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Board Exam > Heme/Onc > Flashcards

Heme/Onc Flashcards

1
Q

Normal Hgb

A

Males: 14-18 g/100ml
Females: 12-16 g/100ml

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2
Q

Normal Hct

A

Males: 40-54%
Females: 37-47%

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3
Q

Normal TIBC

A

250-450 ug/dl

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4
Q

High TIBC indicates..

A

increased need for iron

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5
Q

Normal serum iron

A

50-150 ug/dl

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6
Q

normal MCV

A

80-100 um3

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7
Q

normal MCHC

A

26-34 pg

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8
Q

normal MCHC

A

32-36%

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9
Q

thalassemia:
- H/H
- MCV
- MCHC
- TIBC
- serum ferritin
- alpha or beta chains

A

H/H low
MCV low
MCHC low
TIBC normal
ferritin normal
alpha or beta chains decreased

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10
Q

iron deficiency anemia:
- H/H
- MCV
- MCHC
- RBC
- Serum iron
- serum ferritin
- TIBC
- RDW

A

H/H low
MCV low
MCHC low
RBC low
serum iron low
serum ferritin low
TIBC high
RDW high

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11
Q

Pernicious anemia (B12 deficiency):
- H/H
- MCV
- MCHC
- RBC
- serum B12
- Anti-IF (intrinsic factor) and anti-parietal antibody test

A

H/H low
MCV high
MCHC normal
RBC low
serum B23 low (<200 pg/ml)
Anti-IF and anti-parietal cell antibody test

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12
Q

folate deficiency:
- H/H
- MCV
- MCHC
- serum folate
- RBC folate

A

H/H low
MCV high
MCHC normal
serum folate decreased
RBC folate <100 ng/ml

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13
Q

alcoholism:
- H/H
- MCV

A

H/H low
MCV high

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14
Q

liver failure:
- H/H
- MCV

A

H/H low
MCV high

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15
Q

anemia of chronic disease
- H/H
- MCV
- MCHC
- serum iron
- TIBC
- serum ferritin

A

H/H low
MCV normal
MCHC normal
serum iron low
TIBC low
serum ferritin high (>100ng/ml)

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16
Q

sickle cell disease
- H/H
- MCV
- peripheral smear

A

H/H low
MCV normal
peripheral smear shows classic distorted sickle-shaped RBCs and Howell-Jolly bodies

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17
Q

renal failure
- H/H
- MCV

A

H/H low
MCV normal

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18
Q

blood loss
- H/H
- MCV

A

H/H low
MCV normal

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19
Q

most common cause of anemia

A

iron deficiency anemia

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20
Q

iron deficiency anemia: causes

A

blood loss
inadequate iron intake
impaired iron absorption

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21
Q

iron deficiency anemia: S/Sx

A

Usually slow in onset

As Hct falls:
- Pica: unusual food cravings
- dyspnea, pallor
- weakness, mild fatigue with exercise
- headache
- palpitations, tachycardia, postural hypotension
- koilonychia (spoon-shaped nails)

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22
Q

iron deficiency anemia: treatment

A

Oral iron 325mg TID for 3-6 months after restoration of normal lab values
Parenteral iron (iron dextran or sodium ferric gluconate) can be given if GI absorption of iron seems to be the problem

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23
Q

anemia of chronic disease: categories

A

Associated with chronic inflammation, infection, renal failure, malignancy

Anemia of inflammation
-chronic inflammatory conditions such as RA or IBD interfere with hepcidin activity

Anemia of organ failure
-liver or kidney failure suppress erythropoietin activity and therefore the bone marrow is not properly stimulated for erythropoiesis

Anemia of older adults
-anemia that is found in those over age 85 where any other cause is completely lacking

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24
Q

anemia of chronic disease: management

A

Manage underlying cause
Nutritional support

Severe symptoms:
-transfusion
-recombitant erythropoietin (epoetin alfa or darbopoetin)

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25
Q

Sickle cell anemia

A

Type of hemolytic anemia
Mutation that causes unstable hemoglobin which denatures under stressors such as hypoxia or acidosis, leading to deformation of the RBC into a sickle shape, and then hemolysis
Results in chronic anemia

