3 Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What is the presentation of glucose–6–phosphate dehydrogenase deficiency?,

A

Sudden, severe, intravascular hemolysis; jaundice, dark urine, weakness, and tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the treatment for glucose–6–phosphate dehydrogenase deficiency?,

A

Hydration and transfusion. Avoid oxidant stress.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is aplastic anemia?,

A

Failure of bone marrow, resulting in anemia, leukopenia, and thrombocytopenia (pancytopenia). The marrow is empty.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the treatment for aplastic anemia?,

A

Bone marrow transplantation or immunosuppressive agents.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the causes of acute leukemia?,

A

Most cases are idiopathic; radiation exposure, benzene, melphalan and etoposide, retroviruses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the presentation of acute leukemia?,

A

Fatigue from anemia. Bleeding from thrombocytopenia. Infection from the underproduction of white blood cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the markers of acute myelogenous leukemia?,

A

AML is characterized by Auer rods, myeloperoxidase, and esterase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the markers of acute lymphocytic leukemia?,

A

ALL is characterized by common ALL antigen and terminal deoxynucleotidyl transferase (TdT).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is chronic myelogenous leukemia (CML)?,

A

Massive overproduction of myeloid cells. Philadelphia chromosome is characteristic, producing tyrosine kinase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is chronic lymphocytic leukemia?,

A

Massive overproduction of mature; lymphocytes from production of B lymphocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is multiple myeloma?,

A

Plasma cell overproduction, replacing the bone marrow; large quantities of functionless immunoglobulins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is Bence–Jones protein?,

A

Urinary Bence–Jones protein is nonfunctional gamma globulin found in multiple myeloma. It will not react with urine dipstick test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the treatment for multiple myeloma?,

A

Bone marrow transplantation. Older patients should receive melphalan and prednisone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is monoclonal gammopathy of uncertain significance?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is Hodgkin disease?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the presentation of Hodgkin disease?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the treatment for Hodgkin disease?,

A

Localized disease is managed with radiation. All patients with symptoms and stage III or stage IV disease are managed with chemotherapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is non–Hodgkin lymphoma?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What conditions predispose to non–Hodgkin lymphoma?,

A

Infections such as HIV, hepatitis C, Epstein–Barr, HTLV–I, and Helicobacter pylori predispose to the development of NHL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the presentation of non–Hodgkin lymphoma?,

A

Enlarged, rubbery, nonerythematous, nontender lymph nodes. symptoms are night sweats, weight loss, fevers. Pruritus may occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What sites are affected by non–Hodgkin lymphoma?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the treatment for non–Hodgkin lymphoma?,

A

Local disease is treated with radiation, and those with symptoms or Stages III and IV receive combination chemotherapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

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?,

A

Idiopathic thrombocytopenic purpura. Also known as primary immune thrombocytopenic purpura.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is idiopathic thrombocytopenic purpura?,

A

Thrombocytopenia caused by idiopathic production of an antibody to platelets; often associated with lymphoma, chronic lymphocytic leukemia, HIV, and connective tissue diseases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the presentation of idiopathic thrombocytopenic purpura?,

A

Bleeding skin, nasal, oral, GI, urine, vagina. Young, female; epistaxis, bruising, hematuria, uterine and GI bleeding. Petechiae, purpura, ecchymoses. Splenomegaly absent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How is idiopathic thrombocytopenic purpura diagnosed?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the treatment for idiopathic thrombocytopenic purpura?,

A

Prednisone. Splenectomy if very low platelet counts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is Von Willebrand disease?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the presentation of Von Willebrand disease?,

A

Epistaxis, petechiae, bruising, and menstrual abnormalities; gastrointestinal and urinary tract bleeding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How is Von Willebrand disease diagnosed?,

A

Platelet count is normal. The bleeding time is increased. Von Willebrand factor is low. Ristocetin platelet aggregation test is abnormal. PTT may be elevated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the treatment for von Willebrand disease?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Which coagulopathies cause a prolonged prothrombin time?,

A

Factor VII deficiency, vitamin K deficiency, liver disease, warfarin use, factor VII inhibitor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Which coagulopathies cause a prolonged PTT?,

A

vWF and factors VIII, IX, XI, or XII deficiencies; heparin, antiphospholipid antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Which coagulopathies cause a prolonged PT and PTT?,

A

Prothrombin, fibrinogen, factor V, factor X or combined factor deficiencies, liver disease, DIC, supratherapeutic heparin or warfarin; combined heparin and warfarin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is hemophilia?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Why does hemophilia not express in females?,

A

Females do not express the disease because homozygosity results in intrauterine death of the fetus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the presentation of hemophilia?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What type of bleeding is associated with factor deficiency?,

A

Factor deficiencies cause hemarthrosis, hematoma, gastrointestinal bleeding, urinary bleeding, bruising, CNS bleeding. Severe hemophilia presents by age two or circumcision.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How is hemophilia diagnosed?,

A

A prolonged PTT with a normal PT. Specific factor VIII or IX levels allow for a precise diagnosis of hemophilia A or B.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the treatment of hemophilia?,

A

Mild hemophilia can be treated with desmopressin (DDAVP). Severe deficiencies are treated with replacement of the specific factor. Desmopressin is ineffective for hemophilia B.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What factor deficiency results from vitamin K deficiency?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the presentation of vitamin K deficiency?,

A

Bleeding may occur at any site. Oozing at venipuncture sites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How is vitamin K deficiency diagnosed?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the treatment for vitamin K deficiency?,

A

Severe bleeding is treated with fresh frozen plasma. Vitamin K is given at the same time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Why do patients with liver disease have increased PT and PTT?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the effects of coagulopathy of liver disease?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the treatment of coagulopathy of liver disease?,

A

Fresh frozen plasma severe bleeding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is disseminated intravascular coagulation?,

A

Consumptive coagulopathy from major illness, resulting in consumption of platelets and clotting factors; bleeding with a microangiopathic hemolysis and fibrin products; occasionally thrombosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the causes of disseminated intravascular coagulation?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the presentation of disseminated intravascular coagulation?,

A

Bleeding from any site. Thrombosis is less common. Hemolysis often may lead to acute renal failure, jaundice, confusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How is disseminated intravascular coagulation diagnosed?,

A

Serious underlying disorder with bleeding, elevation PT, PTT; decrease platelets. Fibrinogen low. D–dimers and fibrin– split products are increased. Schistocytes with intravascular hemolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the treatment for disseminated intravascular coagulation?,

A

Fresh frozen plasma and platelet transfusions. Heparin is rarely used except in thrombosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the names of the semisynthetic penicillinase–resistant penicillins?,

A

Oxacillin, cloxacillin, dicloxacillin, methicillin, nafcillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Which bacteria are susceptible to the semisynthetic penicillins?,

A

Staphylococci and streptococci. Oxacillin, nafcillin, dicloxacillin, cloxacillin. Exclusively effective against Gram–pos cocci, particular staph. Methicillin not used because interstitial nephritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the indications for the semisynthetic penicillins?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What antibiotic is used to treat resistant–resistant Staph aureus?,

A

MRSA is treated primarily with vancomycin. Oral linezolid or IV quinupristin–dalfopristin are alternatives for MRSA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the coverage of linezolid?,

A

Drug–resistant enterococcus, staphylococcus, and pneumococcus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Which bacteria are sensitive to penicillin G, penicillin VK, ampicillin, and amoxicillin?,

A

Effective against streptococci, such as S. pyogenes, viridans group streptococci, and S. pneumonia, but not against staphylococci.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

When can ampicillin and amoxicillin be used against staphylococcal infections?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the coverage of ampicillin against E coli?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the first–generation cephalosporins?,

A

Cefazolin, cefadroxil, cephalexin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the second–generation cephalosporins?,

A

Cefoxitin, cefotetan, cefuroxime, cefprozil, loracarbef.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the coverage of the first–generation cephalosporins?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the coverage of second–generation cephalosporins?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the coverage of the third–generation cephalosporins?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the allergic cross–reactivity of penicillins with cephalosporins?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What antibiotic should be used in patients with a history of an anaphylactic reaction to a penicillin?,

