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ITE '23 > Ch. 9 Heme/Onc, Allergy, Immunology > Flashcards

Ch. 9 Heme/Onc, Allergy, Immunology Flashcards

1
Q

What are 5 causes of microcytic anemia?

A
  1. Iron deficiency
  2. Thalassemia
  3. lead poisoning
  4. sideroblastic anemia
  5. chronic disease
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2
Q

What are 5 causes of normocytic anemia?

A
  1. hemorrhage
  2. hemolysis
  3. aplastic anemia
  4. sickle cell disease
  5. anemia of chronic disease/renal disease
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3
Q

What are 4 causes of macrocytic anemia?

A
  1. Vitamin B12 deficiency
  2. Folate deficiency
  3. Sulfa drugs
  4. EtOH abuse
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4
Q

What are normal fasting serum iron levels?

A

60-180 ug/dL

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5
Q

How will TIBC be changed in iron deficiency anemia?

A

increased, >400 ug/dL

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6
Q

What route causes lead poisoning in adults?

A

inhalation
(whereas in children, it is ingestion)

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7
Q

What causes sideroblastic anemia?

A

acquired or congenital defect in porphyrin synthesis.

Often related to toxins (like chloramphenicol,
isoniazid, cycloserine, lead); infections; malignancy; rheumatologic disease;
or hemolytic anemia.

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8
Q

What congenital disorder commonly causes aplastic anemia?

A

Fanconi anemia

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9
Q

What medications commonly cause aplastic anemia?

A

NSAIDs, chloramphenicol, sulfonamides, antiepileptics drugs, nifedipine

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10
Q

What viral infection most commonly causes aplastic anemia?

A

Parvovirus B19
(HIV and hepatitis also implicated)

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11
Q

Dark urine related to hemoglobinuria usually indicates ______ hemolysis

A

intravascular

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12
Q

Splenomegaly is more common in _______ hemolysis

A

extravascular

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13
Q

In _______ hemolysis, look for increased LDH, decreased haptoglobin,
hemoglobinuria, and schistocytes.

A

intravascular

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14
Q

In _______ hemolysis, look for indirect hyperbilirubinemia, increased
LDH, and spherocytes.

A

extravascular

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15
Q

Autosomal dominate disease caused by a defect in red cell membrane protein.

A

Hereditary spherocytosis

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16
Q

What is a risk factor for hereditary spherocytosis?

A

More common among persons of Northern European decent

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17
Q

What causes anemia in Hereditary Spherocytosis?

A

RBCs take on a microspherocytic shape that is unable to pass through the spleen leading to RBC destruction

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18
Q

How is Hereditary Spherocytosis diagnosed?

A

■ Peripheral smear with spherocytes.
■ Negative Coombs test (to rule out autoimmune hemolytic anemia).
■ Osmotic fragility test is confirmative.

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19
Q

What is the treatment for Hereditary Spherocytosis?

A

Folic acid supplementation in mild-moderate disease; splenectomy is curative
and indicated for severe anemia.

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20
Q

This X-linked recessive disorder results in RBCs that are more susceptible to oxidant stress.

A

G6PD Deficiency

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21
Q

What are risk factors for G6PD?

A

African, Asian, and Mediterranean descent

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22
Q

How does G6PD lead to anemia?

A

Oxidant stress leads to hemoglobin precipitation within the RBC and subsequently both intravascular cell lysis and removal of cell from circulation via spleen

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23
Q

What drugs/oxidizing agents commonly precipitate hemolysis in G6PD deficiency?

A

Dapsone, methylene blue, nitrofurantoin, phenazopyridine (Pyridium), primaquine sulfonamides, antimalarials

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24
Q

What are signs and symptoms of hemolytic crisis in G6PD deficiency?

A

severe hemolysis with dark urine (hemoglobinuria), jaundice, pallor, splenomegaly, dyspnea, and possible vascular collapse

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25
Q

How is G6PD diagnosed?

A

■ Laboratory findings of both intravascular and extravascular hemolysis.
■ Peripheral smear showing Heinz bodies (RBCs with precipitated hemoglobin) and degmacytes (aka “bite cell”)

Heinz bodies appear similar to Howell-Jolly bodies, but Heinz bodies will be stained with methylene blue and therefore be bluer in color rather than red/pink

■ Confirm diagnosis with G6PD enzyme activity; should delay testing by 3 weeks after acute event because reticulocytes have more normal levels of G6PD enzyme.

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26
Q

anemia caused by antibodies formed against native RBC antigens

A

Autoimmune (warm and cold antibody) hemolytic anemia

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27
Q

Which type of Autoimmune hemolytic anemia is caused by IgG antibodies form against native RBC antigens?

A

Warm antibody – bind at body temperature

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28
Q

Which type of Autoimmune hemolytic anemia is caused by IgM antibodies form against native RBC antigens?

A

Cold antibody – bind at cool temperatures

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29
Q

What commonly triggers Warm antibody autoimmune hemolytic anemia?

A

lymphoproliferative disorders?

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30
Q

What commonly triggers Cold antibody autoimmune hemolytic anemia?

A

Acute: mycoplasma pneumonia or Epstein-Barr infection
Chronic: Lymphoma or Waldenstrom macroglobulinemia

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31
Q

What do you call anemia caused by Antibodies form in response to foreign RBC antigens?

A

Alloimmune hemolytic anemia

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32
Q

What medications commonly cause auto-immune hemolytic anemia?