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26
Q

sickle cell anemia: signs

A

Signs of disease develop in infancy or childhood
Delayed growth and development
Increased susceptibility to infections
Hct 20-30% at baseline
Jaundice
hepatosplenomegaly
non-healing ulcers on the legs
retinopathies
cardiomegaly

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27
Q

sickle cell crisis

A

When exposed to triggers, sickling is influenced by expression of the gene
The rate of sickling overwhelms the spleen’s ability to compensate and painful vaso-occlusive events occur

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28
Q

sickle cell crisis: treatment

A

Identify precipitating factor

IV hydration: priority
Supplemental O2
Generous analgesia
Transfusion with careful monitoring for iron overload

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29
Q

sickle cell crisis: prevention

A

Appropriate vaccination
Avoidance of physiologic stress
Hydroxyurea (500-700mg PO daily)

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30
Q

What offers about an 80% cure rate for sickle cell anemia

A

bone marrow transplant

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31
Q

Immune thrombocytopenic purpura

A

Formerly “idiopathic”
Results from autoimmune destruction of platelets with or without suppression of thrombopoiesis

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32
Q

Immune thrombocytopenic purpura: diagnosis

A

Diagnosis of exclusion
bone marrow analysis
low platelet count with other causes ruled out

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33
Q

Immune thrombocytopenic purpura: Symptoms

A

spontaneous bruising
petechial rash
spontaneous bleeding from the nose, gums, or vagina

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34
Q

Immune thrombocytopenic purpura: labs

A

Plt <20 or too low to measure

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35
Q

Immune thrombocytopenic purpura: treatment

A

Treatment is not universal, and some patients are not treated at all and the condition resolves on its own in about 1-2 months

If treatment is given, it focuses on:
-mitigation of bleeding complications
-High dose steroids (e.g.Prednisone 1mg/kg/day) to elevate platelet count
-IV gamma globulin
-Consider platelet transfusion, but these transfused platelets are generally subject to the same immune attack
-splenectomy may be considered in patients who are either unresponsive to steroid treatment, have frequent relapses, or cannot be tapered off steroids after a few months

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36
Q

heparin-induced thrombocytopenia: mechanism

A

Immune system forms antibodies against heparin when it is bound to platelet factor 4 (PF4) and has a cascading effect:
1. The IgG antibodies form a complex with heparin and PF4
2. The tail of the antibody binds to a protein on the surface of the platelet
3. This results in platelet activation and the formation of platelet microparticles, which initiate the formation of blood clots
4. The platelet count falls as a result, leading to thrombocytopenia

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37
Q

heparin-induced thrombocytopenia: what lab do you send if suspected?

A

PF4 ELISA

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38
Q

heparin-induced thrombocytopenia: presentation

A

Hallmark: decrease in platelet count by 30-50% within 5-10 days following expsure to heparin

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39
Q

heparin-induced thrombocytopenia: management

A

Stop the heparin if platelet counts are dropping within 5 days of administration of heparin
-hold warfarin, because of the high risk of warfarin necrosis
-start alternative AC: bivalirudin, argatroban, fondaparinux (to treat the clots formed during HIT)

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40
Q

Disseminated intravascular coagulation

A

Acquired condition that results in thrombocytopenia but also involves the clotting cascade being inappropriately activated either locally or systemically

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41
Q

Disseminated intravascular coagulation: causes

A

Always secondary to something else, so treat the cause
-sepsis
-malignancy, often acute leukemia
-retained products of conception
-liver disease
-massive trauma
-extensive burns
-shock

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42
Q

Disseminated intravascular coagulation: mechanism

A
  1. Inappropriate activation of the clotting cascade and platelet activation
  2. Tons of microvascular clotting
  3. As DIC progresses, clotting factors and platelets are exhausted and spontaneous bleeding begins
  4. The organs and body where clotting occurred become ischemic then infarct, which further accelerates the process
  5. The bleeding results in massive anemia, further starving organs of oxygen
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43
Q

