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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
with Burkitt lymphoma. HIV can also be associated with immunoblastic lymphoma. The
main point of knowing this is that they are both high-grade lymphomas with an aggressive
progression of disease.
Clinical Presentation. Enlarged, painless, rubbery, nonerythematous, nontender lymph nodes
are the hallmark of the disease. Patients may also develop what are labeled “B” symptoms, which
are drenching night sweats, 10% weight loss, and fevers. Although pruritus is common in the
disease, it is not one of the “B” symptoms. In this sense, NHL is the same as Hodgkin disease. The
difference is that Hodgkin disease is localized to cervical and supraclavicular nodes 80–90% of
the time, whereas NHL is localized only 10–20% of the time. NHL is far more likely to involve
extralymphatic sites as well as to have blood involvement similar to chronic lymphocytic leukemia. CNS involvement is also more common with NHL. HIV-positive patients often have CNS
involvement.
The staging system for NHL is the same as that for Hodgkin disease as described above.
Diagnosis. The diagnosis of NHL rests initially on an excisional lymph node biopsy. After
this, the most important step is to determine the stage of the disease to determine therapy.
Although this is quite similar to that described above for Hodgkin disease, there are several
significant differences because NHL is far more likely to be widespread at initial presentation.
Lymphangiography is never necessary, and staging laparotomy is rarely needed. The bone marrow biopsy is more central as an initial staging tool. Because the presence of marrow involvement
means the patient has Stage IV disease and therefore needs combination chemotherapy, further
invasive testing such as the laparotomy is not necessary. As with Hodgkin disease anemia, leukopenia, eosinophilia, high LDH, and high ESR often accompany the disease. PET scanning is
highly sensitive and specific for nodal and extranodal sites but not for bone marrow disease.
Note
Knowing each of the
histologic subtypes of NHL is
not necessary for the exam.
Treatment. As with Hodgkin disease, local disease such as stage IA and stage IIA are treated
predominantly with radiation, and all those with “B” symptoms as well as stages III and IV
receive combination chemotherapy. Given the frequency of more widespread disease with
NHL, however, this means few NHL patients are treated with radiation alone. The initial chemotherapeutic regimen for NHL is still CHOP (cyclophosphamide, hydroxy-adriamycin, oncovin [vincristine], prednisone). More elaborate chemotherapeutic regimens for NHL, of which
there are many, are beyond the scope of what is necessary to know for the Step 2 exam.
CNS lymphoma is often treated with radiation, possibly in addition to CHOP. Relapses of
NHL can be controlled with autologous bone marrow transplantation. Some patients with
NHL express CD20 antigen in greater amounts. When this occurs, monoclonal antibody
rituximab should be used. Rituximab is an anti-CD20 antibody that has limited toxicity and
adds survival benefit to the use of CHOP. Thus, R-CHOP would then become first-line therapy. Prior to using R-CHOP, always test completely for hepatitis B and C, as rituximab can
cause fulminant liver injury in those with active hepatitis B or C disease.
Tumor lysis syndrome
Tumor lysis syndrome (TLS) is an oncologic emergency caused by massive tumor cell lysis,
with the release of large amounts of potassium, phosphate, and uric acid into the systemic circulation. Uric acid excretion can result in the precipitation of uric acid in the renal tubules; it
can also induce renal vasoconstriction, reduced renal blood flow, and inflammation, resulting
in acute kidney injury. Hyperphosphatemia with calcium phosphate deposition in the renal
tubules can also cause acute kidney injury.
200
TLS most often occurs after the initiation of cytotoxic therapy in patients with high-grade lym-
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phoma (particularly Burkitt’s and acute lymphoblastic leukemia), though it can occur spontaneously and with other tumor types having a high proliferative rate or large tumor burden.
Patients about to receive chemotherapy for a cancer with a high cell turnover rate--especially
lymphomas and leukemias--should receive prophylactic oral or IV allopurinol plus adequate
IV hydration to maintain high urine output (>2.5 L/day). Rasburicase maybe used as an alternative to allopurinol and is reserved for those at high-risk for developing TLS. Alkalization of
the urine as a treatment of TLS is controversial.
