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Blood Module > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is Primaquine?

A
  • It is an oral drug
  • Tissue schizonticide & gametocide
  • Exact mechanism is unknown (Its metabolite act as an oxidant)
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2
Q

what are the therapeutic uses of primaquine?

A
  1. Radical cure of relapsing malaria
  2. Terminal prophylaxis of relapsing malaria (given after
    leaving the endemic area to ensure that dormant forms are eradicated)
    * 3. Prevents transmission of disease to mosquito
    (gametocide)
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3
Q

what are the adverse effects of primaquine?

A
  • Adverse effects
  • Haemolytic anemia (in G6PDD)
  • Methaemoglobinemia
  • Teratogenic
  • Resistance could develop
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4
Q

what is chloroquine?

A

➢ Mainstay of malaria treatment
➢ Blood schizonticide
➢ Moderately effective gametocidal (in all species except falciparum)

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5
Q

what are the therapeutic uses of chloroquine?

A
  1. Prophylaxis & treatment of chloroquine sensitive malaria
  2. Amoebic hepatitis and amoebic liver abscess
  3. Rheumatoid arthritis (anti- inflammatory effect)
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6
Q

Describe the pharmacokinetics of chloroquine

A

1) Absorption: Rapidly and completely absorbed after
oral administration
➢2) Distribution:
▪ Has very large volume of distribution
▪ Concentrated in the RBCs liver, spleen, lung, leukocytes and melanin containing tissues
▪ Cross BBB
▪ Cross placenta
➢ 3) Metabolized in the liver & 4) excreted via kidney

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7
Q

what are the adverse effects of chloroquine?

A
  1. Headache – pruritis
  2. Eye: Corneal opacity - blurred vision and retinopathy
    * 3. Hemolytic Anemia: in G6PD-deficient subjects
    * 4. C.V.S: quinidine like action → prolong QT interval (hypotension & arrhythmias)
    * 5. GIT: Nausea-vomiting and diarrhea
    * 6. Resistance
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8
Q

what is quinine?

A

➢ Blood schizonticide
➢ Plant in origin
➢ Absorbed well after oral administration
➢ Exact mechanism of action is unknown
➢ Interfere with heme polymerization → death of RBCs
-Used in sever infestation and treatment of chloroquine resistant falciparum
➢ Has no role as prophylaxis (too toxic)
➢ weak muscle relaxant effect (potentiate the action of neuromuscular blockers)

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9
Q

what are the adverse effects of quinine?

A
  1. Quinidine like action → hypotension & arrhythmias
  2. Eye → blurred vision and blindness
  3. Cinchonism: tinnitus - headache - dizziness and visual disturbances
  4. Black water fever & hemolysis (hold medication)
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10
Q

what is mefloquine?

A
  • Mechanism: Same as quinine but
    ➢ More effective
    ➢ Longer acting
    ➢ Less toxic
  • Uses: Treatment & prophylaxis of chloroquine
    resistant falciparum
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11
Q

what is Amodiaquine?

A

*Used in treatment of chloroquine resistant falciparum

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12
Q

what are the side effects of amodiaquine?

A
  1. Aplastic anemia
  2. Agranulocytosis
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13
Q

give examples of 4-aminoquinolines

A

Chloroquine, Quinine, Mefloquine, Amodiaquine

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14
Q

what is halofantrine?

A
  • Structurally related to 4-aminoquinolines
  • Interferes with the degradation of haemoglobin
  • Blood schizonticide, active in all types & in multi resistant falciparum
  • Prolonged QT interval → sudden cardiac death
    limit its use to treatment of chloroquine resistant falciparum
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15
Q

what is Artemisinin?

A

➢ Plant in origin
➢ Free radicals resulting from cleavage of the drug
endoperoxide bridge by heme iron in the parasite food vacuole
➢ Interferes with Hb digestion
➢ Bind and damage specific malarial protein
➢ Available oral, rectal, IV
➢ Recommended for ttt of multidrug resistance P.
falciparum
➢ Can cause nausea, vomiting, diarrhea, prolonged QT interval

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16
Q

what is atovaquone?