Disseminated intravascular coagulation: labs/Dx

A

-Presence of a known trigger

-low RBCs
-Prolonged PT and aPTT (reflect underlying consumption and impaired synthesis of the coagulation cascade)
-low fibrinogen (reflecting exhaustion of the finite supply of it)
-rapidly declining platelet count
-elevated FDP
-elevated D-dimer d/t the body trying to stop the massive clotting
-schistocytes on peripheral blood smear

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44
Q

Disseminated intravascular coagulation: management

A

Treat the trigger

Establish baseline Plt, PT, PTT, D-dimer, fibrinogen

Transfuse:
- platelets for thrombocytopenia
- FFP to replace clotting factors
- cryoprecipitate to maintain fibrinogen levels

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45
Q

Disseminated intravascular coagulation: Platelet transfusion goals

A

> 20 in most patients
50 in patients with GI or CNS bleeding

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46
Q

Disseminated intravascular coagulation: cryoprecipitate transfusion goals

A

Fibrinogen >80-100

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47
Q

Disseminated intravascular coagulation: Fresh frozen plasma transfusion goals

A

PT, PTT <1.5x normal

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48
Q

Disseminated intravascular coagulation: PRBC transfusion goals

A

Hgb >8

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49
Q

Von Willebrand Disease: diagnosis

A

vWF activity assay
platelet function assay

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50
Q

Von Willebrand Disease: treatment

A

DDAVP
more severe bleeding: Factor VIII (Humate P)

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51
Q

Von Willebrand Disease: Type I

A

mild to moderate bleeding, often never diagnosed

Treatment: DDAVP, only use Factor VIII if bleeding is severe

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52
Q

Von Willebrand Disease: Type II

A

Moderate to severe bleeding can occur

Treatment: combo of DDAVP and Factor VIII for any type of bleeding

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53
Q

Von Willebrand Disease: Type III

A

severe bleeding to even minor trauma

Treatment: always Factor VIII regardless of the severity of bleeding

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54
Q

acute leukemia

A

Rapid increase in the number of immature blood cells
Immediate treatment is required because of the rapid progression and accumulation of blasts, which then spill over into the blood stream and spread to other organs

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55
Q

chronic leukemia

A

Excessive buildup of relatively mature, but still abnormal, white blood cells
Typically takes months or years to progress

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56
Q

What happens if CML is left untreated?

A

It will progress to an acute form that appears like AML with a proliferation of blast cells and becomes fatal

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57
Q

What causes CML?

A

Overproduction of the myeloid cell d/t chromosomal abnormality called the Philadelphia chromosome

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58
Q

CML: presentation

A

Fatigue
bone pain
splenomegaly
leukocytosis in the absence of obvious infection; WBC often >150
thrombocytosis

Anemia is not usually present
Mature myeloid cell types (neutrophils, basophils, eosinophils, monocytes) predominate

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59
Q

CML: diagnosis

A

bone marrow biopsy with genomic testing will reveal bcr/abl genotype

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60
Q

CML: treatment

A

Often affects the old, so usually just monitor

Treatment:
-tyrosine kinase inhibitors (e.g. imatinib)
-hydroxyurea
-bone marrow transplant (curative)

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61
Q

CML: Management if it transforms to an acute phase

A

Rising numbers of immature forms in peripheral blood

Tyrosine kinase inhibitors are augmented with a myelosuppressive agent (chemo, radiation) to determine response

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62
Q

blast crisis

A

Final phase in the evolution of CML
Rapid progression, short survival (behaves like acute leukemia)

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63
Q

Blast crisis: diagnosis

A

> 20% blasts in the blood or bone marrow
Presence of an extramedullary proliferation of blasts
Based on symptoms and the blast cell percentage, not on the total WBC count

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64
Q

Blast crisis: presentation

A

Hyperviscosity of the blood, resulting in decreased tissue perfusion

CNS:
-reduced cerebral blood flow can lead to stroke-like symptoms

Cardiopulmonary system:
-acute respiratory failure
-congestive heart failure
-MI

Additional end organ damage
-renal failure
-priapism
-limb ischemia
-bowel infarction

