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Pharm hemato Flashcards

1
Q

Anemia basics

A

Bleeding-a/c

decreased production

increased destruction

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2
Q

requirements for RBC production

A

Iron
B12
Folic acid
Heme

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3
Q

Heme vs non heme fe

A

Meat products vs plants/lentils

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4
Q

Site of absorption of iron

A

Duodenum and jejunum

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5
Q

What is the regulatory hormone of iron

A

hepcidin

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6
Q

iron losses

A

sweat, feces, menses

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7
Q

How do we replace iron?

A

Oral - most preferred
Intravenous-> those intolerant to oral, Malabsorption (Gastric bypass), nonadherence, refusal for blood transfusions

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8
Q

names of oral iron

A

ferrous fumarate 106 mg per 325 mg
ferrous gluconate 35 mg per 325 mg
ferrous sulfate 65 mg per 325 mg
ALL TRIDAILY WITH LIGHT MEAL AND MAYBE VITA C FOR ABSORP

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9
Q

What decreases iron absorption?

A

Other medications should b given 1 hour apart
ion antacids (Calcium, magnesium)
tetracycline
Histamine H2 antagonists
Proton pump

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10
Q

IV preparations

A

all different times and speeds, all affordability driven

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11
Q

GI,GI, GI

AE iron replacement

A

Oral: GI GI GI
* nausea
* constipation
* tarry stools

IV
* Infusion reactions
* arthralgia= younger ——> use benadryl incase

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12
Q

F/u for Iron def Anemia

A

Oral: 2 wks w/ CBC + retic, acess tolerability
IV: 4-8 wks w/ CBC, Retic, Iron panel
Repeat/refractory iron deficiency
* compliance, correct diagnosis, referral for chronic bleeding, unexplained= REFER TO GI

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13
Q

USPSTF rec for CRC

A

@ age 45-50
(cancer rates are rising in young adults)

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14
Q

Acute iron poisoning

cause and tx

A

Accidental overdose by young children-> direct caustic injury to gi mucosa-> cellular toxin impairing metabolism

toxic dose: 20-60 mg/kg……>60 is serious

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15
Q

tx for acute iron poisoning

A

whole bowel irrigation
IV iron chelating agents
supportive therapy

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16
Q

Stages of iron toxicity

A

Stage 1
* 0.5-6 hours
* Local toxicity: n/v, diarrhea, abdominal pain, GI bleeding

Stage 2
* 6-24 hours
* Latent toxicity: resolved Local with ongoing cellular toxicity, hypovolemia, poor perfusion

Stage 3
* 12-24 hours
* Systemic toxicity: shock, acidosis, coagulopathy, coma, system failure

Stage 4
* 2-3 days
* Hepatic failure

Stage 5
* 3-6 weeks
* Long term sequelae: Gastric outlet obstruction, small bowel obstruction, CNS

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17
Q

Megaloblastic anemia

Macrocytic anemias

A

Vitamin B12, Folate, Copper deficiency
Meds that interfere with DNA synthesis-> chemo, rheum drugs

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18
Q

Macrocytic anem Patho and Symptoms

A

Patho
* b12 and folate essential vitamins
* complex absorption
* B12 Pernicious anemia (AutoAB-> Parietal cells-> intrinsic factors-> cant absorb)
* Gastric bypass, small bowel disease, diet/etoh, drugs

Symptoms
* decreased WBC
* Neurocognitive changes

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19
Q

Vitamin B12 deficiency tx

cobalamin

A

PO-> 1,000 mcg PO (higher if impaired absorption)
IM-1,000 mcg weekly x 4 then monthly (preferred for neuro changes and cant do oral)

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20
Q

Folate deficiency

B9 or pteroylglutamic acid

A

PO or IV (unable to take or emergency situations)
1-4 months for replacement
CHRONIC ANEMIA= REPLACEMENT CONSTANT

(medications that mess with folate metabolism?)

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21
Q

Pernicious anemia

what does folate do?

A

Concomitant B12/folate deficiency
(folate may reverse hemat abnormalities, WILL NOT CORRECT NEURO MANIFESTATIONS)

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22
Q

Meds that interfere with folate metabolism?

cause folate deficiency

AMA

A

Methotrexate (MTX)- inhibits dihydrofolate reductase (DHFR)
Antibiotics- some inhibit DHFR- trimethoprim, pyrimethamine
Antiseizure agents-some affect folate absorption &/or cellular utilization-> phenytoin, valproate, carbamazepine

folic acid supplementation-> does not interfere with effectiveness of th

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23
Q

Erythropoietin stimulating agents

all SQ

aLPHA PEG

A

Epoetin Alfa
Epoetin alfa-epbx
Darbepoetin alfa
Methoxy PEG- epoetin beta

3x weekly to monthly

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24
Q

Black box warning for EPO stimulating agents

A

CKD greater risk for death, serious cardiovascular reactions, stroke-»» when targeting hgb higher than 11 g/dL