A
  • Inhibit mitochondrial electron transport
  • No ATP
    -Affection of pyrimidine biosynthesis
  • Usually combined with proguanil
  • Combination used to treat chloroquine resistant strain of P. falciparum
  • Prevention and treatment of malaria
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17
Q
A
  • Pyrimethamine - Proguanil - Sulfadoxine
  • Fansidar (pyrimethamine + sulfadoxine)
  • Blood schizonticides (mainly) –tissue schizonticides- sporontocides
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18
Q

what is the mechanism of action of antifolate antimalarial drugs?

A
  1. Sulfonamides inhibit synthesis of folate by competition with PABA
  2. Pyrimethamine & proguanil inhibit dihydrofolate reductase → inhibit formation of active folic acid→ inhibit synthesis of DNA& RNA
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19
Q

what are the therapeutic uses of antifolate antimalarial drugs?

A
  1. Treatment of chloroquine resistant falciparum (fansidar plus quinine)
  2. Chemoprophylaxis in all types
  3. Toxoplasmosis (pyrimethamine + sulfadiazine)
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20
Q

what are the side effects of antifolate antimalarial drugs?

A
  1. GIT upset – hypersensitivity
    * 2. Megaloblastic anemia - haemolytic anemia (in G6PDD)
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21
Q

what are Tetracycline, doxycycline and clindamycin?

A
    • Inhibit protein synthesis
    • Blood schizonticide
    • Not used alone
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22
Q

how is malaria treated?

A

According to WHO guidelines
* Uncomplicated P. Falciparum
* ACT (Artemisinin Based Combination Therapy)
* Artemisinin or its derivatives plus
* Lumefantrine or amodiaquine or mefloquine or sulfadoxine and proguanil
* For 3 days followed by single dose Primaquine (Gametocide)

  • Uncomplicated P. Vivax, Ovale and Malariae
  • ACT (Artemisinin Based Combination Therapy ) or
    Chloroquine for 3 days
  • Followed by Primaquine for 14 days (for radical cure)
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23
Q

how is chloroquine resistant falciparum treated?

A

*Quinine + sulfadoxine pyrimethamine (or doxycycline)
or
* Atovaquone + proguanil
or
* Mefloquine

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24
Q

how is severe malaria treated?

A

*IV or IM Artesunate for 24 hours then complete with ACT
*Or Quinine

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25
Q

Describe the prevention of malaria

A
  • Artemisinin
  • or
  • Chloroquine
  • or
  • Mefloquine
  • or
  • Proguanil + Atovaquone
  • or
  • Doxycycline
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26
Q

how is malaria prevented during travel?

A

Drugs for chemoprophylaxis are given for 2 weeks (chloroquine, mefloquine) or for 2 days (proguanil or doxycycline) before
travel & during the stay
& for 4 weeks after leaving an endemic area

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27
Q

what are the types of anemia?

A

Under production
* Bone marrow suppression
* Problems with Hg synthesis
(Problems with iron {iron deficiency anemia, anemia of chronic inflammation}, problems with globin
synthesis {thalassemia}, problems with protoporphyrin {sideroblastic
anemia})

  • Problems with cell division (DNA problems; vit B12 & Folate deficiency)
  • Chronic kidney disease

Destruction/blood loss
* Due to intrinsic factors
Haemoglobinopathies
(Thalassemia, sickle cell
anemia) Enzymopathies
(G6PD deficiency)
Membranopathies
(spherocytosis, elliptocytosis)
* Due to extrinsic factors
Immune mediated, Malaria,
DIC, ITP, Rh incompatibilities,
Blood transfusion

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28
Q

how is iron deficiency anemia confirmed?

A

Iron deficiency anemia causes:
–sudden increase in blood formation
–Chronic blood loss
–Increased Demand
–Decreased Absorption

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29
Q

what are the indications of iron therapy?

A

Treatment of Iron-Deficiency Anemia:
(200-400 mg/day
elemental iron)

Prophylactic to prevent Iron-Deficiency Anemia
(30-60 mg/day elemental iron)

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30
Q

what is meant by elemental iron

A

It Is the total amount of iron in the supplement available for absorption.
Each type of iron has a different percentage of
elemental iron

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31
Q

how is the required iron dose calculated?