A

A macrolide (clarithromycin or azithromycin) or levofloxacin, gatifloxacin, or moxifloxacin can be used. For serious infections, use vancomycin, linezolid, or daptomycin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are the indications for macrolides (erythromycin, clarithromycin, azithromycin), extended fluoroquinolones (levofloxacin, gatifloxacin, moxifloxacin), and clindamycin?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Why should ciprofloxacin not be used to treat pneumonia?,

A

Ciprofloxacin does not cover Strep pneumoniae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are the indications for vancomycin, linezolid, quinupristin, dalfopristin?,

A

Alternatives for Gram–pos infections when penicillin allergy or MRSA. Linezolid is the only oral MRSA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the coverage of linezolid, quinupristin, dalfopristin?,

A

Linezolid, quinupristin, dalfopristin are effective against MRSA and vancomycin–resistant enterococci.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the activity of antipseudomonal penicillins (piperacillin, ticarcillin, mezlocillin) against Gram–negative bacilli?,

A

Fully active against range of Gram–negative bacilli, such as the Enterobacteriaceae including Pseudomonas. Enterobacteriaceae include E. coli, Proteus, Enterobacter, Citrobacter, Morganella, Serratia, Klebsiella.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is the activity of ticarcillin and mezlocillin against MSSA?,

A

Antipseudomonal penicillins are only active against staph when combined with a beta–lactamase inhibitor, such as piperacillin/tazobactam or ticarcillin/clavulanate. Not MRSA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the coverage of ampicillin/sulbactam and amoxicillin/clavulanate?,

A

Cover strep and staph and Gram–neg bacilli, but not Pseudomonas. All penicillins will cover sensitive streptococci.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the third–generation cephalosporins?,

A

Ceftazidime, cefotaxime, ceftriaxone, cefotaxime.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the fourth generation cephalosporin?,

A

Cefepime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the coverage of third– and fourth–generation cephalosporins?,

A

Fully active against full range of Gram–neg bacilli, such as the Enterobacteriaceae. Only ceftazidime and cefepime will cover Pseudomonas. Cefepime also covers staph.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is the Gram–negative coverage of second–generation agents?,

A

Cover some of the Enterobacteriaceae, but not Pseudomonas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the coverage of the third generation cephalosporins?,

A

Predominantly for use against Gram–negative organisms. Ceftriaxone and cefotaxime cover best for penicillin–insensitive pneumococci which cause meningitis or pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the coverage of quinolones (ciprofloxacin, levofloxacin, gatifloxacin, moxifloxacin, ofloxacin)?,

A

Cover most Enterobacteriaceae, such as E. coli, Proteus, Enterobacter, Haemophilus, Moraxella, Citrobacter, Morganella, Serratia, and Klebsiella. Only ciprofloxacin will cover Pseudomonas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is the coverage of extended–spectrum quinolones?,

A

Moxifloxacin, levofloxacin, gatifloxacin are also active against Gram–positive cocci, in particular Strep pneumoniae. Good for pneumonia because also cover Mycoplasma, Chlamydia, Legionella.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is the coverage of aminoglycosides (gentamicin, tobramycin, amikacin)?,

A

Gram–negative coverage. Aminoglycosides are synergistic with ampicillin in treatment of staph.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is the coverage of monobactams?,

A

Aztreonam is exclusively a Gram–negative agent, with no strep or staph coverage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is the coverage of carbapenems (imipenem, meropenem, ertapenem)?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What agent is most active against intraabdominal anaerobes?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the coverage of clindamycin?,

A

Clindamycin may have some advantages over metronidazole against the anaerobic streptococci found in the mouth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What agents have intraabdominal anaerobic coverage?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

A 15–year–old male with fever, headache, nausea, and vomiting. Neck stiffness and photophobia. What is the next step?,

A

Lumbar puncture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is the most common cause of meningitis after the neonatal period?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What factors predispose to listeria monocytogenes meningitis?,

A

Listeria monocytogenes is more common with immune system defects, HIV, steroid use, leukemia, lymphoma, and various chemotherapeutic agents. Neonates and the elderly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is the most common cause of meningitis in the elderly and infants?,

A

Streptococcus pneumoniae is the most common etiology. Listeria is more common in the very old and infants.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Which patients are at risk for staphylococcal meningitis?,

A

Staphylococcus aureus is more common in those who have had any form of neurosurgery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Which patients are at risk for cryptococcus meningitis?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Which persons are at risk for Rocky Mountain spotted fever meningitis?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What area is associated with Lyme meningitis?,

A

Lyme disease can also cause meningitis and is more common in the Northeast. Tuberculosis and syphilis are also associated with meningitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the CSF characteristics in aseptic meningitis?,

A

CSF has lymphocytic pleocytosis and bacterial cultures are negative.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are the causes of aseptic meningitis?,

A

Enteroviruses, arboviruses (St. Louis encephalitis virus, West Nile virus), HIV, herpes simplex, and lymphocytic choriomeningitis virus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is the most common cause of neonatal meningitis?,

A

Group B Streptococcus (Streptococcus agalactiae) is the most common cause of meningitis in the neonatal period.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is the clinical presentation of meningitis?,

A

Fever, photophobia, headache, nuchal rigidity (Kernig, Brudzinski), nausea, vomiting, seizures. The most common deficit from meningitis is damage to 8th cranial nerve (hearing).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What type of meningitis is associated with a petechial rash?,

A

Neisseria. A rash on the wrists and ankles with centripetal spread toward the body suggests Rocky Mountain spotted fever.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What type of meningitis is associated with facial palsy?,

A

Facial nerve palsy is suggestive of Lyme disease. Pulmonary symptoms or an abnormal chest x–ray suggest tuberculosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

When should a CT scan be done before lumbar puncture in patients with suspected meningitis?,

A

CT should be done before lumbar puncture if papilledema, focal motor deficits, new onset seizures, mental status abnormalities, or immunocompromise (HIV, immunosuppressive).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What should be done if the lumbar puncture is delayed more than 20–30 minutes?,

A

An empiric dose of antibiotics should be given.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What are the CSF findings in bacterial meningitis?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What types of meningitis are associated with an elevation in lymphocytes?,

A

Viral infection, Rickettsia, Lyme disease, tuberculosis, syphilis, or fungal (cryptococcal) etiology. Normal CSF cell count is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the empiric treatment of bacterial meningitis in adults?,

A

Vancomycin (pneumococci are resistant penicillin) plus a 3rd gen cephalosporin, such as ceftriaxone. Ampicillin is added to cover Listeria if immune defects, >50, or

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is the treatment of Lyme meningitis?,

A

Lyme disease is treated with ceftriaxone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is the treatment of Cryptococcal meningitis?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is the treatment of neurosyphilis?,

A

Neurosyphilis is treated with high–dose intravenous penicillin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What is the treatment of tuberculosis meningitis?,

A

TB meningitis is treated the same as pulmonary tuberculosis (though a longer duration of 9–12 months).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What are the indications for corticosteroid in meningitis?,

A

Steroid use in adult meningitis is appropriate for TB meningitis and bacterial meningitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What are the recommendations for adjunctive dexamethasone for bacterial meningitis?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What is encephalitis?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is the presentation of encephalitis?,

A

Altered mental status with fever and headache. Confusion to lethargy or coma. Focal deficits. Neck stiffness. Seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

How is HSV encephalitis diagnosed?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What is the treatment for HSV encephalitis?,

A

Intravenous acyclovir.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What is the treatment of cytomegalovirus encephalitis?,

A

Ganciclovir or foscarnet are active against CMV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

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?,

A

Brain abscess.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What are the causes of brain abscesses?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Which organisms cause brain abscesses?,

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is the presentation of brain abscess?,

A

Headache. Fever, focal neurologic deficits, seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