PLATELET DISORDERS
Immune Thrombocytopenic Purpura (ITP)
Definition. Thrombocytopenia of unknown etiology.
Etiology. The idiopathic production of an antibody to the platelet, leading to removal of plate-
lets from the peripheral circulation by phagocytosis by macrophages. The platelets are bound
by the macrophage and brought to the spleen, leading to low platelet counts. ITP is often associated with lymphoma, CLL, HIV, and connective tissue diseases.
Chapter 6
l Hematology
Clinical Presentation. Like all platelet disorders, the patient presents initially with signs of
bleeding from superficial areas of the body such as the skin, nasal and oral mucosa, GI tract,
urine, and vagina. The patient is generally young, more often female, and complains of epistaxis,
bruising, hematuria, dysfunctional uterine bleeding, and sometimes GI bleeding. Petechiae,
purpura, and ecchymoses are often found on exam. The patient is generally otherwise healthy.
Splenomegaly should be absent.
Diagnosis. Thrombocytopenia is the major finding. A normal spleen on exam and on imaging studies such as an U/S is characteristic. Antiplatelet antibodies have a high sensitivity but
poor specificity. The bone marrow should be filled with megakaryocytes indicating that there
is a problem with platelet destruction and not platelet production. The bone marrow will also
exclude other causes of thrombocytopenia such as primary or metastatic cancer, infiltration by
infections such as tuberculosis or fungi, or decreased production problems such as drug, radiation, or chemotherapy effect on the bone marrow. The peripheral smear and creatinine should
be normal, excluding other platelet destruction problems such as hemolytic uremic syndrome,
thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation.
Treatment. Prednisone is the initial therapy in almost all patients. Splenectomy is used in
patients in whom very low platelet counts <10,000–20,000/mm
repeated courses of steroids. IVIG or RhoGAMTM may be used in patients with profoundly
low platelet counts (<10,000 µL) or in patients at risk for life-threatening bleeding. Note that
RhoGAM may only be used in Rh-positive patients. In those who recur after splenectomy, we
use thrombopoietin agents romiplostim or eltrombopag. Rituximab has also been used.
3
continue to recur despite
Clinical Pearl
Platelet disorders can broadly
be classified into 2 groups:
• Quantitative (low platelet
count, eg, ITP)
• Qualitative (normal platelet
count but abnormal
platelet function, eg,
Von Willebrand, Bernard
Soulier)
201
USMLE Step 2 CK
l Internal Medicine
Von Willebrand Disease (vWD)
A 22-year-old woman comes to the emergency department with epistaxis and
heavy periods. She has a PT of 11 seconds (normal), a PTT of 40 seconds
3
(prolonged), and 217,000/mm
Definition. An increased predisposition to platelet-type bleeding from decreased amounts of
von Willebrand factor.
Etiology. An autosomal dominant disorder resulting in a decreased amount of von
Willebrand factor. This is the most common congenital disorder of hemostasis. vWD results
in a decreased ability of platelets to adhere to the endothelial lining of blood vessels. This is
different from platelets aggregating with each other, which is mediated by fibrinogen. In vWD,
aggregation is normal, whereas adherence is abnormal. It is not necessary to know the difference between the different subtypes of vWD for the Step 2 exam.
Clinical Presentation. Patients with vWD manifest platelet-type bleeding such as that
described above for ITP. This is mucosal and skin bleeding such as epistaxis, petechiae, bruising, and menstrual abnormalities. Both platelet problems as well as clotting factor abnormalities can result in GI and urinary tract bleeding. There is often a marked increase in bleeding
after the use of aspirin.
platelets.
Diagnosis. The platelet count and appearance are normal. The bleeding time is increased particularly after the use of aspirin. The level of von Willebrand factor, also known as factor VIII
antigen, is low. The ristocetin platelet aggregation test, which examines the ability of platelets
to bind to an artificial endothelial surface (ristocetin), is abnormal. The PTT may be elevated
in some patients because of a concomitant decrease in levels of factor VIII coagulant portion.
Treatment. Desmopressin acetate (DDAVP) is used for mild bleeding or when the patient
must undergo minor surgical procedures. It releases subendothelial stores of von Willebrand
factor. Factor VIII replacement is used if desmopressin is not effective and the bleeding continues. Factor VIII replacement contains von Willebrand factor. This replaces the use of cryoprecipitate, which is now seldom necessary. Patients should not use aspirin. FFP is not useful.