A

➢ Normally 3-6% (5-10%) of inorganic iron (non-heme iron) is absorbed
➢ In response to low iron stores or increased
iron requirements it reaches up to 25-30%
➢ In iron deficient individuals, about 50-100
mg of iron can be incorporated into
hemoglobin daily

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32
Q

Describe oral iron therapy

A

-Route of choice
-Effective & cheap
Preparations:
1) Ferrous sulfate, gluconate or fumarate (vary in
elemental iron content -12-33%)
2) Polysaccharide-iron complex 150mg, carbonyl iron
-150 mg contain 100% elemental iron
3) Heme iron polypeptide – more expensive

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33
Q

what are the adverse effects of oral iron therapy?

A

-GIT disturbances: nausea, epigastric pain, constipation
-Black stool
-Black staining of
teeth

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34
Q

when should oral iron be taken?

A

Given after meals to decrease GIT disturbances- Start with small dose then gradually increase.

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35
Q

what is the recommended duration of oral iron therapy?

A

➢ Treatment continued till hemoglobin level is normal
➢ It takes from 7-10 days to increase hemoglobin level by 1g/dl
➢ Then for an extra 2-3 months to replenish
stores

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36
Q

what is the follow up procedure of oral iron therapy?

A

➢ An increase in reticulocytes 5-10 days after the initiation of iron therapy
➢ The hemoglobin concentration increases by
about 1 g/dL (7-10 days)
➢ Until normal values are restored 2-3 months
later, measure serum ferritin

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37
Q

what are the types of parenteral iron therapy?

A

–IMZ – track injection
technique

–IV Infusion

38
Q

what are the adverse effects of parenteral iron therapy?

A

IM - local pain - tissue
staining
IV: headache, fever, urticaria,
lymphadenopathy &
anaphylactic shock

39
Q

what are the indications of parenteral iron therapy?

A
  • Non-compliance to oral therapy
  • Mal-absorption syndrome
  • Severe anemia
  • Anemia of chronic kidney disease
    (especially in patient on dialysis and receiving erythropoietin)
40
Q

What are the indications of using iron therapy in patient with chronic kidney disease on dialysis and erythropoietin?

A

-↓ erythropoietin → under
production of RBCs
-When this patient is on dialysis and on erythropoietin treatment:
-Increase in blood formation –Chronic blood loss

41
Q

what are the preparations of parenteral iron therapy?

A

A) Iron dextran (given IM & IV)
B) Iron sucrose complex &
Iron sodium gluconate
complex
C) Newer preparations:
Ferric carboxymaltose,
Ferumoxytol
(given IV)

Iron could be taken IV as a total dose infusion (TDI)

42
Q

what are the advantages of TDI (total dose infusion)

A

➢ Avoids non-compliance of the patient
➢ Avoids unpleasant effects of IMI
➢ Allows delivery of the entire dose of iron necessary at one time

43
Q

how to calculate the parenteral iron dose?

A

Dose (mL) = 0.0442 (Desired Hb - Observed Hb)
x BW + (0.26 x BW)

44
Q

how to calculate total iron deficit?

A

Total iron deficit (mg) = Body weight [kg] x
(Target Hb – Actual Hb) [g/l] x 2.4 + Iron stores
[mg]

45
Q

Describe the symptoms of acute iron toxicity?

A

Abdominal pain, vomiting,
bloody diarrhea, dyspnea
followed by metabolic acidosis,
cardiovascular collapse,
convulsions, coma & death

46
Q

how is acute iron toxicity treated?

A

1) Raw egg or milk - bind and precipitate iron as albuminate or caseinate until chelating agent is available

2) Deferoxamine:
-1-2 g IM or IV - chelates iron promoting its excretion in urine.
5g in 100 ml water swallowed or by stomach tube

3) IV infusion of saline, dextrose or bicarbonate –> correct water and electrolyte disturbance

47
Q

how do patients develop chronic iron toxicity?