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65
Q

Blast crisis: most effective means of treatment

A

Urgent hematology consult for consideration of leukopheresis

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66
Q

Myelodysplastic Syndrome

A

A variety of acquired clonal disorders of the hematopoietic stem cell
Results in cytopenias and hypercellular bone marrow

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67
Q

MDS: biggest risk factor

A

DNA damage
-hydrocarbons
-ionizing radiation
-alkylating chemo agents

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68
Q

MDS: Diagnosis

A

Excluding other causes of cytopenias and:
-bone marrow aspiration
-cytogenics
-flow cytometry

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69
Q

MDS: Treatment

A

Supportive care with blood products and hematopoietic growth factors:
-erythropoetin
-romiplostim
-granulocyte colony stimulating factor (Neupogen)

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70
Q

MDS: complications with therapy

A

iron overload from multiple blood transfusions

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71
Q

acute leukemia: presentation

A

Blast cells >20%

Profound fatigue
Fevers
Spontaneous bleeding

Occasionally infiltration of organs with leukemic cells (chloroma) - forms a solid tumor

Remission rates from 50-85%
Long term survival ~ 40%

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72
Q

AML: labs, Dx

A

Leukocytosis
Severe anemia
Thrombocytopenia
Blasts
-Auer rods present in blasts

Diagnosis: cryogenic testing of a bone marrow aspiration

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73
Q

AML: malignant cell

A

myeloblast

74
Q

AML: Treatment

A

Induction: High-dose Cytarabine (HiDAC) and an anthracycline (usually daunorubicin)
-stops massive proliferation of myeloblasts
-goal: remission

Consolidation:
-goal: remove myeloblasts that may remain in undetectable amounts in the bone marrow

If AML recurs, consider bone marrow transplant, which can be curative

75
Q

APML: Presentation

A

Extremely rapid development and fatality, sometimes in less than a week

Fatigue
Bone pain
Night sweats
Bleeding/petechiae

76
Q

APML: malignant cell

A

promyelocyte

77
Q

APML: treatment

A

all-trans-retinoic acid (ATRA)

78
Q

ALL: malignant cell

A

lymphoblast

79
Q

ALL: mechanism

A

Lymphocytes have a role in the defense of the CNS, so leptomeningeal spread of ALL to the CNS is common

80
Q

ALL: treatment

A

Intrathecal chemo
Cranial radiation

More difficult to treat in adults than children

81
Q

ALL: labs

A

Atypical lymphocytes
Pancytopenia with circulation blasts (immature/poorly differentiated cells)
-Neutropenia
-Anemia
-Thromobocytopenia

82
Q

CLL: malignant cell

A

B cell lymphocytes

83
Q

CLL: labs

A

lymphocytosis
-smudge cells are often present

84
Q

CLL: Presentation

A

Immunosuppression is the biggest clinical factor

Liver and spleen are often enlarged
Occasionally, signs of autoimmune hemolytic anemia

85
Q

CLL: treatment

A

Ibrutinil - has tyrosine kinase inhibition effects

86
Q

Rarely, CLL can transform a lymph node into an aggressive large B-cell lymphoma, called a…

A

Richter Transformation

87
Q

Lymphomas: Presentation, labs

A

Lymphadenopathy
Normal CBC

88
Q

Lymphomas: Diagnosis, Staging

A

lymph node biopsy

Staging:
- Stage I: disease localized to single lymph node or group
-Stage II: more than one lymph node group involved; confined to one side of the diaphragm
-Stage III: lymph nodes or the spleen involved; occurs on both sides of the diaphragm
-Stage IV: liver or bone marrow involvement

89
Q

Diffuse Large B-Cell Lymphoma (DLBCL): presentation

A

Type of Non-Hodgkins Lymphoma

Aggressive tumor which can arise in any part of the body

First sign: rapidly growing mass in a lymph node
Sometimes associated with “B symptoms” (e.g. fever, weight loss, night sweats)

90
Q

Diffuse Large B-Cell Lymphoma (DLBCL): What viral infections are associated?

