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Pharmacology > Lecture 7 (Hem/oncology)-Exam 4 > Flashcards

Lecture 7 (Hem/oncology)-Exam 4 Flashcards

1
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2
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  • What is MCV? What is small and large?
  • What is MCHC? What is hypo/hyperchromic?
  • WHat is MCH?
  • What is RDW?
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5
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HEMOCHROMATOSIS
* What is it?
* What are risk factors?
* What are s/s?

A
  • Iron Overload
  • Risk factors: severe hemoglobinopathies, hematological malignancies, sideroblastic anemias, & multiple RBC transfusions
  • Signs/symptoms: lethargy, hepatomegaly, hepatic cirrhosis, arthropathy/arthritis, diabetes mellitus, heart disease, hypogonadism
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6
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HEMOCHROMATOSIS
* What are the labs?
* What is the imaging/diagnostics?
* What is the txt?

A
  • Labs: serum ferritin level significantly elevated, transferrin saturation elevated, and liver enzymes elevated
  • Imaging/diagnostics: MRI/MRE of liver and liver biopsy
  • Treatment: iron chelation agents (ie IV deferoxamine or PO deferasirox) & supportive treatment of damaged organs
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7
Q

THALASSEMIAS
* Defect in what?
* What is beta thalassemia? Who is it mc in?
* What is alpha thalassemia? Who is it mc in?

A

Defect in the alpha or beta chains of adult hemoglobin
* Beta thalassemia – defect of beta globin chains; low beta chains-> African, Mediterranean descent MC
* Alpha thalassemia - defect of alpha globin chains; low alpha chains->Middle East, North Africa, Southeast Asia descent MC

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8
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THALASSEMIAS
* Imbalance of what?
* Decreased what?

A
  • Imbalance of alpha and beta chain production
  • Decreased RBC survival and short RBC lifespan
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9
Q

Hemoglobin:
* What is it?
* Normal hemoglobin made up of what? What does it do?

A
  • Oxygen carrying component of RBC
  • Normal hemoglobin made of 2 alpha and 2 beta globin chains
  • Each globin chain binds oxygen molecule
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10
Q

Beta thalassemia
* What are the chains like?

A
  • Two normal alpha chains
  • Partial (B+) or complete (B) beta globin deficiency
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11
Q

BETA THALASSEMIA
* What mutation?
* Dominant or recessive?
* Reduced or absent what?
* Increased or unmatched what? What does it cause?

A

Point mutation on chromosome 11

Autosomal recessive
* Two mutated genes required to cause severe disease

Reduced or absent beta globin chain synthesis

Increased, unmatched alpha chains
* Clump together forming inclusion bodies
* Damage RBC cell membranes

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12
Q

BETA THALASSEMIA
* What does deficiency of beta globin chains lead to?

A

Increased free alpha globin chains
* Clump together and form inclusion bodies
* Damage RBC cell membrane causing
* Hemolysis – RBC destroyed in bone marrow
* Extravascular hemolysis – RBC destroyed in spleen

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13
Q

Beta thalassemia
* Hemolysis leads to what?

A
  • Hemoglobin spillage directly into plasma
  • Hypoxia
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14
Q

Beta thalassemia-> hemolysis
* Hemoglobin spillage directly into plasma. Heme gets recycled to where (2)
* Hypoxia increases what? What is enlarged?

A
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15
Q

Beta thalassemia-hemolysis
* What is ineffective?

A

Ineffective erythropoiesis, chronic anemia, hypoxia cause increased iron absorption from duodenum
* Worsens hemochromatosis

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16
Q

Hemochromatosis
* What are the different areas?

A
  • Cardiac (arrhythmias, pericarditis)
  • Liver (cirrhosis)
  • Endocrine (growth retardation, thyroid disorders, diabetes mellitus)
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17
Q

Beta thalassemia:
* Minor: What is the genetic mutation and what are the symptoms?

A
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18
Q

Beta Thalassemia
* Intermedia: what is the genetic mutation? What are the sx?

A
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19
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Beta Thalassemia
* Major: what is the genetic mutation? What are the sx?

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20
Q

transfusion dependent beta thalassemia
* What are the indications for transfusion? (3)
* What is the timing?
* What are the goals (3)?

