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Heme/Onc Flashcards

1
Q

What is the energy source for RBCs?

A

Glucose – undergo glycolysis. Cannot undergo TCA cycle and cannot use fatty acids or ketones since they do not have mitochondria

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2
Q

What activates macrophages?:

A

IFN gamma (released by Th1)

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3
Q

What Ig can cross the placenta?

A

IgG

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4
Q

Hemolytic disease of the newborn

A

in first pregnancy, Rh(-) mom with an Rh(+) fetus will make antibodies against Rh

o The first fetus is unaffected because IgM will not cross the placenta
o The next pregnancy (if Rh+) will be attacked because the anti Rh IgG will cross the placenta and target the fetal erythrocytes
o Tx: give Rh(-) mom anti-D IgG (RhoGAM) to prevent production of anti Rh IgG

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5
Q

What coag factors are affected by vitamin K deficiency?

A

2, 7, 9, 10

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6
Q

What vitamin deficiency can antibiotics cause?

A

Vitamin K deficiency → disruption of the vitamin K producing bacteria in the GI tract

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7
Q

Why do neonates need a shot of vitamin K after birth? What can happen if they dont receive this?

A

Newborns have an inherent lack of GI colonization and therefore can easily become Vitamin K deficient
Lack of clotting factors can lead to intraventricular hemorrhage

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8
Q

Liver failure and coagulation

A

The liver is responsible for making clotting factors → liver failure leads to dec production of clotting factors (will see bleeding)

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9
Q

Factor 5 Leiden

A

Autosomal dominant point mutation in F5, which makes it resistant to inactivation by Protein C → leads to thrombosis

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10
Q

Where does vWF come from?

A

vWF comes from the Weibel-Palade bodies of endothelial cells and a granules of platelets

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11
Q

vWF deficiency mechanism and treatment

A

most common inherited bleeding disorder (autosomal dominant)

o Normally, promotes platelet adhesion to subendothelial collagen through the GP1b receptor
Present with mucocutaneous bleeding

Is also responsible for carrying F8, so if it is deficient, there can be a deficiency in F8 –> inc aPTT

Treatment: vWF concentrate or desmopressin (DDAVP) – inc release of vWF and F8 from endothelial cells

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12
Q

What coag factors does Protein C/Protein S normally regulate?

A

F8 and F5

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13
Q

What coag factors does Antithrombin normally regulate?

A

Mainly thrombin and F10

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14
Q

Lupus anticoagulant aka Antiphospholipid antibody

Do patients present with bleeding or clotting

A

Clotting!

Patients have antiphospholipid antibody in serum and a hx of thrombosis or miscarriage

(Not always in Lupus patients)

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15
Q

How will a patient with a platelet disorder present?

A

mucocutaneous bleeding, petechiae, epistaxis, and inc bleeding time

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16
Q

6 year old child with a history of acute diarrhea presents with thrombocytopenia and renal failure. What do you suspect? How does this syndrome present?

A

Hemolytic Uremic Syndrome – thrombocytopenia, hemolytic anemia, and renal failure

Cytotoxin from bacteria (usually E coli and Shigella) causes endothelial damage and platelet aggregation → formation of microthrombi → decreased platelets and RBC lysis due to shearing

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17
Q

What type of RBCs do you see in a blood smear of someone with HUS or TTP?

A

Schistocytes – due to shearing

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18
Q

What causes thrombotic thrombocytopenic purpura?

A

TTP is caused by decreased ADAMTS13 enzyme – vWF isn’t cleaved to smaller monomers for degradation and instead the large strings of vWF cause abnormal platelet adhesion and formation of microthrombi

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19
Q

Treatment for immune thrombocytopenic purpura

A

IVIG, steroids, splenectomy – this is due to production of auto-antibodies against platelets which causes their destruction by splenic macrophages

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20
Q

Patient presents with widespread sepsis and undergoes antibiotic therapy. She then begins bleeding from her mouth and IV lines.
What do you suspect and what caused this?
What will you see on blood smear?

A

DIC!