A

Cephalosporins, levodopa, methyldopa, penicillin, sulfa, quinidine, oral hypoglycemic agents, some NSAIDs

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33
Q

What is the pathophysiology for Drug-induced hemolytic anemia?

A

Antibody, hapten, or immune complex binding to RBCs leads to rapid cell destruction via complement fixation and/or sequestration by the spleen where affected portions of the RBC membrane are digested by macrophages leading to development of microspherocytes.

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34
Q

_________ on peripheral smear suggest splenic sequestration.

A

Microspherocytes

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35
Q

______ Coombs test measures immunoglobulin G [IgG]-mediated reactions like warm antibody
hemolytic anemia

A

direct

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36
Q

_____ Coombs test measures immunoglobulin M [IgM] or complement mediated reactions like cold antibody hemolytic anemia).

A

indirect

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37
Q

What are 6 causes of microangiopathic hemolytic anemia?

A

DIC
TTP
HUS
Pregnancy
Malignant HTN
Malignancies

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38
Q

Occurs in children and is recognized as microangiopathic anemia, thrombocytopenia, and renal dysfunction following a diarrheal illness

A

HUS

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39
Q

What bacteria are implicated in HUS?

A

classically caused by Shiga toxin–producing bacteria-like Escherichia coli, Shigella, Salmonella

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40
Q

What causes classic TTP?

A

congenital or acquired deficiency in ADAMTS13 protein activity

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41
Q

Besides bacteria, what are some other known causes of TTP-HUS in adults?

A

drugs (quinine, antiplatelet agents, chemotherapeutic agents); malignancy; and pregnancy

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42
Q

How does HUS-TTP cause anemia and thrombocytopenia?

A

Fibrin deposition and platelet aggregation in capillaries and arterioles lead to intravascular
hemolysis (microangiopathic hemolytic anemia) and thrombocytopenia

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43
Q

How does HUS-TTP lead to renal failure?

A

microthrombi in renal vasculature

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44
Q

How does HUS-TTP lead to neurologic symptoms?

A

microthrombi in CNS

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45
Q

What is the classic pentad of TTP?

A

fever, anemia, thrombocytopenia, renal failure,
and neurology problems

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46
Q

What are the three lab findings of microangiopathic hemolytic anemia?

A

anemia with:
1. decreased haptoglobin
2. elevated LDH
3. presence of schistocytes on peripheral smear

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47
Q

What is the treatment for typical HUS?

A

supportive care

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48
Q

What is the treatment for TTP or severe HUS?

A

plasma exchange therapy

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49
Q

What defines a-thalassemia?

A

≥ 1 of the 4 α-globin chain genes fail to function

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50
Q

What defines a-thalassemia carrier state?

A

one mutated gene; asymptomatic, normal CBC

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51
Q

What defines α-Thalassemia minor?

A

two mutated genes; usually asymptomatic, mild
microcytic anemia

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52
Q

What defines Hemoglobin H disease?

A

three mutated a chain genes; splenomegaly, jaundice,
chronic microcytic anemia

(most severe non-fatal form of alpha thalassemia)

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53
Q

What defines α-Thalassemia major/hydrops fetalis?

A

four mutated genes; fetal demise

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54
Q

How is B-Thalassemia minor defined?

A

one mutated gene; asymptomatic, hypochromic,
microcytic anemia

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55
Q

How is B-Thalassemia major/Cooley anemia defined?

A

two mutated genes; severe anemia,
splenomegaly, frontal bossing

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56
Q

What is the treatment for B-Thalassemia major?

A

Patients require transfusions to sustain life
and iron chelation therapy to prevent complications from chronic transfusions.
Splenectomy may reduce transfusion requirements

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57
Q

How is Sickle cell trait defined?

A

caused by defect in only one β-globin chain and produces a less severe form of the disease with sickling only under conditions of severe hypoxia

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58
Q

How is sickle cell disease defined?

A

This autosomal recessive disease is caused by an abnormal structure to BOTH β-globin chains of hemoglobin, resulting in sickling of deoxygenated RBC.

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59
Q

What is the most common manifestation of sickle cell crisis?

A

Vaso-Occlusive pain crisis

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60
Q

How long does pain from vaso-occlusive pain crisis typically last?

A

5-7 days

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61
Q

What is the treatment for vaso-occlusive pain crisis?

A

analgesia +/- IV/PO hydration if dehydrated

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62
Q

When are antibiotics implicated in vaso-occlusive pain crisis?

A

any age with concern for infection
and empirically in children < 2 years old with a temperature ≥ 39.5°C/103.1°F or white blood cells (WBCs) >20,000/μL

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63
Q

When are exchange transfusions indicated for sickle cell patients?

A

cardiopulmonary collapse, acute CNS event, acute chest syndrome, and priapism

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64
Q

What causes acute chest syndrome in sickle cell patients?

A

a combination of pulmonary vascular infarction
and/or infection

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65
Q

What pathogens are most commonly implicated in acute chest syndrome?

A

Chlamydia, Mycoplasma, respiratory syncytial
virus (RSV), Staphylococcus aureus, and Streptococcus pneumoniae

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66
Q

What is the treatment for acute chest syndrome?

A

supportive with O2, IV hydration, analgesia
+Abx (Azithromycin and Cefotaxime)

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67
Q

When is exchange transfusion indicated in acute chest syndrome?

A

multiple lobe involvement, severe
hypoxia, and disease refractory to antibiotics and supportive care

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68
Q

What is splenic sequestration Crisis?