How is brain abscess diagnosed?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What is the treatment for brain abscess?,

A

Surgical drainage. Penicillin, metronidazole, and a third–generation cephalosporin, such as ceftazidime. HIV patients are treated empirically with pyrimethamine and sulfadiazine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What are the causes of otitis media?,

A

The most common organisms are Strep pneumoniae (35–40%), H. influenzae (nontypeable; 25–30%), and Moraxella catarrhalis (15–20%). Viruses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What is the presentation of otitis media?,

A

Ear pain, fever, and decreased hearing. Immobility of the membrane on insufflation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What is the treatment for otitis media?,

A

High–dose amoxicillin. Amoxicillin–clavulanate is used if recent amoxicillin or if no response to amoxicillin. Alternatives: Cefuroxime, loracarbef, cefprozil, or cefdinir or cefixime.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What is the treatment for otitis media in severe allergy to penicillin?,

A

Macrolides, such as azithromycin or clarithromycin. Levofloxacin, moxifloxacin or gatifloxacin are acceptable. TMP/SMZ is poorly active against Streptococcus pneumoniae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What is the most common site of sinusitis?,

A

The most common site of infection is the maxillary sinus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What are the cause of sinusitis?,

A

Viruses are responsible for most cases. Bacterial organisms are strep pneumonia, H influenza (non–typable), Moraxella catarrhalis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What is the presentation of sinusitis?,

A

Facial pain, headache, postnasal drainage, and purulent nasal drainage. Headache, fever, tooth pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

How is sinusitis diagnosed?,

A

If imaging is required because of concern of complications, a CT scan is the best test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What is the treatment for sinusitis?,

A

High–dose amoxicillin. Amoxicillin–clavulanate if recent amoxicillin use or if no response amoxicillin. Alternatives: cefuroxime, loracarbef, cefprozil, cefdinir, cefixime.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What is the treatment of sinusitis in patients with severe penicillin allergies?,

A

Patients with severe penicillin allergies should receive azithromycin or clarithromycin. Levofloxacin, moxifloxacin, or gatifloxacin are acceptable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What are the causes of pharyngitis?,

A

Usually viruses; group A beta–hemolytic streptococci (S. pyogenes) may cause rheumatic fever or glomerulonephritis. S. pyogenes causes 15–20% of cases of pharyngitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What is the presentation of pharyngitis?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

How is pharyngitis diagnosed?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What is the treatment for pharyngitis?,

A

Penicillin or amoxicillin. Azithromycin, clarithromycin, and oral, second–generation cephalosporins are alternatives in penicillin–allergic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What is influenza?,

A

A systemic viral illness from influenza A or B, usually occurring in an epidemic pattern, leading to sinusitis, otitis media, bronchitis, and pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What is the presentation of influenza?,

A

Fever, myalgias, headache, and fatigue. Upper respiratory symptoms predominate. Coryza, nonproductive cough, sore throat, and conjunctival injection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

How is influenza diagnosed?,

A

Rapid antigen detection methods of swabs or washings of nasopharyngeal secretions. Viral culture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is the treatment for influenza?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What are the indications for influenza vaccinations?,

A

>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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

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?,

A

Bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What are the causes of bronchitis?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What is the treatment for acute exacerbations of chronic bronchitis?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

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?,

A

Lung abscess.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What is a lung abscess?,

A

Necrosis of the pulmonary parenchyma caused by microbial infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is the bacteriology of lung abscesses?,

A

90% anaerobes. Peptostreptococcus, Prevotella, and Fusobacterium species (oral anaerobes). Aerobic bacteria, most frequently are S. aureus, E. coli, Klebsiella, and Pseudomonas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What conditions predispose to lung abscess?,

A

Association with periodontal disease or aspiration (e.g., altered sensorium, seizures).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What is the presentation of lung abscess?,

A

Fever, cough, chest pain; putrid, foul–smelling sputum in 60–70%; chronic course with weight loss and fatigue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

How is lung abscess diagnosed?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What is the treatment of lung abscess?,

A

Clindamycin has good empiric coverage for the above the diaphragm anaerobes. Penicillin is also acceptable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What conditions predispose to pneumonia?,

A

Cigarette smoking, diabetes, alcoholism, malnutrition, obstruction from tumors, and immunosuppression. Neutropenia and steroid use predispose to Aspergillus infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What is the most common cause of community–acquired pneumonia in all groups?,

A

S. pneumoniae (viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What conditions predispose to Haemophilus influenzae pneumonia?,

A

Smokers, COPD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What factors are associated with Mycoplasma pneumonia?,

A

Young, otherwise healthy patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What conditions predispose to Legionella?,

A

Epidemic infection in older smokers, particularly when located near infected water sources, such as air–conditioning systems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What conditions predispose to Pneumocystis jiroveci pneumonia?,

A

HIV–positive persons with

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What conditions predispose to Coxiella burnetii (Q–fever) pneumonia?,

A

Exposure to animals, particularly at the time the animals are giving birth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What condition predisposes to Klebsiella pneumonia?,

A

Alcoholics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What condition predisposes to Staphylococcus aureus pneumonia?,

A

Occurs after viral syndromes or viral bronchitis, especially influenza

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What condition predisposes to Coccidioidomycosis pneumonia?,

A

Exposure to the deserts of the American Southwest, particularly Arizona

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What conditions predispose to Chlamydia psittaci pneumonia?,

A

Bird exposure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What conditions predispose to Histoplasma capsulatum pneumonia?,

A

Exposure to bat or bird droppings, spelunking (recreational cave exploration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

What are the clinical signs of Bordetella pertussis pneumonia?,

A

Cough with whoop and post–tussive vomiting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What conditions predispose to Francisella tularensis pneumonia?,

A

Hunters or exposure to rabbits, bioterrorism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What activity predisposes to severe acute respiratory syndrome (SARS, Avian influenza pneumonia)?,

A

Travel to southeast Asia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Which bacteria may be utilized in bioterrorism?,

A

Bacillus anthracis, Yersinia pestis, and Francisella tularensis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What is the clinical presentation of pneumonia?,

A

Cough, fever, sputum, dyspnea. Bacterial infections (pneumoniae, Haemophilus, Klebsiella) have purulent sputum. S. pneumoniae causes rusty hemoptysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What are the characteristics of the sputum in Klebsiella pneumonia?,

A

Klebsiella pneumoniae sputum is like currant jelly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What are the characteristics of pneumonia caused by Pneumocystis jiroveci, viruses, Mycoplasma, and Legionella?,

A

Interstitial infections are caused by Pneumocystis jiroveci pneumonia, viruses, Mycoplasma, and Legionella; often cause nonproductive or dry cough.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What type of pain is associated with pneumococcal pneumonia?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What are the physical signs of pneumonia?,

A

Rales, rhonchi, lung consolidation, dullness to percussion, bronchial breath sounds, increased vocal fremitus, egophony. Severe pneumonia leads to hypoxia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What is the presentation of Mycoplasma pneumonia?,

A

Dry cough and chest soreness. Bullous myringitis; anemia from hemolysis from cold agglutinins. Rarely need to be admitted to the hospital.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What is the presentation of Legionella pneumonia?,

A

Confusion, headache, and lethargy. Diarrhea and abdominal pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What is the presentation of Pneumocystis jiroveci pneumonia?,

A

Marked dyspnea, particularly on exertion, with chest soreness with cough in an HIV–positive person with a CD4 count of

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

Which types of pneumonia are associated with interstitial infiltrates?,

A

Interstitial infiltrates are associated with PJP, viral, Mycoplasma, Chlamydia, Coxiella, and Legionella pneumoniae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

What is the most specific test for lobar pneumonia?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

What is the best diagnostic method for Mycoplasma pneumonia?,

A

Specific serologic antibody titers. Cold agglutinins have limited specificity and sensitivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What are the diagnostic methods for Legionella pneumonia?,

A

Charcoal yeast extract media, urine antigen tests, direct fluorescent antibodies, and antibody titers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