Sepsis triggered widespread activation of the coagulation cascade which then led to a deficiency in clotting factors and caused widespread bleeding

Can also be due to trauma, OB complications, pancreatitis, malignancy, nephrotic syndrome, transfusion

Will see schistocytes

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21
Q

Why is vWF deficiency considered a mixed platelet and coagulation disorder?

A

Because it also is in charge of carrying F8, so if it is deficiency there is a deficiency of F8 –> impaired coagulation

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22
Q

Hemophilia A

Hemophilia B

A

A (more common): defect in F8 (A-ight)

B: defect in F9

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23
Q

What is the genetic cause of alpha thalassemia? B thalassemia?

A

Alpha- caused by a gene deletion

Beta - caused by a point mutation in a splice site or promoter sequence

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24
Q

Lead poisoning effects which enzymes in heme synthesis? What else does it do to cells?

A

ALA dehydratase (ALA –> PBG)
and
Ferrochetalase (Protoporphyrin –> Heme)

Also prevents rRNA degradation, leading to basophilic stippling in RBCs

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25
Q

How can you use labs to differentiate between folate deficiency and vitamin B12 (cobalamin) deficiency?

A

Folate: inc homocysteine

B12: inc homocysteine AND inc methylmalonic acid

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26
Q

What type of anemia does Methotrexate cause?

What drug can you give to reverse this?

A 
Folate deficiency (macrocytic anemia). Methotrexate is a chemotherapy drug that blocks purine synthesis by inhibiting DHF reductase
Reverse myelosuppression with leucovorin

Also trimethoprim and phenytoin cause anemia

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27
Q

Diphyllobothrium latum causes what type of vitamin deficiency

A

Vitamin B12

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28
Q

What is necessary for the absorption of vitamin B12?

A

Intrinsic factor produced by gastric parietal cells (Pernicious anemia= impaired absorption of vitamin B12)

Gastrectomy can also cause B12 deficiency due to lack of parietal cells

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29
Q

Why does B12 deficiency cause neurologic symptoms?

What parts of the spinal cord does it effect?

A

B12 is involved in myelin synthesis.

B12 deficiency will result in dysfunction of the spinocerebellar tract (ataxia), lateral corticospinal tract (weakness), and dorsal column dysfunction (sensory deficits)

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30
Q

How does chronic disease lead to anemia?

A

Production of hepcidin by the liver which sequesters iron in storage sites by binding to ferroportin on intestinal mucosal cells and macrophages, inhibiting iron transport

Dec release of iron from macrophages
Dec iron absorption from the gut

**leads to inc intracellular iron that is stuck there and dec serum iron

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31
Q

What does an elevated MCHC suggest?

A

Hereditary spherocytosis- round RBCs that cannot move through the splenic sinuosoids and are removed by splenic macrophages

Treatment is splenectomy

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32
Q

What do Heinz bodies and bite cells on blood smear suggest?

A

G6PD deficiency

Causes dec glutathione and inc RBC susceptibility to oxidative stress

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33
Q

What drugs can trigger hemolytic anemia in a person with G6PD deficiency?

A

Sulfa drugs
Fava beans
Antimalarials (Primaquine)
Anti leprosy drugs (Dapsone)

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34
Q

Paroxysmal Nocturnal Hemoglobinuria

Mechanism?
What do labs show?

A

complement mediated lysis of RBCs – impaired synthesis of GPI anchor for delay accelerating factor that protects RBC from complement

o Cells are negative for CD55 and CD59

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35
Q

What precipitates sickling of RBCs in sickle cell anemia?

A

Low O2
high altitude
Acidosis

Leads to anemia and vaso-occlusive disease

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36
Q

Patient presentation of acute intermittent porphyria

What causes symptoms?

What precipitates symptoms?

Treatment?

A

Abdominal Pain
Port wine urine
Psych disturbances
Polyneuropathy

Caused by a combination of porphobilinogen deaminase (PBG deaminase) deficiency and induction of ALA synthase

Precipitated by drugs (CYP450 inducers), alcohol, and starvation

Treat with heme and glucose (inhibit ALA synthase activity)

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37
Q

Patient presents with blistering cutaneous photosensitivity and has tea colored urine. Formation of what is likely impaired?