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21
Q

Iron chelation therapy (ICT)
* Prevents accumulation of what?
* Remove what? (2)
* Initiation? What are the indications (ferritin levels and liver iron concentration)?

A
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22
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23
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Iron absorption
* How is heme iron absorbed?
* How is non heme iron absorbed?
* Once absorbed Fe2 is stored by what?
* Once needed-what happens?

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26
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What are the typical sxs of anemia? What are the iron deficiency sxs?

A
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27
Q

Iron deficiency anemia - treatment
* What is first line?
* What is second line?
* What is for unstable patients?

A

First-line:
* oral iron replacement (stable patients)

Second-line:
* parenteral iron replacement (stable patients)

Packed RBC transfusion (unstable patients)
* Reserved for severe anemia (< 7 gm/dL) with symptoms
* Menstruating woman
* Rectal bleeding

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28
Q

Oral iron supplements: General considerations
* Different amounts of what?
* Variable what?
* Best absorption when?
* Avoid taking with what?
* What is common about the treatment?

A
  • Different amounts of elemental iron with each iron salt
  • Variable absorption – improved with acidic environment (Vit C?)
  • Best absorption when taken on empty stomach – most patients cannot tolerate
  • Slow-release, enteric-coated tablets generally not effective
  • Avoid taking with medications that decrease absorption
  • Treatment failure common – noncompliance due to intolerance
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29
Q

Iron replacement PO

Avoid taking with medications that decrease absorption? (3)

A
  • Al, Mg, Ca containing antacids
  • Antihistamines
  • Proton pump inhibitors
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30
Q

Ferrous sulfate:
* What is the dose?
* What are the adverse effects?
* What are the CI?

A
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31
Q

IV iron replacement
* What are the indications? (4)
* Various formulas exist for determining what?
* Specific administration recommendations vary by what?
* _ efficacy

A
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32
Q

IV iron replacement: LMW iron dextran
* What is the disadvange and benefit?

A
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33
Q

Anemia of chronic disease (inflammation):
* What will chronic renal disease have?
* What will chronic inflammation have? What are different causes of chronic inflammation.
* What will be elevated and low?
* What is the txt?

A
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34
Q

Erythropoietin
* How does erytrohopietin work?

A
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35
Q

Recombinant erythropoietin (EPO)
* What are Erythropoietin stimulating agents (ESAs)? What are two examples?
* What is the indication?

A

Erythropoietin stimulating agents (ESAs) are recombinant EPO produced pharmacologically via recombinant DNA technology
* epoetin alfa (Procrit)
* darbepoetin (Aranesp)

Indication: anemia from CKD or malignancies with hemoglobin < 10 g/dL

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36
Q

EPO dosing:
* CKD:
* Chemo related anemia:
* Surgery associated transfusion reduction: ⭐️

A
  • CKD: 50 to 100 units/kg IV or SC three days/week
  • Chemo-related anemia: Start with 40,000 units subcutaneously every week or 150 units/kg/dose subcutaneously three times weekly
  • Surgery-associated transfusion reduction: 300 units/kg/dose subcutaneously daily for 15 days before surgery
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37
Q

Dosing of darbepoetin:
* Chronic kidney disease-associated anemia
* Chemo-related anemia:

A

JUST KNOW THIS ONE WAS MARKETED FOR A WEEK
* Chronic kidney disease-associated anemia:Start with 0.45 mcg/kg IV or subcutaneously weekly.
* Chemo-related anemia: Start with2.25 mcg/kg/dose subcutaneously every week or 500 mcg subcutaneously every three weeks

38
Q

Recombinant erythropoietin (EPO)
* What are the adverse effects?

A
  • Risk of thrombotic events – increased blood viscosity
  • Increased risk of tumor progression – not indicated for myelosuppressive chemotherapy if cure is anticipated outcome
39
Q

Recombinant erythropoietin (EPO)
* What are the goals (4)

A
  • Lowest dose to reduce RBC transfusions
  • Hb level should be no greater than 11g/dL
  • Monitor Hb at least weekly
  • Consider addition of iron if no effect
40
Q

Fill in for normocytic anemias

A
41
Q

Sickle cell anemia
* What type of disease?
* Most common with what population?
* What results in sickle hemoglobin?

