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Hematology and Oncology Flashcards

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1
Q

What do mast cells do?

A

Release histamine and heparin, and trypase

They are involved in type 1 hypersensitivity

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2
Q

What do dendritic cells do?

A

Highly phagocytic

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3
Q

What do lympocytes include?

A

Can be B cells, T cells, NK cells

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4
Q

Where do B cells come from?

What is their function?

A

They are humoral response cells

They function as APC and MHC cells

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5
Q

what do T cells do?

where do they come from?

A

T-cells differentiate into cytotoxic T cells

They develop within the Tymus

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6
Q

what type of cancer is associated with the plasma cell?

A

Multiple mylenoma

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7
Q

What is the difference between the fetal and adult hemoglobin?

A

HbF has higher affinity for O2, and less binding of O2 2, 3 BPF

This allows for higher extraction of O2 from maternal hemoglobin

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8
Q

What are the types of antigens on the blood surface?

A

If have A (then have the A surface antigen) if have AB have both the A and the B

O has no antigen

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9
Q

What type of antibodies will be in the plasma?

A

anti-B (if type A)

Anti-A (if type B)

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10
Q

What happens if you give type A or AB blood to the type B person?

A

will have a hemolytic reaction

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11
Q

Who is the universal recipient?

A

The type AB

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12
Q

Which is the universal donor?

A

The type O

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13
Q

What is the rh hemolytic disease of a newborn?

A

Rh - mothers, had rh+ baby, so made anti-D IgG, so the IgG will cross the placentas and cause hemolytic disease of the newborn

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14
Q

How to prevent hemolytic disease of the newborn?

A

Give Rho-gram (this is an anti-D IgG)

Should be given at the third trimester to avoid production of the anti-D IgG production

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15
Q

What is ABO hemolytic disease of the newborn?

Presentation?

A

Most common form
Usually occurs in mother with type A, B, or AB fetus
Usually presents with mild jaundice (24 hours) . Does not change future pregnancies

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16
Q

How to tell abnormal hemoglobin on the gel?

A

Cathode (neagtive) on the left
Abnotaml will move more on the left, because higher negative charge

Furthest to the left:

Hb SC
SS
HbF
Normal HB

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17
Q

What are deficiency in hemophilia A?
Hemophilia B?
Hemophilia C

A 
Factor VIII
Factor 1X (hempophilia B) 
Factor X1 (Hemophilia C)
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18
Q

What are factors that inhibit coagulation factor Xa?

A

LMWH
heparin
direct Xa inhibitors
fondaparinox

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19
Q

How does heparin work?

A

Inhibits the antithrombin

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20
Q

What are factors that are affected by anti-thrombin?

A

II, VII, IX, X, X1, X11

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21
Q

What are the possible targets of anti-thrombin?

A

Thrombin and factor Xa

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22
Q

How does ASA work?

A

inhibits cyclooxygenase

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23
Q

How does plavix work?

A

Inhibits ADP (expression of GP11B/IIIA)

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24
Q

How does Abciximab, epitafibatide, tirofiban work?

A

GP IIB/IIIA

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25
Q

What pathology associated with acanthocyte (spur cell)?

A

Liver disease

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26
Q

what associated with Basophilic stippling?

A

Lead poisoning
Sideroblastic anemia
Myelodysplasia syndromes

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27
Q

Disease associated with Dacrocyte?

A

Bone marrow infiltration (myelofibrosis)

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28
Q

Disease associated with degmacyte *bite cell)

A

G6PD deficiency

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29
Q

Disease associated with echinocyte? Burr cell

A

end stage renal disease
Liver disease
Pyruvate kinase deficiency

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30
Q

Disease associated with elliptocyte?

A

Heredirary (usually assymptomatic)

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31
Q

Disease associated with ovalcyte?

A

Megaloblastic anemia (bone marrow failure)

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32
Q

Disease associated with ringed sideroblast?

A

Sideroblastic anemica

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33
Q

Disease associated with schistocyte?

A

DIC, TTP, HUS, HELPP syndrome, or mechanical heart valve hemolysis

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34
Q

Disease associated with sphereocyte?

A

Hereditary spherocytosis, drug infection hemolytic anemia

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35
Q

What are the disease associated with the target cell?

A

HbC disease, asplenia, liver disease, thalessemia

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36
Q

Disease associated with Heinz bodies?