A

EBV
CMV
HIV

91
Q

Diffuse Large B-Cell Lymphoma (DLBCL): treatment

A

lymph node resection
chemo (R-CHOP or R-EPOCH, Rituximab)
Radiation
Bone marrow transplant in recurrent disease

92
Q

Cutaneous T-Cell Lymphoma (CTCL)

A

Type of Non-Hodgkin’s Lymphoma

Caused by a mutation of T-cells (unlike most NHL which are generally B-cell related)

93
Q

Cutaneous T-Cell Lymphoma (CTCL): Presentation

A

Generalized erythroderma with lichenification (thick, leathery)
Lymphadenopathy

Atypical T-cells seen in the blood (called Buttock Cells)

Most CTCLs are mistaken for something else, so if the dermatologic condition does not resolve in the usual period of time, CTCL should enter the differential

94
Q

Cutaneous T-Cell Lymphoma (CTCL): treatment

A

Biologic therapy (monoclonal antibodies)
Chemotherapy
Radiation

95
Q

Hodgkin’s Lymphoma: prevalence

A

A type of lymphoma with a bimodal distribution of prevalence (first in the 20s, second in the 50s)

96
Q

Hodgkin’s lymphoma: presentation

A

painful, tender lymph node, usually in one of the cervical chains and spreads in a predictable fashion along lymph node groups
More common in males, average age is 32 years

97
Q

Hodgkin’s lymphoma: diagnosis

A

Biopsy to confirm diagnosis, showing Reed-Sternberg cells (giant lymphocytes with multiple or bilobed nuclei)
- differentiates from non-hodgkin’s lymphoma

CT, X-rays, ultrasound, MRI to locate and stage the disease

98
Q

Hodgkin’s lymphoma: treatment

A

Excision of an affected node
Chemo: ABVD, Stanford V, BEACOPP

99
Q

Plasma Cell Myeloma (aka multiple myeloma)

A

Disease of plasma cells which infiltrate the bone marrow, causing bony destruction and paraprotein formation

100
Q

Plasma Cell Myeloma (aka multiple myeloma): presentation

A

C = hypercalcemia
R = renal failure
A = anemia
B = bony lesions, which cause characteristic “moth-eaten” or “punched out” appearance to large bones (e.g. skull, pelvis, femurs)

101
Q

Plasma Cell Myeloma (aka multiple myeloma): diagnosis

A

proton electrophoresis of urine or blood (SPEP, UPEP) to identify the pathognomonic “Bence-Jones” protein
Serum and urine assessment for monoclonal protein
Serum-free light chain assay
Bone marrow aspiration for increased plasma cells

102
Q

Plasma Cell Myeloma (aka multiple myeloma): treatment

A

Incurable; goal is remission and treat symptoms

Lenalidomide (Revlimid): immunomodulator
Bortezomib (Velcade): proteasome inhibitor
Bone marrow transplant: given as a rescue after a toxic dose of chemotherapy is given to eradicate plasma cells
Orthopedic procedures to help with pathologic fractures

103
Q

Oncologic complications: tumor lysis syndrome - labs

A

hyperuricemia
hyperkalemia
hyperphosphatemia
hypocalcemia

Acute renal failure develops soon after

104
Q

Oncologic complications: tumor lysis syndrome - treatment

A

aggressive IV hydration before, during, and after chemo to maintain urine output and prevent the buildup of cellular materials from destroyed cancer cells

Allopurinol
Rasburicase

NaHCO3 infusions during chemo to alkalinize the urine

Severe: consult nephrologist to determine if emergent HD is needed

105
Q

thalassemia minor: etiology

A

Heterozygous; has only one copy of the beta thalassemia gene

106
Q

thalassemia major: etiology

A

Homozygous; has two genes for beta thalassemia and no normal beta-chain gene

107
Q

thalassemia major: presentation

A

Normal presentation at birth d/t protective effects of fetal hemoglobin
Anemia develops within the first few months of life and becomes progressively severe

Other findings in early life:
- failure to thrive
- feeding difficulties d/t easy fatigue and lack of oxygen
- bouts of fever
- diarrhea
- hepatosplenomegaly and jaundice
- maxillary enlargement

108
Q

folate deficiency: cause

A

inadequate intake or malabsorption of folic acid (needed for RBC production)