ie: ONLY IF HB < 10 gm/dL and use smallest dose

Contraindicated for active or recent malignancy due to progression

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25
Clotting........basics to process | hemostasis
Hemostasis: process of blood clot formation at the site of vessel injury * quick, localize, carefully regulated->to prevent abnormal clotting/bleeding response
26
primary hemostasis
Injury leads to platelet * adhesion-> platelet VWF * activation-> alpha granules + ADP ejected into circulation-> TXA2 * aggregation-> fibrinogen Platelet plug Petechiae and mucocutaneous bleeding | Prolonged BT, Normal PT and aPTT ## Footnote Diseases of Primary= ITP, TTP, HUS, DIC
27
2ndary Hemostasis
Clotting factors lead to fibrin formation= strengthen platelet plug Intrinsic (PTT prolonged) and Extrinsic (PT prolonged) | Diseases: Hemophilias, DIC ## Footnote DRAW OUT THE CASCADE DUFUS
28
Thrombosis types
Arterial-> platelet rich (platelets>fibrin) Venous->coagulation factors(fibrin>platelets)
29
3 types of antithrombotic drugs
1. Antiplatelets-> arterial thromboses 2. Anticoagulants-> venous thromboembolism 3. Fibrinolytics-> selective venous thromboemb
30
where do we use antiplatelet drugs
Peripheral arterial disease acute coronary syndromes secondary prevention of ACS ischemic stroke/TIA stable ischemic heart disease
31
where do we use anticoagulants?
DVT and prophylaxis atrial fibrillation PE
32
Where do we use fibrinolytics
1. Acute ischemic stroke (nonhemorrhagic) 2. Acute myocardial infection 3. massive PE
33
Types of antiplatelet drugs
1. Aspirin (ASA) * aspirin or dipyridamole + ASA 2. P2Y12 inhibitors (receptor for ADP- activated platelet) * Clopidogrel (plavix) * Prasugrel (effient) * Ticagrelor 3. GP 2b/3a Inhibitors * Eptifibatide * Tirofiban
34
Aspirin used for what | Acetylsalicylic acid ## Footnote Antiplatelet therapy
1st line for Acute coronary syndroms 2nd line for Atherosclerotic cardiovascular disease or stroke
35
MOA aspirin + SE
Irreversibly binds to cooxygenase (COX)1 enzyme on platelets preventing arachidonic acid turning into thromboxane A2 S: GI upset and bleeding
36
P2Y12 inhibitors indications
Clopidogrel Prasugrel Ticagrelor Used for Acute coronary syndrome, MI, stroke, Peripheral artery disease
37
P2Y12 classes and SE
Clopidogrel and Prasugrel= Thienopyridine Class Ticagrelor=Cyclopentyltriazolopyrimidine Class SE: Bleeding-> can be fatal | all bind irreversibly and block ADP P2Y12 receptor on platelets ## Footnote all require loading dose and maintenance REQ 5-7 DAY PERIPROCEDURAL HOLD (LIFESPAN OF PLATELET)
38
Glycoprotein 2b/3a inhibitors indications/MOA/SE
CERTAIN situations acute coronary syndromes-> cath lab high risk patients MOA: monoclonal ab that bind to glyc receptor blocking fibrinogen to the receptor which is final step of aggregation SE: bleeding, hypotension, bradycardia, Drug induced ITP
39
Risk factors for venous thrombosis
acquired: * recent surgery * trauma * cancer * pregnancy * fractures * immobilization * meds genetic=5: * Factor 5 leiden * Prothrombin gene mutation * Protein C def * Protein S def * Antithrombin lll def
40
Virchow's Triad
1. Hypercoagulable state * malignancy, pregnancy, trauma, sepsis 2. Vascular wall injury * Venepuncture, chemical irritation, heart valve replacement, surgery 3. Circulatory Stasis * Atrial fibrillation * Paralysis * Left ventricular dysfunction
41
Oral Anticoagulants | classes and names
1. Xa inhibitors -aban (rivaroxaban) 2. thrombin Dabigatran 3. Vita K antagonist Warfarin
42
Factor drug targets
Warfarin- 2, 7, 9, 10 all activated LMWH and Antithrombin- 10a Xa inhibitors -aban- 10a Dabigatran- 2a
43
MOA of Heparin, LMWH, and Fondaparinux
all cause Thrombin (2a) or Factor Xa to bind to antithrombin by adding a halter of negative charge
44
Unfractionated Heparin Indications/Monitoring/Notes/Reversal agent
Indications: Acute inpatient tx of PE, MI, ACS Monitoring: aPTT or Xa activity Notes: IV, RAPIDLY ELIMINATED Reversal agent: Protamine sulfate works in 5 min lasts for 2 hours= fish sperm AEs: bleeding , HIT
45
Heparin Induced Thrombocytopenia (HIT) diag/tx
Diag: receive heparin-> develop thrombocytopenia or thrombosis * Calc T score - **T**hrombocytopenia, **T**iming, **T**hrombosis, o**T**her causes of low plt * if high= empircally treat * Low= watch and wait TX: Stop Heparin