A

Seen in G6PD deficiency

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37
Q

Disease associated with Howell Jolly bodies?

A

Functiona hyposplenia or asplenia

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38
Q

What are the causes of microcytic anemia?

A 
Iron deficiency 
Alpha thalessemia 
B talessemia
Lead poisoning
Siderblastic anemia
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39
Q

What are the MCV of different types of anemia?

A

Microcytic (less then 80)

Macro > 100

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40
Q

What are symptoms of iron deficiency? (Lab and clinical)

A

Decreased iron
Increased TIBC
Decreased ferritin

Clinical: fatigue, conjunctival pallor, pica

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41
Q

What are the causes of iron deficiency anemia?

A

GI hemorrage
Malnutrition
Absoprtion disorders

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42
Q

What deletions are responsible for alpha thalesemia? What do each deletions mean?

A

4 allele: no alph globin (incompatible with life)
3 allele deletion )very little alpha, a lot of B
2 allele deletions: less clinically severe anemia
1 allele deletion: no anemia (clincally silent)

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43
Q

What is B thalesemia minor?

A

No B chain produces, usually assymptomatic (increased HbA)

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44
Q

What is B thalesemia major?

A

severe microcytic, hypochromic anemia

has target cells, and increased anisopikilocytosis

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45
Q

What is HbS/B thalassemia heterozygote?

A

mild to moderate sickle cell anemia

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46
Q

What are the signs of lead poisoning?

A 
Lead lines of gingiva
Encephalopathy (on erthrocyte basophilic strppling) 
Abdominal colic
Sideroblastic anemia 
Drop waist and foot

How to treat: succimar chelation for kids

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47
Q

What are the causes of siderblastic anemia?

A

Defect in heme synthesis

Caused by: genetic, ETOH, vitamin B6, copper deficiency

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48
Q

What are the lab findings for sideroblastic?

What is the treatment for sideroblastic?

A

Increased iron, decreased TIBC, increased ferritin

Treatement: pyridoxine B6

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49
Q

What are the causes of megaloblastc anemia?

A

Folate deficiency
Vitamin B 12 (cobalamine deficiency)
Orotic aciduria
Diamond Blackfan anemia

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50
Q

What are causes of folate deficiency?

What are the findings?

A 
Malnutrition 
Malabsoporption
Drugs
Phenytoin 
Pernacious anemia

Findings:
Homocystein increased
Normal methylmalonic acid
No neurological deficieny

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51
Q

What are causes and findings of Vitamin B deficiency?

A

Insufficient uptake
Malabsorption
Pernacious anemia

Findings:
increased homocysteine, increased methlmalonic acid

Neurological symptoms: neuro degeneration ( in fatty acid pathways, and in myelin synthesis)

How to diagnosis the vitamin B deficiency?
With a Schilling test

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52
Q

What is orotic aciduria?

A

Can’t convert orotic acid to UMP
Diagnosis: orotic acid in urine
Treatement: uridine monophosphate to bypass the mutated enzyme

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53
Q

What is Diamond blackfan anemia?

A

Rapid onset anemia due to defect with progenitor cells

Clincial: short stature craniofacial abnormalities, and upper extremities are deformed

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54
Q

What is non-megaloblastic anemia?

A

Macrocytic anemia in which the DNA synthesis is unimpaired

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55
Q

What are the types of normocytic, normochromic anemia?

A

Are classified as non-hemolytic or hemolytic
Caused by:
Intravasular hemolysis
Extravasculat hemolysis

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56
Q

What are findings of intravascular hemolysis?

A 
Decreased haptoglibun 
Increased LDG
schistocytes
Increased reticulocytes
Increased unconjugated bilirubin 
Hemogloginuria
microangiopathic anemia
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57
Q

What are signs of extravascular hemolysis?

A

Spherocytes in periphereal smear
increased LDH
No hemoglobinuria/hemosiderinuria
Increased unconjugated bilirunin (jaunedice)

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58
Q

What are causes of nonhemolytic, normocytic anemia?

A

Anemia of chronic disease

Aplastic anemia

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59
Q

What are the signs the signs of Anemia of chronic disease?

A

Inflammation (increased hepcidin), decreased iron absorption
findings: decreased iron, decreased TIBC, icnreased ferrtiin

Treatment: EPO

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60
Q

What are causes of aplastic anemia?

A

Radiation, drugs
Viral agens (B19, EBV, HIV)
Fanconi anemia
Idiopathic

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61
Q

What are lab findings of aplastic anemia?