109
Q

folate deficiency: S/Sx

A

fatigue
dyspnea on exertion
pallor
headache
tachycardia
anorexia
glossitis

** no neurological signs ** – differentiates B12 from folate deficiency

110
Q

folate deficiency: management

A

folate 1mg PO daily
foods high in folic acid: bananas, peanut butter, fish, green leafy vegetables, iron-fortified breads and cereals

111
Q

Pernicious anemia (B12 deficiency): management

A

B12 (cyanocobalamin) 100mg IM daily x 1 week, then x1/month and lifelong monitoring

112
Q

Von Willebrand Disease

A

genetic disorder that results in the reduced ability to create blood clots, caused by deficiency or mutation in von Willebrand factor and clotting factor VIII

113
Q

Von Willebrand Disease: S/Sx

A

frequent, prolonged, severe episode of bleeding
easy bruising

114
Q

leukemias: S/Sx

A

may be asymptomatic
fatigue
weakness
anorexia
generalized lymphadenopathy
weight loss

115
Q

leukemias: labs, Dx

A

CBC with subnormal RBCs and neutrophils
elevated ESR
peripheral blood smear to distinguish acute and chronic leukemia
bone marrow aspiration to confirm Dx

116
Q

leukemias: treatment

A

chemotherapy
- allopurinol to reduce tumor lysis syndrome in high-risk patients
- bone marrow transplant
- control symptoms

117
Q

lymphomas: management

A

radiation
chemotherapy
bone marrow transplant

118
Q

immune thrombocytopenia purpura: other considerations

A

thrombocytopenic precautions
- avoid constipation (increase fiber, laxatives, etc)
- no flossing
- no shaving
- hold pressure for 5 mins or more for cuts, line insertion, etc.

heparin- induced thrombocytopenia purpura
- stop the heparin
- argatroban (Acova), lepirudin (Refludan) - reverse HIT while offering AC properties

119
Q

How to differentiate ITP from SLE? They both have thrombocytopenia

A

bone marrow analysis

120
Q

Patients with which selective immunoglobulin deficiency have a high risk of reaction when receiving blood products?

A

IgA
risk for anaphylaxis

121
Q

Which immunoglobulin deficiency is associated with repeated infections?

A

IgM
IgG

122
Q

Schistocytes

A

RBC fragments

Result of mechanical destruction (fragmentation hemolysis) of a normal RBC when there is damage to the blood vessel and a clot begins to form

Often seen when there is something implanted in circulation (balloon pump, VAD, mechanical valve, etc.)

Always pathological
Suggests some degree of hemolysis

123
Q

Howell-Jolly bodies

A

Nuclear remnants in the cityplasm
Generally indicate splenic dysfunction

124
Q

Dohle bodies

A

Rough endoplasmic reticulum remnants in neutrophils
Seen in infections and inflammatory conditions

125
Q

Bands

A

Abnormal cells
Cell undergoing granulopoiesis, derived from a myelocyte, and leading to a mature granulocyte
Seen in infections

126
Q

What does a “shift to the left” mean?

A

There is a greater than normal count of neutrophils and the presence of immature neutrophils such as bands and metamyelocytes

127
Q

Blasts

A

Unipotent stem cells
Seen in the peripheral blood
Usually indicates a leukemia or severe myelodysplastic syndrome

128
Q

hemachromatosis

A

iron overload

129
Q

hemachromatosis: causes

A

primary causes: gene mutation of hepcidin common in Celtic, English, and Scandinavian people

secondary causes: excessive blood transfusions, too much iron supplementation

130
Q

results of hemachromatosis

A

cirrhosis
bronzing of the skin
systolic CHF, arrhythmias
endocrine problems

131
Q

How is hemachromatosis diagnosed?

A

Ferritin >300 in males and post-menopausal females, >200 in premenopausal females
TIBC very low
genetic testing if the cause is thought to be primary

132
Q

How is hemachromatosis treated?

A

Phlebotomy to reduce ferritin
Primary hemachromatosis can be treated with chelating agents such as Deferasirox (Exjade)

133
Q

hemolytic anemia

A

due to increased RBC destruction (usually prematurely), faster than the body’s ability to replace them

134
Q

All of the hemolytic anemias cause..