46
Pathogenesis of HIT
Heparin causes the release of PF4 from platelets that complex with IgG-> binds to Fc receptor to further release PF4 from alpha granules further complexing with IgG
47
LMWH Enoxaparin (lovenox) indications/monitoring/reversible/Black Box warning
Treatment for DVT, PE, anticoag during pregnancy, BRIDGING for procedures Monitoring: NO MONITORING Black Boxed warning: **epidural or spinal hematomas**
48
Pros and Cons of LMWH
Pros: * better bioavailability->no resistance * used outpatient * fixed dose without monitoring * lower risk of HIT Cons: * slower onset * longer duration * less reversible with protamine * longer half life in CKD patients
49
Fondaparinux (Arixtra) Indications/Monitoring/ETC/MOA/Black box
Tx: DVT, PE, ACS, HIT Monitoring: none Reversal: none MOA: binds to antithrombin with a greater affinity than LMWH, DOES NOT INTERACT WITH PF4 Black box: LMWH- spinal hematoma
50
Warfarin (coumadin) Indications/MOA/Monitoring/Reversal agents/Warnings
Indications: DVT, PE, Prosthetic valves, PREFERRED FOR ANTIPHOSPHOLIPID ANTIBODY SYNDROME MOA: Vitamin K antagonist-> inhibit 2,7,9,10,C, S Monitoring: PT/INR 2.0-3.0 and check 72 hours after starting Reversal agents: Vitamin K, PCC, FFP DO NOT USE PREGO-> CROSSES PLACENTA
51
Warfarin interactions and mechanisms
Decrease INR: (rich in vitamin k)- eaten consistency * Leafy greens, broccoli, asparagus Increase risk of bleeding: * Alcohol effects from drug interactions Prolonged PT/INR-> inhibit CYP, warfarin interrupts vitamin K recycling, alters intestinal flora Decreased PT/INR-> induction of hepatic CYP= faster metabolism and less available
52
DOAC TYPES
1. Direct Thrombin Inhibitors- (Dabigatran) 2. Factor Xa inhibitors- Rivaroxaban, Apixaban, Edoxaban
53
Direct Thrombin inhibitors (DTI) MOA
MOA: binds to clot bount thrombin and inhibit cleaving of fibrinogen to fibrin Parenteral options: Bivalirudin, Argatroban Oral: Dabigatran Etexilate (Pradaxa)
54
Dabigatran (Pradaxa)indications, monitoring, etc
Indications: 1st line VTE prophylaxis in post surgical patients, stroke prevention Monitoring: None Reversal agent: Idarucizumab AE: dyspepsia- nausea that wont go away BLEEDING RISK CLOSE TO HEPARIN but less cranial bleeding
55
Direct Xa inhibitors Indications/MOA,/Monitoring/reversal agent/etc
Indications: 1st line VTE prophylaxis in post surgical, stroke prevention MOA: inactivation of clot bound Xa Monitoring: none Reversal agent: Andexanet alfa, PCC coumadin or hep are better for prego, mechanical heart, and noncompliance
56
3 Direct Xa inhibitors and pearls
1. Rivaroxaban/Xarelto- loading period needed 2. Apixaban/Eliquis- loading period plus LEAST SENSITIVE TO CrCL 3. Edoxaban/Savaysa- parenteral bridging needed
57
DOAC compared to Warfarin
Doacs: * very expensive * less drug interactions * limited reversal agent Coumadin: * Cheap * many interactions * no renal/weight concerns * higher bleeding risks
58
Overall risk factors and prevention of bleeding
risks: drug choice, first 3 months of use, dosage, age, hx of bleeding, comorbities, thrombocytopenia Reduction of risks: control BP, optimize renal and hepatic fxn, fall prevention, ID cards
59
what is Tissue Plasminogen activator (tPA)? Indications
DRAINO 1. tPA is a serine protease-> converts plasminogen to plasmin-> the main ezyme with dissolving blood clots 2. Synthetic version= recombinant tissue plasminogen activator (rtPA) Indications: 1. Ischemic stroke 2. MI 3. PE 4. Thrombolysis for central lines
60
Fibrinolytic therapies | RAT
1. Alteplase/Activase 2. Reteplase/Retavase 3. Tenecteplase/TNKase
61
Alteplase/Activase Indications etc
ST Elevation MI (STEMI) **Acute ischemic stroke** Fibrin specific Results in systemic lytic state-> increase fibrin degradation (D-Dimer)-> substantial risk of systemic bleeding
62
Reteplase (Retavase)/indications
Indications: STEMI 2nd gen fibrinolytic faster onset and lower bleeding risk than Alteplase
63
Tenecteplase/TNKase Indications
Indications: STEMI DRUG OF CHOICE FOR ACUTE MI FOR MOST CARDIOLOGISTS greater fibrin specificity, longer plasma halflife, decreased bleeding SE than Alteplase

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