A
  • Patients receiving many red
    cell transfusions
  • Patients with hemochromatosis:
  • an inherited disorder characterized by increased Fe absorption —> hemosiderosis
48
Q

describe the treatment of chronic iron toxicity?

A

1) Venesection (500 ml blood
removes 200 mg iron) - weekly.

2) Iron chelators
- Deferoxamine: (IM or SC)
- Deferasirox: oral iron chelator

3) Large intake of tea - binds iron

49
Q

what is Anemia of Chronic Illness?

A
  • It is a functional iron deficiency anemia
  • occurs when there is infection and inflammation with release of cytokines that stimulate hepcidin release from the liver.
    -High
50
Q

describe the importance of vitamin B12

A

➢ Essential for Cell
growth and DNA synthesis
➢ Maintenance of
normal myelin sheath
➢ Normal metabolic
functions of folic acid

51
Q

how is vitamin b12 prepared?

A

A. Cyanocobalamin
B. Hydroxocobalamin (preparation of
choice)
1. More slowly absorbed
2. More bound to plasma proteins
3. Slowly excreted
4. More sustained rise in serum level

52
Q

uses of vitamin b12

A

treatment of:
A) Megaloblastic anemia:

1)Pernicious anemia (lifelong treatment by IMI)
2) Megaloblastic anemia due to diphylobothriasis: Treated by VB12 and praziquantel

B) Drug induced megaloblastic anemia: Neomycin, colchicine and antiepileptics reduce absorption of VB12

C) Neurological Conditions:
-Peripheral neuritis in diabetes & retrobulbar neuritis in heavy smokers

53
Q

what are the causes of folic acid deficiency?

A
  1. Inadequate dietary supply or increased demand (e.g. Pregnancy, lactation)
  2. Diseases in small intestine
  3. Alcoholism
  4. Drug-induced folic acid
    deficiency
54
Q

what are the therapeutic uses of folic acid?

A

*- Megaloblastic anemia
* - Malabsorption syndrome
* - In alcoholics and pregnant women
* - Patients with liver disease & with hemolytic anemia
* - Patients on dialysis (as folic acid is removed each time)
* - With anticonvulsant drugs

55
Q

Describe the Treatment of aplastic Anemia (SEA BICE)

A

1) Supportive treatment
2) Eliminate underlying cause
3) Anabolic agents
4) Bone marrow transplantation
5) Intravenous Anti thymocyte immunoglobulin
6) Corticosteroids (reduce bleeding due to thrombocytopenia)
7) Erythropoietin

56
Q

Describe the uses of erythropoietin

A

➢ IV or SC
➢ Acts as regulator of erythropoiesis
➢ Used in anemia of chronic renal failure & severe anemia of cancer & AIDS
➢ It decreases the need for
transfusion as it elevates red blood cell level
➢ Hypertension and thrombosis

57
Q

Describe platelet activation

A

Damage of vessel wall → exposure of collagen in
subendothelium →
platelet adhesion (enhanced by factor VIII and von Willebrand factor) followed by activation→
release reaction (ADP, fibrinogen TXA2
, etc.….).
ADP binds to its receptor on platelets →
exposure of glycoprotein GP IIb/IIIa receptor on platelet membrane.
Fibrinogen binds to the GP IIb/IIIa receptor linking adjacent platelets → aggregation

58
Q

what are the therapeutic uses of antiplatelet drugs?

A

(mainly in arterial thrombosis)
1. High risk of myocardial infarction (AMI): e.g., previous attack of angina (aspirin).

  1. Acute coronary syndrome (aspirin +clopidogrel).
  2. Coronary bypasses grafting, angioplasty & stent insertion
    (aspirin plus clopidogrel or abciximab).
  3. Prosthetic heart valves: ↓thrombo-embolism (dipyridamole plus warfarin).
  4. Thrombotic stroke (dipyridamole plus aspirin).
  5. Hemodialysis (epoprostenol)
59
Q

Describe the mechanism of action of low dose aspirin
(Acetylsalicylic Acid)

A

➢ Irreversible inhibition of cyclooxygenase enzyme (COX-1 ) via acetylation.

