3 Flashcards
(500 cards)
1
Q
What is the presentation of glucose–6–phosphate dehydrogenase deficiency?,
A
Sudden, severe, intravascular hemolysis; jaundice, dark urine, weakness, and tachycardia.
2
Q
How is glucose–6–phosphate dehydrogenase deficiency diagnosed?,
A
High LDH, bilirubin, and reticulocyte count with a normal MCV and hemoglobinuria. Heinz bodies are inclusions in red cells. Definitive test is the G6PD level.
3
Q
What is the treatment for glucose–6–phosphate dehydrogenase deficiency?,
A
Hydration and transfusion. Avoid oxidant stress.
4
Q
What is aplastic anemia?,
A
Failure of bone marrow, resulting in anemia, leukopenia, and thrombocytopenia (pancytopenia). The marrow is empty.
5
Q
What are the causes of aplastic anemia?,
A
Radiation, benzene, NSAIDs, chloramphenicol, alcohol, chemotherapeutics. Tb, lymphoma. Hepatitis, HIV, CMV, EBV, Parvovirus B19. The most common etiology is idiopathic.
6
Q
What is the presentation of aplastic anemia?,
A
Bleeding from thrombocytopenia. Fatigue from anemia and infections from neutropenia. Pancytopenia on CBC. Marrow biopsy confirms.
7
Q
What is the treatment for aplastic anemia?,
A
Bone marrow transplantation or immunosuppressive agents.
8
Q
What is acute leukemia?,
A
Derangement of pluripotent stem cell, resulting in the destruction of marrow. Leukemic blasts crowd out marrow cells, resulting in pancytopenia. Blood cells lose the ability to mature and function.
9
Q
What are the causes of acute leukemia?,
A
Most cases are idiopathic; radiation exposure, benzene, melphalan and etoposide, retroviruses.
10
Q
What is the presentation of acute leukemia?,
A
Fatigue from anemia. Bleeding from thrombocytopenia. Infection from the underproduction of white blood cells.
11
Q
Which type of anemia is more common in children?,
A
Acute lymphocytic leukemia (ALL) is more common in children. Acute myelogenous leukemia (AML) is more common in adults. Enlargement of the liver, spleen, and lymph nodes and bone pain are common at presentation.
12
Q
How is acute leukemia diagnosed?,
A
WBC can be low, normal, or elevated. Thrombocytopenia, anemia; leukemic blasts in peripheral blood. Marrow biopsy >20% blasts confirms.
13
Q
What are the markers of acute myelogenous leukemia?,
A
AML is characterized by Auer rods, myeloperoxidase, and esterase.
14
Q
What are the markers of acute lymphocytic leukemia?,
A
ALL is characterized by common ALL antigen and terminal deoxynucleotidyl transferase (TdT).
15
Q
What is chronic myelogenous leukemia (CML)?,
A
Massive overproduction of myeloid cells. Philadelphia chromosome is characteristic, producing tyrosine kinase.
16
Q
What is the presentation of chronic myelogenous leukemia?,
A
Markedly elevated white blood cell count fatigue, night sweats, and low–grade fever. Abdominal pain from massive enlargement of the spleen. Bone pain.
17
Q
How is chronic myelogenous leukemia diagnosed?,
A
Elevated WBC consisting of neutrophils. Leukocyte alkaline phosphatase score is diminished. Basophilia characteristic of CML and all myeloproliferative disorders such as polycythemia vera. Platelets elevated.
18
Q
What is the treatment for chronic myelogenous leukemia?,
A
Imatinib which is direct inhibitor of the tyrosine kinase produced by the Philadelphia chromosome. 90% hematologic response.
19
Q
What is chronic lymphocytic leukemia?,
A
Massive overproduction of mature; lymphocytes from production of B lymphocytes.
20
Q
What is the presentation of chronic lymphocytic leukemia?,
A
CLL can often present as an asymptomatic elevation of white cells. 90% being over the age of 50. Fatigue, lethargy, and enlargement of lymph nodes. Infiltration of spleen, liver, and bone marrow.
21
Q
How is chronic lymphocytic leukemia diagnosed?,
A
Older patient with a marked elevation in the white cell count with a marked lymphocytic predominance. The marrow is infiltrated with the leukemic lymphocytes with CD19 antigen.
22
Q
What is multiple myeloma?,
A
Plasma cell overproduction, replacing the bone marrow; large quantities of functionless immunoglobulins.
23
Q
What is the presentation of multiple myeloma?,
A
Bone pain. Pain in back, ribs; fractures. Radiculopathy. Encapsulated organisms (Pneumococcus, Haemophilus). Renal failure, anemia. Hypercalcemia: polyuria, polydipsia, altered mental. Weakness, pallor.
24
Q
How is multiple myeloma diagnosed?,
A
Normochromic, normocytic anemia. Protein electrophoresis monoclonal immunoglobulin spike. Skull punched out lesions. beta2 microglobulin. Hypercalcemia from bone destruction. Elevated BUN, creatinine from kidney damage. Biopsy: 10% plasma cells.
25
What is Bence–Jones protein?,
Urinary Bence–Jones protein is nonfunctional gamma globulin found in multiple myeloma. It will not react with urine dipstick test.
26
What is the treatment for multiple myeloma?,
Bone marrow transplantation. Older patients should receive melphalan and prednisone.
27
What is monoclonal gammopathy of uncertain significance?,
Overproduction of immunoglobulin by plasma cells without manifestations MGUS is present in 1% \> 50 and in 3% of those \> age 70. Monoclonal immunoglobulin spike on electrophoresis. Treatment is not necessary.
28
What is Hodgkin disease?,
A neoplastic transformation of lymphocytes in the lymph node with Reed–Sternberg cells; spread to contagious areas of lymph nodes. Bimodal age peaks in the 20s and 60s.
29
What is the presentation of Hodgkin disease?,
Enlarged, rubbery, nonerythematous, nontender lymph nodes. symptoms are night sweats, weight loss, fevers. Pruritus; cervical, supraclavicular, axillary lymphadenopathy most common. Spleen, skin, gastric, lung, CNS.
30
What is the treatment for Hodgkin disease?,
Localized disease is managed with radiation. All patients with symptoms and stage III or stage IV disease are managed with chemotherapy.
31
What is non–Hodgkin lymphoma?,
Neoplastic transformation of B and T lymphatic cells. Accumulation of neoplastic cells in both the lymph nodes and diffusely in extra–lymphatic organs and the bloodstream. Reed–Sternberg cell is absent.
32
What conditions predispose to non–Hodgkin lymphoma?,
Infections such as HIV, hepatitis C, Epstein–Barr, HTLV–I, and Helicobacter pylori predispose to the development of NHL.
33
What is the presentation of non–Hodgkin lymphoma?,
Enlarged, rubbery, nonerythematous, nontender lymph nodes. symptoms are night sweats, weight loss, fevers. Pruritus may occur.
34
What sites are affected by non–Hodgkin lymphoma?,
NHL is the same as HD except that HD is localized to cervical and supraclavicular nodes. NHL involves extra–lymphatic sites and blood. CNS is more common NHL. HIV patients often have CNS NHL.
35
What is the treatment for non–Hodgkin lymphoma?,
Local disease is treated with radiation, and those with symptoms or Stages III and IV receive combination chemotherapy.
36
A 21–year–old woman with epistaxis and heavy periods. She has a PT of 12 seconds, a PTT of 40 seconds (prolonged), and 200,000/mm3 platelets. What is the diagnosis?,
Idiopathic thrombocytopenic purpura. Also known as primary immune thrombocytopenic purpura.
37
What is idiopathic thrombocytopenic purpura?,
Thrombocytopenia caused by idiopathic production of an antibody to platelets; often associated with lymphoma, chronic lymphocytic leukemia, HIV, and connective tissue diseases.
38
What is the presentation of idiopathic thrombocytopenic purpura?,
Bleeding skin, nasal, oral, GI, urine, vagina. Young, female; epistaxis, bruising, hematuria, uterine and GI bleeding. Petechiae, purpura, ecchymoses. Splenomegaly absent.
39
How is idiopathic thrombocytopenic purpura diagnosed?,
Thrombocytopenia. Antiplatelet Ab have a high sensitivity, poor specificity. Marrow filled with megakaryocytes, indicating platelet destruction. Smear and creatinine are normal, excluding HUS, TTP, DIC.
40
What is the treatment for idiopathic thrombocytopenic purpura?,
Prednisone. Splenectomy if very low platelet counts.
41
What is Von Willebrand disease?,
Platelet–type bleeding, autosomal dominant, decreased von Willebrand factor; VWD is the most common congenital disorder of hemostasis. Decreased ability of platelets to adhere to endothelial lining of blood vessels.
42
What is the presentation of Von Willebrand disease?,
Epistaxis, petechiae, bruising, and menstrual abnormalities; gastrointestinal and urinary tract bleeding.
43
How is Von Willebrand disease diagnosed?,
Platelet count is normal. The bleeding time is increased. Von Willebrand factor is low. Ristocetin platelet aggregation test is abnormal. PTT may be elevated.
44
What is the treatment for von Willebrand disease?,
Desmopressin acetate (DDAVP) for mild bleeding. Factor VIII replacement is used if desmopressin is not effective and the bleeding continues. Aspirin contraindicated. FFP is not useful.
45
Which coagulopathies cause a prolonged prothrombin time?,
Factor VII deficiency, vitamin K deficiency, liver disease, warfarin use, factor VII inhibitor.
46
Which coagulopathies cause a prolonged PTT?,
vWF and factors VIII, IX, XI, or XII deficiencies; heparin, antiphospholipid antibody
47
Which coagulopathies cause a prolonged PT and PTT?,
Prothrombin, fibrinogen, factor V, factor X or combined factor deficiencies, liver disease, DIC, supratherapeutic heparin or warfarin; combined heparin and warfarin.
48
What is hemophilia?,
Deficiency of clotting factor 8 in hemophilia A and deficiency of factor 9 in hemophilia B resulting in increased bleeding. X–linked recessive, resulting in disease in males. Females are carriers. Hemophilia A is far more common than B.
49
Why does hemophilia not express in females?,
Females do not express the disease because homozygosity results in intrauterine death of the fetus.
50
What is the presentation of hemophilia?,
Mild deficiencies result in absence of symptoms or with symptoms only during surgery or trauma. Severe deficiency results in spontaneous bleeding. Factor–type bleeding is deeper than bleeding caused by platelets.
51
What type of bleeding is associated with factor deficiency?,
Factor deficiencies cause hemarthrosis, hematoma, gastrointestinal bleeding, urinary bleeding, bruising, CNS bleeding. Severe hemophilia presents by age two or circumcision.
52
How is hemophilia diagnosed?,
A prolonged PTT with a normal PT. Specific factor VIII or IX levels allow for a precise diagnosis of hemophilia A or B.
53
What is the treatment of hemophilia?,
Mild hemophilia can be treated with desmopressin (DDAVP). Severe deficiencies are treated with replacement of the specific factor. Desmopressin is ineffective for hemophilia B.
54
What factor deficiency results from vitamin K deficiency?,
The deficiency of vitamin K results in decreased production of factors 2, 7, 9, and 10. Caused by dietary deficiency, malabsorption, and antibiotics that kill the colon bacteria that produce vitamin K.
55
What is the presentation of vitamin K deficiency?,
Bleeding may occur at any site. Oozing at venipuncture sites.