What is the best diagnostic method for Pneumocystis jiroveci pneumonia?,

A

Bronchoalveolar lavage; increased LDH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

What is the best diagnostic method for Chlamydia pneumoniae, Coxiella, Coccidioidomycosis, and Chlamydia psittaci?,

A

Specific antibody titers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

What are the signs of severe pneumonia?,

A

pO2 30, disorientation, uremia, systolic BP 125), hyponatremia, dehydration, elevated BUN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

Which pneumonia patients should be hospitalized?,

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

What is the empiric therapy for outpatient pneumonia?,

A

Macrolide, azithromycin or clarithromycin. Levofloxacin, moxifloxacin, gatifloxacin are alternatives. Cephalosporins and amoxicillin/clavulanate do not cover atypical pathogens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

What is the treatment for hospitalized patients with community–acquired pneumonia?,

A

Levofloxacin, moxifloxacin, or gatifloxacin or cefotaxime or ceftriaxone combined with a macrolide such as azithromycin or clarithromycin (or doxycycline).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

What organisms cause hospital–acquired pneumonia?,

A

Drug–resistant, Gram–negative bacilli (Pseudomonas, Klebsiella, E. coli), or gram–positives, including methicillin–resistant Staphylococcus aureus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

What is the treatment of hospital–acquired pneumonia?,

A

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
Q

What is the specific coverage for Haemophilus influenzae?,

A

Second– or third–generation cephalosporin.

203
Q

What is the specific coverage for Mycoplasma pneumoniae?,

A

Macrolide, doxycycline, or a quinolone.

204
Q

What is the specific coverage for Legionella?,

A

Macrolide, doxycycline, or a quinolone

205
Q

What is the specific coverage for pneumocystis jiroveci pneumonia?,

A

Trimethoprim/sulfamethoxazole. Steroids should be used if arterial pO2

206
Q

What is the specific coverage for Coxiella burnetii (Q–fever)?,

A

Doxycycline (or erythromycin)

207
Q

What is the specific coverage for klebsiella?,

A

Third–generation cephalosporin.

208
Q

What is the specific coverage for staphylococcus aureus?,

A

Semisynthetic penicillin (nafcillin) if methicillin sensitive. In the nosocomial setting, isolates are methicillin–resistant, and vancomycin or linezolid is used.

209
Q

What is the specific coverage for coccidioidomycosis?,

A

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
Q

Which patients should receive pneumococcal vaccine?,

A

>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
Q

What is bacillus Calmette–Guerin?,

A

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
Q

Which persons are at risk for tuberculosis infection?,

A

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
Q

What is the clinical presentation of tuberculosis?,

A

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
Q

What sites may be affected by extrapulmonary tuberculosis?,

A

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
Q

How is tuberculosis diagnosed?,

A

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
Q

What is the treatment of tuberculosis?,

A

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
Q

What is the length of treatment of tuberculosis meningitis?,

A

12 mths. TB in pregnancy is treated for 9 mths. HIV– positive treated for 6–9 months.

218
Q

What drug should be taken with isoniazid?,

A

INH use should generally be combined with vitamin B6 (pyridoxine) to prevent peripheral neuropathy.

219
Q

Which antituberculosis drugs are contraindicated in pregnancy?,

A

Pregnant patients should not receive PZA or streptomycin.

220
Q

When are steroids used in tuberculosis?,

A

Steroids are used for TB meningitis and TB pericarditis.

221
Q

What are the side effects of antituberculosis medications?,

A

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
Q

What are the adverse effects of ethambutol?,

A

Ethambutol is associated with optic neuritis, color blindness and other visual disturbances. PZA can cause a benign hyperuricemia, which does not require treatment.

223
Q

What is the PPD test?,

A

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
Q

What is the physical indication of a positive PPD?,

A

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
Q

What is two–stage PPD testing?,

A

Those in whom there has not been a recent PPD test and now show some reactivity that is

226
Q

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?,

A

>5 mm

227
Q

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?,

A

>10 mm

228
Q

What is the criteria for a positive PPD in low risk populations?,

A

>15 mm

229
Q

What is the management of a positive PPD?,

A

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
Q

What is the treatment for patients with positive PPD and no evidence of active disease (negative chest x–ray)?,

A

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
Q

What is the cause of most infectious diarrhea?,

A

Contaminated food and water. Bacillus cereus and Staphylococcus aureus, food poisoning present predominantly with vomiting. Food poisoning is most commonly Campylobacter.

232
Q

What type of diarrhea is associated with poultry and eggs?,

A

Salmonella is most commonly associated with contaminated poultry and eggs.

233
Q

What is the most common cause of travelers’ diarrhea?,

A

E. coli is the most common cause of travelers’ diarrhea. E. coli 0157:H7 is associated with eating undercooked hamburger meat.

234
Q

What organism is associated with fried rice?,

A

Bacillus cereus is associated with fried rice.

235
Q

What types of diarrhea are associated with water from streams?,

A

Giardia lamblia and cryptosporidiosis are acquired from contaminated water from streams.

236
Q

What type of diarrhea is associated with AIDS?,

A

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
Q

What type of diarrhea is associated with shellfish?,

A

Vibrio parahaemolyticus is associated with contaminated shellfish.

238
Q

What is the most common cause of diarrhea in children?,

A

Viral infections such as with rotavirus or Norwalk agents are associated with outbreaks in children.

239
Q

What type of diarrhea is associated with previous antibiotic use?,

A

Clostridia difficile is associated with previous antibiotic use.

240
Q

What type of food is associated with clostridia botulinum?,

A

Clostridia botulinum is associated with ingestion of infected canned foods, and Clostridia perfringens is associated with meats that have been contaminated with spores.

241
Q

What organisms are associated with blood in the stool?,

A

Blood in the stool is most commonly associated with invasive enteric pathogens, such as Salmonella, Shigella, Yersinia, invasive E. coli, and Campylobacter.

242
Q

What type of diarrhea is associated with Guillain–Barre syndrome?,

A

Campylobacter is rarely associated with Guillain–Barre syndrome.

243
Q

What are the symptoms of ciguatera toxin poisoning?,

A

Ingestion of barracuda, red snapper, grouper within 2 h; paresthesias, numbness, nausea, vomiting, cramps; weakness, reversal of hot–cold, hypotension.

244
Q

What is the treatment for ciguatera toxin poisoning?,

A

No therapy.

245
Q

Which infectious agents are associated with hemolytic uremic syndrome?,

A

E. coli 0157:H7 and Shigella are associated with hemolytic uremic syndrome.

246
Q

What is the presentation of staphylococcal food poisoning?,

A

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
Q

What is the characteristic of viral diarrhea?,

A

Viruses can cause voluminous watery diarrhea but do not result in bloody diarrhea.

248
Q

What type of diarrhea occurs after ingestion of tuna, mackerel, or mahi mahi?,

A

Scombroid poisoning from histamine in flesh. Minutes: rash, diarrhea, vomiting, wheezing, burning in mouth, dizziness, paresthesias.

249
Q

How is infectious diarrhea diagnosed?,

A

Test the stool for white blood cells with methylene blue testing. WBCs indicate an invasive pathogen. Culture is necessary to determine specific type.

250
Q

Which test is used to detect Giardia and Cryptosporidium?,

A

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
Q

What is the treatment of infectious diarrhea?,

A

More severe infections with high fever, abdominal pain, tachycardia and hypotension, require intravenous fluids and oral ciprofloxacin.

252
Q

What are the causes of viral hepatitis?,

A

Viral hepatitis is an infection of the liver caused by hepatitis A, B, C, D, or E.

253
Q

What are the symptoms of hepatitis A?,

A

Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice.

254
Q

What are the symptoms of hepatitis B?,

A

Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice, 10–20% with serum sickness–like (joint pain, rash).

255
Q

What are the symptoms of hepatitis C?,

A

Only 20% are acutely symptomatic with fever, malaise, headache, jaundice.

