Hematology

Front 1

WBC differential

Back 1

• Neutrophils (54–62%)
• Lymphocytes (25–33%)
• Monocytes (3–7%)
• Eosinophils (1–3%)
• Basophils (0–0.75%)

"Neutrophils like making everything better"

Front 2

Important neutrophil chemotactic agents other than C5a, IL-8, LTB4

Back 2

kallikrein, platelet-activating factor

Front 3

Lipid A from bacterial LPS binds _______ on

macrophages to initiate septic shock

Back 3

CD14

Front 4

Causes of eosinophilia

Back 4

Neoplasia
Asthma
Allergic processes
Chronic adrenal insufficiency

Parasites (invasive)

Front 5

__________________ prevents mast cell degranulation (used for asthma prophylaxis)

Back 5

Cromolyn sodium

Front 6

___________ activates bradykinin; ______ inactivates bradykinin

Back 6

Kallikrein; ACE

Front 7

Principal targets of antithrombin

Back 7

thrombin and factor Xa

Front 8

When would you see Acanthocytes (“spur cells”)?

Back 8

Liver disease, abetalipoproteinemia (states of cholesterol dysregulation)

Front 9

When would you see basophilic stippling?

Back 9

Lead poisoning; lead inhibits rRNA degradation, causing RBCs to retain aggregates of rRNA (basophilic stippling)

Front 10

When would you see degmacytes (“bite cells”)?

Back 10

G6PD deficiency

Front 11

When would you see macro-ovalocytes?

Back 11

Megaloblastic anemia (also hypersegmented PMNs), marrow failure

Front 12

When would you see dacrocytes (“teardrop cells”)?

Back 12

Bone marrow infiltration (e.g., myelofibrosis)

RBC “sheds a tear” because it’s mechanically squeezed out of its home in the bone marrow

Front 13

In which conditions do you see target cells?

Back 13

HbC disease, Asplenia, Liver disease, Thalassemia

"HALT,” said the hunter to his target

Front 14

What are Heinz bodies?

Back 14

• Oxidation of Hb -SH groups to -S—S- → Hb precipitation (Heinz bodies A ), with subsequent phagocytic damage to RBC membrane → bite cells

• Seen in G6PD deficiency; Heinz body–like inclusions seen in α-thalassemia

Front 15

What kind of anemia is seen in copper deficiency?

Back 15

Microcytic sideroblastic anemia

Front 16

What causes normocytic anemia with a decreased or normal reticulocyte count?

Back 16

• ACD
• Aplastic anemia
• Chronic kidney disease
• Iron deficiency (early)

Front 17

What causes non-megaloblastic macrocytic anemia?

Back 17

• Liver disease
• Alcoholism
• Reticulocytosis

Front 18

Clinical signs of lead poisoning

Back 18

• Lead Lines on gingivae (Burton lines) and on

metaphyses of long bones D on x-ray.

• Encephalopathy and Erythrocyte basophilic

stippling.

• Abdominal colic and sideroblastic Anemia.
• Drops—wrist and foot drop. Dimercaprol and EDTA are 1st line of treatment.
• Succimer used for chelation for kids (It “sucks” tobe a kid who eats lead)

Front 19

Orotic aciduria

Back 19

• Inability to convert orotic acid to UMP

(de novo pyrimidine synthesis pathway) because of defect in UMP synthase.

• Autosomal recessive.
• Presents in children as failure to thrive, developmental delay, and megaloblastic anemia refractory to folate and B12.
• No hyperammonemia (vs. ornithine transcarbamylase deficiency— ↑ orotic acid with hyperammonemia)

Front 20

Causes of aplastic anemia

Back 20

• Radiation and drugs (benzene,

  
  

  chloramphenicol, alkylating agents,

  
  

  antimetabolites)

• Viral agents (parvovirus B19, EBV, HIV,

  
  

  HCV)

• Fanconi anemia (DNA repair defect)

• Idiopathic (immune mediated, 1° stem cell

  
  

  defect); may follow acute hepatitis

Front 21

Pyruvate kinase deficiency (E)

Back 21

• Autosomal recessive.
• Defect in pyruvate kinase leads to decreased ATP, resulting in rigid RBCs

Front 22

What is given to treat Paroxysmal nocturnal hemoglobinuria (I)?