A

Rapid sequestration of RBCs in spleen causing splenomegaly and severe anemia;
(usually 6 months-6 years old in setting
of viral illness)

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69
Q

How is Splenic Sequestration Crisis diagnosed?

A

Very low hemoglobin with evidence for reticulocytosis and palpable splenomegaly

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70
Q

What is aplastic crisis in sickle cell patients?

A

Sudden decrease in hemoglobin production by bone marrow resulting in severe anemia; usually precipitated by infection (parvovirus B19).

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71
Q

What is the treatment for stroke caused by Sickle Cell disease?

A

Exchange transfusions to HbS < 25%.

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72
Q

How is aplastic crisis diagnosed?

A

Hemoglobin fall > 2 g/dL from baseline without reticulocytosis (< 2%)

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73
Q

How is polycythemia defined?

A

an increase in RBC count to:
Women: Hgb > 16.5 g/ dL (Hct > 48%)
Men: Hgb > 18.5 g/dL (Hct > 52%)

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74
Q

What are some causes of secondary polycythemia?

A

conditions that increase erythropoietin levels such as:
lung disease, heart disease, high altitude, and erythropoietin-secreting tumors.

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75
Q

What are symptoms of polycythemia?

A

pruritus, headache, dizziness, blurry vision, plethora

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76
Q

How is primary polycythemia (vera) differentiated from secondary polycythemia?

A

primary polycythemia will have decreased serum EPO level, whereas it will be elevated in secondary polycythemia

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77
Q

What is the treatment for polycythemia? Treatment goal?

A

Phlebotomy
Goal Hct of 55%

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78
Q

How is methemoglobinemia defined?

A

Hemoglobin-containing ferric iron (Fe3+) – wont bind O2

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79
Q

What are common causes of methemoglobinemia?

A

Nitrates (in well water or vegetables)
Medications: Lidocaine, benzocaine, nitrates, nitroglycerin, nitroprusside, sulfonamides, dapsone, phenazopyridine (Pyridium), inhaled nitric oxide

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80
Q

Describe pulse ox in context of methemoglobinemia?

A

Classically see pulse oximetry of 80%-85% without response to supplemental O2

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81
Q

What causes classic chocolate brown blood on venipuncture?

A

methemoglobinemia

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82
Q

At what methemoglobin levels do you become symptomatic?

A

levels >20%;
levels >40% leads to significant mortality

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83
Q

What is the treatment for methemoglobinemia?

A

Methylene blue (1-2 mg/kg IV) facilitates the reduction of Fe3+ to Fe2+

BUT IS CONTRAINDICATED IN G6PD PATIENTS (bc may cause hemolysis and worsen symptoms)

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84
Q

Methemoglobinemia causes a ____ shift in the oxygen dissociation curve.

A

Leftward (cannot bind O2, therefore decreased delivery/dissociation)

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85
Q

How is leukemoid reaction differentiated from CML?

A

leukemoid reaction = normal leukocyte alkaline phosphatase (LAP) level
CML = low LAP

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86
Q

In which form of leukemia is the Philadelphia chromosome uniformly present (translocation between chrom. 9 and 22)?

A

CML

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87
Q

What is the most common ACUTE leukemia in adults?

A

AML

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88
Q

What is the most common leukemia in adults?

A

CLL (aka SLL)

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89
Q

How are AML and ALL diagnosed?

A

Bone marrow biopsy

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90
Q

How is CLL diagnosed?

A

flow cytometry

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91
Q

Which leukemia is known for being a malignancy of childhood with most cases occurring in children from 2-5 years old?

A

ALL

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92
Q

Malignant proliferation of a single plasma cell clone with subsequent uncontrolled
production of a single immunoglobulin

A

Multiple myeloma

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93
Q

How is multiple myeloma diagnosed?

A

anemia + renal failure
elevated protein:albumin ratio

Confirmation: serum/urine electrophoresis

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94
Q

A group of lymphoid malignancies characterized by the presence of Reed-Sternberg cells (owl eye cells) contained within a reactive cellular background

A

Hodgkin Lymphoma

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95
Q

What is the age distribution for Hodgkin Lymphoma?

A

bimodal: young adults (20s-30s) and adults >50 yrs old

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96
Q

Heterogeneous group of B-cell and T-cell malignancies that range from indolent
to highly aggressive and rapidly fatal. This is generally a disease of the elderly.

A

Non-Hodgkin Lymphoma (NHL)

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97
Q

Which type of lymphomas often have extranodal disease (GI and skin)?

A

Non-Hodgkin Lymphomas

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98
Q

What is the treatment for aggressive NHL?

A

Chemo: CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone)
+/- rituximab (an anti-CD20 monoclonal antibody)

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99
Q

How is the intrinsic pathway of coagulation measured?

A

activated partial thromboplastin time (aPTT).

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100
Q

How is the extrinsic pathway of coagulation measured?

A

prothrombin time (PT).

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101
Q

What causes prolonged PT?

A

vitamin K deficiency
Warfarin
DIC
factor deficiency
liver disease

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102
Q

What causes prolonged PTT

A

Hemophilia A (Factor VIII)
Hemophilia B (Factor IX)
von Willebrand disease
Heparin
Factor deficiency
Liver disease

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103
Q

What is the mechanism of action of tPA?

A

released from endothelial cells, activates
plasminogen to plasmin leading to breakdown of fibrinogen and cross-linked fibrin (creating the degradation product d-dimer)

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104
Q

What should you be thinking about in a patient with petechiae, epistaxis, gum bleeding, or vaginal bleeding?