256
Q

What are the symptoms of hepatitis D?,

A

Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice

257
Q

What are the symptoms of hepatitis E?,

A

Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice

258
Q

What types of hepatitis have a carrier state?,

A

Hepatitis B, C, D. There is no carrier state for hepatitis A or hepatitis E.

259
Q

What is the serology of hepatitis A?,

A

Anti–HAV, IgM fraction, IgG fraction.

260
Q

What is the serology of hepatitis B?,

A

HBsAg, HBsAb, HBeAg, anti–HBs, anti–HBc, anti–HBe

261
Q

What is the serology of hepatitis C?,

A

Antibody to hepatitis C, PCR–RNA

262
Q

What is the serology of hepatitis D?,

A

Anti–delta, IgM fraction, IgG fraction

263
Q

What is the serology of hepatitis E?,

A

Anti–Hep E IgM, IgG

264
Q

What is the mode of transmission of hepatitis A and E?,

A

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
Q

What is the mode of transmission of hepatitis B, C and D?,

A

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
Q

What is the most common disease leading to the need for liver transplantation?,

A

Hepatitis C. All forms of hepatitis can occasionally present with fulminant hepatic necrosis and acute liver failure.

267
Q

What is the presentation of acute hepatitis?,

A

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
Q

How is acute hepatitis diagnosed?,

A

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
Q

What is the significance of a positive IgM antibody in the diagnosis of hepatitis?,

A

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
Q

What is the first hepatitis B marker to elevate?,

A

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
Q

What is the significance of the hepatitis B e antigen?,

A

The e antigen indicates high levels of viral replication and increased infectivity.

272
Q

What laboratory findings indicate resolution of hepatitis B?,

A

Resolution of the infection is definitively indicated by the loss of surface antigen activity and the development of hepatitis B surface antibody.

273
Q

What is the significance of the hepatitis B core IgG antibody?,

A

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
Q

What is the treatment for chronic hepatitis B?,

A

Interferon, entecavir, adefovir, or lamivudine.

275
Q

What is the treatment of chronic hepatitis C?,

A

Chronic hepatitis C is treated with interferon combined with ribavirin. The only therapy for cirrhosis is liver transplantation.

276
Q

What is the postexposure prophylaxis after hepatitis B needlestick?,

A

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
Q

What is the postexposure prophylaxis for hepatitis C?,

A

There is no effective postexposure prophylaxis to hepatitis C, and there is no vaccine?

278
Q

What are the indications for hepatitis B vaccine?,

A

All healthcare workers, IV drug users, and others at risk should be vaccinated. Newborn children are vaccinated.

279
Q

What are the causes of urethritis?,

A

Neisseria gonorrhoeae or nongonococcal urethritis is caused by either Chlamydia trachomatis (50%), Ureaplasma urealyticum (20%), Mycoplasma hominis (5%), Trichomonas (1%), or herpes simplex.

280
Q

What are the clinical signs of urethritis?,

A

Purulent urethral discharge; dysuria, urgency, and frequency in urination

281
Q

How is urethritis diagnosed?,

A

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
Q

What is the treatment of urethritis?,

A

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
Q

What is pelvic inflammatory disease?,

A

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
Q

What are the clinical signs of pelvic inflammatory disease?,

A

Pelvic pain on palpation of the cervix, uterus, or adnexa; fever, and leukocytosis. Cervical motion tenderness. Discharge from the cervix.

285
Q

How is pelvic inflammatory disease diagnosed?,

A

Cervical culture on Thayer–Martin for gonococcus. Laparoscopy. A pregnancy test should be done.

286
Q

What is the therapy for pelvic inflammatory disease?,

A

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
Q

What are the sequelae of pelvic inflammatory disease?,

A

Infertility and ectopic pregnancy.

288
Q

A 22–year–old man with painless, ulcerated genital lesion, adenopathy. What is the next step?,

A

Dark–field microscopy for syphilis, VDRL.

289
Q

What are the clinical signs of primary syphilis?,

A

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
Q

What are the signs of secondary syphilis?,

A

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
Q

What are the signs of latent syphilis?,

A

Asymptomatic; persist for life, and one–third develop late or tertiary syphilis.

292
Q

What are the signs of late or tertiary syphilis?,

A

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
Q

What is the Argyll Robertson pupil?,

A

Small irregular pupil that accommodates but does not react to light.

294
Q

What are the signs of tabes dorsalis?,

A

Tabes dorsalis (locomotor ataxia) is pain, ataxia, sensory changes, and loss of tendon reflexes.

295
Q

How is syphilis diagnosed?,

A

Screening tests are VDRL and RPR; specific tests are FTA–ABS, MHA–TP, and Darkfield exam of chancre.

296
Q

What are the causes of a false positive VDRL?,

A

False positives VDRL occurs with EBV, collagen vascular disease, TB, subacute bacterial endocarditis.

297
Q

What is the Jarisch–Herxheimer reaction?,

A

Malaise, fever, headache, sweating rigors, and temporary exacerbations of the syphilitic lesions 6–12 hours after initial treatment.

298
Q

What is the treatment of primary, secondary, and latent syphilis?,

A

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
Q

What is the treatment for tertiary syphilis?,

A

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
Q

What is chancroid?,

A

Acute, localized, contagious disease of painful genital ulcers and suppuration of the inguinal lymph nodes caused by Haemophilus ducreyi (Gram negative bacillus)

301
Q

What are the clinical signs of chancroid?,

A

Small, soft, painful papules that become shallow ulcers with ragged edges. Inguinal lymph nodes become very tender and enlarged.

302
Q

How is chancroid diagnosed?,

A

Gram stain shows Gram–negative bacillus, culture; PCR testing.

303
Q

What is the treatment of chancroid?,

A

Azithromycin single dose or ceftriaxone intramuscularly (single dose). Erythromycin for 7 days or Cipro for 3 days are alternatives.

304
Q

What is lymphogranuloma venereum?,

A

Contagious, sexually transmitted disease with primary lesion followed by suppurative lymphangitis caused by chlamydia trachomatis.

305
Q

What are the clinical signs of lymphogranuloma venereum?,

A

Small, transient, nonindurated, ulcerates, heals; tender, unilateral enlargement inguinal nodes; multiple draining sinuses (buboes); scar, sinuses; fever, malaise, joint pains, headaches.

306
Q

How is lymphogranuloma venereum diagnosed?,

A

Complement fixing antibodies; isolate chlamydia from pus in buboes

307
Q

What is the treatment of lymphogranuloma venereum?,

A

Doxycycline or erythromycin.

308
Q

What is granuloma inguinale?,

A

Chronic granulomatous condition, spread by sexual contact; caused by Donovania granulomatis, Calymmatobacterium granulomatis

309
Q

What are the clinical signs of granuloma inguinale?,

A

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
Q

How is granuloma inguinale diagnosed?,

A

Giemsa or Wright stain (Donovan bodies) or smear of lesion; punch biopsy. Treatment with doxycycline ceftriaxone, TMP/SMZ, or erythromycin.

311
Q

What virus causes genital herpes?,

A

Herpes virus, type II; type I can be seen in genital herpes.

312
Q

What are the clinical signs of genital herpes?,

A

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
Q

How is genital herpes diagnosed?,

A

Tzanck test and viral culture.

314
Q

What is the treatment of genital herpes?,

A

Acyclovir, famciclovir, or valacyclovir. Herpes may recur; sexual contacts should be examined. Acyclovir–resistant herpes is treated with foscarnet.

315
Q

What are genital warts?,

A

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
Q

What is the treatment of genital warts?,

A

Destruction (curettage, trichloroacetic acid), cryotherapy, podophyllin, imiquimod for 14 weeks (an immune stimulant), laser.

317
Q

What conditions predispose to cystitis?,

A

Predisposed by tumors, stones, strictures, prostatic hypertrophy, neurogenic bladder. Sexual intercourse in women. Catheters.

