
be asymptomatic but can be picked up on microfilament testing by evidence of decreased
sensation. Patients with decreased sensation are at risk for limb-threatening infections as well
as ischemia.
Studies show that nearly half of the amputations caused by neuropathy and poor circulation
could have been prevented by careful foot care. Do monofilament testing once a year and teach
the patient adequate foot care (inspect feet and toes every day for erythema, swelling, calluses,
fungal infections; wear shoes or slippers to protect feet from injuries; wear shoes that fit well,
etc.). The pain caused by diabetic peripheral neuropathy is treated with amitriptyline and
gabapentin.
CLINICAL PEARL
Outpatient management for type 2 diabetes is as follows:
Final Diagnosis
Uncontrolled type 2 diabetes
Monitor effectiveness with A1C and fasting glucose
Metformin is first-line treatment alone or in combination with sulfonylureas
Add insulin to regimen if oral hypoglycemic agents are ineffective
Do not use sulfonylureas or metformin in patients with renal failure
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