Back 22

eculizumab (terminal complement

inhibitor)

Front 23

Acute intermittent porphyria

Back 23

• Problem with Porphobilinogen deaminase

• Painful abdomen

• Port wine–colored urine

• Polyneuropathy

• Psychological disturbances

• Precipitated by drugs (e.g., cytochrome

  
  

  P-450 inducers), alcohol, starvation

Front 24

How is acute intermittent porphyria treated?

Back 24

glucose and heme, which inhibit ALA synthase

Front 25

Porphyria cutanea tarda

Back 25

• Problem with uroporphyrinogen decarboxylase

• Blistering cutaneous photosensitivity

• Build up of uroporphyrin produces tea- colored urine

• Most common porphyria

Front 26

Why would you give frozen fresh plasma?

Back 26

• It increases coagulation factor levels

• DIC, cirrhosis, immediate warfarin reversal

Front 27

Cryoprecipitate

Back 27

• Contains fibrinogen, factor VIII, factor XIII,

  
  

  vWF, and fibronectin

• Coagulation factor deficiencies involving fibrinogen and factor VIII

Front 28

When is heparin indicated?

Back 28

Immediate anticoagulation for pulmonary embolism (PE), acute coronary syndrome, MI, deep venous thrombosis (DVT). Used during pregnancy (does not cross placenta). Follow PTT.

Front 29

What is used as an antidote in heparin overdose?

Back 29

protamine sulfate (positively charged molecule that binds negatively charged heparin)

Front 30

Why would a LMWH be used instead of heparin?

Back 30

Low-molecular-weight heparins (e.g., enoxaparin, dalteparin) and fondaparinux act more on factor Xa, have better bioavailability, and 2–4 times longer half-life; can be administered subcutaneously and without laboratory monitoring. Not easily reversible.

Front 31

Argatroban, bivalirudin, dabigatran

Back 31

• Bivalirudin is related to hirudin, the anticoagulant used by leeches
• Inhibit thrombin directly
• Alternatives to heparin for anticoagulating patients with HIT

Front 32

When is warfarin indicated?

Back 32

• Chronic anticoagulation (e.g., venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation).
• Not used in pregnant women (because warfarin, unlike heparin, crosses placenta).
• Follow PT/INR.

Front 33

Apixaban, rivaroxaban

Back 33

• Direct factor Xa inhibitors

• Treatment and prophylaxis for DVT and PE (rivaroxaban); stroke prophylaxis in patients with atrial fibrillation.

• Oral agents do not usually require coagulation monitoring

Front 34

Name the thrombolytic drugs

Back 34

Alteplase (tPA), reteplase (rPA), streptokinase, tenecteplase (TNK-tPA)

Front 35

Name the ADP receptor inhibitors

Back 35

Clopidogrel, prasugrel, ticagrelor (reversible), ticlopidine

Front 36

How do ADP receptor inhibitors work?

Back 36

Inhibit platelet aggregation by irreversibly blocking ADP receptors. Prevent expression of glycoproteins IIb/IIIa on platelet surface

Front 37

When are ADP receptor inhibitors indicated?

Back 37

• Acute coronary syndrome; coronary stenting.
• Decrease incidence or recurrence of thrombotic stroke

Front 38

MOA for Cilostazol, dipyridamole

Back 38

Phosphodiesterase III inhibitor; increase cAMP in platelets, resulting in inhibition of platelet aggregation; vasodilators.

Front 39

When would Cilostazol/dipyridamole be indicated?

Back 39

• Intermittent claudication
• Coronary vasodilation
• Prevention of stroke or TIAs (combined with aspirin)
• Angina prophylaxis

Front 40

MOA of abciximab, eptifibatide, tirofiban

Back 40

• GP IIb/IIIa inhibitors

• Bind to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation.

• Abciximab is made from monoclonal antibody Fab fragments

Front 41

When would abciximab be used?

Back 41

Unstable angina, percutaneous transluminal coronary angioplasty