A

Decreased reticulocyte count
Pancytopenia
Fatigue, malaise, pallor, purpura,

TreatmentL withdraw the agent, immunosuppression regimes, RBC/platelet tranfusion, bone marrow stimulation with GM-CSF

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62
Q

What are causes of intrinsic hemolytic anemia?

A 
Hereditery spherocytosis
G6PD
Pyruvate deficiency 
HbC disease
Paroxymal nocturnal hemoglobinuria 
Sickle cell anemia
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63
Q

What are characteristics of hereditery spherecytosis?

A

Extravascular hemolysis
Small RBC with less surface area
Premature removal by splee
Spleenomegaly and aplastic crisis

Lab: osmotic fragility test +
Treatment: spleenectomy

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64
Q

What are characteristic of G6PD?

A

Causes intra and extravascular hemolysis
X-linked recessive
Will have hemolytic anemia following oxident stress (sulfa, anti-maleria, infections)

What are the lab values? Heinz bodies,

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65
Q

What are HbC disease?

A

Homozygots will have hemoglobin crystals inside the RBC

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66
Q

What is the paradoxymal nocturnal hemoglobinuria?

A

Complement mediated RBC lysis
Increased incidence of leukemia

Clinical: Coombs negative hemolytic anemia, pancytopenia, venous thrombosis

Treatment: eculizumab terminal complement inhibition

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67
Q

What are the characteristics of sickle cell anemia?

A

Point mutation with B chain substitute
At low O2, high altitude or acidosis can cause anemia and vaso-occlusive disease

Newborns are initially symptomatic because HBF is decresed and HBS is decreased

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68
Q

What are the complications of sickle cell disease?

A 
Aplastic crisis
Autosplenectomy
Splenic infarct
salmonella
Painful crisis 
Renal papillary necorsis
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69
Q

What trait to hetrozygotes for sickle cell anemia have?

A

They tend to be resistant to maleria

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70
Q

What are the types of extrinsic suckle cell anemia?

A

Warm IgG (chronic seen in SLE, and CLL): usually Coombs test +

Cold IgM and complement: anemia triggered by cold seen in CLL (findings: direct coombs test anti-Ig antibody

Can be seen in mycoplasma pneumonia infections

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71
Q

What is the coombs vs indirect ?

A

Coombs direct: put the anti-Ig antibody
Indirect coombs: normal RBC added to the patient serum. If serum has anti-RBC then will agglutinate when Coombs reagent added.

72
Q

What are characteristics of microangiopathic anemia?

A

RBC are damaged when passing through the vessel lumina

Seen in DIC, TTP/HUS, SLE and malignant HTN

Will see schistocytes

73
Q

What are characteristics of macroangiopathic anemia ?

A

Prosthetic heart valves
Aortic stenosis
Will have schistocytes on periphereal blood smear

74
Q

How do infections cause extrinsic hemolytic anemia?

A

destroy RBC (Maleria, Babesia)

75
Q

What happens to the iron, ferrtin transferrin, and % of saturation in iron deficiency, chronic disease, hemochromatosis, pregancy?

A 
Iron deficiency anemia:
Iron decreased
transferrin increased
ferritin decreased
percentage of transferrin saturation decreased

Chronic disease:
Serum iron decreased
Transferrin decreased
Ferritin increased

Hemochromatosis: 
Iron increased
Transferrin decreased
Ferritin increased
Percentage of saturation increased
76
Q

What are the causes of neutropenia?

A

Neutophil count less then 1500
Severe infection occurs then
Causes of neurtopenia: sepsis, post infection, drugs (chemotherapy) aplastic anemia, radiation

77
Q

What are causes of lymphopenia?

A 
Lymphocyte count less the 1500
HIV, DiGeorges, SCID
Radiation
Sepsis 
Post op
78
Q

What are charactertics of eosinopenia?

A

Cushings, coticosteroids

79
Q

What is a left shift of the WBC?

A

Inceased neutrophil precursosrs such as band cells and metamyleocytes in periphereal blood

Neutrophilia caused in response to infection or inflammation

More immatyre cells

80
Q

What is the enzyme and the substrate/symptoms of lead poisoning?

A

enzyme: ferrochlatase and ALA dehydratase
Accumulated substance: protophyrin ALA
Symtoms: microcytic anemia, children with exposure to lead paint
Adults: envrionemental exposure (leads to memory loss,demyelination)

81
Q

Enzyme, accumulated substance and symptoms of acute intermittant porphyria?