56
How is vitamin K deficiency diagnosed?,
PT and PTT are elevated. A correction of PT and PTT in response to giving vitamin K is the most common method of confirming the diagnosis.
57
What is the treatment for vitamin K deficiency?,
Severe bleeding is treated with fresh frozen plasma. Vitamin K is given at the same time.
58
Why do patients with liver disease have increased PT and PTT?,
Coagulopathy is caused by decreased production of clotting factors by the liver. Any severe liver disease or cirrhosis can cause decreased production of clotting factors.
59
What are the effects of coagulopathy of liver disease?,
Bleeding at any site, gastrointestinal tract is the most common site. Vitamin K does not result in improvement. Low platelet counts are often caused by hypersplenism that accompanies the liver disease.
60
What is the treatment of coagulopathy of liver disease?,
Fresh frozen plasma severe bleeding.
61
What is disseminated intravascular coagulation?,
Consumptive coagulopathy from major illness, resulting in consumption of platelets and clotting factors; bleeding with a microangiopathic hemolysis and fibrin products; occasionally thrombosis.
62
What are the causes of disseminated intravascular coagulation?,
Sepsis is most common. Any cell destruction and release of tissue factor. Rhabdomyolysis, adenocarcinomas, heatstroke, transfusion reactions, burns, head trauma, abruption, amniotic embolism, trauma, pancreatitis, snakebites, leukemia.
63
What is the presentation of disseminated intravascular coagulation?,
Bleeding from any site. Thrombosis is less common. Hemolysis often may lead to acute renal failure, jaundice, confusion.
64
How is disseminated intravascular coagulation diagnosed?,
Serious underlying disorder with bleeding, elevation PT, PTT; decrease platelets. Fibrinogen low. D–dimers and fibrin– split products are increased. Schistocytes with intravascular hemolysis.
65
What is the treatment for disseminated intravascular coagulation?,
Fresh frozen plasma and platelet transfusions. Heparin is rarely used except in thrombosis.
66
What are the names of the semisynthetic penicillinase–resistant penicillins?,
Oxacillin, cloxacillin, dicloxacillin, methicillin, nafcillin
67
Which bacteria are susceptible to the semisynthetic penicillins?,
Staphylococci and streptococci. Oxacillin, nafcillin, dicloxacillin, cloxacillin. Exclusively effective against Gram–pos cocci, particular staph. Methicillin not used because interstitial nephritis.
68
What are the indications for the semisynthetic penicillins?,
Used when Staphylococcus is sensitive to the semisynthetic penicillins and if concurrent Gram–negative infection is not suspected. More efficacious than vancomycin when the organism is sensitive.
69
What antibiotic is used to treat resistant–resistant Staph aureus?,
MRSA is treated primarily with vancomycin. Oral linezolid or IV quinupristin–dalfopristin are alternatives for MRSA.
70
What is the coverage of linezolid?,
Drug–resistant enterococcus, staphylococcus, and pneumococcus.
71
Which bacteria are sensitive to penicillin G, penicillin VK, ampicillin, and amoxicillin?,
Effective against streptococci, such as S. pyogenes, viridans group streptococci, and S. pneumonia, but not against staphylococci.
72
When can ampicillin and amoxicillin be used against staphylococcal infections?,
Ampicillin and amoxicillin are only effective against staph when ampicillin is combined with the beta–lactamase inhibitor sulbactam or when amoxicillin is combined with clavulanate.
73
What is the coverage of ampicillin against E coli?,
Ampicillin also has some activity against E. coli. Ampicillin and amoxicillin are effective against enterococci and Listeria. Useful against Gram–negative bacteria, such as Neisseria.
74
What are the first–generation cephalosporins?,
Cefazolin, cefadroxil, cephalexin.
75
What are the second–generation cephalosporins?,
Cefoxitin, cefotetan, cefuroxime, cefprozil, loracarbef.
76
What is the coverage of the first–generation cephalosporins?,
Same organisms that the semisynthetic penicillins will cover. In addition to staphylococci and streptococci, 1st and 2nd gen cephalosporins will also cover some Gram–neg. 1st gen agents will only reliably cover Gram–neg Moraxella and E. coli.
77
What is the coverage of second–generation cephalosporins?,
Cover everything a first–generation cephalosporin covers, as well as a few more Gram–negative bacilli such as Providencia, Haemophilus, Klebsiella, Citrobacter, Morganella, and Proteus.
78
What is the coverage of the third–generation cephalosporins?,
3rd gen, particularly ceftazidime, are not reliable against staphylococcus. 4th gen cephalosporin, cefepime, will cover staph and strep, but should not be used for exclusively Gram–pos infections.
79
What is the allergic cross–reactivity of penicillins with cephalosporins?,
For persons allergic to penicillin, there is only 5% risk of cross–reaction with cephalosporins. When the allergic reaction was a rash, a cephalosporin can be used. When the reaction was anaphylaxis, a cephalosporin should not be used.
80
What antibiotic should be used in patients with a history of an anaphylactic reaction to a penicillin?,
A macrolide (clarithromycin or azithromycin) or levofloxacin, gatifloxacin, or moxifloxacin can be used. For serious infections, use vancomycin, linezolid, or daptomycin.
81
What are the indications for macrolides (erythromycin, clarithromycin, azithromycin), extended fluoroquinolones (levofloxacin, gatifloxacin, moxifloxacin), and clindamycin?,
Alternatives to penicillin and cephalosporins for Gram–pos infection. Macrolides should not be used for serious staph. Extended quinolones very good for strep, particularly S pneumoniae in absence of penicillin resistance. Good against staph; not MRSA.
82
Why should ciprofloxacin not be used to treat pneumonia?,
Ciprofloxacin does not cover Strep pneumoniae.
83
What are the indications for vancomycin, linezolid, quinupristin, dalfopristin?,
Alternatives for Gram–pos infections when penicillin allergy or MRSA. Linezolid is the only oral MRSA.
84
What is the coverage of linezolid, quinupristin, dalfopristin?,
Linezolid, quinupristin, dalfopristin are effective against MRSA and vancomycin–resistant enterococci.
85
What is the activity of antipseudomonal penicillins (piperacillin, ticarcillin, mezlocillin) against Gram–negative bacilli?,
Fully active against range of Gram–negative bacilli, such as the Enterobacteriaceae including Pseudomonas. Enterobacteriaceae include E. coli, Proteus, Enterobacter, Citrobacter, Morganella, Serratia, Klebsiella.
86
What is the activity of ticarcillin and mezlocillin against MSSA?,
Antipseudomonal penicillins are only active against staph when combined with a beta–lactamase inhibitor, such as piperacillin/tazobactam or ticarcillin/clavulanate. Not MRSA.
87
What is the coverage of ampicillin/sulbactam and amoxicillin/clavulanate?,
Cover strep and staph and Gram–neg bacilli, but not Pseudomonas. All penicillins will cover sensitive streptococci.
88
What are the third–generation cephalosporins?,
Ceftazidime, cefotaxime, ceftriaxone, cefotaxime.
89
What is the fourth generation cephalosporin?,
Cefepime
90
What is the coverage of third– and fourth–generation cephalosporins?,
Fully active against full range of Gram–neg bacilli, such as the Enterobacteriaceae. Only ceftazidime and cefepime will cover Pseudomonas. Cefepime also covers staph.
91
What is the Gram–negative coverage of second–generation agents?,
Cover some of the Enterobacteriaceae, but not Pseudomonas.
92
What is the coverage of the third generation cephalosporins?,
Predominantly for use against Gram–negative organisms. Ceftriaxone and cefotaxime cover best for penicillin–insensitive pneumococci which cause meningitis or pneumonia.
93
What is the coverage of quinolones (ciprofloxacin, levofloxacin, gatifloxacin, moxifloxacin, ofloxacin)?,
Cover most Enterobacteriaceae, such as E. coli, Proteus, Enterobacter, Haemophilus, Moraxella, Citrobacter, Morganella, Serratia, and Klebsiella. Only ciprofloxacin will cover Pseudomonas.
94
What is the coverage of extended–spectrum quinolones?,
Moxifloxacin, levofloxacin, gatifloxacin are also active against Gram–positive cocci, in particular Strep pneumoniae. Good for pneumonia because also cover Mycoplasma, Chlamydia, Legionella.
95
What is the coverage of aminoglycosides (gentamicin, tobramycin, amikacin)?,
Gram–negative coverage. Aminoglycosides are synergistic with ampicillin in treatment of staph.
96
What is the coverage of monobactams?,
Aztreonam is exclusively a Gram–negative agent, with no strep or staph coverage.
97
What is the coverage of carbapenems (imipenem, meropenem, ertapenem)?,
Enterobacteriaceae and Pseudomonas with Gram–neg coverage. Excellent staph and anaerobic coverage. Used in Gram–negative infections, but also effective polymicrobial. Ertapenem not cover Pseudomonas.
98
What agent is most active against intraabdominal anaerobes?,
Metronidazole. Clindamycin is less active against intraabdominal anaerobes. Metronidazole has good anaerobic Gram– neg in bowel, such as B fragilis. Metronidazole is first–line against C difficile.
99
What is the coverage of clindamycin?,
Clindamycin may have some advantages over metronidazole against the anaerobic streptococci found in the mouth.
100
What agents have intraabdominal anaerobic coverage?,
Metronidazole, carbapenems and beta–lactam/beta–lactamase combinations (piperacillin/tazobactam, ticarcillin/clavulanate, ampicillin/sulbactam, or amoxicillin/clavulanate). 2nd gen cephalosporins cefoxitin and cefotetan, have fair activity against.
101
A 15–year–old male with fever, headache, nausea, and vomiting. Neck stiffness and photophobia. What is the next step?,
Lumbar puncture.
102
What is the most common cause of meningitis after the neonatal period?,
Streptococcus pneumoniae is the most common cause of meningitis for all patients beyond the neonatal period. Neisseria meningitidis is the most common cause of meningitis in adolescents.
103
What factors predispose to listeria monocytogenes meningitis?,
Listeria monocytogenes is more common with immune system defects, HIV, steroid use, leukemia, lymphoma, and various chemotherapeutic agents. Neonates and the elderly.
104
What is the most common cause of meningitis in the elderly and infants?,
Streptococcus pneumoniae is the most common etiology. Listeria is more common in the very old and infants.
105
Which patients are at risk for staphylococcal meningitis?,
Staphylococcus aureus is more common in those who have had any form of neurosurgery.
106
Which patients are at risk for cryptococcus meningitis?,
Cryptococcus is more common in those who are HIV positive and who have profound decreases in their T–cell counts to levels less than 100 cells/mm3.
107
Which persons are at risk for Rocky Mountain spotted fever meningitis?,
Rocky Mountain spotted fever is common in those who have been exposed to ticks in the mid–Atlantic areas, such as the Carolinas, Kentucky, Tennessee, Delaware, Maryland, Virginia, Georgia, Florida, Oklahoma, etc.
108
What area is associated with Lyme meningitis?,
Lyme disease can also cause meningitis and is more common in the Northeast. Tuberculosis and syphilis are also associated with meningitis.
109
What are the CSF characteristics in aseptic meningitis?,
CSF has lymphocytic pleocytosis and bacterial cultures are negative.
110
What are the causes of aseptic meningitis?,
Enteroviruses, arboviruses (St. Louis encephalitis virus, West Nile virus), HIV, herpes simplex, and lymphocytic choriomeningitis virus.