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BLEEDING
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Chapter 6
l Hematology
Symptoms
• Petechiae
• Purpura
• Ecchymosis
• Epistaxis
• Gingival bleed
• Menstrual bleeding
Decreased Platelet Count Normal Platelet Count
Causes
• ITP (IgM auto Ab
against GP2B3A rec)
• TTP (auto Ab against
Adams factor TS 13)
• HUS (EHEC 0157:H7)
• DIC
Superficial Bleeding
Check
Bleeding Time
Prolonged
Check
Platelet Count
Reversible
Causes
• Uremia
(inhibits
platelet
degranulation)
• Drugs (NSAIDs,
aspirin)
• ADP rec
blocker
(clopidogrel,
ticlopidine)
• GP2B3A rec
blocker
(abciximab)
• Von Willebrand
• Bernard Soulier
• Glanzmann’s
Deep Bleeding
PTT, PT, & INR
Hemophilia A
(Factor 8 deficiency)
Hemophilia B
(Factor 9 deficiency)
Hemophilia C
(Factor 11 deficiency)
Irreversible
Causes
disease
disease (GP1B
defect)
Thrombasthenia
(GP2B3A rec
defect)
Check
Symptoms
• Hemarthrosis
• Deep muscle
bleeding
• Organ bleeding
• PTT (prolonged)
• PT/INR (normal)
Figure 6-7. Evaluation of Patients with Bleeding
COAGULOPATHY
Hemophilia A and B
Definition. The deficiency of factor VIII in hemophilia A and factor IX in hemophilia B
resulting in an increased risk of bleeding.
Etiology. Both hemophilia A and B are X-linked recessive disorders resulting in disease in
males. Females are carriers of the disease. Females do not express the disease because they
would have to be homozygous, which is a condition resulting in intrauterine death of the
fetus. Hemophilia A is far more common than B.
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USMLE Step 2 CK
l Internal Medicine
Clinical Presentation. Mild deficiencies (25% or greater activity) result in either the absence
of symptoms or with symptoms only during surgical procedures or with trauma. More severe
deficiency (<5–10% activity) can result in spontaneous bleeding. Factor-type bleeding is generally deeper than that produced with platelet disorders. Examples of the type of bleeding found
with factor deficiencies are hemarthrosis, hematoma, GI bleeding, or urinary bleeding. Bruising
and central nervous system bleeding can also occur. Severe hemophilia is obvious in most
patients by the age of two. The disorder becomes apparent often at the time of circumcision.
Diagnosis. A prolonged PTT with a normal PT is expected. A factor deficiency is strongly suspected when a 50:50 mixture of the patient’s blood is created with a normal control and the PTT
drops to normal. This is known as a “mixing study.” If the PTT does not correct with mixing,
then an antibody inhibitor of the factor is suspected. The mixing study will only tell you that a
deficiency is present; it will not tell you which specific factor is deficient. Specific factor VIII or IX
levels are necessary to determine a precise diagnosis. This is true of both hemophilia A and B.
Treatment. Mild hemophilia can be treated with desmopressin (DDAVP). Desmopressin can
also be used prior to surgical procedures in mild hemophiliacs. Desmopressin works by releasing subendothelial stores of factor VIII. More severe deficiencies are treated with replacement
of the specific factor. Desmopressin does not work for hemophilia B.
Table 6-3. Causes of Prolonged PT or PTT
Prolonged PT Prolonged PTT Prolonged PT and PTT
Inherited causes Factor VII deficiency vWF and factors VIII, IX,
XI, or XII deficiencies
Acquired causes • Vitamin K deficiency
• Liver disease
• Warfarin use
• Factor VII inhibitor
PT, prothrombin time; PTT, partial thromboplastin time; vWF, von Willebrand factor.
• Heparin
• Antiphospholipid
antibody
Vitamin K Deficiency
Definition. The deficiency of vitamin K resulting in decreased production of factors II, VII,
IX, and X.