A 
Enzyme: porphobilinogen deaminase
Symptoms: painful abdomen
wine colored urine
Polyneuropathy
Psychological disturbances
Drugs: cytrochrome P450 
Treatment: glucose, heme
82
Q

Enzyme, accumulated substrate, and symptoms of porphyria cutanea tarda?

A

Enzyme: Uroporphyrinogen decarcobylase
Substrate: Uroporphyrin (tea colored urine)
Symtoms: photosensitivity (most lcommon)

83
Q

Mechanism/symptoms/treatement of lead poisoning?

A

Usually due to accidental ingestion (has high mortality)

cell death due to peroxidation of membranes

Symptoms: nausea, vomiting, gastric bleeding, lethargy and scarring

Treatment: chelation

84
Q

What do PT tests function on?

A 
I
II
V
Vll
X
85
Q

What test does PTT function on?

A

Acts on all of the intrinsic pathways except Vll and Xlll

86
Q

What happens to PT and PTT in hemophilia? Which factors are affected?

A

PT remains the same
PTT increases

Hemophilia A: factor VIII
Hemophilia B IX
Hemophilia C XI

87
Q

How to treat hemophilia?

A

Desmopressin
Factor VIII
factor IX concentrates
Factor XI concentrates

88
Q

What are some symptoms of hemophilia?

A

macrohemorrage (hemarthoses, bleeding into the jonts) easy bruising, bleeding after trauma or surgery

89
Q

What happens when you have a general coagulation defect?

A

Decrease in activity factors II, VII, IX, X protein C and protein S

90
Q

What happens to platelet count and bleeding time within Bernard Soulier syndrome?

A

Decreased platelet count
Increased bleeding time
Defect in platelt plug formation (large platelets)

91
Q

What happens in Glanzman thrombasthenia?

A

Platelet count unchanged
Bleeding time increased
Defect in plug formation
Lab: blood smear will show no clumping

92
Q

What happens to bleeding time and platelet count in Immune Thrombocytopenia?

A

Decreased platelet count
Increased bleeding time
Labs: increased megakaryocytes on bone marrow biopsy
Treatment: IVIG, splenectomy (for refractory ITP)

93
Q

What happens to bleeding time and platelet count in hemolytic-uremic syndrome?

A

Decreased platelet count
Increased bleeding time
HUS in children accompanied by diarrhea and caused by Shiga toxin E coli

IN adults: STEC infection (usually no diarrehea)

94
Q

What happens to platelet count, and bleeding time in thrombotic thrombocytopenic purpura?

A 
Degredation of vWF
Labs: shistocytes and increased LDH
Symptoms: neurological and renal symptoms
Fever
Thrombocytopenia
Microangiopathic hemolytic anemia 
Treatment: plasmaphaeresis and seteroids
95
Q

What happens to platelet count and bleeding time with von Willebrand disease?

A

Platelet count unchanged
Bleeding time increased
PT stays the same
PTT increased

Defect in plug formation, but usually mild
Treatment with desmopressin (releases the vWF stored within)

96
Q

what happens to platelet count, bleeding time, and PT and PTT in disseminated intravasular coagulation?

A 
Decreased platelet count
Increased bleeding time
Increased PT
Increased PTT
Widespread activation of clotting factors 
Causes: 
Sepsis
Trauma
Obstetrics
Malignancy
Nephrotic syndrome 
Transfusions
Labs show: shcistocytes, fibrin degredation, D-Dimer, decreased fibrinogen, decreased factor V and VIII
97
Q

What is description of antithrombin deficeincy?

A

No antithrmobin
No direct effect on PT and PTT
(less increase in PTT when give heparin)
Can be acquired from renal failure, nephorotic syndrome, and antithrombin loss in the urine

98
Q

What about factor V leiden?

A

Production of mutant factor V
Most common cause of hypercoagulability
Results in DVT, cerebral vein thrmobosis, and recurrent pregnancy loss

99
Q

what occurs in protein C and S deficiency?

A

Inability to activate factor V and VIII

ncreased risk of thrombotic skin necrosis with hemmorage when given warfarin

100
Q

What are characteristics of prothrombin gene mutation?

A

Mutation in the untranslated 3’ region
Increase production of prothrombin
Increase venous clots

101
Q

What are blood transfusion therapy?