111
What is the most common cause of neonatal meningitis?,
Group B Streptococcus (Streptococcus agalactiae) is the most common cause of meningitis in the neonatal period.
112
What is the clinical presentation of meningitis?,
Fever, photophobia, headache, nuchal rigidity (Kernig, Brudzinski), nausea, vomiting, seizures. The most common deficit from meningitis is damage to 8th cranial nerve (hearing).
113
What type of meningitis is associated with a petechial rash?,
Neisseria. A rash on the wrists and ankles with centripetal spread toward the body suggests Rocky Mountain spotted fever.
114
What type of meningitis is associated with facial palsy?,
Facial nerve palsy is suggestive of Lyme disease. Pulmonary symptoms or an abnormal chest x–ray suggest tuberculosis.
115
When should a CT scan be done before lumbar puncture in patients with suspected meningitis?,
CT should be done before lumbar puncture if papilledema, focal motor deficits, new onset seizures, mental status abnormalities, or immunocompromise (HIV, immunosuppressive).
116
What should be done if the lumbar puncture is delayed more than 20–30 minutes?,
An empiric dose of antibiotics should be given.
117
What are the CSF findings in bacterial meningitis?,
Protein elevated with bacterial meningitis. Opening pressure elevated. Gram stain has a limited sensitivity; positive 50%. The most useful test is the cell count. Only bacterial meningitis causes thousands of cells, all neutrophils.
118
What types of meningitis are associated with an elevation in lymphocytes?,
Viral infection, Rickettsia, Lyme disease, tuberculosis, syphilis, or fungal (cryptococcal) etiology. Normal CSF cell count is
119
What is the empiric treatment of bacterial meningitis in adults?,
Vancomycin (pneumococci are resistant penicillin) plus a 3rd gen cephalosporin, such as ceftriaxone. Ampicillin is added to cover Listeria if immune defects, \>50, or
120
What is the treatment of Lyme meningitis?,
Lyme disease is treated with ceftriaxone.
121
What is the treatment of Cryptococcal meningitis?,
Cryptococcus is treated with amphotericin. Followed by fluconazole in HIV–positive patients for life or until the patient is on HAART and is asymptomatic with a CD4 count \>100.
122
What is the treatment of neurosyphilis?,
Neurosyphilis is treated with high–dose intravenous penicillin.
123
What is the treatment of tuberculosis meningitis?,
TB meningitis is treated the same as pulmonary tuberculosis (though a longer duration of 9–12 months).
124
What are the indications for corticosteroid in meningitis?,
Steroid use in adult meningitis is appropriate for TB meningitis and bacterial meningitis.
125
What are the recommendations for adjunctive dexamethasone for bacterial meningitis?,
Reduces inflammatory response to bacterial lysis; given with antibiotics for 4 days if bacterial meningitis is confirmed by positive Gram stain or \>1000 WBCs in CSF.
126
What is encephalitis?,
Infection of brain parenchyma usually caused by any viruses. The most common cause is HSV type 1. Varicella–zoster virus, CMV, enteroviruses, Eastern and Western equine encephalitis, St. Louis, and West Nile.
127
What is the presentation of encephalitis?,
Altered mental status with fever and headache. Confusion to lethargy or coma. Focal deficits. Neck stiffness. Seizures.
128
How is HSV encephalitis diagnosed?,
Lumbar puncture PCR has eliminated the need for biopsy. PCR for HSV has a 98% sensitivity and \>95% specificity. HSV has a predilection for temporal lobes.
129
What is the treatment for HSV encephalitis?,
Intravenous acyclovir.
130
What is the treatment of cytomegalovirus encephalitis?,
Ganciclovir or foscarnet are active against CMV.
131
An HIV–negative man with a seizure. Aphasia and weakness of the right hand and leg. A CT scan of the head with contrast shows a ring enhancing lesion. What is the diagnosis?,
Brain abscess.
132
What are the causes of brain abscesses?,
Bacteria can spread into the brain from otitis media, sinusitis, mastoiditis, or dental infections. Organisms may also spread through the bloodstream from endocarditis or pneumonia.
133
Which organisms cause brain abscesses?,
Brain abscesses most commonly Streptococcus 60–70%, Bacteroides 20–40%, Enterobacteriaceae 25–35% and Staph 10%, often polymicrobial. Toxoplasmosis can reactivate in HIV when CD4
134
What is the presentation of brain abscess?,
Headache. Fever, focal neurologic deficits, seizures.
135
How is brain abscess diagnosed?,
Brain abscess and malignancy enhance with contrast. MRI more accurate than CT. Stereotactic aspiration for Gram stain, culture. In HIV, 90% of brain lesions will be toxoplasmosis or lymphoma.
136
What is the treatment for brain abscess?,
Surgical drainage. Penicillin, metronidazole, and a third–generation cephalosporin, such as ceftazidime. HIV patients are treated empirically with pyrimethamine and sulfadiazine.
137
What are the causes of otitis media?,
The most common organisms are Strep pneumoniae (35–40%), H. influenzae (nontypeable; 25–30%), and Moraxella catarrhalis (15–20%). Viruses.
138
What is the presentation of otitis media?,
Ear pain, fever, and decreased hearing. Immobility of the membrane on insufflation.
139
What is the treatment for otitis media?,
High–dose amoxicillin. Amoxicillin–clavulanate is used if recent amoxicillin or if no response to amoxicillin. Alternatives: Cefuroxime, loracarbef, cefprozil, or cefdinir or cefixime.
140
What is the treatment for otitis media in severe allergy to penicillin?,
Macrolides, such as azithromycin or clarithromycin. Levofloxacin, moxifloxacin or gatifloxacin are acceptable. TMP/SMZ is poorly active against Streptococcus pneumoniae.
141
What is the most common site of sinusitis?,
The most common site of infection is the maxillary sinus.
142
What are the cause of sinusitis?,
Viruses are responsible for most cases. Bacterial organisms are strep pneumonia, H influenza (non–typable), Moraxella catarrhalis.
143
What is the presentation of sinusitis?,
Facial pain, headache, postnasal drainage, and purulent nasal drainage. Headache, fever, tooth pain.
144
How is sinusitis diagnosed?,
If imaging is required because of concern of complications, a CT scan is the best test.
145
What is the treatment for sinusitis?,
High–dose amoxicillin. Amoxicillin–clavulanate if recent amoxicillin use or if no response amoxicillin. Alternatives: cefuroxime, loracarbef, cefprozil, cefdinir, cefixime.
146
What is the treatment of sinusitis in patients with severe penicillin allergies?,
Patients with severe penicillin allergies should receive azithromycin or clarithromycin. Levofloxacin, moxifloxacin, or gatifloxacin are acceptable.
147
What are the causes of pharyngitis?,
Usually viruses; group A beta–hemolytic streptococci (S. pyogenes) may cause rheumatic fever or glomerulonephritis. S. pyogenes causes 15–20% of cases of pharyngitis.
148
What is the presentation of pharyngitis?,
Sore throat with cervical adenopathy and inflammation of the pharynx with an exudate is highly suggestive of S. pyogenes. Viruses do not cause an exudate.
149
How is pharyngitis diagnosed?,
Rapid Streptococcal antigen test is 60–100% sensitive and \>95% specific. A positive test can be considered the equivalent of a positive culture, whereas a negative test should be confirmed with a culture.
150
What is the treatment for pharyngitis?,
Penicillin or amoxicillin. Azithromycin, clarithromycin, and oral, second–generation cephalosporins are alternatives in penicillin–allergic.
151
What is influenza?,
A systemic viral illness from influenza A or B, usually occurring in an epidemic pattern, leading to sinusitis, otitis media, bronchitis, and pneumonia.
152
What is the presentation of influenza?,
Fever, myalgias, headache, and fatigue. Upper respiratory symptoms predominate. Coryza, nonproductive cough, sore throat, and conjunctival injection.
153
How is influenza diagnosed?,
Rapid antigen detection methods of swabs or washings of nasopharyngeal secretions. Viral culture.
154
What is the treatment for influenza?,
Specific antiviral medications for both influenza A and B are the neuraminidase inhibitors: oseltamivir and zanamivir. Amantadine and rimantadine are only effective against influenza A.
155
What are the indications for influenza vaccinations?,
\>50 chronic lung and cardiac disease, pregnant in the second and third trimesters; chronic facilities, health–care workers, immunosuppressed, diabetes, renal dysfunction. Contraindicated in allergy to eggs.
156
A 63–year–old man with a cough sputum smoked 30 years. Temperature of 100 degrees F. Chest x–ray is normal. What is the diagnosis?,
Bronchitis
157
What are the causes of bronchitis?,
Viruses. Small percentage caused by M. pneumoniae, C. pneumoniae, B. pertussis. Most common organisms responsible for chronic bronchitis are S pneumoniae, H influenzae, and Moraxella. CXR normal.
158
What is the treatment for acute exacerbations of chronic bronchitis?,
Amoxicillin, doxy, or TMP/SMZ. Patients not responding to amoxicillin should be treated with amoxicillin/clavulanate, clarithromycin, azithromycin, 2nd/3rd–gen cephalosporins, or gatifloxacin, levofloxacin, or moxifloxacin.
159
A 65–year–old alcoholic with cough, sputum, fever. Lost 15 pounds. Febrile. Poor dentition. Putrid, foul breath. CXR: cavitary lesion. What is the diagnosis?,
Lung abscess.
160
What is a lung abscess?,
Necrosis of the pulmonary parenchyma caused by microbial infection.
161
What is the bacteriology of lung abscesses?,
90% anaerobes. Peptostreptococcus, Prevotella, and Fusobacterium species (oral anaerobes). Aerobic bacteria, most frequently are S. aureus, E. coli, Klebsiella, and Pseudomonas.
162
What conditions predispose to lung abscess?,
Association with periodontal disease or aspiration (e.g., altered sensorium, seizures).
163
What is the presentation of lung abscess?,
Fever, cough, chest pain; putrid, foul–smelling sputum in 60–70%; chronic course with weight loss and fatigue.
164
How is lung abscess diagnosed?,
Sputum Gram stain and culture. Cavitary lesion. Lower lobes in upright patients, and the posterior right upper lobe in supine patients. Aspiration of abscess fluid is necessary for diagnosis.
165
What is the treatment of lung abscess?,
Clindamycin has good empiric coverage for the above the diaphragm anaerobes. Penicillin is also acceptable.
166
What conditions predispose to pneumonia?,
Cigarette smoking, diabetes, alcoholism, malnutrition, obstruction from tumors, and immunosuppression. Neutropenia and steroid use predispose to Aspergillus infection.
167
What is the most common cause of community–acquired pneumonia in all groups?,
S. pneumoniae (viruses
168
What conditions predispose to Haemophilus influenzae pneumonia?,
Smokers, COPD.
169
What factors are associated with Mycoplasma pneumonia?,
Young, otherwise healthy patients.
170
What conditions predispose to Legionella?,
Epidemic infection in older smokers, particularly when located near infected water sources, such as air–conditioning systems.
171
What conditions predispose to Pneumocystis jiroveci pneumonia?,
HIV–positive persons with
172
What conditions predispose to Coxiella burnetii (Q–fever) pneumonia?,
Exposure to animals, particularly at the time the animals are giving birth.