Etiology. Vitamin K deficiency can be produced by dietary deficiency, malabsorption, and the
use of antibiotics that kill the bacteria in the colon that produce vitamin K. The antibiotics
most commonly associated are broad-spectrum drugs such as fluroquinolones, cephalosporins, and other penicillin derivatives.
Prothrombin, fibrinogen, factor V,
factor X, or combined factor deficiencies
• Vitamin K deficiency
• Liver disease
• Disseminated intravascular coagulation
• Supratherapeutic heparin or warfarin
• Combined heparin and warfarin use
• Direct thrombin inhibitors
• Inhibitor of prothrombin, fibrinogen,
or factor V or X
204
Clinical Presentation. Bleeding may mimic that of hemophilia and may occur at any site.
Look for oozing at venapuncture sites.
Diagnosis. Both the PT and PTT are elevated. The PT usually elevates first and more severely.
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A correction of the PT and PTT in response to giving vitamin K is the most common method
of confirming the diagnosis.
Treatment. Severe bleeding is treated with infusions of fresh frozen plasma. Vitamin K is
given at the same time to correct the underlying production defect.
Liver Disease
Definition. Coagulopathy from the decreased production of clotting factors by the liver.
Etiology. Any severe liver disease or cirrhosis leads to a decreased production of the major-
ity of clotting factors that are generally all made in the liver, except for factor VIII and von
Willebrand factor. Factor VII is first factor to be depleted.
Clinical Presentation. Bleeding may occur at any site, but the GI tract is the most common site.
Diagnosis. Patients have an elevation of both the PT and PTT, but the PT elevates first and
is often more severely affected. The disorder is clinically indistinguishable from vitamin
K deficiency except that there is no improvement when vitamin K is given. A clear history of
liver disease is often present, suggesting the diagnosis. Low platelet counts are often present
from the hypersplenism that accompanies the liver disease.
Chapter 6
l Hematology
Treatment. Fresh frozen plasma is used acutely to correct severe bleeding such as melena.
Long-term management is based on the nature of the liver disease.
Disseminated Intravascular Coagulation (DIC)
Definition. Consumptive coagulopathy from major underlying illness resulting in consumption of both platelet and clotting factor type and occasionally thrombosis. The bleeding is associated with a marked production of fibrin degradation products such as d-dimers.
Etiology. Although essentially an idiopathic disorder, there is almost always a major underlying disease in the case history. Look for evidence of sepsis most commonly. Almost any disorder that results is cellular destruction and the release of tissue factor can initiate the cascade
of consumption of platelets as well as clotting factors. These problems include rhabdomyolysis, adenocarcinomas, heatstroke, hemolysis from transfusion reactions, burns, head trauma,
obstetrical disasters such as abruptio placenta and amniotic fluid embolism, as well as trauma,
pancreatitis, and snakebites. Promyelocytic leukemia (M3) is a classic association.
Gram-negative sepsis causes DIC by the releasing endotoxin. In acute promyelocytic leukemia (M3), the destruction of leukemic granulocyte precursors results in the release of large
amounts of proteolytic enzymes from their storage granules, causing microvascular damage.
Other malignancies may also cause DIC by augmenting the expression of various oncogenes
that result in the release of tissue factor. DIC exists in acute and chronic forms.
• Acute DIC develops when sudden exposure of blood to procoagulants (tissue factor,
tissue thromboplastin) generates intravascular coagulation. The compensatory hemostatic mechanisms are quickly overwhelmed, and, as a consequence, a severe consumptive coagulopathy leading to hemorrhage develops.
• In contrast, chronic DIC reflects a compensated state that develops when blood
is continuously or intermittently exposed to small amounts of tissue factor.
Compensatory mechanisms are not overwhelmed. Chronic DIC is more frequently
observed in patients with solid tumors and in those with large aortic aneurysms.
205
USMLE Step 2 CK
l Internal Medicine
Clinical Presentation. Bleeding from any site in the body is possible because of a decrease in
both the platelet as well as clotting factor levels. Thrombosis is less common. Hemolysis is often
present and may lead to acute renal failure, jaundice, and confusion.