A

think platelet problems not coagulation factor disorders

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105
Q

What are some disorders of increased platelet destruction?

A

ITP, TTP, HUS, DIC, HELLP

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106
Q

At what platelet count should you transfused platelets in non-bleeding patient?

A

<10,000/uL

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107
Q

At what age(s) is peak incidence of ITP?

A

children 2-6 years old and adults 20-50 years old

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108
Q

What are common signs and symptoms of ITP?

A

Petechiae, gingival bleeding, epistaxis, menorrhagia, and GI bleeding

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109
Q

How is ITP diagnosed?

A

diagnosis of exclusion
isolated thrombocytopenia on CBC, and peripheral smear with a small
number of well-granulated platelets.

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110
Q

What is the treatment for ITP?

A

Children –> avoid physical activity and NSAIDs
Adults –> Prednisone 1-1.5 mg/kg/d PLUS IVIG or anti-D Ig
(platelets if hemorrhaging)

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111
Q

What is the treatment for TTP?

A

Exchange transfusions

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112
Q

What are the most common causes of DIC?

A

Infection; specific pathogens
gram- positive and gram-negative sepsis,
meningococcemia, typhoid fever, and
Rocky Mountain spotted fever

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113
Q

What is purpura fulminans?

A

protein C deficiency, often seen with meningococcemia
treat with protein C concentrate

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114
Q

What is the most common hereditary bleeding disorder?

A

von Willebrand disease

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115
Q

Bleeding disorder with normal platelet
count, PT, and PTT, but INCREASED bleeding time

A

Von Willebrand disease

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116
Q

How is von Willibrand diagnosed?

A

Abnormal assay of vWF activity, vWF antigen, or factor VIII coagulant (C) activity.

117
Q

How is von willebrand disease treated?

A

DDAVP
and/or vWF concentrate
+/- Cryoprecipitate

118
Q

What is the mechanism of action of DDAVP in the treatment of von willebrand disease?

A

Stimulates release of vWF (and factor VIII) stored in vascular endothelial cells

119
Q

What are signs and symptoms of Hemophilia A and B?

A

Easy bruising, hemarthrosis, hematuria, and muscle hematoma are most common. May also see excessive bleeding after procedures, severe and/or delayed bleeding after apparent minor trauma (including intracranial hemorrhage and retroperitoneal hematoma formation).

120
Q

How are hemophilia A and B diagnosed?

A

Prolonged PTT, normal PT, abnormal factor specific assay.

121
Q

What is the treatment for Hemophilia A?

A

DDAVP (–>release of vWF and Factor VIII from endothelial cells)
and
Factor VIII replacement

122
Q

What is the treatment for Hemophilia B?

A

Factor IX replacement

123
Q

What should be given to Hemophilia A or B patients with bleeding refractory to first line treatments?

A

PCCs or Factor VIIa (to overcome inhibitors)

124
Q

What anticoagulant primarily works through antithrombin III to inhibit thrombin and factor Xa (to prevent clot propagation)?

A

Unfractionated Heparin

125
Q

What is the therapeutic range of unfractionated heparin?

A

aPTT (1.5-2.5x normal)

126
Q

What should be administered in someone on Heparin with major bleeding?

A

Protamine Sulfate
(1 mg for every 100 unit of heparin administered over the previous 4 hours, max 50 mg)

127
Q

When is the typical onset of HIT Syndrome?

A

within 5-7 days of initiating heparin therapy

128
Q

What is the treatment in HIT SYndrome?

A

anticoagulation with direct thrombin inhibitors (eg bivalirudin) or heparinoids

129
Q

Anticoagulant that works by primarily inhibiting factor Xa activity

A

LMWH (enoxaparin, dalteparin,
and ardeparin)

130
Q

What must be considered in dosing LMWH?

A

renal function – renally cleared

131
Q

What anticoagulant is a synthetic heparin derivative; inhibits activated factor X?

A

Fondaparinux

132
Q

How should bleeding while on Fondaparinux be treated?

A

if severe, recombinant Factor VIIa

133
Q

What medications are the traditional direct thrombin inhibitors? (list 4)

A

lepirudin, desirudin, argatroban, and bivalirudin

134
Q

What is the primary use for direct thrombin inhibitors?

A

in patients with HIT

135
Q

Argatroban is _____ metabolized so should be used with caution in patients with _____ failure.

A

hepatically, liver

136
Q

Lepirudin and desirudin are_____ cleared so should be used with caution in patients with___ failure.

A

renally, renal

137
Q

Oral anticoagulant that inhibits formation and activation of vitamin K–dependent coagulation factors

A

Warfarin

138
Q

What coag factors are Vitamin K dependent?

A

II, VII, IX, X; also the anticoagulant factors protein C and protein S

139
Q

What are contraindications to Warfarin?

A

Medication allergy, active bleeding, pregnancy, liver failure.

140
Q

What INR is considered therapeutic for Warfarin?

A

2.0 - 3.0; for mechanical valves it is 2.5-3.5

141
Q

What medications/supplements commonly increase INR?

A

Acetaminophen, amiodarone, amoxicillin,
antifungals, cimetidine, doxycycline,
fluoroquinolones, macrolides,
metronidazole, sulfonamides, SSRIs, garlic,
ginger, ginkgo biloba

142
Q

What medications/supplements commonly decrease INR?