173
What condition predisposes to Klebsiella pneumonia?,
Alcoholics
174
What condition predisposes to Staphylococcus aureus pneumonia?,
Occurs after viral syndromes or viral bronchitis, especially influenza
175
What condition predisposes to Coccidioidomycosis pneumonia?,
Exposure to the deserts of the American Southwest, particularly Arizona
176
What conditions predispose to Chlamydia psittaci pneumonia?,
Bird exposure.
177
What conditions predispose to Histoplasma capsulatum pneumonia?,
Exposure to bat or bird droppings, spelunking (recreational cave exploration)
178
What are the clinical signs of Bordetella pertussis pneumonia?,
Cough with whoop and post–tussive vomiting.
179
What conditions predispose to Francisella tularensis pneumonia?,
Hunters or exposure to rabbits, bioterrorism.
180
What activity predisposes to severe acute respiratory syndrome (SARS, Avian influenza pneumonia)?,
Travel to southeast Asia.
181
Which bacteria may be utilized in bioterrorism?,
Bacillus anthracis, Yersinia pestis, and Francisella tularensis.
182
What is the clinical presentation of pneumonia?,
Cough, fever, sputum, dyspnea. Bacterial infections (pneumoniae, Haemophilus, Klebsiella) have purulent sputum. S. pneumoniae causes rusty hemoptysis.
183
What are the characteristics of the sputum in Klebsiella pneumonia?,
Klebsiella pneumoniae sputum is like currant jelly.
184
What are the characteristics of pneumonia caused by Pneumocystis jiroveci, viruses, Mycoplasma, and Legionella?,
Interstitial infections are caused by Pneumocystis jiroveci pneumonia, viruses, Mycoplasma, and Legionella; often cause nonproductive or dry cough.
185
What type of pain is associated with pneumococcal pneumonia?,
Pleuritic pain is associated with lobar pneumonia, caused by Pneumococcus, because of inflammation of the pleura. S. pneumoniae usually causes a lobar pneumonia with pleural effusion.
186
What are the physical signs of pneumonia?,
Rales, rhonchi, lung consolidation, dullness to percussion, bronchial breath sounds, increased vocal fremitus, egophony. Severe pneumonia leads to hypoxia.
187
What is the presentation of Mycoplasma pneumonia?,
Dry cough and chest soreness. Bullous myringitis; anemia from hemolysis from cold agglutinins. Rarely need to be admitted to the hospital.
188
What is the presentation of Legionella pneumonia?,
Confusion, headache, and lethargy. Diarrhea and abdominal pain.
189
What is the presentation of Pneumocystis jiroveci pneumonia?,
Marked dyspnea, particularly on exertion, with chest soreness with cough in an HIV–positive person with a CD4 count of
190
Which types of pneumonia are associated with interstitial infiltrates?,
Interstitial infiltrates are associated with PJP, viral, Mycoplasma, Chlamydia, Coxiella, and Legionella pneumoniae.
191
What is the most specific test for lobar pneumonia?,
Sputum culture and Gram stain. S pneumoniae, Staph, Klebsiella, Haemophilus. Viral, Mycoplasma, Chlamydia, Coxiella (atypicals) will not appear on a Gram stain or bacterial culture.
192
What is the best diagnostic method for Mycoplasma pneumonia?,
Specific serologic antibody titers. Cold agglutinins have limited specificity and sensitivity.
193
What are the diagnostic methods for Legionella pneumonia?,
Charcoal yeast extract media, urine antigen tests, direct fluorescent antibodies, and antibody titers.
194
What is the best diagnostic method for Pneumocystis jiroveci pneumonia?,
Bronchoalveolar lavage; increased LDH.
195
What is the best diagnostic method for Chlamydia pneumoniae, Coxiella, Coccidioidomycosis, and Chlamydia psittaci?,
Specific antibody titers.
196
What are the signs of severe pneumonia?,
pO2 30, disorientation, uremia, systolic BP 125), hyponatremia, dehydration, elevated BUN.
197
Which pneumonia patients should be hospitalized?,
Patients with severe pneumonia or serious underlying diseases such as cancer, liver disease, renal disease, or chronic lung disease should be hospitalized for intravenous medications.
198
What is the empiric therapy for outpatient pneumonia?,
Macrolide, azithromycin or clarithromycin. Levofloxacin, moxifloxacin, gatifloxacin are alternatives. Cephalosporins and amoxicillin/clavulanate do not cover atypical pathogens.
199
What is the treatment for hospitalized patients with community–acquired pneumonia?,
Levofloxacin, moxifloxacin, or gatifloxacin or cefotaxime or ceftriaxone combined with a macrolide such as azithromycin or clarithromycin (or doxycycline).
200
What organisms cause hospital–acquired pneumonia?,
Drug–resistant, Gram–negative bacilli (Pseudomonas, Klebsiella, E. coli), or gram–positives, including methicillin–resistant Staphylococcus aureus.
201
What is the treatment of hospital–acquired pneumonia?,
3rd gen cephalosporin with antipseudomonal activity (ceftazidime, cefotaxime) or carbapenems (imipenem) or beta–lactam/beta–lactamase combinations (piperacillin/tazobactam), and vancomycin or linezolid. Gentamicin added for Gram–neg synergy.
202
What is the specific coverage for Haemophilus influenzae?,
Second– or third–generation cephalosporin.
203
What is the specific coverage for Mycoplasma pneumoniae?,
Macrolide, doxycycline, or a quinolone.
204
What is the specific coverage for Legionella?,
Macrolide, doxycycline, or a quinolone
205
What is the specific coverage for pneumocystis jiroveci pneumonia?,
Trimethoprim/sulfamethoxazole. Steroids should be used if arterial pO2
206
What is the specific coverage for Coxiella burnetii (Q–fever)?,
Doxycycline (or erythromycin)
207
What is the specific coverage for klebsiella?,
Third–generation cephalosporin.
208
What is the specific coverage for staphylococcus aureus?,
Semisynthetic penicillin (nafcillin) if methicillin sensitive. In the nosocomial setting, isolates are methicillin–resistant, and vancomycin or linezolid is used.
209
What is the specific coverage for coccidioidomycosis?,
Treatment only for disseminated disease or pulmonary disease with immunosuppression. Life–threatening disease is treated with amphotericin. Mild disease is treated with fluconazole or itraconazole.
210
Which patients should receive pneumococcal vaccine?,
\>65. Lung, cardiac, liver, renal disease. Immunocompromised. Re–dosing in 5 y is only necessary with severe immunocompromise or if vaccinated 65, a single dose confers lifelong immunity.
211
What is bacillus Calmette–Guerin?,
Bacillus Calmette–Guerin vaccination is used outside the United States to prevent tuberculosis. Only 50% effective and is never used in the US. BCG vaccination does not alter PPD test interpretation.
212
Which persons are at risk for tuberculosis infection?,
Immigrants, alcoholics, healthcare workers, prisoners, homeless shelters, nursing homes, chronically debilitated, impairment of T–cell immunity. Steroid use, organ transplantation, leukemia, lymphoma, and HIV.
213
What is the clinical presentation of tuberculosis?,
Cough, sputum, fever, and an abnormal lung examination. Weight loss. Tuberculosis usually takes up to five years to become fatal. Night sweats. TB occurs outside of the lungs in 15–20%.
214
What sites may be affected by extrapulmonary tuberculosis?,
Any part of the body, although the lymph nodes, meninges, GI and GU are the most frequent extrapulmonary TB. Adenitis is the most common extrapulmonary site.
215
How is tuberculosis diagnosed?,
CXR: apical infiltrates, cavitation. Adenopathy, effusion, calcified nodules (Ghon). 3 sputum smears 90% sensitive. Culture is most specific; 4 wks. PPD not used to diagnose acute TB unless other tests neg.
216
What is the treatment of tuberculosis?,
Initial 4–drug: INH, rifampin, pyrazinamide, ETB. 4 drugs continued for 2 mo or until sensitivity known. PZA/ETB are discontinued, and continue INH, rifampin for 4 mo. ETB given if sensitivity not known.
217
What is the length of treatment of tuberculosis meningitis?,
12 mths. TB in pregnancy is treated for 9 mths. HIV– positive treated for 6–9 months.
218
What drug should be taken with isoniazid?,
INH use should generally be combined with vitamin B6 (pyridoxine) to prevent peripheral neuropathy.
219
Which antituberculosis drugs are contraindicated in pregnancy?,
Pregnant patients should not receive PZA or streptomycin.
220
When are steroids used in tuberculosis?,
Steroids are used for TB meningitis and TB pericarditis.
221
What are the side effects of antituberculosis medications?,
All TB medications can cause liver toxicity, except streptomycin. INH causes peripheral neuropathy because of pyridoxine deficiency. Rifampin is associated with orange/red bodily fluids .
222
What are the adverse effects of ethambutol?,
Ethambutol is associated with optic neuritis, color blindness and other visual disturbances. PZA can cause a benign hyperuricemia, which does not require treatment.
223
What is the PPD test?,
PPD test is used to screen asymptomatic populations at risk of TB to determine if they have been exposed and are at increased risk of re–activating. PPD should not be used to diagnose TB in an acutely ill patient.
224
What is the physical indication of a positive PPD?,
A PPD test is positive if there is induration of the skin 48–72 h after intradermal injection. A positive PPD test indicates a 10% risk of TB in HIV–negative. BCG vaccination does not alter recommendations.
225
What is two–stage PPD testing?,
Those in whom there has not been a recent PPD test and now show some reactivity that is
226
What is the criteria for a positive PPD in close contacts of active TB cases, HIV–positive persons, persons with an abnormal chest x–ray consistent with old TB, and steroid use or organ transplantation recipients?,
\>5 mm
227
What is the criteria for a positive PPD in high–risk groups, such as healthcare workers, prisoners, nursing home residents; immigrants; homeless; leukemia, lymphoma, diabetics, dialysis, IVDU who are HIV–neg; and children exposed to adults at high risk?,
\>10 mm
228
What is the criteria for a positive PPD in low risk populations?,
\>15 mm
229
What is the management of a positive PPD?,
Chest x–ray to determine if they have early signs of TB. Those with abnormal chest x–rays should have sputum AFB stains to see if they have active disease. Positive AFB smears need the start of four TB drugs.
230
What is the treatment for patients with positive PPD and no evidence of active disease (negative chest x–ray)?,
9 months of INH and vitamin B6. A normal chest x–ray or an abnormal x–ray and three negative AFB stains of sputum are sufficient to exclude active disease.
231
What is the cause of most infectious diarrhea?,
Contaminated food and water. Bacillus cereus and Staphylococcus aureus, food poisoning present predominantly with vomiting. Food poisoning is most commonly Campylobacter.
232
What type of diarrhea is associated with poultry and eggs?,
Salmonella is most commonly associated with contaminated poultry and eggs.
233
What is the most common cause of travelers' diarrhea?,
E. coli is the most common cause of travelers' diarrhea. E. coli 0157:H7 is associated with eating undercooked hamburger meat.
234
What organism is associated with fried rice?,
Bacillus cereus is associated with fried rice.
235
What types of diarrhea are associated with water from streams?,
Giardia lamblia and cryptosporidiosis are acquired from contaminated water from streams.
236
What type of diarrhea is associated with AIDS?,
Cryptosporidiosis is associated with HIV, particularly when the CD4 count has dropped below 50 cells. Vibrio cholera is very rare in the United States.
237
What type of diarrhea is associated with shellfish?,
Vibrio parahaemolyticus is associated with contaminated shellfish.