A

Packed RBC: increased Hb and O2 carrying capacity

102
Q

What does platelet transfucion do?

A

Give if significant bleeding

If there are qualitative platelets re low

103
Q

What does FFP do?

A

Increase in coagulation levels

USE of DIC, cirrhosis, and to reverse the warfarin

104
Q

What does cryoprecipitate do?

A 
Contains fibrinogen
Factor VIII
Factor XIII
vWF
fibronectin

Give in coagulation factor deficiencies involving fibrinogen or factor VIII

105
Q

What are signs associated with the leukemia?

A

lymphoid and myeloid neoplasm with involvement of the bone marrow

Tumor cells are found in the peripheral blood

106
Q

What is lymphoma?

A

Tumor mass arising in the lymph nodes

107
Q

What are the differences between Hodgekin and non hodgkin lymphoma?

A

Hodgekin:
Localized, single node
Goof prognosis
Reed-sternberg cells
Bimodal distribution (> 55 or young adults)
Assocaited with EBV
have low grade fever, night sweats and weight loss

Non Hodgkins:
Multiple lymph nodes involed (non contiguous spread)
Mostly B cells, and a few T cells
Can occur in children and adults
May be associated with HIV and autoimmune disease
May have constitutional signs and symptoms

108
Q

What is a reed steinberg cellÉ

A

Giant tumor cell in Hodgekinsès Lymphoma (looks like owl) due to bilobed. Necessary but not sufficiant to make diagnosis of Hodgekins

109
Q

What are the genetics and occurrence of Burkitt’s lymphoma?

A

Adults or young children
Caused by transolocation of 8:14 (c-myc) gene
Associated with EBV
Has characteristic jaw lesion which is endemic in Africa

110
Q

Genetics and occurrence of B cell lymphoma?

A

Usually in older adults, but 20% in children

Is the most common type of Non_hodgekin’s lymphoma

111
Q

Genetics and occurrence of Follicular lymphoma?

A

Occurs in adults
Due to 14:18 translocation
Indolent course (Bcl-2 inhibits apopotosis)
Has painless waxing and waning lymphadenopathy
If have follicular architecture, small cleaved cells (grade 1)

Large cells (grade 3) 
Mixture of cells (grade 2)
112
Q

What is mantle cell lymphoma?

A

Usually occurs in adult males
Translocation 11:14 cycli D1 and heavy chain Ig
Very aggressive, and typically present with late stage disease

113
Q

What is primary central nervous system lymphoma?

A

Occurs in adults
Usually associated with HIV and aids
Considered an aids defining illness
Variable presentation: confusion, memory loss
Will have a mass on MRI
Can be distinguished from toxoplasmosis via CSF analysis or other lab tests

114
Q

What are the two Neoplasms of the mature T cells?

A

Adult T cell lymphoma

Mycosis fungoides/Sezary syndrome

115
Q

How is adult T cell lymphoma caused?

A

By adult HTLV (associated with IV drug use)
Adults present with cutanesous lesions in Africa, Japan, and Carribean

Are lytic bone leisions
Associated with hypercalcemia

116
Q

What is mycosis fungoides/Sezary syndrome?

A

Caused in adults
Presents with skin patches (plaques(
Has atypical CD4+ cells (cerebriform nuclei)
May progress to Sezry syndrome

117
Q

What are the characteristics of multiple myeloma?

A

Monoclonal plasma cell (fried egg appearance)
Cancer arises in the marrow and produces large amounts of IgG (55%) or IGA (25%)

Most common primary tumor arising within bone of people > 40-50 years of age

Associated with:
Increased infection
Primary amylooidosis
Punched out leisions on x-ray
M spike on the serum protein (electrophoresis
Ig Light chains in urnine (Bence Jones protein)
Rouleauc formation (RBC stacked like poker chips)
Numerous plasma cells with clock face chromatin and intracytoplasmic inclusions containing immunoglobulin

118
Q

What is Monoclonal gammopathy of undetermined significance?

A

Monoclonal expansion of plasma cells (assymptomatic)
May lead to multiple myeloma.
Not associated with CRAB findings

119
Q

What are the CRAB findings associated with multiple myeloma?

A

Hypercalcemia
Renal involvement
Lytic bone pain/Back pain
Have the multiple myeloma M spike on protein

120
Q

How to distinguish between Walderstrom macroglobinemia and Multiple Myeloma?

