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HEMATOLOGY AND ONCOLOGY > HEMATOLOGY AND ONCOLOGY- Pharmacology > Flashcards

HEMATOLOGY AND ONCOLOGY- Pharmacology Flashcards

1
Q

Mechanism of action of Heparin

A

Cofactor for the activation of antithrombin, ↓ thrombin, and ↓ factor Xa

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2
Q

Clinical use of Heparin

A

Immediate anticoagulation for Pulmonary embolism, acute coronary syndrome, MI, deep venous thrombosis (DVT)

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3
Q

Can heparin be used during pregnancy?

A

Yes. (does not cross placenta)

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4
Q

What need to be followed when using Heparin?

A

PTT

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5
Q

Secondary effects due to use of Heparin

A

Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drgu interactions

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6
Q

What is the rapid reversal antidote for Heparin?

A

Use protamine sulfate

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7
Q

How does protamine work?

A

Positively charged molecule that binds negatively charged heparin

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8
Q

Which are low molecular weight heparin?

A

Enoxaparin

Dalteparin

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9
Q

Which is the benefict of Low weght heparin?

A

Act more on factor Xa, have better bioavilability and 2-4 times longer half life

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10
Q

How is low molecular weight heparin administered?

A

Subcutaneously

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11
Q

Does low molecular weight heparin require monitoring?

A

No

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12
Q

Which is the risk when using low molecular weight heparin?

A

Not easily reversible

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13
Q

What is HIT?

A

Heparin Induced Thrombocytopenia

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14
Q

Pathophysiology of Heparin Induced Thrombocytopenia

A

Development of IgG antibodies against heparin bound to platelet factor 4. Antibody- Heparin- PF4 coplex activates platelets→ Thrombosis and thrombocytopenia

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15
Q

Derivates of hirudin

A

Argatroban, bivalirudin

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16
Q

Which anticoagulant is used by leeches?

A

Hirudin

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17
Q

What is the effect of Argatroban, bivalirudin?

A

Inhibit thrombin directly

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18
Q

When is recommended to use Argatroban, bivalirudin?

A

Used instead of heparin for anticoagulating patients with Heparin Induced Thrombocytopenia

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19
Q

What is the coumadin?

A

Warfarin

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20
Q

What is the mechanism of action of Warfarin?

A

Inteferes with normal synthesis and γ carboxylation of vitamin K dependent clotting factors II, VII, IX and X and proteins C and S

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21
Q

Who metabolizes Warfarin?

A

By cytochrome P 450 pathway

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22
Q

What do laboratory assay stbalish about Warfarin?

A

Warfain has effect on extrinsic pathway

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23
Q

Which lab study is modified with Warfarin?

A

↑ PT

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24
Q

How is the half life of Warfarin?

A

Long half life

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25
Q

Clinical use for Warfarin

A

Chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation)

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26
Q

What main difference does Warfarin has compared to Heparin?

A

Warfarin is not used in pregnant women (because warfarin, unlike heparin, can cross the placenta)

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27
Q

How is Warfarin monitored?

A

Follow PT/ INR values

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28
Q

Toxic effects of Warfarin

A

Bleeding, teratogenic, skin/ tissue necrosis, drug interactions

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29
Q

What is used fro reversal of warfarin overdose?

A

Give vitamin K

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30
Q

What is used for rapid reversal of severe warfarin overdose?

A

Frozen plasma

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31
Q

Direct Factor Xa inhibitors

A

Apixaban, rivaroxaban

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32
Q

Mechanism of action of Apixaban, rivaroxaban

A

Bind and Directly inhibit Factor Xa

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33
Q

Which Direct Factor Xa inhibitors is used in Pulmonary embolism?

A

rivaroxaban

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34
Q

Clinical use for Apixaban, rivaroxaban

A

Treatment and prophylaxis of DVT, stroke prophylaxis in patient with atrial fibrillation

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35
Q

What is a benefict of Apixaban, rivaroxaban ?

A

Oral agents do not require coagulation monitorin

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36
Q

Toxic effect of Apixaban, rivaroxaban

A

Bleeding

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37
Q

Which is the antidote for Direct Factor Xa inhibitors?

A

No specific reversal agent available

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38
Q

How is the structure of Heparin?

