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Pharm > Pharm hemato > Flashcards

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
Q

Clotting……..basics to process

hemostasis

A

Hemostasis: process of blood clot formation at the site of vessel injury
* quick, localize, carefully regulated->to prevent abnormal clotting/bleeding response

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26
Q

primary hemostasis

A

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

Diseases of Primary= ITP, TTP, HUS, DIC

27
Q

2ndary Hemostasis

A

Clotting factors lead to fibrin formation= strengthen platelet plug
Intrinsic (PTT prolonged) and Extrinsic (PT prolonged)

Diseases: Hemophilias, DIC

DRAW OUT THE CASCADE DUFUS

28
Q

Thrombosis types

A

Arterial-> platelet rich (platelets>fibrin)
Venous->coagulation factors(fibrin>platelets)

29
Q

3 types of antithrombotic drugs

A
  1. Antiplatelets-> arterial thromboses
  2. Anticoagulants-> venous thromboembolism
  3. Fibrinolytics-> selective venous thromboemb
30
Q

where do we use antiplatelet drugs

A

Peripheral arterial disease
acute coronary syndromes
secondary prevention of ACS
ischemic stroke/TIA
stable ischemic heart disease

31
Q

where do we use anticoagulants?

A

DVT and prophylaxis
atrial fibrillation
PE

32
Q

Where do we use fibrinolytics

A
  1. Acute ischemic stroke (nonhemorrhagic)
  2. Acute myocardial infection
  3. massive PE
33
Q

Types of antiplatelet drugs

A
  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
Q

Aspirin used for what

Acetylsalicylic acid

Antiplatelet therapy

A

1st line for Acute coronary syndroms
2nd line for Atherosclerotic cardiovascular disease or stroke

35
Q

MOA aspirin + SE

A

Irreversibly binds to cooxygenase (COX)1 enzyme on platelets preventing arachidonic acid turning into thromboxane A2

S: GI upset and bleeding

36
Q

P2Y12 inhibitors indications

A

Clopidogrel
Prasugrel
Ticagrelor
Used for Acute coronary syndrome, MI, stroke, Peripheral artery disease

37
Q

P2Y12 classes and SE

A

Clopidogrel and Prasugrel= Thienopyridine Class

Ticagrelor=Cyclopentyltriazolopyrimidine Class

SE: Bleeding-> can be fatal

all bind irreversibly and block ADP P2Y12 receptor on platelets

all require loading dose and maintenance
REQ 5-7 DAY PERIPROCEDURAL HOLD (LIFESPAN OF PLATELET)

38
Q

Glycoprotein 2b/3a inhibitors indications/MOA/SE

A

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
Q

Risk factors for venous thrombosis

A

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
Q

Virchow’s Triad

A
  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
Q

Oral Anticoagulants

classes and names

A
  1. Xa inhibitors
    -aban (rivaroxaban)
  2. thrombin
    Dabigatran
  3. Vita K antagonist
    Warfarin
42
Q

Factor drug targets

A

Warfarin- 2, 7, 9, 10 all activated
LMWH and Antithrombin- 10a
Xa inhibitors -aban- 10a
Dabigatran- 2a

43
Q

MOA of Heparin, LMWH, and Fondaparinux

A

all cause Thrombin (2a) or Factor Xa to bind to antithrombin by adding a halter of negative charge

44
Q

Unfractionated Heparin Indications/Monitoring/Notes/Reversal agent

A

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
Q

Heparin Induced Thrombocytopenia (HIT) diag/tx

A

Diag: receive heparin-> develop thrombocytopenia or thrombosis
* Calc T score - Thrombocytopenia, Timing, Thrombosis, oTher causes of low plt
* if high= empircally treat
* Low= watch and wait

TX: Stop Heparin

46
Q

Pathogenesis of HIT

A

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
Q

LMWH Enoxaparin (lovenox) indications/monitoring/reversible/Black Box warning

A

Treatment for DVT, PE, anticoag during pregnancy, BRIDGING for procedures
Monitoring: NO MONITORING
Black Boxed warning: epidural or spinal hematomas

48
Q

Pros and Cons of LMWH

A

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
Q

Fondaparinux (Arixtra) Indications/Monitoring/ETC/MOA/Black box

A

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
Q

Warfarin (coumadin) Indications/MOA/Monitoring/Reversal agents/Warnings

A

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
Q

Warfarin interactions and mechanisms

A

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
Q

DOAC TYPES

A
  1. Direct Thrombin Inhibitors- (Dabigatran)
  2. Factor Xa inhibitors- Rivaroxaban, Apixaban, Edoxaban
53
Q

Direct Thrombin inhibitors (DTI) MOA

A

MOA: binds to clot bount thrombin and inhibit cleaving of fibrinogen to fibrin
Parenteral options: Bivalirudin, Argatroban
Oral: Dabigatran Etexilate (Pradaxa)

54
Q

Dabigatran (Pradaxa)indications, monitoring, etc

A

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
Q

Direct Xa inhibitors Indications/MOA,/Monitoring/reversal agent/etc

A

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
Q

3 Direct Xa inhibitors and pearls

A
  1. Rivaroxaban/Xarelto- loading period needed
  2. Apixaban/Eliquis- loading period plus LEAST SENSITIVE TO CrCL
  3. Edoxaban/Savaysa- parenteral bridging needed
57
Q

DOAC compared to Warfarin

A

Doacs:
* very expensive
* less drug interactions
* limited reversal agent

Coumadin:
* Cheap
* many interactions
* no renal/weight concerns
* higher bleeding risks

58
Q

Overall risk factors and prevention of bleeding

A

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
Q

what is Tissue Plasminogen activator (tPA)? Indications

A

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
Q

Fibrinolytic therapies

RAT

A
  1. Alteplase/Activase
  2. Reteplase/Retavase
  3. Tenecteplase/TNKase
61
Q

Alteplase/Activase Indications etc

A

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
Q

Reteplase (Retavase)/indications

A

Indications: STEMI
2nd gen fibrinolytic
faster onset and lower bleeding risk than Alteplase

63
Q

Tenecteplase/TNKase Indications

A

Indications: STEMI
DRUG OF CHOICE FOR ACUTE MI FOR MOST CARDIOLOGISTS
greater fibrin specificity, longer plasma halflife, decreased bleeding SE than Alteplase

Pharm (9 decks)

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