A

Walderstrom will have hyperviscosity syndrome (blurred vision), Raynaud phenomenon, and will NOT have CRAB

121
Q

What are the myelodysplastic syndromes?

A

Stem cell disorders with ineffective hemtopoiesis
Defecrs in cell maturation of cells NON-lymphoid lineages
Caused by new mutations or environmental exposure

122
Q

What is the Pseudo-Pelger-Huet anomaly?

A

Neutrophils with bilobed nuclei

Usually are seen after chemotherapy

123
Q

What are the characteristics of Leukemias?

A

Unregulated growth and differentiation of WBC in the bone marrow
Usually has marrow failure
Anemia, decreased mature WBC causing infecion, hemorrage due to decreased platelets

Will have malignant WBC in body (immature ones)

In some rare cases can cause the normal WBC to decrease

Can have cell infiltation of the liver, spleen, lymph nodes and cause skin leukemias

124
Q

What are characteristics of the acute lymphoblastic leukemia/lymphoma?

A

Most often occurs in children (if in adult has bad prognosis)

Tcell ALL can present as a mediastinal mass (SVC syndrome)

Can be associated with Down’s syndrome

Peripheral blood and bone marrow will have increased in lymphoblasts

TdT+ marker of preT and preB cells (most responsive to therapy)

May spread to the CNS and the Testes

translocation 12:21 has a better prognosis

125
Q

What are characteristics of Chronic lymphocytic leukemia/small lypmhocytic lymphoma?

A 
Age more the 60 years 
Most common adult leukemia 
CD 20+ CD5+ B cell neoplasm 
Are assymptomatic and progress slowly 
Autoimmune hemolytic anemia
126
Q

What is a Richter transformation of CLL/SLL?

A

There is transformation to an aggressive lymphoma (most commonly diffuse large B cell lymphoma)

127
Q

What is hairy cell leukemia?

A 
Usually in adult males 
Mature B cell neoplasm 
Usually assymptomatic 
Have hair like projections on the cell
Causes marrow fibrosis

Treatment: Cladribine and pentostatin

128
Q

What is acute myelogenous leukemia?

A

Median onset is 65 years old
Has Auer rods and myeloperoxidase (cytoplasmic inclusions are seen)

Will have increased circulating myeloblasts on periphereal smear

Risk factors: 
Prior akylating chemotherapy 
Radiation 
Myeloproliferative disorders 
Down's syndrome  (15:17)

APL subtype responds to all Trans-retinoic acids
DIC is common presentation or promyelocytes

129
Q

What is chronic myelogenous leukemia?

A

Occurs accross the peak spectrum of 45-85 years of age
Defined by the philidelphia chromosome (translocation of (9:22) BCR-ABL

Has a slow progression with very low LAP as a result of low activity in malignant neutrophils

Responds to bcr-abl tyrosine inhibitors (imatinib)

130
Q

What are the common chromosomal translocations?

A

8: 14 Burkitt’s lymphoma
9: 22 (Philedelphia chromosom) CML, rarely ALL
11: 14 Mantle cell
14: 18 Follicular lymphoma
15: 17 APL ( a type of AML)n

131
Q

What is Langerhans cell histiocytosis?

A

Proliferative disorders of the dendritic (Langerhans cells)

Presents with:
Skin rash
Lytic boneleisions
Otitis media (mass around the mastoid bone)
Cells are immature and do not effectively stimulate T cells
Cells will express S-100 mesodermal origin (tennis racket looking cell)

132
Q

What are examples of Chronic myeloproliferative disorders?

A

Polycythemia vera
Essential thrombocytopenia
Myelofibrosis

133
Q

What are characteristics of polycthemia vera?

A

Increased hematocrit
May present with itching after hot shower
Classic symptom: erythomelagia ( severe burning pain with blue discolaration)
Can have blood clots
Treat with ASA

134
Q

What are characteristics of esstential thrombocytopenia?

A

Have proliferation of megakaryocytes and platelets
Have bleeding and thrombosis
Blood smear has increased platelets
Can have erythromelagia

135
Q

What are characteristics of Myelofibrosis?

A

Obliteration of the bone marrow with fibrosis due to fibroblast activity

Can have splenomegaly and teardrop RBC

136
Q

What are the essential differentating characteristics between polycythemia, essential thrombocytopenia and myelofiborisis?

