Hematology Flashcards

1
Q

What is the Intrinsic pathway?

What is the Extrinsic pathway?

What is the common pathway? What is Clotting factor 1?

What are the Vitamin K dependent Clotting factors?

What is thrombin? What does it do?

What is antithrombin? What does it do?

How do healthy cells keep from clotting?

How does damaged cells/adhered platelets create clotting?

What does Plasmin do?

A

TE-EN (2 above and below 10; VIII, IX, XI, XII); PTT (patatatatata)

Tissue trauma 3 + 7 = 10 = PT

The rest, 13 is the cross-linker. Factor 1 = fibrin = tissue factor

Cunts and Sluts created in 1972 (C, S, 10, 9, 7, 2(thrombin))

CF 2; activates V, VIII, and XI. Also C/S to keep it in control

CF 3; irreversibly inactivates thrombin

Negative-Negative charge repelling platelets

Thromboplastin; converts Prothrombin => Thrombin

Causes clot to retract

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2
Q

What is Transferrin when is it seen?

What is Ferritin when is it seen?

A

Transportation of iron in blood (seen when iron demand is high, but not seen in anemia of chronic disease)

Primary iron storage (seen when iron is high and in anemia of chronic disease)

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3
Q

What are the three main types of blood transfusions? When are they used?

A
  • Packed RBCs = concentrated Hb for increased oxygen in acute blood loss/anemia
  • “6-pack” Platelet and freshly frozen plasma = increased coagulation for severe bleed
  • Cryoprecipitate = Fibrinogen, CF VIII/XIII for deficiencies
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4
Q

What is the Flow cytometry value for B-cell cancer?

A

20 (like B = 2)

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5
Q

What is Felty’s syndrome?

A

Severe Rheumatoid arthritis => granulocytopenia/splenomegaly/neutropenia. I felt your belly too long and your spleen enlarged and made you susceptable like AIDS

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6
Q

What is the pathology of Mononucleosis?

A

URI => lymphadenopathy => splenomegaly

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7
Q

What is the most common cause of parasitic cysts in the spleen? What is a key feature of it? How many people have accessory spleen? What is natural Asplenia associated with?

A

Echinococcus. NO epithelial lining. 20-35%. Situs inversus and cardiac malformations.

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8
Q

What does Hydroxyurea do? What is that a treatment for?

How do I remember that?

A

Increases fetal hemoglobin, is an antineoplastic, and antiretroviral. Sickle/HbC/β-thallasemia/Cancer/AIDS

Hy** _dro_oling **XY** baby. I want to go back to you carelessly **ureating, before I knew about cancer and AIDS

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9
Q
  • What does Cyclosporine inhibit? When would you not use it? What are the side effects? What is special about its number 1 side effect? How do I remember this shit?
  • What does Tacrolimus inhibit? What are the side effects of Tacrolimus? How do I remember this shit?
  • Sirolimus(rapamycin)? What are the side effects? How do I remember this shit?
A

Cyclo**phillin from activating calcineurin => IL-2. Young/Acute immune attack/Side effects too much. _**N****ephrotoxic**(treated with mannitol),gingival hyperplasia, hirsutism, liver dysfunction, andGout. I besportinea new kidney and have to protect it from myhairy/big gummed_**self even if it means Gout.

FKBP => calcineurin => IL-2. Nephrotoxic**, linked to cancer (lymph/skin), PNS neuropathy, HTN, pleural effusion, **hyperglycemia**. Oh **Limus**, I need to **Tackle you down for not treating your kidney right, you have DM/HTN and possibly PNS neuropathy/Pleural effusion from me tackling you. I hope you get cancer.

FKBP (mTOR**) => **Cdk 2** => blocks proliferation (IL-2). Hyperlipidemia and profound **Myelosuppression. Sirons must block T**h**or**’s reproduction by Fu_ck_ing his **fat** _d_ick with **2 at a time

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10
Q

What is Azathioprine? What does it do? When do you use it? What are the side effects? What is the major drug interaction to look out for? How do I remember this shit?
What is ALG and ATG used for? What are they especially good for? How do I remember between the two?

A

Pro-drug for mercaptopurine**. Inhibits **DNA synthesis** (**T-cells**) for A/G. T-cell cancer and stopping acute autoimmune reaction. **Bone marrow inhibition**, linked to cancer, GI toxicity. **Allopurinol** blocks **Xanthine oxidase** => toxic levels. **Aza** **thi** was saying **o**’ lack of _purine_s can prevent **T**-cells from attacking transplants. Blocks **All** **o****purines metabolism even the purine blockers metabolism.

kidney transplants** and **acute rejection episodes** respectively. Polyclonal, good for steroid resistance. _A_l is a _Lucky orGan receiver, unT_il he **Gets a rejection episode.