A

Heme synthesis (Porphyria cutanea tarda)

Due to a defect in uroporphyrinogen decarboxylase

Tea colored urine is due to accumulation of uroporphyrinogen

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38
Q

Autoimmune hemolytic anemias are usually Coombs positive or negative?

A

Positive

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39
Q

Warm vs cold autoimmune hemolytic anemia immunoglobulins

A

Warm (IgG) – warm weather is great

Cold (IgM) – cold weather is miserable

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40
Q

Warm vs cold autoimmune hemolytic anemia: presentation

A

Warm: chronic anemia seen in SLE and CLL and with certain drugs

Cold: acute anemia triggered by cold. Seen in CLL, Mycoplasma pneumonia infections, and mononucleosis – cam cause painful blue fingers and toes with cold exposure

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41
Q

Direct Coombs test

A

anti-Ig antibody (Coombs reagent) is added to patient blood. RBCs agglutinate if patient’s RBCs are coated with anti-RBC antibody

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42
Q

Indirect Coombs test

A

normal RBCs from a donor are added to the patient’s serum. If serum has anti-RBC surface Ig, the RBCs will agglutinate

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43
Q

Mutation in sickle cell anemia

A

Point mutation in the B globin gene (valine for glutamic acid)

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44
Q

Drugs used in tumor lysis syndrome to prevent uric acid induced renal dysfunction

A

Allopurinol (xanthine oxidase inhibitor)

Rasburicase (solubilizes uric acid to allantoin for excretion)

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45
Q

Complications in tumor lysis syndrome

A

K+ is released from cells and can cause a fatal arrhythmia

Uric acid formation due to breakdown of released nucleic acid can cause uric acid deposition in the kidney

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46
Q

Haptoglobin levels in hemolytic anemia (inc or dec?)

A

Decreased
As the RBC is lysed and hemoglobin is released into the blood, it is scaveneged by haptoglobin (“suicide protein”) → haptoglobin (+hemoglobin) is engulfed by macrophages, which leads to decreased serum levels of haptoglobin

47
Q

diagnosis of vWF deficiency

A

Dx with ristocetin aggregation test:

Ristocetin activates GP1b receptors on platelets and makes them available for vWF bindings → When the vWF level is decreased, there is poor platelet aggregation in the presence of ristocetin

48
Q

Child presents with bleeding gums. Has small wide thumbs and small eyes and pigmented patches on abdomen. He has not met cognitive milestones. Labs show pancytopenia and high fetal hemoglobin levels. What is this congenital disorder?

A

Fanconi anemia

The most common cause of inherited aplastic anemia and is characterized by defective DNA repair that results in inc chromosomal breakage, rearrangements, and deletions → causes bone marrow failure

o Patients have short stature, ic incidence of tumors/leukemia, café au lait spots and thumb/radial defects

49
Q

What is the cause of almost all of the Myeloproliferative Neoplasms?

A

JAK2 kinase mutation: cytoplasmic tyrosine kinase

(Polycythemia Vera, Essential Thrombocythemia, and Primary Myelofibrosis, but NOT seen in Chronic Myelogenous Leukemia)

CML is t(9,22) philadelphia chromosome

50
Q

Erythropoitetin levels in polycythemia vera

A

Decreased. Due to negative feedback that suppresses renal EPO production

  • In contrast, EPO is elevated in malignancy (renal cell carcinoma, hepatocellular carcinoma) due to ectopic EPO production
51
Q

Patient has a platelet levels >450,000. What myeloproliferative neoplasm do you suspect?

A

Essential Thrombocythemia (JAK2 kinase mutation)

52
Q

Patient presents with intense itchiness after taking a warm shower. She also reports episodes of burning pain in her hands with red discoloration. What do you suspect and what is a common complication of this disorder?