A

Poly inc RCB, Inc WBC, Inc Platelet Phil chrom -, JAK 2 +
Essential No change RBC, NC WBC,Inc Plt, Phil -, 30-50% Jak 2,

Myelofibrosis: Dec RBC, Variable WBC, Var Plt, negative phil, + Jak (30-50)

CML: Decreased RBC, Inc WBC, increased Plt, +Phil, -JAk

137
Q

what are the characteristics of the different types of polycythemia?

A

Relative:have a decrease in plasma volume (due to dehtydration)

Appropriate (absolute) 
increased RBC mass
decreased O2 saturation
EPO increased
Due to lung disease, congenital heart disease 
Inappropriate absolute
no change in plasma volume
increased RBC mass
no change in O2 saturaton
 increased EPO leves (malignancy, hydronephrosis)

Polycythemia vera: increased plasma volume, increased RBC mass
no change in O2
EPO is decreased (polycythemia suppresses EPO production)

138
Q

What is the mechanism of Heparine?

What are side effects of heparine?

A 
Lowers the activity of thrombin and factor X
Side effects:
Bleeding
HIT
Osteoporosis
139
Q

The difference between low molecular weight heparine and heparine (enoxaparin, dalteparin, fondaparinox) ?

A 
More active on factor X
They have a better bioavailability
2-4 times longer half life 
Does not need monitoring
Difficult to reverse
140
Q

How does heparin induced thrombocytopenia occur?

A

developpement of IgG against heparine bound platelet factor 4
Causes thrombosis and thrombocytopenia

141
Q

What are examples of direct thrombin inhibitors?

A

Bivalirudin (related to hirudin)
Directly inhibits activity of free and associated thrombin
Can be used in atrial fibrillation, DVT
no lab monitoring
no reversal agent ( use fibrinolytics and tranexamic acid

142
Q

What is the mechanism of warfarin?

A

Factors II, VII, IX, X, protein C and protein S

Increased PT

143
Q

What are adverse effects of warfarin?

A

Bleeding
Teratogenic skin necrosis (due to microthrombosis)
Hypercoagulobility

144
Q

What are the differences in heparin vs warfarin?

A

Warfarin works in the liver, heparine in the blood
Warfarin slow action, heparine is quick
Warfarin lasts for days, heparin is hours
Heparine inhibits coagulation in vitro
Heparine PTT (intrinsic pathway), PT, INR (extrinsic pathway)

145
Q

what are example of direct factor Xa inhibitors?

what is the mechanism?

A

Apixaban, Rivaroxaban
Binds directly to factor Xa
No reversal agent exists

146
Q

Thrombolytics: mechanism, clinical use, and adverse effects?

A

Alteplase, reteplase, streptokinase, tenectaplase
Aids conversion of plasminogen to plasmin (cleaves thrombin to fibrin)
Use: early MI, ischemic stroke or PE
Contraindications: bleeding, intracranial, recent surgery, bleeding diathesis
Treat toxicity: aminocarpoic acid, fibrinolysis
FFP

147
Q

What are examples of ADP receptor inhibitors?

Clinical uses/ adverse effects?

A

Plavix, prasugrel, tricagrelor, ticlopidine
Clinical uses: MI, coronary stenting, decrease thrombotic stroke
Adverse: neutropenia

148
Q

What are examples of phosphodiesterase III inhibitors?

A

Increase cAMP in platelets leading to platelet aggregation
Clinical use is acute coronary syndrome, stroke
Adverse: Nausea, headache, facial flushing, hypotension

149
Q

What are examples pf glycoprotein IIB/IIIb inhibitors?

A

Abciximab, eptifibatide, tirofiban
Binds to glycoprotien IIB/IIIA on activated platelets
Clinical use: unstable angina, PTCA
Adverse: Bleeding and thrombocytopenia

150
Q

what are the different types of cancer drugs, and what cell cycle do they act on?

A

G1:
Bleomycin
Topoisomerase inhibitors (etoposide, teniposide)

Antimetabolites (DNA synthesis)
Azathiopine
Cladribine
Cytarabine
Fluorouracil 
Hydroxyurea

Microtubule inhibitors:
Paclitaxel
Vinblastine

151
Q

Mechanism, clinical, adverse effect of azathiorpine?

A

Purine analog
Prevents rejection, RA, IBD, SLE
Adverse: myelosuppression, GI, liver,
Increased toxicity when combined with allopurinol

152
Q

Mechanism, clinical, adverse of cladribine?