318
Q

What is the etiology of cystitis?,

A

E. coli in >80%; second are other coliforms (Gram–negative bacilli) such as Proteus, Klebsiella, Enterobacter; enterococci occasionally; Staph saprophyticus in young women.

319
Q

What are the symptoms of cystitis?,

A

Dysuria, frequency, urgency, and suprapubic pain. Hematuria, low–grade fever; foul–smelling and cloudy urine. Suprapubic tenderness without flank tenderness.

320
Q

How is cystitis diagnosed?,

A

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
Q

What is the treatment of cystitis?,

A

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
Q

What are the predisposing factors for pyelonephritis?,

A

Strictures, tumors, calculi, prostatic hypertrophy, or neurogenic bladder, vesicoureteral reflux; more common in women, childhood, pregnancy, after urethral catheterization or instrumentation

323
Q

What are the clinical signs of pyelonephritis?,

A

Chills, fever, flank pain, nausea, vomiting, costovertebral angle tenderness, increased frequency in urination, and dysuria.

324
Q

How is pyelonephritis diagnosed?,

A

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
Q

What is the treatment of pyelonephritis?,

A

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
Q

What is the bacteriology of pyelonephritis?,

A

E. coli is the most common pathogen, others include: Klebsiella, Proteus, and Enterococcus. Immunosuppressed and indwelling catheters are more prone to Candida.

327
Q

What is perinephric abscess?,

A

Infected material surrounding kidney and within the Gerota fascia; from pyelonephritis. Stones in 20–60%. Other structural abnormalities, recent surgery, trauma, diabetes.

328
Q

What is the microbiology of perinephritic abscess?,

A

E. coli most common, then Klebsiella, Proteus; Staph aureus sometimes accounts for hematogenous cases.

329
Q

How is perinephritic abscess diagnosed?,

A

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
Q

What is the treatment of perinephric abscess?,

A

Third–generation cephalosporins, antipseudomonal penicillin, or ticarcillin/clavulanate with an aminoglycoside percutaneous drainage

331
Q

What is impetigo?,

A

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
Q

What are the clinical signs of impetigo?,

A

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
Q

What is the treatment of impetigo?,

A

Oral first–generation cephalosporin or semisynthetic penicillin (oxacillin, cloxacillin, dicloxacillin). Topical mupirocin or bacitracin. Penicillin–allergic: clarithromycin or azithromycin.

334
Q

What is erysipelas?,

A

Superficial cellulitis caused by group A beta–hemolytic Streptococcus.

335
Q

What are the clinical signs of erysipelas?,

A

Bilateral, shiny, red, indurated, edematous, tender lesions on the face, arms, and legs. Lesions are sharply demarcated.

336
Q

What is the treatment of erysipelas?,

A

Semisynthetic penicillin or first–generation cephalosporin; penicillin.

337
Q

What are dermatophyte infections?,

A

Superficial infection caused by a dermatophyte fungus that invades outer layer of skin nails, hair, stratum corneum; caused by microsporum, Trichophyton, and Epidermophyton

338
Q

How are dermatophyte infections diagnosed?,

A

Potassium hydroxide (10%) prep; culture.

339
Q

What are the signs of tinea corporis?,

A

Papulosquamous annular lesions of the body with a raised border, which expands peripherally and clear centrally.

340
Q

What are the signs of tinea pedis?,

A

Macerated and scaling borders (third and fourth interdigital space) of the foot.

341
Q

What are the signs of tinea unguium?,

A

Thickened and lusterless nails.

342
Q

What are the signs of tinea capitis?,

A

Small, scaly, semi–bald, grayish patches with broken lusterless hair on head

343
Q

What are the signs of tinea cruris?,

A

Ringed lesion that extends from the crural folds over the adjacent inner thigh

344
Q

What are the signs of tinea barbae?,

A

Inflammatory, deep plaques and noninflammatory patches on the bearded area of the face.

345
Q

What is the treatment for dermatophyte infections?,

A

Terbinafine or itraconazole orally for capitis, corporis, and unguium. Miconazole, clotrimazole and ketoconazole in cream or lotion for mild cruris, pedis, and corporis.

346
Q

What is candidiasis?,

A

Infection of skin, mucous membranes by Candida albicans. Immunodeficiency antibacterial therapy, obesity, diabetes, corticosteroid, antimetabolite, pregnancy, debilitate, blood dyscrasias, HIV.

347
Q

What are the clinical signs of candidiasis?,

A

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
Q

What are the signs of candida vulvovaginitis?,

A

White discharge with inflammation of the vaginal and vulva. Pregnancy and diabetes mellitus.

349
Q

What are the signs of oral candidiasis (thrush)?,

A

White patches of exudates on tongue or buccal mucosa.

350
Q

What is candidal paronychia?,

A

Painful red swelling around the nail.

351
Q

How is candidiasis diagnosed?,

A

Potassium hydroxide exam. Culture is definitive.

352
Q

What is the treatment of candidiasis?,

A

Topical nystatin, clotrimazole, miconazole, ciclopirox, econazole, terconazole. Amphotericin for invasive infection. Fluconazole for less serious infections and paronychia.

353
Q

What is tinea versicolor?,

A

Multiple macules (usually asymptomatic), varying in color from white to brown caused by Pityrosporum orbiculare (Malassezia furfur)

354
Q

What are the clinical signs of tinea versicolor?,

A

Tan, brown, white, scaling macular lesions that tend to coalesce; found on chest, neck, abdomen, or face. Lesions do not tan.

355
Q

How is tinea versicolor diagnosed?,

A

Skin scrapings with 10% KOH. spaghetti and meatballs, appearance of hyphae and spores.

356
Q

What is the treatment of tinea versicolor??,

A

Topical selenium sulfide, clotrimazole, ketoconazole, or oral itraconazole.

357
Q

What are the signs of scabies?,

A

Skin infection with superficial burrows, intense pruritus, and secondary infections, caused by Sarcoptes scabiei; skin–to–skin transmission.

358
Q

What are the clinical signs of scabies?,

A

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
Q

How is scabies diagnosed?,

A

Parasite in scrapings in mineral oil.

360
Q

What is the treatment of scabies?,

A

Permethrin, lindane (Kwell). Ivermectin oral therapy if the disease is extensive. Lindane in contraindicated in pregnancy.

361
Q

What is pediculosis?,

A

Skin infestation caused by lice. Itching, excoriations, erythematous macules and papules; secondary bacterial infection

362
Q

How is pediculosis diagnosed?,

A

Examination of the pubic area, axillae, scalp, and other hair–bearing surfaces for the louse or nits.

363
Q

What is the treatment for pediculosis?,

A

Permethrin or lindane (Kwell).

364
Q

What is molluscum contagiosum?,

A

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
Q

What is the treatment of molluscum contagiosum?,

A

Freezing, curettage, electrocautery, or cantharidin.

366
Q

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?,

A

Osteomyelitis

367
Q

What is acute hematogenous osteomyelitis?,

A

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
Q

What is the most common organism in osteomyelitis that is caused by spread of a contiguous infection?,

A

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
Q

What is vascular insufficiency osteomyelitis?,

A

Majority over 50, with diabetes or peripheral vascular disease. Bones of the lower extremities. Polymicrobial, but most common organism is S. aureus.

370
Q

What is the presentation of osteomyelitis?,

A

Pain, erythema, swelling, and tenderness. Nearby ulceration or wound. Draining sinus tract.

371
Q

How is osteomyelitis diagnosed?,

A

Technetium bone scan and MRI. Plain x–ray: Periosteal elevation. Bone biopsy and culture is the best test.

372
Q

What is the treatment of osteomyelitis?,

A

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
Q

70–year–old woman with a swollen right knee; effusion and decreased mobility. Redness and tenderness. What is the next step?,

A

Arthrocentesis.

374
Q

What are the causes of septic arthritis?,

A

Neisseria gonorrhoeae, staphylococci or streptococci; Rickettsia, viruses, spirochetes. Bacterial arthritis is divided into gonococcal and nongonococcal types?