A

Polycythemia vera (inc risk of venous thrombosis, like Budd Chiari syndrome)

53
Q

t(9,22)

A

Chronic myelogenous leukemia (CML)

Philadelphia chromosome t(9,22) which generates a BCR-ABL fusion protein with inc tyrosine kinase activity – drives overproduction of neoplastic cells

54
Q

Teardrop RBCs on bloodsmear

A

Primary myelofibrosis
(JAK2 kinase mutation)

Obliteration of the bone marrow with fibrosis (due to inc fibroblast activity)

55
Q

Auer rods seen on histo

A

Needle shaped cytoplasmic structures (crystal aggregates of myeloperoxidase)

Seen in Acute Myelogenous Leukemia

56
Q

t(15, 17)

A

Acute promyelocytic leukemia (M3 subtype of AML)

Defect is in retinoic acid receptor (PML/RARA fusion protein blocks maturation)

treat with vitamin A derivatives

57
Q

Cells express TdT (terminal deoxynucleotidyl transferase)– what does this indicate about the cells? What is the role of TdT?

A

They are immature B or T cells (mature cells do not express TdT)

TdT is responsible for adding nucleotides to the V, D, and J regions of the antibody gene for antibody diversity

58
Q

A young male presents with an anterior mediastinal mass involving thymic tissue. What do you suspect?

A

T cell acute lymphoblastic lymphoma (T-ALL)

symptoms of superior vena cava syndrome

59
Q

“Crew cut” on skull Xray

A

due to marrow expansion from inc erythropoiesis – seen in Sickle cell and B thalassemia major

60
Q

Where can ALL spread?

A

To the CNS or to the testes

61
Q

Histo shows smudge cells

A

Chronic lymphocytic leukemia

CLL = Crushed Little Lymphocytes

62
Q

What can happen with CLL/SCL in terms of progression?

A

Richter transformation: CLL/SCL can transform into an aggressive lymphoma (diffuse large B cell lymphoma)

63
Q

What stains TRAP positive?

A

Hairy cell leukemia (mature B cell tumor)

64
Q

What are heme/onc causes of a dry tap?

A

Primary myelofibrosis (obliteration of the bone marrow with fibrosis- inc fibroblast activity)

Hairy cell leukemia (mature B cell tumor)

65
Q

Reed Sternberg cells are positive for which cytologic markers

A

CD15 and CD30

(2 owls eyes x 15 = 30)

Seen in Hodgkin Lymphoma

66
Q

What drugs can you give to help tx Sickle Cell patients and how do they work?

A

Hydroxyurea: increases production of HbF

Gardos channel blockers (calcium dependent K+ channel): hinders the efflux of K+ and water from the cell, preventing the dehydration and RBCs and reducing the polyermization of HbS

67
Q

Electrolyte changes in blood transfusion

A

Hypocalcemia: citrate is a calcium chelator (will also see dec Mg for the same reasons)
Hyperkalemia: RBCs may lyse in older blood unites

68
Q

SLE effects on RBCs

A

Autoimmune hemolytic anemia

Warm hemolytic anemia (IgG)

69
Q

t(8;14)

A

Burkitt lymphoma

translocation of c-myc (8) and heavy chain Ig(14)
Transcription factor that causes rapid tumor cell proliferation

70
Q

How to differentiate between benign neutrophilia (leukemoid reaction) and chronic myelogenous leukemia?

A

CML has a low leukocyte alkaline phosphatase due to low activity of malignant neutrophils

Benign neutrophilia will have high LAP

71
Q

Cells express S-100 and CD1a

A

Langerhans cell histiocytosis

Have characteristic Birbeck granules in the cytoplasm

72
Q

Blotting procedures: Southern vs Western vs Northern

A

SNoW DRoP

Southern = DNA sample
Northern = RNA sample
Western = protein sample
73
Q

Multiple myeloma key clinical presentation

A 
CRAB
hyperCalcemia
Renal dysfunction
Anemia
Bone lesions and back pain
74
Q

t(14, 18)

A

Follicular lymphoma
translocation of heavy Ig chain and BCL2

Inhibition of apoptosis

75
Q

t(11; 14)

A

Mantle cell lymphoma

Translocation of cyclin D1 and heavy chain Ig

76
Q

Why are people with multiple myeloma at inc risk of infection?