A

Purine analog
Hairy cell leukemia
Adverse: myelofibrosis, nephrotoxocity, neurotoxicity

153
Q

Mechanism, clinical, adverse Cytarabine?

A

Pyrimidine analog
Used in leukemias
Myelofiboris, nephortoxicity, and neurotoxicity

154
Q

Mechanism, clinical use, adverse effects of 5-fluorouracil?

A 
Pyrimidine analog 
Colon cancer, pancreatic cancer 
Cancer
Basal cell carcinoma 
Adverse: Myelosuppression (worsened with addition of leucovorin)
155
Q

Adverse, clinical, of methotrexate?

A

Folic acid analog
Cancers: leukemia, lymphomas, choriocarcinoma, sarcomas, ectopic pregnancy, medical abortion, arthritis, psoriasis , IBD, vasculitis
Adverse: Myelosuppression (which is REVERSED by leucovorin…this is opposite of the effect on 5-fluorourcil
Hepatoxicity
Mucositis
Pulmonary fibrosis

156
Q

Adverse, clinical of bleomycin?

A

Induces free radical formation
Testicular cancer
Hodgkins Lymphoma
Adverse effects: pulmonary fibrosis

157
Q

Adverse, clinical of dactinomycin?

A

Intercalates DNA
Wilms tumor, Ewing Sarcoma
Rhabdomyosarcoma
Adverse: Myelosuppression

158
Q

Adverse, Clinical of Doxorubicin?

A

Generates free-radicals
Solid tumors, leukemia, lymphoma
Adverse:Cardiotoxicity, myelosuppression

159
Q

Adverse, clinical Busulfan?

A

CML
Also to abalate the bone marrow before transplant
Adverse: severe myelosuppression

160
Q

Adverse, clinical of cyclophosphamide?

A

Cross-link DNA
Solid tumors:leukemia, lymphomas
Adverse: Myelosuppression, cystitis

161
Q

Adverse, clinical of nitrosourreas?

A

Used for brain tumors (glioblastoma multiforms)
Crosses blood brain barrier
Adverse: CNS toxicity (convulsions, ataxia)

162
Q

Clinical use/adverse effects if Paclitaxel ?

A

Ovarian and breast carcinoma

Adverse effects: Myelosuppression, neuropathy, hypersensitivity

163
Q

Adverse effetcs of Etoposide, teniposide?

A

Used for solid tumoirs (testicular and small cell lung cancer) leukemia, lymphomas

164
Q

Adverse effects, and uses for Irinotecan, topotecan?

A

Inhibits Topoisomerase
Used for colon cancer
Severe myelosuppression, diarrihea

165
Q

Adverse effect, uses for hydroxyurea

A

Melanoma, CML, sickle cell

Adverse: severe myelosuppression

166
Q

What are the adverse effects and uses or prednisone, prednisolone?

A 
Used in chemotherapy for CLL, non Hodgkins's lymphoma, immunosuprresants in autoimmune disease 
Adverse effects: 
Cushing like symptoms 
Osteoporosis
Hypertension
Peptic Ulcer
167
Q

What are the effects of Bevaciszumab?

A 
Monoclonal antibody 
Solid tumores (colorectal and renal cell carcinoma)
168
Q

Clinical adverse of erlotinib?

A

Non cell carcinoma

169
Q

Cetruximab?

A

Stage IV colorectal cancer

Adverse effect: rash, elevated LFT

170
Q

Rituximab?

A

Non Hodgekin’s lymphoma, CLL and ITP, Rhumatoid

171
Q

Tamoxifen and raloxifene?

A

Selective estrogen recpetors
Clinical use: Breast cancer treatement
Raloxifene can also be useful to prevent osteoporosis

172
Q

Trastuzumab?

A

For Her-2 breast Ca and gastric Ca

Adverse effect: cardiotoxicity

173
Q

Vemurafenib?

A

Inhibits BRAF oncogene + melonomal

For use in metastatic melatnoma

174
Q

What are drugs that give ototoxicity and nephrotoxicity?

A

Cisplatin/Carboplatin

175
Q

What is common side-effect of cyclophosphamide?

A

Hemorraghic cystitis

176
Q

Most common side effect of 5-Fu and 6-MP?

A

Myelosuppression

177
Q

Common effect of methotrexate?

A

Myelosuppression

US (17 decks)

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