A
  • Autosomal recessive
  • Most common with African heritage (1:400 African American births)
  • Substitution of valine for glutamic acid on the beta-hemoglobin chain resulting in sickle hemoglobin (HbS)
42
Q
  • Sickle cell trait (SCT) –
  • Sickle cell SS –
  • Sickle cell SC –
  • How is diagnosed?
A
  • Sickle cell trait (SCT) – one normal, one sickle gene (HbA, HbS)
  • Sickle cell SS – two sickle genes (homozygous); more severe (HbS, HbS)
  • Sickle cell SC – one HbS, one HbSC; less severe
  • Diagnosed at birth or via hemoglobin electrophoresis
43
Q

Newborn screening
* Screening for what?
* What is not required

A
  • Screening for sickle cell mandated in all states
  • Thalassemia is not core
44
Q

Sickle Cell Anemia
* What does HbS cells carry like?
* What causes the HbS cells to sickle?
* What can sickle cells do after?
* What is repeat sickle?

A
  • HbS cells carry oxygen just like HbA
  • Deoxygenation, dehydration, acidosis cause HbS cells to sickle
  • Sickled cells can return to normal once reoxygenated
  • Repeat sickle – unsickle results in damage and premature destruction
45
Q

Repeat sickle – unsickle results in damage and premature destruction
* What are the examples of damage?

A

Anemia

Hyperbilirubinemia (hemolysis)
* Jaundice
* Scleral icterus
* Gallstones

46
Q

What is the normal hemoglobin throughout the years?

A
47
Q

Sickle cell anemia
* What do sickled cells not do well!
* What leads to pain?

A
  • Sickled cells do not move through capillaries well
  • vaso-occlusion -> hypoxia -> tissue ischemia ->PAIN
48
Q

Sickle cell anemia: Vaso-occlusion
* MC where?
* What bones?
* What happens in spleen?
* CNS?
* Lungs?
* kidneys?
* Penis?

A
49
Q

Sickle cell anemia: Effects on the spleen
* What happens to cause spleen sequestration?

A

Spleen sequestration (mild to severe)
* RBCs trapped in spleen
* Medical emergency

50
Q

Sickle cell anemia: Effects on the spleen
* How does spleen infaract happen?
* What is there an increase risk of?

A

Infarction – scarring and fibrosis causing auto-splenectomy (aka: functional asplenia)
* Increased risk of infection with encapsulated organs
* S. pneumonia, H. influenza, N. meningitis, Salmonella spp

51
Q

What is the treatment strategies of effects on the spleen from sickle cell anemia?

A
  • Penicillin or amoxicillin prophylaxis for children < 5 years
  • 23-valent pneumococcal vaccine after age 2 years
  • Close monitoring for patients with fever
52
Q

VOC treatment
* Where is treatment for mild?
* What is the txt for moderate to severe?

A
52
Q
A
53
Q

Acute txt of SC:
* What is the cause, txt, and notes for anemia, vaso-occlusive crisis, splenic sequestration?

A
54
Q

Acute txt of SC:
* What is the cause, txt, and notes for splenic auto infaraction, stoke and acute chest syndrome?

A
55
Q

What is the VOC prevention?
* How does it work?
* Approved for who?
* Can decrease what?

A
  • hydroxyurea
  • Increases HbF by stimulating HbF production->Exact mechanism unknown
  • Approved for children and adolescents
  • Can decrease vaso-occlusive episodes by up to 50%
56
Q

What are the adverse effects of Hydroxyurea? What is the monitoring?

A
57
Q

Fill in for the macrocytic anemias?

A
58
Q

Macrocytic anemias (MCV > 100𝜇𝑀3)
* What are the causes of vit b12 cobalamin?

A
59
Q

What is pernicious Vitamin B12 Deficiency?
* Vitamin B12 (cobalamin) is a precursor for what? What happens when there is a deficiency?
* What happens to blood cells?
* What happens to oral mucosa?

A
60
Q

Vitamin B12 Deficiency
* What lab levels are increased?
* What are they and what do they cause?

A
61
Q

What are the s/s of vit b12 deficiency?

A
62
Q

What are the labs you need to order for vitamin b12 diangosis?

A
  • CBC
  • Periferal blood smear
  • Vitamin B12 and folate levels
63
Q

What will the cbc and peiferal blood smear show in a pt with vit b12 anemia?