A

They overproduce abnormal Igs and do not produce enough normal Igs

77
Q

Heparin: use, mechanism and antidote

A

Use for immediate anticoagulation

activates antithrombin, which then decreases the activity of thrombin and factor 10a (monitor PTT)

o Rapid onset, short t ½
o Safe to use in pregnancy
o Antidote = protamine sulfate

78
Q

LMWH (Enoxaparin, Dalteparin) and Fondaparinux

A

act more on factor 10a, have better bioavailability, and have a longer half life

79
Q

Warfarin mechanism of action and antidote

A

Warfarin: interferes with γ-carboxylation of vitamin K-dependent clotting factors (2, 7, 9, 10) and Protein C/S

o Inc PT
o Not safe for pregnancy
o Antidote: Vitamin K and fresh frozen plasma
o Can cause a transient hypercoagulable state due to inhibition of protein C and S – start patients on Heparin first and then warfarin

80
Q

Factor 10 inhibitors

A

Factor X inhibitors: Rivaroxaban, Apixaban

o have an X in the name

81
Q

Heparin Induced Thrombocytopenia:

A

IgG is formed against the heparin-platelet factor 4 complex and results in platelet activation and aggregation → clotting
o Can see DVT and PE in this patient
o Seen 5-14 days after exposure to heparin

DO NOT GIVE PATIENTS WARFARIN - inhibition of protein C and S can worsen the clotting

82
Q

B thalassemia trait

A

Inc HbA2 (a2d2)

83
Q

Coarse basophilic stippling in RBCs seen in blood smear

A

Lead poisoning

Lead prevents the breakdown of rRNA

84
Q

Which neoplasm has a common presentation of DIC?

A

Acute myelogenous leukemia (AML) - especially the acute promyelocytic leukemia subtype

85
Q

B symptoms

A

Reed Sternberg cells (Hodgkin lymphoma) secrete cytokines which can cause fever, chills, weight loss, and night sweats

86
Q

How do RBCs generate NADPH

A

via the HMP shunt, necessary to maintain glutathione in a reduced state by the action of glutathione reductase

o HMP shunt is the only major pathway that makes NADPH in erythrocytes so if there are defects then the RBC is susceptible to free radical and oxidant stress

87
Q

What factors promote angiogenesis in neoplastic and granulation tissue?

A

VEGF and Fibroblast growth factor (FGF)

o Pro-inflammatory cytokines can indirectly promote angiogenesis through inc VEGF production

88
Q

What cells stain positive for major basic protein?

A

Eosinophils

helps defend against parasites

89
Q

What cells stain positive for peroxidase?

A

Myeloblasts (auer rods)

90
Q

CML treatment

A

Imantinib (inhibits the BCR-ABL fusion protein)

91
Q

Blood smear shows stacked RBCs

A

Multiple myeloma (Rouleaux formation)

92
Q

What are thymomas associated with?

A

Myasthenia gravis and pure red cell aplasia

93
Q

Are multiple myeloma bone lesions osteolytic or osteoblastic? What other cancers can cause this type of lesion?

A

Osteolytic

Non small cell lung cancer (squamous cell carcinoma secretes PTHrP)
Renal cell carcinoma (secretes PTHrP)
Melanoma
Non hodgkin lymphoma

94
Q

What type of bone lesions are caused by prostate cancer?

A

Osteoblastic bone lesions

95
Q

What causes cachexia in cancer patients?

A

Cytokine release (TNFa, IL1, IL6)

TNFa acts on the hypothalamus to dec appetite and increase metabolic rate

96
Q

Mechanism of apoptosis

How does translation of apoptotic proteins occur?

A

Bcl2 in the cytoplasm is inactivated, cytochrome c can exit the mitochondria and enter the cytoplasm where it activates caspases that initiate apoptosis

Caspases are proteolytic enzymes that destroy cell components. They contain cysteine and are able to cleave aspartic acid residues (cysteine-aspartic-acid-proteases)

o In order to translate proteins necessary for apoptosis, an alternative method known as internal ribosome entry is used → a distinct nucleotide sequence called the internal ribosome entry site attacts the eukaryotic ribosome to mRNA and allows translation to begin in the middle of the mRNA sequence

97
Q

What drugs have increased activity when given with Allopurinol or Febuxostat? Why?