A

hyperbilirubinemia

135
Q

hemolytic anemia: labs

A

low haptoglobin
high LDH (lactate dehydrogenase)
Elevated LFTs with normal GGT

136
Q

Carcinoid crisis

A

Rare and extremely dangerous manifestation that occurs in patients with neuroendocrine tumors
Sudden onset of hemodynamic instability

137
Q

carcinoid crisis: treatment

A

octreotide to control symptoms
glucocorticoids to abort the episode

138
Q

Carcinoid crisis: S/Sx

A

diarrhea
flushing
wheezing
bronchospasm
hypotension refractory to IV fluids

139
Q

Thrombotic thrombocytopenic purpura

A

Results in blood clots forming in small blood vessels throughout the body

Results in low platelet count, low RBCs due to their breakdown, and often kidney/heart/brain dysfunction

140
Q

Thrombotic thrombocytopenic purpura: known triggers

A

bacterial infections
certain medications
autoimmune diseases such as lupus
pregnancy

Triggers form an autoantibody against vWF, which in turn prevents proper platelet adhesion

141
Q

Thrombotic thrombocytopenic purpura: labs/Dx

A

thrombocytopenia
normal or slightly elevated PT/PTT
normal FDP

142
Q

Thrombotic thrombocytopenic purpura: presentation

A

fever
AMS
acute renal failure
hemolytic anemia

143
Q

Thrombotic thrombocytopenic purpura: When to start treatment

A

High mortality – presumptive diagnosis of TTP is made and therapy is started even when only hemolytic anemia and thrombocytopenia are seen.

144
Q

Thrombotic thrombocytopenic purpura: treatment

A

Transfusion is contraindicated as it fuels the coagulopathy

Treatment of choice: plasmapheresis
-Rituximab is often given to augment treatment
-steroids are also helpful

145
Q

Thrombotic thrombocytopenic purpura: monitoring

A

Monitor levels:
-lactate dehydrogenase
-platelets
-schistocytes

146
Q

TTP is a rare complication of which medication?

A

clopidogrel (Plavix)

147
Q

Neoplasm that arises from the endocrine and nervous systems
Commonly in GI tract, lung, pancreas
Most common small bowel tumor

A

neuroendocrine tumor

148
Q

most common primary malignancy affecting the duodenum and jejunum

A

adenocarcinoma

149
Q

Management for pulmonary nodules based on size

A

> 4mm or high risk: serial chest CTs

<6mm: serial chest CTs not required if low risk

<1 cm: intermediate probability of being malignant; serial chest CTs

> 1cm: intermediate probability of being malignant; evaluate by PET
-Positive PET: excise nodule
-Negative PET: serial chest CTs

150
Q

Pulmonary nodules: criteria for low probability of malignancy

A

small size
higher density
discrete and smooth border

benign pattern of calcification
- popcorn calcification
- central calcification
- diffuse homogenous calcification
- concentric calcification

151
Q

Peutz-Jeghers syndrome is a hereditary disorder that increases risk for several cancers, especially…

A

ovarian
endometrial
breast
colorectal
liver
lung
testicular

152
Q

familial adenomatous polyposis is associated with what types of cancer

A

papillary thyroid cancer
adrenal carcinomas
CNS tumors

153
Q

multiple endocrine neoplasia type 1 (MEN1) is associated with what disorders

A

pitutary adenomas
primary hyperparathyroidism
GI tumors

154
Q

Von Hippel-Lindau (VHL) is associated with what types of cancer

A

RCC
end-lymphatic sac tumors
pheochromocytomas
angiomatosis
hemagioblastomas

155
Q

form of intrinsic hemolytic anemia caused by a defect in the RBC membrane, resulting in small spherical erythrocytes that lack central pallor on a peripheral smear

A

spherocytosis

156
Q

spherocytosis: labs

A

increased indirect bilirubin
increased reticulocyte count
+ osmotic fragility test