A

Carbamazepine, phenytoin, phenobarbital,
cholestyramine, dicloxacillin, griseofulvin,
haloperidol, nafcillin, ranitidine, rifampin

143
Q

When is warfarin-induced skin necrosis most common?

A

2-10 days after initiation of warfarin

144
Q

What is the treatment for Warfarin use, INR 5-9 without major bleeding?

A

Hold dose, consider oral vitamin K 1-2.5 mg PO, recheck INR in 24 h

145
Q

What is the treatment for Warfarin use, INR >9 without major bleeding?

A

Hold dose, vitamin K 2.5-5 mg PO, recheck INR in 24 h

146
Q

What is the treatment for any INR with major bleeding in context of Warfarin use?

A

Hold dose, vitamin K 10 mg slow IV or sub Q, administer FFP, PCC, or recombinant factor VIIa

147
Q

What side effect/reaction does IV Vitamin K commonly produce?

A

anaphylaxis

148
Q

What is the mechanism of action of ASA?

A

irreversibly inhibits cyclooxygenase (COX-1), which prevents synthesis of thromboxane A2 and associated platelet aggregation

149
Q

What medications fall under the drug class, thienopyridines?

A

clopidogrel (Plavix), prasugrel (Effient), and ticlopidine (Ticlid)

150
Q

What is the mechanism of thienopyridines, aka Plavix?

A

Irreversibly inhibit platelet aggregation via adenosine diphosphate receptor antagonism

151
Q

What medications are GP IIb/IIIa inhibitors?

A

abciximab, tirofiban, and eptifibatide

152
Q

What is the Hct of PRBC units?

A

55-80%

153
Q

How many mLs are in 1 adult unit of PRBCs?

A

350mL

154
Q

How many mLs are in 1 pediatric unit of blood?

A

60 mL

155
Q

How is massive transfusion defined?

A

> 10 units of PRBCs in 24 hours for adult patients

156
Q

What causes hypocalcemia in MTP?

A

binding to citrate preservative

157
Q

If massive transfusion and INR >1.5, how many units of FFP be should be transfused?

A

2-4 units

158
Q

If MTP and platelets <50,000, how many units of platelets should be transfused?

A

1 unit

159
Q

If MTP and fibrinogen <100mg/dL, how many units of cryoprecipitate should be transfused?

A

10 units

160
Q

In MTP, how is symptomatic hypocalcemia treated?

A

calcium gluconate

161
Q

Most common transfusion reaction; characterized by fevers/chills, malaise.
Treatment is symptomatic, usually with Tylenol

A

Febrile transfusion reaction

162
Q

Most serious transfusion reaction, typically due to clerical error. ABO incompatibility leads to lysis of transfused RBCs with associated hemoglobinemia and hemoglobinuria.

A

Acute hemolytic transfusion reaction

163
Q

What is the treatment for Acute hemolytic transfusion reaction?

A

stopping the transfusion, immediate vigorous
crystalloid infusion, and diuretic therapy to maintain urine output at 1-2 mL/kg/h.

164
Q

Usually urticaria or hives only (rarely anaphylaxis). Treatment is symptomatic,
usually with Benadryl.

A

Allergic reaction

165
Q

Can occur with any plasma-containing blood transfusion, however is most common with FFP or platelets. Usually occurs within 6 hours
of transfusion. Signs and symptoms are indistinguishable from acute respiratory distress syndrome.

A

Transfusion-related acute lung injury (TRALI)

166
Q

What is the treatment for Transfusion-related acute lung injury (TRALI)?

A

Stop transfusion. Treatment is otherwise primarily supportive, no evidence
for use of steroids, antihistamines, or diuretics

167
Q

Characterized by delayed extravascular hemolysis due to presence of small amounts of RBC antibodies (not detected on blood-type screening) directed against transfused RBC antigens.

A

Delayed transfusion reaction

168
Q

What is the treatment for Delayed transfusion reaction?

A

supportive

169
Q

Occurs when immunocompromised patients are transfused with PRBC containing immunocompetent T lymphocytes, effectively resulting in an unintentional bone marrow transplant. Carries 80% mortality.

A

Transfusion-associated graft-versus-host disease

170
Q

How can Transfusion-associated graft-versus-host disease be prevented?

A

use irradiated blood products in immunocompromised patients

171
Q

One unit of platelets is sufficient to raise platelet count by ______/μL.

A

30,000

172
Q

One unit of fresh frozen plasma (FFP) contains __ U/mL of each clotting factors in addition to
__-__mg/mL of fibrinogen.

A

1, 1-2

173
Q

How is FFP typically dosed?

A

It must be ABO compatible
and is typically dosed as 4-6 units (200-250 mL volume per unit) in adults or
15 mL/kg in children.

174
Q

What 4 things does cryoprecipitate contain?

A

Factors VIII, XIII, fibrinogen, and vWF

175
Q

What is the standard dose of cryoprecipitate?

A

Standard dosage is 6-10 units (10-40 mL volume per unit). Does not require ABO matching.

176
Q

What is contained in PCC?

A

vitamin K–dependent factors II, VII, IX, and X.

177
Q

When is recombinant factor VIIa indicated?

A

approved only for the control of bleeding in hemophiliacs with inhibitors

178
Q

What are the symptoms of hypercalcemia of malignancy?

A

anorexia, abdominal pain, nausea and vomiting,
constipation, polyuria/polydipsia, hypertension, weakness, confusion, and generalized itching

179
Q

What ECG finding is consistent with hypercalcemia?

A

shortened QT interval

180
Q

How is hypercalcemia of malignancy treated?