Diagnosis. DIC is suspected when a patient has a serious underlying disorder as described
above with bleeding and there is elevation in both the PT and PTT with a decrease in the
platelet count. The fibrinogen level is often low because it has been consumed. D-dimers
and fibrin-split products are present in increased amounts, suggesting the consumption of
all available elements of the coagulation system. The peripheral blood smear often shows the
schistocytes as fragmented cells consistent with intravascular hemolysis.
Treatment. Because most patients present with severe bleeding, fresh frozen plasma (FFP)
and sometimes platelet transfusions are necessary to correct the bleeding. Heparin is controversial and is rarely used except in those patients presenting predominantly with thrombosis.
Don’t forget to correct the underlying disorder.
Thrombotic Thrombocytopenic Purpura/Hemolytic Uremic
Syndrome
Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are
two varieties of the same disease process with considerable overlap. There is no specific diagnostic test, so the diagnosis is based on the clinical triad (HUS) or pentad (TTP).
• Most cases of TTP are idiopathic and arise from inhibition of the enzyme ADAMTS13,
which is responsible for cleaving large multimers of von Willebrand factor into smaller
units. The increase in circulating multimers of vWF increase platelet adhesion to areas
of endothelial injury, particularly the arteriole-capillary junctions.
• Some cases of TTP are associated with specific diseases (cancer, HIV) and drugs
(ticlopidine, clopidogrel, cyclosporine, and interferon) and are referred to as secondary
TTP. ADAMTS13 activity is generally not as depressed in secondary TTP.
HUS predominantly affects children. Most cases are caused by a shiga-like toxin produced by
E. coli O157:H7 although Campylobacter, shigella and some viruses have also been implicated.
It is one of the most common causes of acute renal failure in childhood and carries up to 10%
mortality.
HUS consists of a triad of hemolytic anemia, uremia, and thrombocytopenia. TTP has the same
3 findings, and is also associated with fever and neurologic problems. You do not have to have
all 5 findings simultaneously to be considered to have TTP. The anemia in both will be intravascular in nature and will have an abnormal blood smear showing schistocytes, helmet cells, and
fragmented red cells. LDH and reticulocyte count will be elevated and haptoglobin decreased.
Treatment for TTP is plasmapheresis. Plasmapheresis is used to treat severe cases of HUS
but is not established in the treatment of mild disease. Mild disease resolves spontaneously.
Dipyridamole may help treat TTP by preventing platelet aggregation.
Do not give antibiotics to those with possible HUS; if antibiotics are given, organism may
release more toxins as it dies and may worsen the disease.
Do not transfuse platelets. Even if the platelet count is low, administering platelets can actually worsen the CNS and renal abnormalities by giving more platelets as a substrate to precipitate. Small platelet plugs are actually the cause of the problem.
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Heparin-Induced Thrombocytopenia
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Heparin-induced thrombocytopenia (HIT), a complication of heparin therapy, can occur
with any form of heparin. It is more common with IV unfractionated heparin than with low
molecular weight (LMW) heparin.
Type 1 HIT presents within first 2 days after exposure to heparin.
• Non-immune-mediated disorder that results from the direct effect of heparin on
platelet activation
• This form of thrombocytopenia is benign, self-limited, and not associated with bleeding or increased risk of thrombosis
Type 2 HIT (generally referenced as HIT) occurs 4-10 days after exposure to heparin.
• Immune-mediated disorder
• Has life- and limb-threatening thrombotic complications (low platelet count causes
embolism, paradoxically)
Suspect HIT when a patient who is receiving heparin has a decreased platelet count, particularly if the drop is >50% of the baseline count, even if the platelet count nadir remains
>150,000. Clinically, HIT is not often marked by bleeding; the most common complication is
venous thromboembolism (deep venous thrombosis, pulmonary embolism), and less often,
arterial thrombosis (stroke, myocardial infarction). For that reason, the disorder is sometimes
called heparin-induced thrombocytopenia and thrombosis (HITT). Thrombosis develops in
approximately 20% of patients with HIT, with mortality as high as 30%.
Chapter 6
l Hematology
Diagnosis of HIT is based on the combined clinical findings, thrombocytopenia characteristics,
and lab studies of HIT antibodies (positive in ~85% of patients with type 2 HIT). Treatment
begins with discontinuation of all heparin products (including heparin flushes of intravenous
catheters), and later the administration of an alternative anticoagulant such as argatroban or
lepirudin. Patients diagnosed with HIT should avoid all forms of heparin for life.