➢Small dose inhibits thromboxane (TXA2) synthesis in platelets But not prostacyclin
(PGI2) synthesis in endothelium (larger dose).

60
Q

what are the Side effects of low dose aspirin?

A

-Increased incidence of GIT bleeding (aspirin prolongs
bleeding time)
GIT irritation
Hyperuricemia
Hypersentivity

61
Q

how is clopidogrel given?

A

-Clopidogrel is given orally and has a slow onset of action (3 - 5 days).
-It is a Prodrug so avoid taking with omeprazole as it inhibits its activation in liver

62
Q

what are the Adverse effects of ADP pathway inhibitors?

A

Ticlopedine –> neutropenia, bleeding, GIT irritation (rarely used)

Clopidogrel –>
➢Bleeding (prolong bleeding time)
➢G.I.T : nausea, dyspepsia, diarrhea.
➢Prodrug
➢Less neutropenia

63
Q

Describe the mechanism of action of Dipyridamole

A

Inhibits phosphodiestrase thus increase cAMP
–>
Vasodilator and antiplatelet

64
Q

Dipyridamole uses

A

➢ Given orally.
➢Week antiplatelet, so usually combined

65
Q

Adverse effects of Dipyridamole

A
  • Headache
  • Postural hypotension
  • Coronary Steal phenomenon
    -GIT irritation
66
Q

what are the side effects of Glycoprotein IIb/ IIIa receptor inhibitors?

A

bleeding, thrombocytopenia,
arrhythmia

67
Q

Drugs used in Thrombotic Disorders

A

Anticoagulants
Antiplatelets –>
Prevention and treatment of
thromboembolic

Fibrinolytics= Thrombolytic
–> Fibrin lysis
Acute treatment

68
Q

what is thrombosis?

A

Pathological condition from inappropriate activation of platelet aggregation
and coagulation cascades

69
Q

what are the types of thrombosis?

A

Arterial thrombus:
Mainly from platelets in a fibrin mesh, associated with
atherosclerosis and interrupted blood flow resulting in ischemia
–Treated mainly by
antiplatelet and fibrinolytic

Venous thrombus:
Mainly of fibrin tail with white head (platelet)→→→
stasis and detached leads to emboli (DVT and pulmonary
embolism)
–Treated mainly by
anticoagulants

70
Q

Describe the primary and secondary prevention of thrombosis

A

■ Primary prevention: prevent the initial formation
of blood clots in patients with recognised risk
factors
■ Secondary prevention chronically to treat and
prevent recurrence of thrombi and their
associated complications

71
Q

Describe the parenteral treatment of thrombosis

A

Indirect thrombin inhibitors:
Heparin, LMWH

Direct thrombin inhibitors:
Bivalirudin, argatroban, desirudin

Inhibitor of factor Xa
(Indirect)
Fondaparinux

72
Q

Describe the oral treatment of thrombosis

A

Inhibitors of synthesis of
clotting factor II, VII, IX, X
–Warfarin

Direct thrombin inhibitors
–Dabigatran

inhibitor of factor Xa (Direct)
–Rivaroxaban, apixaban, edoxaban

73
Q

Describe the mechanism of heparin action

A

Indirect Thrombin Inhibitor (indirectly by increasing the activity of the endogenous
anticoagulant “antithrombin III” (1000 folds) on activated clotting factors especially: Factor IIa (Thrombin) - factor
IXa - factor Xa

Heparin binds to both antithrombin III and thrombin to form a complex
❑ Heparin dissociates leaving them
❑ Once dissociated, Heparin is free to bind to another antithrombin

-Slight vasodilator
-Stimulates lipoprotein lipase

74
Q

describe the pharmacokinetics of heparin

A

– Immediate onset of action after IV injection and short duration (4-6 h).
– 80 % hepatic metabolism, 20 % excreted renally, unchanged.
– Does not cross placenta & is not secreted in milk (high MW)
 can be used during
lactation or pregnancy

75
Q

what are the heparin routes of administration?

A

■ IV
■ SC
■ Never IM may lead to
hematoma

76
Q

Control of heparin therapy

A

aPTT (activated partial thromboplastin time) should be kept as close as possible
to twice normal value (normal value 30-35 seconds)

77
Q

what are the adverse effects of heparin?