A

aggressive rehydration
bisphosphonates (pamidronate, zoledronate)
Calcitonin

avoid – thiazide diuretics or lithium

181
Q

What are common causes of hyperviscosity syndrome?

A

Waldenström macroglobulinemia
(increased IgM), multiple myeloma (increased IgG or immunoglobulin A [IgA]), leukemias with blast transformation, or polycythemia vera

182
Q

How does hyperviscosity syndrome classically present?

A

Blurred vision, mucosal bleeding, and neurologic
symptoms (headache, dizziness, AMS, dyspnea)

183
Q

What might you see on peripheral smear in hyperviscosity syndrome?

A

rouleaux formation

184
Q

What is the treatment for hyperviscosity syndrome?

A

■ Two units of phlebotomy with IV fluids hydration can be temporizing measure (and is definitive therapy for polycythemia).
■ Emergent plasmapheresis for dysproteinemias.
■ Emergency leukapheresis for blast transformations.
■ Chemotherapy.

185
Q

How is neutropenic fever defined?

A

sustained temperatures > 38.0°C/100.4°F
or single temperature > 38.3°C/101.0°F in the presence of neutropenia (ANC < 500 cells/μL).

186
Q

What is the treatment for neutropenic fever?

A

empiric broad-spectrum antibiotic:
Monotherapy with cefepime (or equivalent).
Add vancomycin if methicillin-resistant Staphylococcus aureus (MRSA) suspected or in presence of vascular catheter or soft tissue
infection.
Add other agents depending on clinical suspicion regarding source of infection.

187
Q

What is the most common site of spinal cord compression due to malignancy (Rubin Syndrome)?

A

thoracic spine

188
Q

What is superior vena cava syndrome?

A

Obstruction may be due to external pressure on the SVC or invasion of the SVC by tumor and resultant thrombosis

189
Q

What is a risk factor for tumor lysis syndrome?

A

pre-existing renal failure

190
Q

What metabolic derangements are commonly seen in tumor lysis syndrome?

A

Hyperuricemia, hyperkalemia, hyperphosphatemia, and associated
hypocalcemia

191
Q

How does tumor lysis syndrome lead to renal failure?

A

Oliguric renal failure results from uric acid precipitation in the renal tubules.

192
Q

How is hyperuricemia treated in Tumor Lysis Syndrome?

A

vigorous IV hydration and allopurinol
(to reduce production of uric acid).

Many sources recommend alkalization of urine to pH > 7, but this should be done with caution because it can exacerbate other metabolic abnormalities

193
Q

For what uric acid level might hemodialysis be necessary?

A

> 10mg/dL

194
Q

For what phosphate level might hemodialysis be necessary?

A

> 10 mg/dL

195
Q

What malignancies are associated with acanthosis nigricans?

A

Gastrointestinal (GI) malignancies primarily, lung and breast cancer

196
Q

What malignancies are associated with Dermatomyositis?

A

Breast, ovarian, stomach, colon, and lung cancer

197
Q

What malignancies are associated with Erythema multiforme?

A

Leukemias and Hodgkin lymphoma

198
Q

What malignancies are associated with Erythema nodosum?

A

Leukemia, Hodgkin lymphoma, and metastatic cancer

199
Q

What is erythroderma?

A

Diffuse erythema of the skin. Associated with intractable pruritus

200
Q

What malignancies are associated with erythroderma?

A

Hodgkin lymphoma, leukemia, and mycosis fungoides

201
Q

What is icthyosis?

A

Diffuse, dry scaling lesions; hyperkeratosis of palms and soles

202
Q

What malignancies are associated with acquired icythyosis?

A

Hodgkin lymphoma; breast, cervical, lung, and colon cancer

203
Q

What malignancies are associated with pruritus?

A

Hodgkin lymphoma, leukemia, multiple myeloma, polycythemia vera, adenocarcinoma, carcinoid syndrome

204
Q

What malignancies are associated with Sister mary joseph nodule?

A

Advanced adenocarcinoma (gastric or ovarian)

205
Q

What malignancies are associated with Urticaria?

A

Hodgkin lymphoma, leukemia, internal malignancy, multiple myeloma

206
Q

What malignancies are associated with Purpura?

A

Hodgkin lymphoma, leukemias, lymphoma, multiple myeloma, polycythemia vera

207
Q

What is the mechanism of a Type I hypersensitivity reaction?

A

IgE-mediated degranulation of mast
cells with release of mediators

208
Q

What is the mechanism of a Type II hypersensitivity reaction?

A

IgG or IgM antibodies react with
cell antigens with resultant
complement activation

209
Q

What is the mechanism of a Type III hypersensitivity reaction?

A

Immune complex deposition and
subsequent complement activation

210
Q

What is the mechanism of a Type IV hypersensitivity reaction?

A

Activated T cells against cell surface
bound antigens

211
Q

Anaphylaxis is an example of which type of hypersensitivity reaction?

A

Type I

212
Q

Angioedema is an example of which type of hypersensitvity reaction?

A

Type I

213
Q

Autoimmune hemolytic anemia is an example of which type of hypersensitvity reaction?

A

Type II

214
Q

SLE is an example of which type of hypersensitvity reaction?

A

Type III

215
Q

Contact Dermatitis is an example of which type of hypersensitvity reaction?

A

Type IV

216
Q

What is pediatric dosing for epinephrine in anaphylaxis?