375
Q

What is the pathogenesis of gonococcal septic arthritis?,

A

Sexual activity is risk factor for gonococcal septic arthritis. 1–5% of people with gonorrhea will develop disseminated disease.

376
Q

What is the pathogenesis of nongonococcal bacterial arthritis?,

A

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
Q

What is the microbiology of nongonococcal arthritis?,

A

Gram–positive (>85); (S. aureus [60%], Streptococcus [15%], Pneumococcus [5%]), Gram–negative (10–15%), polymicrobial (5%).

378
Q

What is the presentation of nongonococcal septic arthritis?,

A

Monoarticular in >85%, with a swollen, tender, erythematous joint with decreased range of motion. Knee most common. Petechiae or purpura?

379
Q

How is nongonococcal septic arthritis diagnosed?,

A

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
Q

How is gonococcal septic arthritis diagnosed?,

A

Only 50% of aspirates have positive culture. Less than 10% of blood cultures are positive. Cervix, pharynx, rectum, and urethra may be positive.

381
Q

What is the treatment for nongonococcal septic arthritis?,

A

Good empiric coverage is nafcillin or oxacillin (or vancomycin if MRSA is suspected) combined with an aminoglycoside or a third–generation cephalosporin.

382
Q

What is the treatment for gonococcal septic arthritis?,

A

Ceftriaxone is the drug of choice.

383
Q

What is gas gangrene (clostridial myonecrosis)?,

A

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
Q

What are the signs and symptoms of clostridial myonecrosis?,

A
385
Q

How is clostridial myonecrosis diagnosed?,

A

Gram–positive rods, but no white cells. Culture positive for C. perfringens.

386
Q

What is the treatment for clostridial myonecrosis?,

A

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
Q

What is the next step?,

A

Blood cultures for infective endocarditis.

388
Q

Which heart valves are most frequently affected by endocarditis?,

A

Left–sided lesions of the aortic and mitral valves are the most common.

389
Q

What procedures are associated with infective endocarditis?,

A

Invasive and dental procedures. Oral and upper respiratory tract surgery. GI procedures. GU surgery. Alimentation catheters. Pressure–monitoring catheters. IV drug use.

390
Q

What is the most common cause of acute infective endocarditis?,

A

S. aureus is the most common cause. Seed previously normal valves. IV drug use is the major risk factor.

391
Q

What are the signs of acute infective endocarditis?,

A

Rapid onset of fever and sepsis. Splenomegaly of invasion of myocardium and rapid valve destruction. Embolic complications.

392
Q

What is the most common cause of subacute infective endocarditis?,

A

4–5% have negative blood cultures. Viridans group streptococci is the most common organism; low virulence. Seed abnormal valves.

393
Q

Which cardiac conditions are risk factors for infective endocarditis?,

A

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
Q

What are the clinical signs of subacute infective endocarditis?,

A

Slow onset with vague symptoms of malaise, low–grade fever, weight loss; and survival 80–90% with treatment.

395
Q

What are the complications of infective endocarditis?,

A

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
Q

How is infective endocarditis diagnosed?,

A

Positive blood cultures; transesophageal echo is >90% sensitive.

397
Q

What is the treatment of infective endocarditis?,

A

Empiric therapy with antistaphylococcal drug (nafcillin), and streptococcal drug (ampicillin and gentamicin). Vancomycin and gentamicin are empiric treatment if MRSA suspected.

398
Q

What is the prophylactic treatment of bacterial endocarditis?,

A

Dental procedures: Amoxicillin. For penicillin–allergic patients: clindamycin or (azithromycin, or clarithromycin or cephalexin). Urinary or gastrointestinal procedures: no prophylaxis is required.

399
Q

What cardiac conditions require prophylactic antibiotics?,

A

Prosthetic cardiac valves. Previous bacterial endocarditis, even in the absence of heart disease. Congenital cardiac malformations.

400
Q

What cardiac conditions do not require prophylactic therapy?,

A

Rheumatic and other acquired valvular disease. Hypertrophic cardiomyopathy; mitral valve prolapse with valvular regurgitation; surgically repaired shunts or intracardiac defects.

401
Q

What are the causes of pericarditis?,

A

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
Q

What is the clinical presentation of pericarditis?,

A

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
Q

What is pulsus paradoxus?,

A

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
Q

What are the ECG signs of pericarditis?,

A

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
Q

What is the treatment for viral pericarditis?,

A

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
Q

What is myocarditis?,

A

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
Q

What are the signs of myocarditis?,

A

Myocardial dysfunction, dyspnea and fatigue. Asymptomatic, subclinical infection or a rapid progression to chest pain, arrhythmia, and death. S–3 gallop and murmurs.

408
Q

How is myocarditis diagnosed?,

A

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
Q

What is the vector for Lyme disease?,

A

Lyme disease is spread by the bite of the Ixodes scapularis tick.

410
Q

What is the clinical presentation of lyme disease?,

A

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
Q

What are the neurologic symptoms of lyme disease?,

A

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
Q

What are the cardiovascular signs of lyme disease?,

A

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
Q

What is the diagnostic criteria of Lyme disease?,

A

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
Q

What is the treatment of Lyme disease?,

A

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
Q

Which cell is the primary target of HIV?,

A

The primary mechanism of HIV is to infect a subset of T lymphocytes called CD4 cells, often just referred to as T cells.

416
Q

What are the symptoms of pneumocystis jiroveci pneumonia?,

A

CD4 count

417
Q

What is the diagnostic test for PJP?,

A

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
Q

What is the treatment of pneumocystis jiroveci pneumonia?,

A

Trimethoprim–sulfamethoxazole (TMP–SMZ) IV is the first–line therapy for mild–severe disease and may cause a rash.

419
Q

What is the alternative treatments for PJP if TMP–SMZ is not tolerated?,

A

For mild–moderate disease: dapsone and trimethoprim, or primaquine and clindamycin; or atovaquone, or trimetrexate (with leucovorin).

420
Q

What are the adverse effects of pentamidine?,

A

Pancreatitis, hyperglycemia, hypoglycemia.

421
Q

What are the indications for steroids in PJP?,

A

Steroids are used as adjunctive therapy for any patient with severe pneumonia. Severe is defined with a PaO2 of 35 mm Hg.

422
Q

How is cytomegalovirus diagnosed?,

A

Funduscopy; colonoscopy with biopsy for diarrhea; or upper gastrointestinal endoscopy with biopsy of ulcers.

423
Q

What is the treatment of cytomegalovirus retinitis and esophagitis?,

A

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
Q

What are the side effects of ganciclovir?,

A

Ganciclovir may cause neutropenia.

425
Q

What is the prophylactic therapy for cytomegalovirus retinitis?,

A

Valganciclovir can be used for maintenance therapy.

426
Q

What is Mycobacterium avium complex?,

A

Occurs in HIV infected with CD4

427
Q

What is the testing for Mycobacterium avium complex?,

A

Blood culture, culture of bone marrow, liver, or other body tissue or fluid.

428
Q

What is the treatment of Mycobacterium avium complex?,

A

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
Q

At what level of CD4 cell count does toxoplasmosis occur?,

A

Occurs in HIV infected patients with CD4

430
Q

What are the signs of cerebral toxoplasmosis?,

A

Brain mass lesion: Headache, confusion, seizures, and focal neurologic deficits

431
Q

What tests are used to detect toxoplasmosis?,

A

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
Q

What is the treatment of toxoplasmosis?,

A

Pyrimethamine and sulfadiazine. Clindamycin can be substituted for sulfadiazine. Leucovorin prevents marrow suppression. Prophylaxis with TMP/SMZ or dapsone/pyrimethamine.

433
Q

What is cryptococcosis?,

A

Occurs in HIV infected persons with CD4

434
Q

How is cryptococcosis diagnosed?,

A

Lumbar puncture with India ink and cryptococcal antigen testing. Serum cryptococcal antigen testing.