157
Q

spherocytosis: S/Sx

A

anemia
jaundice
splenomegaly

158
Q

sickle cell crisis: triggers

A

Dehydration (most common)
Hypoxia
Infections
High altitudes
Physical or emotional stress
Acidosis
Surgery
Blood loss

159
Q

advanced ovarian cancer: treatment

A

surgical debulking, followed by cisplatin or carboplatin plus paclitaxel chemotherapy regimen

160
Q

Von Willebrand Disease: S/Sx

A

easy bruising
mucosal bleeding
prolonged bleeding after minimal trauma
severe bleeding after major surgery

Women: menorrhagia is a common presenting complaint

161
Q

Plasma Cell Myeloma (aka multiple myeloma): S/Sx

A

bone pain (most common presenting symptom)
renal failure
anemia
hypercalcemia
pathologic fractures
weakness
infection (often pneumococcal)
spinal cord compression

162
Q

Glucose-6-phosphate deficiency

A

Most commonly affects African Americans and persons of Mediterranean descent
Hemolytic anemia results from oxidative stress that is induced by sulfonamides, quinine, primaquinine, dapsone, and fava beans

163
Q

Glucose-6-phosphate deficiency: S/Sx

A

Typically asymptomatic until they encounter a triggering agent, then present with jaundice, back pain, dark urine, fatigue

164
Q

Glucose-6-phosphate deficiency: labs

A

Hgb: low
Retics: high
Unconjugated bilirubin: high

165
Q

Drug of choice for DVT prophylaxis for bed ridden patients

A

LMW Heparin

166
Q

Most common cause of thrombocytopenia

A

idiopathic thormbocytopenic purpura

167
Q

acute chest syndrome

A

Major complication of sickle cell disease
May be the result of trigger vasooclusion d/t pneumonia, asthma, hypoventilation

Characterized by:
-fever
-pleuritic chest pain
-low oxygen saturation
-multilobar infiltrates

168
Q

malignancy-associated hypercalcemia: management

A

Goal: restore a eucalcemic state while inhibiting bone resorption
- IV hydration with NS to provide resuscitation and re-establish renal perfusion with calciuresis
- bisphosphonates given within 24 hours if no improvement
- calcitonin as an adjuvant to inhibit osteoclastic bone resorption

169
Q

Henoch-Schonlein purpura

A

IgA vasculitis

Characterized by:
-purplish rash
-abdominal pain
-glomerulonephritis

170
Q

adrenal insufficiency: diagnosis

A

ACTH stimulation test
-cosyntropin (Cortrosyn), a form of synthetic ACTH, is given IV push and cortisol levels are drawn at 0, 30, and 60 minutes
-cortisol levels normally rise to >20mg/dL
-If the levels fail to rise by >5-10% of the baseline, the test is diagnostic for adrenal insufficiency

171
Q

hemolytic uremic syndrome: presentation

A

renal failure
neurologic abnormalities
hemolytic anemia
thrombocytopenia

171
Q

hemolytic uremic syndrome: labs/Dx

A

FDP normal
thrombocytopenia

172
Q

hemolytic uremic syndrome is most often associated with…

A

diarrheal illness caused by a Shiga toxin-producing E. coli

173
Q

protein C deficiency is a disorder associated with increased risk for…

A

VTE

174
Q

neutropenic fever

A

Sign of severe infection in patients with ANC<1000
Rapidly fatal if left untreated

175
Q

neutropenic fever: management

A

Urine, sputum, blood cultures
Empiric broad-spectrum ABx as soon as possible
Neutropenic isolation precautions
Private room with positive pressure air ventilation

176
Q

SVC syndrome

A

partial or complete obstruction of blood flow through the SVC

177
Q

SVC syndrome: causes

A

Most common: tumor
infection
thrombus

178
Q

SVC syndrome: S/Sx

A

Develop slowly

Cough
Face or neck swelling
Feeling of fullness in your upper body
Upper extremity swelling
SOB, cyanosis
Chest pain
Horner’s syndrome

179
Q

SVC syndrome: management

A

Treat underlying cause

180
Q

SVC syndrome: diagnosis

A

xray
CT
venography

Board Exam (18 decks)

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