A

0.01 mg/kg, max 0.5mg

217
Q

_____ can be used for anaphylaxis patients on β-blockers with symptoms refractory to fluids and epinephrine

A

Glucagon

218
Q

What causes hereditary angioedema?

A

an autosomal dominant hereditary disorder
associated with C1-inhibitor deficiency

219
Q

What causes medication-related angioedema?

A

Mediated through bradykinin and substance P.

220
Q

Hereditary Angioedema is clinical diagnosis but what lab value may be diagnostic?

A

Low C1 level

221
Q

How is angioedema treated?

A

supportive & stop offending med
(Limited benefit: antihistamines, epi, steroids)
Severe attacks: purified human C1 inhibitor, icatibant (a bradykinin B2-receptor agonist),
or ecallantide (a kallikrein inhibitor).

FFP contains C1 inhibitor and is an alternative when these medications are not available

222
Q

What type of hypersensitivity reaction is serum sickness?

A

type III (immune complex)

223
Q

What is serum sickness?

A

when injection of an offending agent results in antigen-antibody complex formation. These complexes deposit in vessel walls and
result in activation of the complement cascade.

224
Q

When does serum sickness typically occur?

A

7-10 days after exposure to causative agent

225
Q

What are signs and symptoms of Serum SIckness?

A

a pruritic rash and flulike symptoms (fever, malaise, arthralgia, myalgia)

226
Q

How is Serum Sickness diagnosed?

A

clinically; C3, C4 levels will be decreased

227
Q

What is the treatment for Serum Sickness?

A

Generally self-limited – stops within 1-2 weeks of stopping offending agent.
Can give: antihistamines, NSAIDs, and steroids.

Plasmapheresis has been used for severe cases with symptoms that are not responsive to other treatments or when causative agent cannot be
withdrawn.

228
Q

What medications are known to cause serum sickness?

A

Abx– PCN, sulfonamides
phenytoin
thiazide diuretics
barbiturates

Horse serum antivenom

229
Q

What type of rash is seen in Drug hypersensitivity reaction?

A

widespread, symmetrical maculopapular rash
affects mucous membranes

230
Q

What is treatment for Drug Hypersensitivity reaction?

A

withdraw offending agents
+antihistamines
+/- steroids

231
Q

What type of rash is seen in DRESS?

A

Widespread rash, mucous membranes spared

232
Q

How is DRESS diagnosed?

A

clinically based on rash, eosinophilia, and end organ damage

233
Q

How is DRESS treated?

A

withdraw offending agent
antihistamines, glucocorticoids

234
Q

How is DRESS treated?

A

withdraw offending agent
antihistamines, glucocorticoids

235
Q

Which medications are commonly implicated in DRESS?

A

allopurinol, antiepileptic medications (carbamazepine, lamotrigine, phenytoin), sulfasalazine, vancomycin, minocycline, dapsone, and sulfamethoxazole

236
Q

Describe the rash of SJS-TENS

A

Severe, acute, widespread blistering rash that often includes mucous membrane
lesions.

SJS is defined by sloughing of < 10% total body surface area, and TENS is defined by sloughing of > 10% of total body surface area

237
Q

How is SJS differentiated from TENS?

A

SJS is defined by sloughing of < 10% total body surface area, and TENS is defined by sloughing of > 10% of total body surface area

238
Q

What medications are commonly implicated in SJS-TENS?

A

allopurinol, antiepileptic medications, sulfa
medications

239
Q

How is SJS-TENS treated?

A

withdraw offending agent
wound management, fluid and electrolyte management, infection prevention

(steroids, IVIG, immunomodulators controversial)

240
Q

What prevention advice should be given to those with reynauds?

A

cold avoidance, smoking cessation, maintaining whole body warmth, and avoiding sympathomimetic medications.

241
Q

How are acute Reynauds attacks treated?

A

rewarming

242
Q

What typically causes reactive arthritis?

A

usually preceded by 1-4 weeks by a GI or GU infections caused by Chlamydia, Yersinia,
Shigella, Salmonella, Campylobacter, or Clostridium difficile

243
Q

What are signs/symptoms of Reactive arthritis?

A

Asymmetric oligoarthritis, predominantly of weight bearing joints of lower extremities, including hips, knees, and heels (“lover’s heels”).

+/- urethritis, conjunctivit, and/or uveitis, mucocutaneous lesions, fever, malaise

244
Q

Describe joint involvement in rheumatoid arthritis.

A

typically symmetric and starts with small joints, including MCP and PIP joints

245
Q

What hand deformities are classically seen in RA?

A

Swan-neck deformities, Boutonniere deformity

246
Q

How is RA diagnosed?

A

inflammatory arthritis involving >/= 3 joints
Elevated CRP or ESR
+RF and anti-CCP antibodies

247
Q

What is treatment for RA?

A

NSAIDs and low dose oral prednisone for arthritis, arthralgias, serositis

Additional disease-modifying antirheumatic drugs (DMARDs) include methotrexate,
tumor necrosis factor (TNF)-blockers, and monoclonal antibodies.

248
Q

What medications are commonly implicated in drug-induced SLE?

A

HIPPS
hydralazine
isoniazid
phenytoin
procainamide
sulfonamides

249
Q

What antibodies are seen in SLE?

A

+anti-dsDNA
or
+anti-Sm

ANA+

250
Q

How do complement and inflammatory markers change in acute SLE flares?

A

During acute flares, there is a decrease in C3, C4 levels but an increase in ESR and CRP levels.

251
Q

What is treatment for SLE?