A

6-Mercaptopurine and Azathioprine

These drugs are also metabolized by xanthine oxidase – thus have increased toxicity when taken with allopurinol or Febuxostat (because less xanthine oxidase is available to metabolize 6-MP or Azathioprine)

98
Q

Heme precursors

A

Glycine and Succinyl CoA

99
Q

Tumor invasion of basement membrane

A
  1. Tumor cells detach from surrounding cells due to decreased expression of E-cadherin
  2. Tumor cells adhere to the basement membrane via increased expression of laminin and other adhesion molecules
  3. Tumor cells invade the basement membrane via enhanced secretion of proteolytic enzymes (metalloproteinases)
100
Q

Patient ingests rat poison – what should you do to treat them?

A

Rat poison = super warfarin – give them FFP!

101
Q

Retinoblastoma is associated with what other cancer?

A

Osteosarcoma

Both have mutation in RB gene (G1/S transition inhibitor)

102
Q

Warfarin induced skin necrosis: mechanism and treatment

A

happens in patients who are protein C or S deficient – following the initiation of warfarin, a rapid drop in factor 7 and protein C levels occurs. If a protein C deficiency is present, the transient procoagulant/anticoagulant balance is futther exaggerated, causing a hypercoagulable state with thrombotic occlusion of microvasculature and skin necrosis

Tx: stop warfarin and give FFP to replenish protein C concentrations

103
Q

What cytokine stimulates the release of acute phase reactants?

A

IL-6

104
Q

Inheritance of G6PD

A

X linked recessive

105
Q

What is the mechanism by which the human multidrug resistance (MDR1) gene works in chemotherapy resistance?

A

The MDR1 gene codes for P-glycoprotein, a transmembrane ATP dependent pump protein that increases efflux of drugs from the cytosol and decreases influx of drugs into the cytosol

106
Q

What is responsible for converting pro-carcinogens into carcinogens – promoting the formation of cancers?

A

Cytochrome P450 monooxygenase

107
Q

Li Fraumeni

A

Mutation in TP53 (tumor suppressor)
Autosomal dominant – inc risk of cancer in childhood or as yound adults

SBLA syndrome: sarcomas, breast/brain tumors, leukemia, and adrenocortical carcinoma

108
Q

Uremic platelet dysfunction
Cause?
Labs?
Tx?

A

due to renal failure

Accumulation of uremic toxins impair platelet aggregation and adhesion, resulting in prolonged bleeding time with normal platelet count, PT, and aPTT

Can be improved with dialysis as it removes the toxins and partially reverses the bleeding abnormality

109
Q

How do the RBCs of alcoholic look?

A

Macrocytic with or without anemia (usually due to poor diet – folate)

110
Q

Role of Kallikrien in the coagulation cascade

A

accelerates the activation of F12

o Positive feedback: starts being made when there is some F12 present, and then induces more formation of activated F12

111
Q

Sideroblastic anemia

A

defect in heme synthesis due to defect in ALA synthase

Can be caused by genetic defect (X linked), alcohol abuse, lead, vitamin B6 deficiency, copper deficiency, isoniazid

o Treatment: vitamin B6 (cofactor for ALA synthase)
o Histo shows ringed siderblasts with iron laden, Prussian blue-stained mitochondria

112
Q

Which microcytic anemia can cause hydrops fetalis?

A

alpha thalassemia

–/– = severe anemia, stillborn – Hydrops fetalis

113
Q

Roles of transferrin and ferritin?

A

Transferrin: transports iron in blood (transferrin transports)

  • Inc in iron deficiency anemia (looking for more iron)
  • Dec in anemia of chronic disease

Ferritin: stores iron in cells

  • Dec in iron deficiency anemia (not a lot of iron intracellularly)
  • Inc in chronic disease anemia (hepcidin sequesters iron in cells and prevents release)

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