238
What is the most common cause of diarrhea in children?,
Viral infections such as with rotavirus or Norwalk agents are associated with outbreaks in children.
239
What type of diarrhea is associated with previous antibiotic use?,
Clostridia difficile is associated with previous antibiotic use.
240
What type of food is associated with clostridia botulinum?,
Clostridia botulinum is associated with ingestion of infected canned foods, and Clostridia perfringens is associated with meats that have been contaminated with spores.
241
What organisms are associated with blood in the stool?,
Blood in the stool is most commonly associated with invasive enteric pathogens, such as Salmonella, Shigella, Yersinia, invasive E. coli, and Campylobacter.
242
What type of diarrhea is associated with Guillain–Barre syndrome?,
Campylobacter is rarely associated with Guillain–Barre syndrome.
243
What are the symptoms of ciguatera toxin poisoning?,
Ingestion of barracuda, red snapper, grouper within 2 h; paresthesias, numbness, nausea, vomiting, cramps; weakness, reversal of hot–cold, hypotension.
244
What is the treatment for ciguatera toxin poisoning?,
No therapy.
245
Which infectious agents are associated with hemolytic uremic syndrome?,
E. coli 0157:H7 and Shigella are associated with hemolytic uremic syndrome.
246
What is the presentation of staphylococcal food poisoning?,
Bacillus cereus and Staphylococcus predominantly present with vomiting within 1–6 hours of their ingestion because they contain a preformed toxin. Diarrhea occurs later.
247
What is the characteristic of viral diarrhea?,
Viruses can cause voluminous watery diarrhea but do not result in bloody diarrhea.
248
What type of diarrhea occurs after ingestion of tuna, mackerel, or mahi mahi?,
Scombroid poisoning from histamine in flesh. Minutes: rash, diarrhea, vomiting, wheezing, burning in mouth, dizziness, paresthesias.
249
How is infectious diarrhea diagnosed?,
Test the stool for white blood cells with methylene blue testing. WBCs indicate an invasive pathogen. Culture is necessary to determine specific type.
250
Which test is used to detect Giardia and Cryptosporidium?,
Giardia and Cryptosporidium are detected by direct examination for ova and parasites, as well as for their eggs. A special modified AFB stain is necessary to detect Cryptosporidium.
251
What is the treatment of infectious diarrhea?,
More severe infections with high fever, abdominal pain, tachycardia and hypotension, require intravenous fluids and oral ciprofloxacin.
252
What are the causes of viral hepatitis?,
Viral hepatitis is an infection of the liver caused by hepatitis A, B, C, D, or E.
253
What are the symptoms of hepatitis A?,
Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice.
254
What are the symptoms of hepatitis B?,
Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice, 10–20% with serum sickness–like (joint pain, rash).
255
What are the symptoms of hepatitis C?,
Only 20% are acutely symptomatic with fever, malaise, headache, jaundice.
256
What are the symptoms of hepatitis D?,
Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice
257
What are the symptoms of hepatitis E?,
Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice
258
What types of hepatitis have a carrier state?,
Hepatitis B, C, D. There is no carrier state for hepatitis A or hepatitis E.
259
What is the serology of hepatitis A?,
Anti–HAV, IgM fraction, IgG fraction.
260
What is the serology of hepatitis B?,
HBsAg, HBsAb, HBeAg, anti–HBs, anti–HBc, anti–HBe
261
What is the serology of hepatitis C?,
Antibody to hepatitis C, PCR–RNA
262
What is the serology of hepatitis D?,
Anti–delta, IgM fraction, IgG fraction
263
What is the serology of hepatitis E?,
Anti–Hep E IgM, IgG
264
What is the mode of transmission of hepatitis A and E?,
Transmitted by contaminated food and water. Incubation period 2–6 weeks. Hepatitis A and E cause symptomatic disease for several days to weeks, no chronic form, cause cirrhosis or hepatocellular CA.
265
What is the mode of transmission of hepatitis B, C and D?,
Transmitted parenterally, perinatally, or through sexual contact; blood transfusion, needlestick, and needle sharing. Hepatitis B and C cause a chronic form, cirrhosis and hepatocellular carcinoma.
266
What is the most common disease leading to the need for liver transplantation?,
Hepatitis C. All forms of hepatitis can occasionally present with fulminant hepatic necrosis and acute liver failure.
267
What is the presentation of acute hepatitis?,
Jaundice, dark urine, light stool, fatigue, malaise, weight loss, tender enlarged liver. B and C can also cause joint pain, rash, vasculitis, glomerulonephritis. B with polyarteritis nodosa.
268
How is acute hepatitis diagnosed?,
Viral and drug hepatitis cause elevated bilirubin. Viral hepatitis causes elevation of ALT and AST, but the ALT is greater than AST. AST is more elevated in alcohol hepatitis.
269
What is the significance of a positive IgM antibody in the diagnosis of hepatitis?,
Hepatitis A, C, D, and E are diagnosed by acute IgM antibody. IgG antibody to hepatitis A, C, D, and E indicates old, resolved. Hepatitis C can be followed with a PCR–RNA viral load.
270
What is the first hepatitis B marker to elevate?,
Hepatitis B is diagnosed as acute with the presence of the hepatitis B surface antigen, which is the first viral marker to elevate. The hepatitis B e antigen and the IgM core antibody also indicate an acute infection.
271
What is the significance of the hepatitis B e antigen?,
The e antigen indicates high levels of viral replication and increased infectivity.
272
What laboratory findings indicate resolution of hepatitis B?,
Resolution of the infection is definitively indicated by the loss of surface antigen activity and the development of hepatitis B surface antibody.
273
What is the significance of the hepatitis B core IgG antibody?,
B core IgG and e antibody indicate that the acute infection is about to resolve and may be the only markers present in window period 2–6 weeks between loss of surface antigen and development of surface Ab.
274
What is the treatment for chronic hepatitis B?,
Interferon, entecavir, adefovir, or lamivudine.
275
What is the treatment of chronic hepatitis C?,
Chronic hepatitis C is treated with interferon combined with ribavirin. The only therapy for cirrhosis is liver transplantation.
276
What is the postexposure prophylaxis after hepatitis B needlestick?,
If surface–antigen–positive patient, the person stuck should receive hepatitis B immunoglobulin (HBIg) and B vaccine. If the person stuck already has protective levels of surface antibody, then no therapy.
277
What is the postexposure prophylaxis for hepatitis C?,
There is no effective postexposure prophylaxis to hepatitis C, and there is no vaccine?
278
What are the indications for hepatitis B vaccine?,
All healthcare workers, IV drug users, and others at risk should be vaccinated. Newborn children are vaccinated.
279
What are the causes of urethritis?,
Neisseria gonorrhoeae or nongonococcal urethritis is caused by either Chlamydia trachomatis (50%), Ureaplasma urealyticum (20%), Mycoplasma hominis (5%), Trichomonas (1%), or herpes simplex.
280
What are the clinical signs of urethritis?,
Purulent urethral discharge; dysuria, urgency, and frequency in urination
281
How is urethritis diagnosed?,
Urethral smear Gram–neg intracellular, coffee bean–shaped diplococci. Fluorescent antibodies for chlamydia by urethral swab, or by ligase chain reaction test of urine. Culture is the most specific test for gonorrhea.
282
What is the treatment of urethritis?,
Combination of ceftriaxone IM and single–dose azithromycin PO. An alternative regimen is ceftriaxone and PO doxycycline for 7 d. Gonorrhea can also be treated with single–dose Cipro or cefixime.
283
What is pelvic inflammatory disease?,
Infection of the fallopian tubes, uterus, ovaries, or ligaments of the uterus caused by N. gonorrhoeae, Chlamydia, Mycoplasma, anaerobic bacteria or Gram–negative bacteria. Intrauterine devices predispose to PID.
284
What are the clinical signs of pelvic inflammatory disease?,
Pelvic pain on palpation of the cervix, uterus, or adnexa; fever, and leukocytosis. Cervical motion tenderness. Discharge from the cervix.
285
How is pelvic inflammatory disease diagnosed?,
Cervical culture on Thayer–Martin for gonococcus. Laparoscopy. A pregnancy test should be done.
286
What is the therapy for pelvic inflammatory disease?,
Doxycycline and cefoxitin (or cefotetan) IV. Outpatient therapy is single–dose ceftriaxone intramuscularly and doxycycline orally for 2 weeks. Outpatient therapy can also be 2 weeks ofloxacin and metronidazole.
287
What are the sequelae of pelvic inflammatory disease?,
Infertility and ectopic pregnancy.
288
A 22–year–old man with painless, ulcerated genital lesion, adenopathy. What is the next step?,
Dark–field microscopy for syphilis, VDRL.
289
What are the clinical signs of primary syphilis?,
Chancre within 3 weeks; disappears 10–90 days; regional lymphadenopathy is painless, nontender. Chancres on penis, anus, rectum, vulva, cervix, perineum. Caused by the spirochete, Treponema pallidum.
290
What are the signs of secondary syphilis?,
6–12 wks after infection, symmetrical rash more on flexor and volar (pinkish in whites; copper blacks). Lymphadenopathy; papules at mucocutaneous junctions and moist areas are condylomata lata (extremely infectious), alopecia.
291
What are the signs of latent syphilis?,
Asymptomatic; persist for life, and one–third develop late or tertiary syphilis.
292
What are the signs of late or tertiary syphilis?,
Most neurologic. Symptomatic but not contagious. Tertiary develops 3–20 y after initial infection, and the typical lesion is the gumma (chronic granulomatous reaction); any tissue or organ. Cardiovascular syphilis.
293
What is the Argyll Robertson pupil?,
Small irregular pupil that accommodates but does not react to light.
294
What are the signs of tabes dorsalis?,
Tabes dorsalis (locomotor ataxia) is pain, ataxia, sensory changes, and loss of tendon reflexes.
295
How is syphilis diagnosed?,
Screening tests are VDRL and RPR; specific tests are FTA–ABS, MHA–TP, and Darkfield exam of chancre.
296
What are the causes of a false positive VDRL?,
False positives VDRL occurs with EBV, collagen vascular disease, TB, subacute bacterial endocarditis.
297
What is the Jarisch–Herxheimer reaction?,
Malaise, fever, headache, sweating rigors, and temporary exacerbations of the syphilitic lesions 6–12 hours after initial treatment.
298
What is the treatment of primary, secondary, and latent syphilis?,
Im benzathine penicillin once a week. Primary and secondary syphilis require one week of therapy. Late latent syphilis is treated for three weeks and diagnosed when VDRL or RPR \>1:8 without symptoms.
299
What is the treatment for tertiary syphilis?,
Penicillin 10–20 million units/day IV for 10. Penicillin–allergics receive doxycycline for primary and secondary syphilis, but must be desensitized in tertiary syphilis. Pregnant must also undergo desensitization.
300
What is chancroid?,
Acute, localized, contagious disease of painful genital ulcers and suppuration of the inguinal lymph nodes caused by Haemophilus ducreyi (Gram negative bacillus)
301
What are the clinical signs of chancroid?,
Small, soft, painful papules that become shallow ulcers with ragged edges. Inguinal lymph nodes become very tender and enlarged.
302
How is chancroid diagnosed?,
Gram stain shows Gram–negative bacillus, culture; PCR testing.