A

■ Hemorrhage
■ Hair loss
■ Hematoma
■ Hypersensitivity reaction
■ Hyperkalemia (monitor K level if given > 7
days)
■ Osteoporosis (long term use)
■ Thrombocytopenia (regular platelet count is
needed)

78
Q

Reversal of Heparin Action in hemorrhage

A

■ Discontinuation of the drug
■ Heparin is strongly acidic and isneutralized by i.v. protamine sulfate (a strongly basic protein)
■ It combines with heparin to form a stable complex devoid of anticoagulant
activity
■ 1mg to every 100U heparin,
excessive amount may lead to bleeding

79
Q

what are the types of HIT (heparin induced thrombocytopenia)?

A

Non immune-HIT
■ Start early (within 2 days)
■ Platelet count >100
000/ul
■ Returns to normal within 5
days despite continued
heparin use (or within 2
days if heparin is stopped).

Immune-HIT
■ Start late
■ Potentially catastrophic thrombosis, blood contain
abnormal low platelet (TOO LOW)
■ 30% develop severe venous and/or arterial thrombosis and bleeding uncommon
■ Replace heparin by argatroban or fondaparinux

80
Q

LMWHs mechanism of action

A

■They bind to antithrombin increasing its inhibitory effect on factor Xa and to a lesser extent on thrombin (Factor IIa)

81
Q

Describe low molecular weight heparins

A

■ Have equal efficacy
■ No frequent laboratory monitoring (
suitable for outpatient therapy)
■ Greater bioavailability
■ longer t ½ (sc once/day)
■ Binding to platelets and osteoblasts is reduced with LMWH compared with
Heparin

82
Q

what is Fondaparinux (Indirect Xa inhibitor)?

A

a synthetic compound that inhibits factor Xa by
accelerating antithrombin no effect on thrombin

83
Q

what are the advantages of Fondaparinux?

A

– Long t1/2 (sc once/day)
– Low risk of HIT
– Bleeding is the major side effects, not
antagonized by protamine sulfate
– No need for monitoring

84
Q

what is protamine sulfate?

A

low MW carrying electropositive charge.
Neutralizes heparin (each 1 mg neutralizes ≈ 100 IU heparin).
Partially antagonizes LMWHs but does not antagonize fondaparinux.
Has a slight anticoagulant effect  avoid overdose.

85
Q

describe the mechanism of action of direct thrombin inhibitors

A

■ Directly bind to thrombin independent of antithrombin→ more
inhibition of fibrin bound thrombin

86
Q

How are direct thrombin inhibitors given and what are the side effects?

A

■ Given intravenous
■ Bleeding is the major side effect
■ Argatroban in HIT in patients with renal insufficiency

87
Q

what is an alternative to heparin?

A

Bivalirudin is alternative to heparin in patient with normal kidney
function also inhibit platelet activation

88
Q

what is the mechanism of action of warfarin?

A

Warfarin inhibits the synthesis of biologically active forms of vitamin K-dependent clotting factors II, VII, IX and X
-Inhibition of vitamin K epoxide reductase enzyme g prevention of reactivation of vitamin K. so interference
with hepatic synthesis of vitamin K-dependent clotting factors (II, VII, IX, X)

89
Q

pharmacokinetics of warfarin

A

■ Well absorbed after oral administration(100%
bioavailability).
■ More than 99 % bound to plasma proteins.
■ Metabolized by liver & excreted by kidney.
■ Delayed onset with long duration of action (up to 6
days).
■ Crosses placenta.
■ Secreted in milk (negligible amounts  safe during
lactation)

90
Q

what are the antidotes of warfarin

A

Fresh frozen plasma.
Vitamin K

91
Q

adverse effects of warfarin

A

■Hemorrhage.
■Skin necrosis
■Teratogenic

92
Q

disadvantages of warfarin

A

■ Delayed onset (5-10 days ) requires
overlapping therapy with heparin.
■ Narrow therapeutic index
■ Requires routine monitoring of coagulation.
■ Drug interactions

Blood Module (9 decks)

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