A

NSAIDs for arthritis, arthralgias, and serositis.

Hydroxychloroquine or chloroquine for rash, malaise, arthralgias.

Steroids for life-threatening manifestations, acute flares, and symptoms refractory to conservative therapy.

Moderate cases: azathioprine or methotrexate

Severe cases: immunosuppressive agents such as mycophenolate, cyclophosphamide, or rituximab.

252
Q

What are the two types of scleroderma?

A

systemic sclerosis
limited cutaneous systemic sclerosis

253
Q

CREST is a subgroup of limited cutaneous systemic sclerosis. What does it stand for?

A

Calcinosis cutis,
Raynaud phenomenon,
Esophageal dysmotility,
Sclerodactyly, and
Telangiectasia

254
Q

What is treatment of CREST syndrome?

A

organ specific ie, ACE inhibitors for hypertensive
renal crisis; calcium channel blockers for Raynaud phenomenon

Immunosuppressive therapies are reserved for patients with severe disease
(like interstitial lung disease, myocarditis, severe arthritis) or diffuse skin involvement.

255
Q

How is Giant Cell arteritis diagnosed?

A

Temporal artery biopsy, ESR > 50 mm/h

256
Q

How is Behcet disease diagnosed?

A

Biopsy of affected tissue

257
Q

How is Takayasu diagnosed?

A

Aortic arch arteriogram

258
Q

What are the three main types of large vessel vasculitis?

A

Giant Cell arteritis
Behcet Disease
Takayasu arteritis

259
Q

How is Giant Cell arteritis treated?

A

Prednisone 1-2 mg/kg/d immediately to present irreversible blindness +Low dose ASA

260
Q

Which large vessel vasculitis presents as recurrent painful oral and genital ulcers?

A

Behcet syndrome

261
Q

How is Behcet syndrome treated?

A

Prednisone

262
Q

What are signs and symptoms of Takayasu arteritis?

A

Uveitis, iritis, or optic neuritis

263
Q

What is treatment for Takayasu arteritis?

A

immunosuppressants

264
Q

How is polyarteritis nodosa diagnosed?

A

Biopsy (skin, kidney)
Mesenteric angiogram
HBV/HCV testing

265
Q

What is the treatment for polyarteritis nodosa?

A

Prednisone
cyclophosphamide

266
Q

How is Wegener granulomatosis diagnosed?

A

c-ANCA
Lung biopsy

267
Q

How is Wegener granulomatosis treated?

A

Prednisone
Cyclophosphamide

268
Q

How is Buerger disease (throboangiitis obliterans) diagnosed?

A

MRA or angiography

269
Q

What is the treatment for Buerger disease?

A

Smoking cessation

270
Q

How is Microscopic polyangiitis diagnosed?

A

p-ANCA
Renal biopsy

271
Q

How is microscopic polyangiitis treated?

A

cyclophosphamide

272
Q

What are the 4 predominantly medium vessel vasculitis?

A

Polyarteritis Nodosa
Wegener Granulomatosis
Buerger Disease
Microscopic polyangiitis

273
Q

How is hypersensitivity vasculitis diagnosed?

A

Skin biopsy

274
Q

How is hypersensitivity vasculitis treated?

A

Prednisone

275
Q

How is Henoch-Schonlein purpura diagnosed?

A

skin biopsy
rectal biopsy

276
Q

How is Henoch Schonlein Purpura treated?

A

Supportive
Prednisone

277
Q

How is Goodpasture Syndrome diagnosed?

A

Renal or lung biopsy showing basement membrane antibodies

278
Q

How is Goodpasture syndrome treated?

A

supportive
prednisone
cyclophosphamide
plasmapheresis

279
Q

Which 3 types of vasculitis is predominantly small vessel vasculitis?

A

Hypersensitivity vasculitis
Henoch-Shonlein Purpura
Goodpasture Syndrome

280
Q

What are the two most common etiologies of infection in the first month after transplant?

A
  1. latent acute infections (ie, bacteremia, candida species, antimicrobial resistant bacteria, West Nile virus, HIV), that are in donor tissue infect the host; and
  2. postsurgical infection (cellulitis, abscess, pneumonia, etc).
281
Q

What are the most common causes of infection 1-6 months after transplant?

A

CMV, EBV, P jiroveci, Chagas disease, endemic fungal disease, and tuberculosis (TB) all become common

282
Q

What are the most common causes of infection->6 months after transplant?

A

Usually the lowest levels of immunosuppression so most infections are related to community-acquired agents.

283
Q

How does cyclosporine toxicity present?

A

Acute toxicity causes reversible
vasoconstriction and renal ischemia

284
Q

What medications can cause increase in cyclosporine levels?

A

Calcium channel blockers and antibiotics
(doxycycline, erythromycin)

285
Q

What are side effects of mycophenolate (CellCept)?

A

diarrhea, n/v, leukopenia

286
Q

What are side effects of Tacrolimus (Prograf)?

A

diabetes, nephrotoxicity, seizures, and neuropathy

287
Q

What is the treatment for renal transplant rejection?

A

■ Methylprednisolone, 500 mg IV × 3 days.
■ May wait for results of biopsy before initiating steroids.

288
Q

What are signs/symptoms of IgA deficiency?

A

recurrent sinus and pulmonary infections

289
Q

Which Igs are low or dysfunctional in Common Variable Immunodeficiency (CVID)?

A

Low or dysfunctional levels of IgG, IgA, and IgM antibodies

ITE '23 (20 decks)

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