303
What is the treatment of chancroid?,
Azithromycin single dose or ceftriaxone intramuscularly (single dose). Erythromycin for 7 days or Cipro for 3 days are alternatives.
304
What is lymphogranuloma venereum?,
Contagious, sexually transmitted disease with primary lesion followed by suppurative lymphangitis caused by chlamydia trachomatis.
305
What are the clinical signs of lymphogranuloma venereum?,
Small, transient, nonindurated, ulcerates, heals; tender, unilateral enlargement inguinal nodes; multiple draining sinuses (buboes); scar, sinuses; fever, malaise, joint pains, headaches.
306
How is lymphogranuloma venereum diagnosed?,
Complement fixing antibodies; isolate chlamydia from pus in buboes
307
What is the treatment of lymphogranuloma venereum?,
Doxycycline or erythromycin.
308
What is granuloma inguinale?,
Chronic granulomatous condition, spread by sexual contact; caused by Donovania granulomatis, Calymmatobacterium granulomatis
309
What are the clinical signs of granuloma inguinale?,
A painless, red nodule that develops into an elevated granulomatous mass. In males, on penis, scrotum, groin, thighs; in females on vulva, vagina, perineum. In homosexual males, the anus and buttocks. Scar formation.
310
How is granuloma inguinale diagnosed?,
Giemsa or Wright stain (Donovan bodies) or smear of lesion; punch biopsy. Treatment with doxycycline ceftriaxone, TMP/SMZ, or erythromycin.
311
What virus causes genital herpes?,
Herpes virus, type II; type I can be seen in genital herpes.
312
What are the clinical signs of genital herpes?,
Vesicles skin or mucous membranes; become painful, circular ulcers, red areola. Soreness precedes lesions. Inguinal lymphadenopathy. Lesions on penis or labia, clitoris, perineum, vagina, cervix.
313
How is genital herpes diagnosed?,
Tzanck test and viral culture.
314
What is the treatment of genital herpes?,
Acyclovir, famciclovir, or valacyclovir. Herpes may recur; sexual contacts should be examined. Acyclovir–resistant herpes is treated with foscarnet.
315
What are genital warts?,
Also known as condylomata acuminata; papilloma virus. Soft, moist, minute, pink, or red; grow rapidly and become pedunculated. Cauliflower appearance. Differentiate from flat warts and condylomata lata.
316
What is the treatment of genital warts?,
Destruction (curettage, trichloroacetic acid), cryotherapy, podophyllin, imiquimod for 14 weeks (an immune stimulant), laser.
317
What conditions predispose to cystitis?,
Predisposed by tumors, stones, strictures, prostatic hypertrophy, neurogenic bladder. Sexual intercourse in women. Catheters.
318
What is the etiology of cystitis?,
E. coli in \>80%; second are other coliforms (Gram–negative bacilli) such as Proteus, Klebsiella, Enterobacter; enterococci occasionally; Staph saprophyticus in young women.
319
What are the symptoms of cystitis?,
Dysuria, frequency, urgency, and suprapubic pain. Hematuria, low–grade fever; foul–smelling and cloudy urine. Suprapubic tenderness without flank tenderness.
320
How is cystitis diagnosed?,
Urinalysis for WBCs, RBCs, protein, bacteria. Nitrites indicate Gram–negative. Urine culture with \>100,000 colonies/mL of urine is confirmatory but not always necessary.
321
What is the treatment of cystitis?,
Uncomplicated cystitis: 3 days of trimethoprim/sulfamethoxazole, or any quinolone. Seven days of therapy for cystitis in diabetes. Quinolones should not be used in pregnancy.
322
What are the predisposing factors for pyelonephritis?,
Strictures, tumors, calculi, prostatic hypertrophy, or neurogenic bladder, vesicoureteral reflux; more common in women, childhood, pregnancy, after urethral catheterization or instrumentation
323
What are the clinical signs of pyelonephritis?,
Chills, fever, flank pain, nausea, vomiting, costovertebral angle tenderness, increased frequency in urination, and dysuria.
324
How is pyelonephritis diagnosed?,
Clean–catch urine for urinalysis, culture; \>100,000 bacteria/mL of urine. If the patient does not improve in 48–72 hours, ultrasound or CT scan can be done to detect obstruction renal or perinephric abscess.
325
What is the treatment of pyelonephritis?,
Antibiotics for 10–14 days with fluoroquinolone, or ampicillin and gentamicin, or a third–generation cephalosporin. Most treated as outpatients. Resistance to TMP/SMZ 20%.
326
What is the bacteriology of pyelonephritis?,
E. coli is the most common pathogen, others include: Klebsiella, Proteus, and Enterococcus. Immunosuppressed and indwelling catheters are more prone to Candida.
327
What is perinephric abscess?,
Infected material surrounding kidney and within the Gerota fascia; from pyelonephritis. Stones in 20–60%. Other structural abnormalities, recent surgery, trauma, diabetes.
328
What is the microbiology of perinephritic abscess?,
E. coli most common, then Klebsiella, Proteus; Staph aureus sometimes accounts for hematogenous cases.
329
How is perinephritic abscess diagnosed?,
Urinalysis normal 30% and culture normal 40%. Fever, pyuria with a negative culture or a polymicrobial culture. Ultrasound; CT or MRI scan are better tests. Aspiration of the abscess.
330
What is the treatment of perinephric abscess?,
Third–generation cephalosporins, antipseudomonal penicillin, or ticarcillin/clavulanate with an aminoglycoside percutaneous drainage
331
What is impetigo?,
Superficial, pustular skin infection in children (ecthyma is ulcerative form of impetigo), oozing, crusting, draining; S. aureus (bullous impetigo) and group A beta–hemolytic Streptococcus
332
What are the clinical signs of impetigo?,
Arms, legs, and face after skin trauma. Maculopapules, rapidly progresses to vesicular pustular lesions or bullae. Progress to lymphangitis, furunculosis, or cellulitis, and acute glomerulonephritis.
333
What is the treatment of impetigo?,
Oral first–generation cephalosporin or semisynthetic penicillin (oxacillin, cloxacillin, dicloxacillin). Topical mupirocin or bacitracin. Penicillin–allergic: clarithromycin or azithromycin.
334
What is erysipelas?,
Superficial cellulitis caused by group A beta–hemolytic Streptococcus.
335
What are the clinical signs of erysipelas?,
Bilateral, shiny, red, indurated, edematous, tender lesions on the face, arms, and legs. Lesions are sharply demarcated.
336
What is the treatment of erysipelas?,
Semisynthetic penicillin or first–generation cephalosporin; penicillin.
337
What are dermatophyte infections?,
Superficial infection caused by a dermatophyte fungus that invades outer layer of skin nails, hair, stratum corneum; caused by microsporum, Trichophyton, and Epidermophyton
338
How are dermatophyte infections diagnosed?,
Potassium hydroxide (10%) prep; culture.
339
What are the signs of tinea corporis?,
Papulosquamous annular lesions of the body with a raised border, which expands peripherally and clear centrally.
340
What are the signs of tinea pedis?,
Macerated and scaling borders (third and fourth interdigital space) of the foot.
341
What are the signs of tinea unguium?,
Thickened and lusterless nails.
342
What are the signs of tinea capitis?,
Small, scaly, semi–bald, grayish patches with broken lusterless hair on head
343
What are the signs of tinea cruris?,
Ringed lesion that extends from the crural folds over the adjacent inner thigh
344
What are the signs of tinea barbae?,
Inflammatory, deep plaques and noninflammatory patches on the bearded area of the face.
345
What is the treatment for dermatophyte infections?,
Terbinafine or itraconazole orally for capitis, corporis, and unguium. Miconazole, clotrimazole and ketoconazole in cream or lotion for mild cruris, pedis, and corporis.
346
What is candidiasis?,
Infection of skin, mucous membranes by Candida albicans. Immunodeficiency antibacterial therapy, obesity, diabetes, corticosteroid, antimetabolite, pregnancy, debilitate, blood dyscrasias, HIV.
347
What are the clinical signs of candidiasis?,
Intertriginous infection: Well–demarcated, erythematous, itchy, exudative patches, rimmed with small red–based pustules in the groin, gluteal folds (diaper rash), axilla, umbilicus, and inframammary areas
348
What are the signs of candida vulvovaginitis?,
White discharge with inflammation of the vaginal and vulva. Pregnancy and diabetes mellitus.
349
What are the signs of oral candidiasis (thrush)?,
White patches of exudates on tongue or buccal mucosa.
350
What is candidal paronychia?,
Painful red swelling around the nail.
351
How is candidiasis diagnosed?,
Potassium hydroxide exam. Culture is definitive.
352
What is the treatment of candidiasis?,
Topical nystatin, clotrimazole, miconazole, ciclopirox, econazole, terconazole. Amphotericin for invasive infection. Fluconazole for less serious infections and paronychia.
353
What is tinea versicolor?,
Multiple macules (usually asymptomatic), varying in color from white to brown caused by Pityrosporum orbiculare (Malassezia furfur)
354
What are the clinical signs of tinea versicolor?,
Tan, brown, white, scaling macular lesions that tend to coalesce; found on chest, neck, abdomen, or face. Lesions do not tan.
355
How is tinea versicolor diagnosed?,
Skin scrapings with 10% KOH. spaghetti and meatballs, appearance of hyphae and spores.
356
What is the treatment of tinea versicolor??,
Topical selenium sulfide, clotrimazole, ketoconazole, or oral itraconazole.
357
What are the signs of scabies?,
Skin infection with superficial burrows, intense pruritus, and secondary infections, caused by Sarcoptes scabiei; skin–to–skin transmission.
358
What are the clinical signs of scabies?,
Pruritus, burrows, papules on flexor surfaces of wrists, finger webs, elbows, axilla, areola of breast and genitals. Immunocompromised may develop severe, crusted Norwegian scabies.
359
How is scabies diagnosed?,
Parasite in scrapings in mineral oil.
360
What is the treatment of scabies?,
Permethrin, lindane (Kwell). Ivermectin oral therapy if the disease is extensive. Lindane in contraindicated in pregnancy.
361
What is pediculosis?,
Skin infestation caused by lice. Itching, excoriations, erythematous macules and papules; secondary bacterial infection
362
How is pediculosis diagnosed?,
Examination of the pubic area, axillae, scalp, and other hair–bearing surfaces for the louse or nits.
363
What is the treatment for pediculosis?,
Permethrin or lindane (Kwell).
364
What is molluscum contagiosum?,
Skin–colored, waxy, papules caused by poxvirus. Small papules anywhere on the skin (genital and pubic area). Transmitted by skin–to–skin contact or sexually. Seen in children; increased with HIV.
365
What is the treatment of molluscum contagiosum?,
Freezing, curettage, electrocautery, or cantharidin.
366
61–year–old man with painful leg for 2 weeks. Ulcer over the proximal portion of his tibia just below the knee. Peripheral vascular disease and diabetes. Sinus tract in the ulcer draining purulent material. What is the diagnosis?,
Osteomyelitis
367
What is acute hematogenous osteomyelitis?,
S aureus. Long bones of lower extremities children; tibia, femur, metaphyseal. In adults, hematogenous osteomyelitis accounts for 20%, lumbar vertebrae. Fever, back tenderness. Injection drugs.
368
What is the most common organism in osteomyelitis that is caused by spread of a contiguous infection?,
A contiguous infection after recent trauma or placement of a prosthetic joint may cause osteomyelitis. S. aureus is the most common organism; sometimes polymicrobial.