A
  • CBC – low hemoglobin / hematocrit, MCV > 100
  • Periferal blood smear – large red blood cells
64
Q

Vitamin b12 and folate levels in vit b12 def
* What level is deficient, borderline?

A
  • < 200 pg/mL = deficiency
  • 200 to 300 pg/mL = borderline
65
Q

Consider checking methylmalonic acid (MMA) and homocysteine levels in vitamin b12 diagnosis
* What are the levels in b12 deficiency and folic acid deficiency?

A
  • MMA and homocysteine elevated – B12 deficiency
  • MMA normal, homocysteine elevated – folic acid deficiency
66
Q

Fill in for vitamin b12 txt
only drug and route

A
67
Q

Folic acid (vitamin B9) deficiency
* increase demand cause?
* Decrease intake casue?
* What are dectrease absorption causes?

A
68
Q

What are the drugs that cause folic acid (vit B9) deficiency?

A
  • Phenytoin
  • Trimethoprim
  • Sulfasalazine
  • Methotrexate

Tri sulfing on meth, phen (phone) a friend

69
Q

Folic acid deficiency
* What is folic acid? What does a deficiency cause?
* What happens to Blood cells?
* What happens to the oral mucosa?

A
70
Q

Folic acid deficiency
* What are the homocysteine and methylmalonic acid levels? What do they cause?
* What happens to embyro?

A

Increased levels of homocysteine and normal methylmalonic acid
* Homocysteine = increased release of proinflammatory cytokines in vasculature and clumping of platelets (atherosclerosis, cardiovascular events)

Impaired closure of fetal neuropore

71
Q

Folic acid deficiency diagnosis
* What labs do you need to order?

A
  • CBC
  • Periferal blood smear
  • Vitamin B12 and folate levels (serum)
72
Q

Folic acid deficiency diagnosis
* What does the cbc, periferal blood semear, vitamin b12 and folate levels show?

A
73
Q

Folic acid deficiency diagnosis
* What is the txt?

A
  • Folic acid
  • 1 to 5mg PO daily for 2-4 months
74
Q

Which of the following physical findings suggest pernicious anemia?

  • Splenomegaly
  • Petechiae
  • Loss of vibratory sense
  • Koilonychia
  • Cheilitis
A
  • Loss of vibratory sense
75
Q
A

Ferrous sulfate

76
Q

Autoimmune (Hemolytic anemia)
* What is first line and second line txt?

A
77
Q

Autoimmune (Hemolytic anemia)
* What might you remove and why?

A

Splenectomy
* 60 to 90% response rate; 30% relapse rate
* Response greater in those without underlying malignancies
* Vaccination against encapsulated organisms at least 14 days prior to splenectomy

78
Q

Rituximab:
* What is the MOA?
* What are the BBWs?

A
79
Q

Rituximab SE?

A
80
Q

Glucose-6-phosphate dehydrogenase (G6PD)deficiency
* What type of disease?
* Increases what?
* What does RBC hemolysis cause?
* What is damage?
* What does the perperial blood smear show?
* What does urobilin show?
* most patients are what?

A
81
Q

What does this show?

A

Glucose-6-phosphate dehydrogenase (G6PD)deficiency

82
Q

What are the G6PD triggers?

A
83
Q

Thrombocytopenia
* What is normal platelet count?
* What is thrombocytopenia?
* What is clinically significant?
* Risk of severe post-tramatic bleeding level?
* What is the level for spontaneous bleeding

A
84
Q

What are the causes of Thrombocytopenia

A
85
Q

Immune/Idiopathic Thrombocytopenic Purpura (ITP)
* What type of disease?
* Affects who?
* What do the labs show?
* How do you dx?

A
86
Q

ITP treatments
* What do you need to give to actively bleeding patients?

A
87
Q

ITP treatments
* What do you give a patient not bleeding?
* What is first line? (2)

A
88
Q

ITP treatments – second line
* Thrombopoietin-receptor agonists: What are the tyeps, approved for who?
* What are the adverse effects?

A
89
Q

ITP treatments – third line
* Immune modulators: what is the drug?
* What can you remove? What are the pros and cons?

A
90
Q
A

Pneumococcal 23 valent vaccination IM

Pharmacology (14 decks)

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