435
Q

What is the treatment of cryptococcosis?,

A

Amphotericin intravenously for 10–14 days (with flucytosine), followed by fluconazole orally for suppressive therapy.

436
Q

What is the normal CD4 cell count?,

A

700–1,500/mcL.

437
Q

What CD4 cell count is associated with oral thrush, Kaposi sarcoma, tuberculosis, zoster, lymphoma?,

A

200–500/mcL

438
Q

What CD4 cell count is associated with pneumocystis jiroveci pneumonia, dementia, progressive multifocal leukoencephalopathy, disseminated histoplasmosis and coccidiomycosis?,

A

100–200/mcL

439
Q

What opportunistic infections occur when the CD4 count is

A

Toxoplasmosis, Cryptococcus, cryptosporidiosis, disseminated herpes simplex

440
Q

What opportunistic infections occur when the CD4 count is

A

Cytomegalovirus, Mycobacterium avium complex. Progressive, multifocal leukoencephalopathy, CNS lymphoma.

441
Q

What test indicates an adequate response to antiretroviral therapy in HIV–infected persons?,

A

The goal is complete suppression of viremia with

442
Q

What are the indications for viral sensitivity testing?,

A

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
Q

What are the side effects of zidovudine?,

A

Leukopenia, anemia, gastrointestinal

444
Q

What are the side effects of didanosine (DDI)?,

A

Pancreatitis, peripheral neuropathy.

445
Q

What are the side effects of stavudine (D4T)?,

A

Peripheral neuropathy

446
Q

What are the side effects of lamivudine (3TC)?,

A

No side effects have been reported in additional to placebo.

447
Q

What are the side effects of emtricitabine?,

A

Structurally related to lamivudine; few side effects.

448
Q

What is the structure of tenofovir?,

A

Tenofovir is a nucleotide analog as compared to the others that are nucleoside analogs.

449
Q

What are the side effects of abacavir?,

A

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
Q

What are the side effects of zalcitabine (DDC)?,

A

Pancreatitis, peripheral neuropathy, lactic acidosis

451
Q

What are the nucleoside reverse transcriptase inhibitors?,

A

Zidovudine (ZDV or AZT), didanosine (DDI), stavudine (D4T), lamivudine (3TC), emtricitabine, abacavir, zalcitabine (DDC).

452
Q

What are the side effects of protease inhibitors?,

A

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
Q

What are the side effects of nelfinavir?,

A

Nausea, diarrhea.

454
Q

What are the side effects of indinavir?,

A

Nephrolithiasis (4%), hyperbilirubinemia (10%).

455
Q

What are the side effects of ritonavir?,

A

Severe nausea, diarrhea.

456
Q

What are the side effects of saquinavir?,

A

Gastrointestinal effects.

457
Q

What are the side effects of amprenavir?,

A

Rash, headache, diarrhea, and nausea.

458
Q

What are the side effects of the lopinavir/ritonavir combination?,

A

Diarrhea

459
Q

What are the side effects of atazanavir?,

A

Diarrhea, asymptomatic hyperbilirubinemia.

460
Q

What are the names of the protease inhibitors?,

A

Nelfinavir, indinavir, ritonavir, saquinavir, amprenavir, atazanavir.

461
Q

What are the names of non–nucleoside reverse transcriptase inhibitors?,

A

Efavirenz, nevirapine, delavirdine.

462
Q

What are the side effects of efavirenz?,

A

Neurologic; somnolence, confusion, or psychiatric disturbance; non–nucleoside reverse transcriptase inhibitor.

463
Q

What are the side effects of nevirapine?,

A

Rash, hepatotoxicity.

464
Q

What are the side effects of delavirdine?,

A

Rash.

465
Q

When should antiretroviral therapy be started in HIV infected patients?,

A

Antiretroviral medication should be started when the CD4 count has dropped or the viral load has risen.>55,000 copies/mL of RNA.

466
Q

What antiretrovirals should be started in HIV infected patients?,

A

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
Q

What is highly active antiretroviral therapy?,

A

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
Q

What is boosted protease inhibitor therapy

A

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
Q

What is considered adequate antiretroviral therapy?,

A

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
Q

What percentage of children born to HIV positive mothers will be infected with HIV?,

A

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
Q

What treatment should be given to pregnant HIV infected women?,

A

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
Q

What are the indications for cesarean section in pregnant HIV–infected women?,

A

C–section is used routinely in those whose CD4 count is low or whose viral load >1000 copies.

473
Q

Which antiretroviral in a known teratogen?,

A

The only known teratogen is efavirenz in animal studies.

474
Q

What treatment is recommended for HIV infected pregnant women?,

A

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
Q

What is the effect of breastfeeding on transmission of HIV to the infant?,

A

Breast feeding is associated with transmission of virus to the infant.

476
Q

What postexposure prophylaxis for HIV after needlestick injury should be given?,

A

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
Q

What is Q–Fever?,

A

Coxiella burnetii infection, which is transmitted by inhalation; found in cattle, sheep, and goats.

478
Q

What are the clinical signs of Q–fever?,

A

Febrile illness, atypical pneumonia, hepatitis, and hepatomegaly, endocarditis. Treatment is doxycycline. Diagnosed by specific serology.

479
Q

What is Rocky Mountain spotted fever?,

A

R. rickettsi is transmitted by the wood tick from the mid–Atlantic coast, upper South, and Midwest. In spring and summer.

480
Q

What is the triad of Rocky Mountain spotted fever?,

A

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
Q

How is Rocky Mountain spotted fever diagnosed?,

A

Specific serology; biopsy of skin lesion.

482
Q

What is the treatment of Rocky Mountain fever?,

A

Doxycycline

483
Q

What is toxoplasmosis?,

A

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
Q

What is the presentation of toxoplasmosis?,

A

80–90% asymptomatic in the immunocompetent. In AIDS: chorioretinitis, CNS mass lesion, encephalitis. Headache, fever, nausea. The retinal lesion can cause visual complaints.

485
Q

How is toxoplasmosis diagnosed?,

A

Serology is the most common method used. The best test is to visualize the parasite in biopsy tissue.

486
Q

What is the treatment of toxoplasmosis?,

A

Pyrimethamine and sulfadiazine.

487
Q

What is tetanus?,

A

Infectious complication of wounds caused by the toxin of Clostridium tetani; takes 1–7 days to develop; spore forming, Gram–positive rod.

488
Q

What are the clinical signs tetanus infection?,

A

Tonic spasms of voluntary muscles, respiratory arrest, difficulty in swallowing (dysphagia), restlessness, irritability, stiff neck, arms, and legs; headache, lockjaw, high mortality.

489
Q

What is the prophylaxis of tetanus?,

A

Tetanus toxoid (boosters every 10 years). Débride wound. Antitoxin is tetanus immunoglobulin; penicillin 10–14 days.

490
Q

What is aspergillosis?,

A

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
Q

What are the signs of aspergillosis?,

A

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
Q

What are the risk factors for aspergillosis?,

A

Risks: 1) neutropenia

493
Q

How is aspergillosis diagnosed?,

A

Abnormal chest x–ray and Aspergillus in sputum.

494
Q

What are voriconazole and caspofungin?,

A

Drugs used to treat aspergillosis and other fungal infections.

495
Q

What is the treatment of aspergillosis?,

A

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
Q

What is blastomycosis?,

A

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
Q

What are the signs of blastomycosis?,

A

Fever, cough, chest pain, and weight loss. After inhalation, disseminates anywhere in body, but skin is by far the most common.

498
Q

What is the treatment of blastomycosis?,

A

Prolonged amphotericin for severe disease (8–12 weeks); itraconazole or ketoconazole for mild disease.

499
Q

What is the cause of toxic shock syndrome?,

A

Staphylococcus aureus toxin TSST–1. Infected tampons, sponges, and surgical wound infections.

500
Q

What are the clinical signs of toxic shock syndrome?,

A

Hypotension, fever, mucosal changes, desquamative rash on hands and feet. Gastrointestinal, renal, hepatic, and muscular symptoms.