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11
Q

What are the 1st generation anti-H1?

What are the 2nd generation anti-H1?

A

-phen- -ramine; Chlorpheniramine and Diphenhydramine.

-adine; Fexofenadine and Loratadine

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12
Q

What does COX enzymes do?

What are the COX enzymes?

What does Aspirin do?

What does Ibuprofen do?

What does Tylenol do?

A

Turns Arachidonic acid into PGH2

COX-1 = constitutive (always expressed)
COX-2 = inducible (changes its expression)
COX-3 = brain variant

Irreversibly inhibits all COX enzymes

Competively inhibits all COX enzymes

Blocks COX-3

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13
Q

What are the following drugs a recombination of? What are they used in?

  • Aldesleukin
  • Erythropoeitin
  • Filgrastim
  • Sargramostim
  • α-interferon
  • β-interferon
  • γ-interferon
  • Oprelvekin and Thrombopoietin
A
  • IL-2. Renal cell cancer/melanoma (activates T-cells)
  • epoetin. Anemias (especially in renal failure)
  • Granulocyte colony-stimulating factor. Neutropenia
  • Macrophage colony-stimulating factor. Lack of Macrophages
  • Anti-HBV/HCV, Kaposi’s sarcoma, leukemia, and melanoma
  • Multiple sclerosis
  • Chronic granulomatous diseases
  • IL-11. Thrombocytopenia
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14
Q

What are the following drugs an antibody(-mab) for? What diseases could use them?

  • Muromonab
  • Daclizumab/Basiliximab
  • Infliximab
  • Adalimumab
  • Abciximab
  • Trastuzumab
  • Rituximab
  • Omalizumab
A
  • CD3. Organ rejection (T cells)
  • IL-2 receptor. Organ rejection (T cells)
  • TNF-α. Crohn’s, autoimmune arthritis, ankylosing spondylitis
  • TNF-α. Crohn’s, autoimmune arthritis
  • Glycoprotein IIb/IIIa. Prevent cardiac ischemia in angina
  • erb-B2. HER-2 breast cancer
  • CD20. B-cell non-Hodgkin’s lymphoma
  • IgE. Severe asthma
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15
Q

What does Probenecid do?

What does Allopurinol do?

What does Febuxostat do? How is it different?

A

Prevents the reabsorption of uric acid (Gout).

Inhibits Xanthine oxydase => prevent production of purines.

Above, but liver metabolized and higher CVD risk.

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16
Q

What is a major killer in Rheumatoid arthritis (a non-lethal disease)? What is Misoprostol in regards to that? What is Methotrexate? What is Etanercept?

A

GI/renal toxicity of NSAIDs. Helps prevent GI side effects. Drug of choice for RA. TNF-α modifier for RA.

17
Q

What is the mechanism of action of heparin?

What are the low molecular weight Heparins? What is their significance?

What is the side effect of Heparin that is not in warfarin?

What is protamine sulfate?

What is the very small synthetic heparin? What does it do?

What is Rivaroxaban? What is it used for?

What does Clopidogrel do? What is it good for?

What is Hirudin? What is it used in?

What does Cilostazol and dipyridamole do? What are their side effects?

A

Accelerates reaction of antithrombin and thrombin/blocks CF Xa.

Enoxaparin**, Dalte_parin, Tinzaparin_**. Home form/DOC when pregnant.

Osteoporosis.

Antidote to heparin.

Fondaparinux. Inhibits CF Xa.

Direct** CF Xa inhibitor. **Oral prophylaxis

irreversible blocks P2Y12. Stroke (arterial)

Directly inhibits thrombin. Heparin-induced thrombocytopenia

Phosphodiesterase III inhibitor (stop platelet aggregation and vasodilation). Flushing, headache, hypotension, abd pain.

18
Q

What are the thrombolytics? How do they work? When should they not be used?

A

Streptokinase (gram - toxin), Alteplase**, Re_teplase, and Tenecteplase_ (activates recombinant **t**-PA). Uncontrolled bleeding and **unstable angina.

19
Q

Draw Chemo Man

A
20
Q

Draw Corticosteroid Man

A