369
What is vascular insufficiency osteomyelitis?,
Majority over 50, with diabetes or peripheral vascular disease. Bones of the lower extremities. Polymicrobial, but most common organism is S. aureus.
370
What is the presentation of osteomyelitis?,
Pain, erythema, swelling, and tenderness. Nearby ulceration or wound. Draining sinus tract.
371
How is osteomyelitis diagnosed?,
Technetium bone scan and MRI. Plain x–ray: Periosteal elevation. Bone biopsy and culture is the best test.
372
What is the treatment of osteomyelitis?,
Children treated with antibiotics; osteomyelitis in adults requires surgery and nafcillin or vancomycin (MRSA) plus an aminoglycoside or a 3rd gen cephalosporin for 12 weeks.
373
70–year–old woman with a swollen right knee; effusion and decreased mobility. Redness and tenderness. What is the next step?,
Arthrocentesis.
374
What are the causes of septic arthritis?,
Neisseria gonorrhoeae, staphylococci or streptococci; Rickettsia, viruses, spirochetes. Bacterial arthritis is divided into gonococcal and nongonococcal types?
375
What is the pathogenesis of gonococcal septic arthritis?,
Sexual activity is risk factor for gonococcal septic arthritis. 1–5% of people with gonorrhea will develop disseminated disease.
376
What is the pathogenesis of nongonococcal bacterial arthritis?,
Hematogenous spread. Bites, surgery, trauma, spread from surrounding infection. Normal or damaged joints can be infected after rheumatoid arthritis, osteoarthritis, surgery, prosthesis, gout; sickle, IVDU, diabetes, HIV.
377
What is the microbiology of nongonococcal arthritis?,
Gram–positive (\>85); (S. aureus [60%], Streptococcus [15%], Pneumococcus [5%]), Gram–negative (10–15%), polymicrobial (5%).
378
What is the presentation of nongonococcal septic arthritis?,
Monoarticular in \>85%, with a swollen, tender, erythematous joint with decreased range of motion. Knee most common. Petechiae or purpura?
379
How is nongonococcal septic arthritis diagnosed?,
Nongonococcal. Culture of joint aspirate fluid and Gram stain. The cell count of the synovial fluid is high (\>50,000) and is predominantly PMNs with a low glucose. Blood culture is positive in 50%.
380
How is gonococcal septic arthritis diagnosed?,
Only 50% of aspirates have positive culture. Less than 10% of blood cultures are positive. Cervix, pharynx, rectum, and urethra may be positive.
381
What is the treatment for nongonococcal septic arthritis?,
Good empiric coverage is nafcillin or oxacillin (or vancomycin if MRSA is suspected) combined with an aminoglycoside or a third–generation cephalosporin.
382
What is the treatment for gonococcal septic arthritis?,
Ceftriaxone is the drug of choice.
383
What is gas gangrene (clostridial myonecrosis)?,
Necrotizing infection of muscle by gas–producing organisms with sepsis. 80% caused by the spread of infection from C perfringens after traumatic wound (50%). Postoperative (30%), nontraumatic (20%).
384
What are the signs and symptoms of clostridial myonecrosis?,
385
How is clostridial myonecrosis diagnosed?,
Gram–positive rods, but no white cells. Culture positive for C. perfringens.
386
What is the treatment for clostridial myonecrosis?,
High–dose penicillin or clindamycin; surgical debridement or amputation. Hyperbaric oxygen 38–year–old man with fever, intravenous drug use, systolic murmur at the lower left sternal border?
387
What is the next step?,
Blood cultures for infective endocarditis.
388
Which heart valves are most frequently affected by endocarditis?,
Left–sided lesions of the aortic and mitral valves are the most common.
389
What procedures are associated with infective endocarditis?,
Invasive and dental procedures. Oral and upper respiratory tract surgery. GI procedures. GU surgery. Alimentation catheters. Pressure–monitoring catheters. IV drug use.
390
What is the most common cause of acute infective endocarditis?,
S. aureus is the most common cause. Seed previously normal valves. IV drug use is the major risk factor.
391
What are the signs of acute infective endocarditis?,
Rapid onset of fever and sepsis. Splenomegaly of invasion of myocardium and rapid valve destruction. Embolic complications.
392
What is the most common cause of subacute infective endocarditis?,
4–5% have negative blood cultures. Viridans group streptococci is the most common organism; low virulence. Seed abnormal valves.
393
Which cardiac conditions are risk factors for infective endocarditis?,
1) Ventricular septal defect, 2) stenosis, 3) prosthetic valves, 4) indwelling catheters, 5) bicuspid aortic valve, 6) mitral valve prolapse, and 7) Marfan syndrome
394
What are the clinical signs of subacute infective endocarditis?,
Slow onset with vague symptoms of malaise, low–grade fever, weight loss; and survival 80–90% with treatment.
395
What are the complications of infective endocarditis?,
CHF (most common cause of death). Septic infarctions and metastatic infections to brain; spleen; kidneys; coronary arteries. Glomerulonephritis with nephrotic syndrome or renal failure (immune complex).
396
How is infective endocarditis diagnosed?,
Positive blood cultures; transesophageal echo is \>90% sensitive.
397
What is the treatment of infective endocarditis?,
Empiric therapy with antistaphylococcal drug (nafcillin), and streptococcal drug (ampicillin and gentamicin). Vancomycin and gentamicin are empiric treatment if MRSA suspected.
398
What is the prophylactic treatment of bacterial endocarditis?,
Dental procedures: Amoxicillin. For penicillin–allergic patients: clindamycin or (azithromycin, or clarithromycin or cephalexin). Urinary or gastrointestinal procedures: no prophylaxis is required.
399
What cardiac conditions require prophylactic antibiotics?,
Prosthetic cardiac valves. Previous bacterial endocarditis, even in the absence of heart disease. Congenital cardiac malformations.
400
What cardiac conditions do not require prophylactic therapy?,
Rheumatic and other acquired valvular disease. Hypertrophic cardiomyopathy; mitral valve prolapse with valvular regurgitation; surgically repaired shunts or intracardiac defects.
401
What are the causes of pericarditis?,
Viruses/bacteria/tuberculosis/fungal/spirochetes; viral is most common (Coxsackie, ECHO). Acute HIV, SLE; RA, scleroderma. Uremia; neoplasia adjacent heart; hypothyroidism; irradiation; rheumatic fever, trauma, Dressler.
402
What is the clinical presentation of pericarditis?,
Sharp, pleuritic, chest pain that improves when sitting up and leaning forward. Pericardial rub. Best at the apex with the patient sitting up. Low fever.
403
What is pulsus paradoxus?,
Tamponade causes 10–mm drop in BP with inspiration. Blood is drawn into the right heart. Heart is compressed by fluid around it, and the septum bulges into left. Distended neck veins, tachycardia, hypotension also.
404
What are the ECG signs of pericarditis?,
ST segment elevation in almost every lead, except aVR. The ST elevation progresses to T–wave inversion. PR depression may occur. Electrical alternans. Echocardiogram demonstrates effusion.
405
What is the treatment for viral pericarditis?,
Indomethacin, ibuprofen, or Naprosyn. Prednisone if there is no response, or for tuberculosis with antitubercular medications. Pericardiocentesis and pericardial window for large effusion tamponade.
406
What is myocarditis?,
Infection or inflammation of heart muscle by viruses (Coxsackie B). Other causes: bacteria, Rickettsia, fungi, parasites (Chagas, toxoplasmosis), Lyme. Radiation, drugs, collagen–vascular, hyperthyroidism.
407
What are the signs of myocarditis?,
Myocardial dysfunction, dyspnea and fatigue. Asymptomatic, subclinical infection or a rapid progression to chest pain, arrhythmia, and death. S–3 gallop and murmurs.
408
How is myocarditis diagnosed?,
Nonspecific ST–T changes are most common. Heart block. CK–MB, LDH, troponin elevated. LV systolic dysfunction. Viruses from stool, saliva, nasopharynx. Ab to viruses. Biopsy rarely done.
409
What is the vector for Lyme disease?,
Lyme disease is spread by the bite of the Ixodes scapularis tick.
410
What is the clinical presentation of lyme disease?,
Rash 3–30 d after tick bite. 80% develop erythema migrans rash at bite (red patch, central clearing, bull's–eye). Rash resolves in several weeks. Flulike illness with fever, chills, myalgias.
411
What are the neurologic symptoms of lyme disease?,
Neurologic symptoms in 10–20% of patients, most commonly paralysis of the seventh cranial nerve (facial paralysis), which may be bilateral. Meningitis, encephalitis, headache, and memory disturbance may develop.
412
What are the cardiovascular signs of lyme disease?,
AV heart block, myocarditis, pericarditis, and various arrhythmias. Joint involvement may develop months to years later in up to 60%, most commonly a migratory polyarthritis.
413
What is the diagnostic criteria of Lyme disease?,
Erythema migrans with 1 late manifestation and lab confirmation. Treat based on rash. Serology by ELISA and western blot does not distinguish current and previous infection. Early test is often negative.
414
What is the treatment of Lyme disease?,
The rash, the facial palsy, and joint pain can be treated with oral doxycycline or amoxicillin. Heart block, meningitis, myocarditis, or encephalitis are treated with intravenous ceftriaxone.
415
Which cell is the primary target of HIV?,
The primary mechanism of HIV is to infect a subset of T lymphocytes called CD4 cells, often just referred to as T cells.
416
What are the symptoms of pneumocystis jiroveci pneumonia?,
CD4 count
417
What is the diagnostic test for PJP?,
Bronchoscopy with bronchoalveolar lavage for direct identification of the organism. Chest x–ray reveals bilateral, interstitial infiltrates. PJP may occur with a normal chest x–ray. Serum LDH is usually elevated.
418
What is the treatment of pneumocystis jiroveci pneumonia?,
Trimethoprim–sulfamethoxazole (TMP–SMZ) IV is the first–line therapy for mild–severe disease and may cause a rash.
419
What is the alternative treatments for PJP if TMP–SMZ is not tolerated?,
For mild–moderate disease: dapsone and trimethoprim, or primaquine and clindamycin; or atovaquone, or trimetrexate (with leucovorin).
420
What are the adverse effects of pentamidine?,
Pancreatitis, hyperglycemia, hypoglycemia.
421
What are the indications for steroids in PJP?,
Steroids are used as adjunctive therapy for any patient with severe pneumonia. Severe is defined with a PaO2 of 35 mm Hg.
422
How is cytomegalovirus diagnosed?,
Funduscopy; colonoscopy with biopsy for diarrhea; or upper gastrointestinal endoscopy with biopsy of ulcers.
423
What is the treatment of cytomegalovirus retinitis and esophagitis?,
Valganciclovir, an oral prodrug of ganciclovir; achieves levels comparable to IV ganciclovir. IV ganciclovir is reserved for serious CNS infections; foscarnet and cidofovir for ganciclovir resistance.
424
What are the side effects of ganciclovir?,
Ganciclovir may cause neutropenia.
425
What is the prophylactic therapy for cytomegalovirus retinitis?,
Valganciclovir can be used for maintenance therapy.
426
What is Mycobacterium avium complex?,
Occurs in HIV infected with CD4
427
What is the testing for Mycobacterium avium complex?,
Blood culture, culture of bone marrow, liver, or other body tissue or fluid.