Warfarin
Warfarin (Coumadin) is the most widely prescribed anticoagulant for the prevention and
treatment of thromboembolic disease. It was initially introduced as a pesticide against
rodents, and long-acting forms of warfarin are still used for this purpose.
Warfarin anticoagulates by inhibiting an enzyme that recycles oxidized vitamin K to its
reduced form. Warfarin does not antagonize the action of vitamin K, but rather antagonizes
vitamin K recycling. Once vitamin K is reduced, the vitamin K dependent factors (factors
2,7,9,10) are eventually reduced (3-5 days).
Despite its efficacy, treatment with warfarin has several limitations.
• Many commonly used medications interact with warfarin, as do some foods—particularly green vegetables—since they typically contain large amounts of vitamin K.
• Warfarin activity has to be monitored by the PT and international normalized ratio
(INR) to ensure an adequate yet safe dose (typically INR 2−3 is considered adequate
and safe anticoagulation). The pharmacologic action of warfarin may always be
reversed by fresh vitamin K.
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USMLE Step 2 CK
l Internal Medicine
Table 6-4. Recommended Management of a Supratherapeutic INR
INR Bleeding Present Recommended Action
<Ther to 5.0 No • Lower warfarin dose, or
• Omit a dose and resume warfarin at a lower dose
when INR is in therapeutic range, or
• No dose reduction needed if INR is minimally
prolonged
>5.0 to 9.0 No • Omit the next 1–2 doses of warfarin, monitor
INR more frequently, and resume treatment at a
lower dose when INR is in therapeutic range, or
• Omit a dose and administer 1–2.5 mg oral
vitamin K*
>9.0 No • Hold warfarin and administer 5–10 oral vitamin
K. Monitor INR more frequently and administer
more vitamin K as needed. Resume warfarin at a
lower dose when INR is in therapeutic range.
>20 — • Hold warfarin and administer 10 mg vitamin
K by slow IV infusion; supplement with fresh
frozen plasma, or recombinant human factor VIIa,
depending on clinical urgency. Monitor and repeat
as needed.
Any Life-threatening As per “INR >20” above
INR: International Normalized Ratio; Ther: therapeutic INR range for the patient in question.
*Preferred in patients at increased risk for bleeding (e.g., history of bleeding, stroke, anemia).
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Infectious Diseases
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Chapter Title
Learning Objectives
❏ Provide an overview of common antibiotics and their uses
❏ Describe the unique conditions and considerations for infections which occur in the
CNS, head, neck, lung, pericardium, endocardium, GI tract, urinary tract, bones, and
joints
❏ Present the treatment of acute herpes viral hepatic infections
❏ Describe the presentation and management of Lyme disease and Rocky Mountain
spotted fever
❏ Describe the epidemiology, presentation, and treatment of genital and sexually
transmitted diseases
❏ Describe the epidemiology, presentation and management of AIDS and related
opportunistic infections
00
7
INTRODUCTION TO ANTIBIOTICS
Antibiotics can be grouped either by the type of organism they are effective against or by the
chemical class of the medication. The organisms that cause specific diseases do not change
very much over time. For example, Staphylococcus aureus is still the most common cause of
osteomyelitis, and Escherichia coli is still the most common cause of pyelonephritis. What
does change over time is the antibiotic that is effective against each organism and the sensitivity pattern of each organism.
Gram-Positive Cocci
Semisynthetic penicillinase-resistant penicillins (oxacillin, cloxacillin,
dicloxacillin, nafcillin)
Staphylococcal and streptococcal organisms are effectively treated by medications such as the
semisynthetic penicillins, including oxacillin, nafcillin, dicloxacillin, and cloxacillin. These
agents are exclusively effective against Gram-positive cocci, in particular staphylococci.
Methicillin belongs to this group of antibiotics as well, and was one of the original drugs developed in the class. Methicillin is not used clinically, however, because it may cause interstitial
nephritis. Hence the term “methicillin-sensitive” or “methicillin-resistant Staphylococcus aureus”
Note
Do not use vancomycin if the
organism is oxacillin-sensitive.
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