428
What is the treatment of Mycobacterium avium complex?,
Clarithromycin, ethambutol, rifabutin. Prophylaxis is azithromycin once a week or clarithromycin bid; rifabutin is alternative. Prophylaxis discontinued if antiretrovirals raise CD4 \>100 for several months.
429
At what level of CD4 cell count does toxoplasmosis occur?,
Occurs in HIV infected patients with CD4
430
What are the signs of cerebral toxoplasmosis?,
Brain mass lesion: Headache, confusion, seizures, and focal neurologic deficits
431
What tests are used to detect toxoplasmosis?,
CT of head showing a ring (contrast enhancing) with edema and mass effect. Trial of anti–toxoplasmosis therapy is given for 2 weeks, and scan repeated. Shrinkage of lesion is diagnostic. Toxoplasmosis serology, CSF PCR.
432
What is the treatment of toxoplasmosis?,
Pyrimethamine and sulfadiazine. Clindamycin can be substituted for sulfadiazine. Leucovorin prevents marrow suppression. Prophylaxis with TMP/SMZ or dapsone/pyrimethamine.
433
What is cryptococcosis?,
Occurs in HIV infected persons with CD4
434
How is cryptococcosis diagnosed?,
Lumbar puncture with India ink and cryptococcal antigen testing. Serum cryptococcal antigen testing.
435
What is the treatment of cryptococcosis?,
Amphotericin intravenously for 10–14 days (with flucytosine), followed by fluconazole orally for suppressive therapy.
436
What is the normal CD4 cell count?,
700–1,500/mcL.
437
What CD4 cell count is associated with oral thrush, Kaposi sarcoma, tuberculosis, zoster, lymphoma?,
200–500/mcL
438
What CD4 cell count is associated with pneumocystis jiroveci pneumonia, dementia, progressive multifocal leukoencephalopathy, disseminated histoplasmosis and coccidiomycosis?,
100–200/mcL
439
What opportunistic infections occur when the CD4 count is
Toxoplasmosis, Cryptococcus, cryptosporidiosis, disseminated herpes simplex
440
What opportunistic infections occur when the CD4 count is
Cytomegalovirus, Mycobacterium avium complex. Progressive, multifocal leukoencephalopathy, CNS lymphoma.
441
What test indicates an adequate response to antiretroviral therapy in HIV–infected persons?,
The goal is complete suppression of viremia with
442
What are the indications for viral sensitivity testing?,
Patient failing a combination of medications and a change in therapy is necessary. Any pregnant woman who has not been fully suppressed on the initial combination of medications.
443
What are the side effects of zidovudine?,
Leukopenia, anemia, gastrointestinal
444
What are the side effects of didanosine (DDI)?,
Pancreatitis, peripheral neuropathy.
445
What are the side effects of stavudine (D4T)?,
Peripheral neuropathy
446
What are the side effects of lamivudine (3TC)?,
No side effects have been reported in additional to placebo.
447
What are the side effects of emtricitabine?,
Structurally related to lamivudine; few side effects.
448
What is the structure of tenofovir?,
Tenofovir is a nucleotide analog as compared to the others that are nucleoside analogs.
449
What are the side effects of abacavir?,
Hypersensitivity reaction in the first 6 weeks of therapy. Rash, fever, nausea/vomiting, muscle and joint aches, dyspnea. The drug should be stopped and never restarted.
450
What are the side effects of zalcitabine (DDC)?,
Pancreatitis, peripheral neuropathy, lactic acidosis
451
What are the nucleoside reverse transcriptase inhibitors?,
Zidovudine (ZDV or AZT), didanosine (DDI), stavudine (D4T), lamivudine (3TC), emtricitabine, abacavir, zalcitabine (DDC).
452
What are the side effects of protease inhibitors?,
Hyperlipidemia, hyperglycemia, elevated liver enzymes; fat loss (lipoatrophy) from the face and extremities with redistribution of fat to the back of the neck and abdominal viscera.
453
What are the side effects of nelfinavir?,
Nausea, diarrhea.
454
What are the side effects of indinavir?,
Nephrolithiasis (4%), hyperbilirubinemia (10%).
455
What are the side effects of ritonavir?,
Severe nausea, diarrhea.
456
What are the side effects of saquinavir?,
Gastrointestinal effects.
457
What are the side effects of amprenavir?,
Rash, headache, diarrhea, and nausea.
458
What are the side effects of the lopinavir/ritonavir combination?,
Diarrhea
459
What are the side effects of atazanavir?,
Diarrhea, asymptomatic hyperbilirubinemia.
460
What are the names of the protease inhibitors?,
Nelfinavir, indinavir, ritonavir, saquinavir, amprenavir, atazanavir.
461
What are the names of non–nucleoside reverse transcriptase inhibitors?,
Efavirenz, nevirapine, delavirdine.
462
What are the side effects of efavirenz?,
Neurologic; somnolence, confusion, or psychiatric disturbance; non–nucleoside reverse transcriptase inhibitor.
463
What are the side effects of nevirapine?,
Rash, hepatotoxicity.
464
What are the side effects of delavirdine?,
Rash.
465
When should antiretroviral therapy be started in HIV infected patients?,
Antiretroviral medication should be started when the CD4 count has dropped or the viral load has risen.\>55,000 copies/mL of RNA.
466
What antiretrovirals should be started in HIV infected patients?,
Use two nucleosides combined with a protease inhibitor or, Use two nucleosides combined with efavirenz or, Use two nucleosides combined with two protease inhibitors.
467
What is highly active antiretroviral therapy?,
Uses medications with activity at different sites; 2 NRTIs (tenofovir/emtricitabine or ZDV/lamivudine) combined with NNRTI (efavirenz) or 2 PI (atazanavir/ritonavir, fosamprenavir/ritonavir, lopinavir/ritonavir).
468
What is boosted protease inhibitor therapy
Practice of giving protease inhibitors in combination with a low dose of ritonavir (a PI). Ritonavir when given in a low dose with other PIs, decreases metabolism of the second PI and increases drug level.
469
What is considered adequate antiretroviral therapy?,
Any regimen that increases the CD4 count and reduces the viral load to undetectable amounts or close to undetectable amounts. Drop of at least 50% of viral load in the first month indicates adequate therapy.
470
What percentage of children born to HIV positive mothers will be infected with HIV?,
Without treatment, 30% of children born to HIV–positive mothers will be infected. All children at birth will carry the maternal antibody by ELISA testing.
471
What treatment should be given to pregnant HIV infected women?,
Women with low CD4 or high viral load should receive triple antiretrovirals. ZDV, a second nucleoside and a protease inhibitor should begin in pregnant women at 14 weeks if not already on therapy.
472
What are the indications for cesarean section in pregnant HIV–infected women?,
C–section is used routinely in those whose CD4 count is low or whose viral load \>1000 copies.
473
Which antiretroviral in a known teratogen?,
The only known teratogen is efavirenz in animal studies.
474
What treatment is recommended for HIV infected pregnant women?,
If already on antiretrovirals, continue. If low CD4 or opportunistic infection, start immediately. If high CD4, combination therapy can begin at 14 weeks. Can deliver vaginally if the viral load
475
What is the effect of breastfeeding on transmission of HIV to the infant?,
Breast feeding is associated with transmission of virus to the infant.
476
What postexposure prophylaxis for HIV after needlestick injury should be given?,
Persons with serious exposure to blood of HIV–pos should receive ZDV, lamivudine, nelfinavir (or any other fully suppressive 3–drug combo) for 4 wks. ZDV alone will decrease the risk of transmission by 80%.
477
What is Q–Fever?,
Coxiella burnetii infection, which is transmitted by inhalation; found in cattle, sheep, and goats.
478
What are the clinical signs of Q–fever?,
Febrile illness, atypical pneumonia, hepatitis, and hepatomegaly, endocarditis. Treatment is doxycycline. Diagnosed by specific serology.
479
What is Rocky Mountain spotted fever?,
R. rickettsi is transmitted by the wood tick from the mid–Atlantic coast, upper South, and Midwest. In spring and summer.
480
What is the triad of Rocky Mountain spotted fever?,
Abrupt fever, headache and erythematous maculopapules. Rash starts wrist, ankles and spreads centripetally, palms and soles. Confusion, lethargy, dizziness, irritability, stiff neck, GI symptoms.
481
How is Rocky Mountain spotted fever diagnosed?,
Specific serology; biopsy of skin lesion.
482
What is the treatment of Rocky Mountain fever?,
Doxycycline
483
What is toxoplasmosis?,
Intracellular parasite. 50% of the US population is antibody positive. Prevalence increases with age. Undercooked meat, especially pork and lamb. Also from domestic cat feces; transplacental infection.
484
What is the presentation of toxoplasmosis?,
80–90% asymptomatic in the immunocompetent. In AIDS: chorioretinitis, CNS mass lesion, encephalitis. Headache, fever, nausea. The retinal lesion can cause visual complaints.
485
How is toxoplasmosis diagnosed?,
Serology is the most common method used. The best test is to visualize the parasite in biopsy tissue.
486
What is the treatment of toxoplasmosis?,
Pyrimethamine and sulfadiazine.
487
What is tetanus?,
Infectious complication of wounds caused by the toxin of Clostridium tetani; takes 1–7 days to develop; spore forming, Gram–positive rod.
488
What are the clinical signs tetanus infection?,
Tonic spasms of voluntary muscles, respiratory arrest, difficulty in swallowing (dysphagia), restlessness, irritability, stiff neck, arms, and legs; headache, lockjaw, high mortality.
489
What is the prophylaxis of tetanus?,
Tetanus toxoid (boosters every 10 years). Débride wound. Antitoxin is tetanus immunoglobulin; penicillin 10–14 days.
490
What is aspergillosis?,
Fungus widespread in environment; pulmonary disease in immunocompromised. 90 species, with A. fumigatus the most common in decaying organic matter, ceiling tile, ventilation systems.
491
What are the signs of aspergillosis?,
Asthma with cough, fever, wheezing. Mycetoma, a fungal ball: in a pre–existing cavity, with hemoptysis. Invasive pulmonary. Disseminates to any organ from lung.
492
What are the risk factors for aspergillosis?,
Risks: 1) neutropenia
493
How is aspergillosis diagnosed?,
Abnormal chest x–ray and Aspergillus in sputum.
494
What are voriconazole and caspofungin?,
Drugs used to treat aspergillosis and other fungal infections.
495
What is the treatment of aspergillosis?,
Invasive disease is treated with voriconazole, a broad–spectrum azole. Itraconazole for very mild disease. Caspofungin is superior to amphotericin. Caspofungin is an echinocandin.
496
What is blastomycosis?,
A fungus that is strongly associated with rotting organic material and soil. Occurs in southeast and central US. It has a 10:1 male:female ratio. Begins with inhalation of decaying wood and vegetation.
497
What are the signs of blastomycosis?,
Fever, cough, chest pain, and weight loss. After inhalation, disseminates anywhere in body, but skin is by far the most common.
498
What is the treatment of blastomycosis?,
Prolonged amphotericin for severe disease (8–12 weeks); itraconazole or ketoconazole for mild disease.
499
What is the cause of toxic shock syndrome?,
Staphylococcus aureus toxin TSST–1. Infected tampons, sponges, and surgical wound infections.
500
What are the clinical signs of toxic shock syndrome?,
Hypotension, fever, mucosal changes, desquamative rash on hands and feet. Gastrointestinal, renal, hepatic, and muscular symptoms.