A

Large anionic, acicid

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39
Q

Route of administering Heparin

A

Parenteral (IV, SC)

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40
Q

Site of action of Heparin

A

Blood

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41
Q

Onset of Action of Heparin

A

Rapid (seconds)

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42
Q

Activates antitrhrombin, which ↓ the action of IIa (thrombin) and factor Xa

A

Heparin

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43
Q

How is the duration of action of Heparin?

A

Acute (hours)

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44
Q

Does Heparin inhibits coagulation in vitro?

A

Yes

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45
Q

Treatment of acute overdose of Heparin

A

Protamine sulfate

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46
Q

How is Heparin monitored?

A

By PTT

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47
Q

Which pathway is altered by Heparin?

A

Intrinsic pathway

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48
Q

Does Heparin crosses placenta?

A

No

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49
Q

Structure of Warfarin

A

Small lipid-soluble molecule

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50
Q

Route of administering Warfarin

A

Oral

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51
Q

Site of action of Warfarin

A

Liver

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52
Q

Onset of action of Warfarin

A

Slow, limited by half lives of normal cloting factors

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53
Q

Impairs the synthesis of vitamin K dependent clotting factors

A

Warfarin

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54
Q

What is the mechanism of action of Warfarin?

A

Vitamin K antagonist

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55
Q

How is the duration of action of Warfarin?

A

Chronic (days)

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56
Q

Does Warfarin inhibits coagulation in vitro?

A

No

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57
Q

Treatment of acute overdose of Warfarin

A

IV vitamin K and fresh frozen plasma

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58
Q

How is Warfarin therapy monitored?

A

With PT/INR

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59
Q

Which pathway is modified with Warfarin therapy?

A

Extrinsic pathway

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60
Q

Does Warfarin crosses placenta?

A

Yes (teratogenic)

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61
Q

Who are Thrombolytics?

A

Alteplase (tPA)
Reteplase (rPA)
Tenecteplase (TNK-tPA)

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62
Q

What is tPA?

A

Tissue plasminogen activator (tPA)

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63
Q

Mechanism of actionof Thrombolytics

A

Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots

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64
Q

How are coagulation times affected by Thrombolytics?

A

↑ PT

↑ PTT

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65
Q

Do thrombolytics affect platelet count?

A

No change in platelet count

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66
Q

Clinical use for Thrombolytics

A

Early MI, early ischemic stroke, direct thrombolysis of severe Pulmonary Embolism

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67
Q

Toxic effect of thrombolytics

A

Bleeding

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68
Q

Contraindications of Thrombolytic drugs

A

In patients with active bleeding, hystory of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension

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69
Q

How is thrombolytic toxicity treated?

A

With Aminocaproic acid

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70
Q

What is aminocaproic acid?

A

An inhibitor of fibrinolysis

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71
Q

What else can be used to correct factor deficiencies?

A

Fresh frozen plasma and cryoprecipitate

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72
Q

What is the mechanism of action of aspirin?

A

Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) enzyme by covalent acetylation

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73
Q

What is the effect of aspirin on platelets?

A

Platelets cannot synthesize new enzyme, so effect lasts until new platelets are produced

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74
Q

What efect does aspirin has?

A

↑ bleeding time, ↓ TXA2 and prostaglandins

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75
Q

How does aspirin affects PT and PTT?

A

No effect on PT or PTT

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76
Q

Clinical use for Aspirin

A

Antipyretic, analgesic, anti-inflammatory, antiplatelet (↓ aggregation)

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77
Q

Toxic effects of Aspirin

A

Gasrtic ulceration, tinnitus (CN VIII)

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78
Q

What does chronic use of aspirin leads to?

A

Acute renal failure, intesrtitial nephritis, and upper GI bleeding

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79
Q

What is the effect of Aspirin in children?

A

Reye syndrome when treating Viral infection

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80
Q

What happens with Aspirin overdose?

A

Causes Respiratory alkalosis initially, which is then superimposed by metabolic acidosis

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81
Q

ADP receptor inhibitors

A

Clopidogrel, ticlopidine, prasugel, ticagrelor

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82
Q

How is clopidogrel consider?

A

ADP receptor inhibitor

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83
Q

Mechanism of action of clopidogrel

A

Inhibit platelet aggreagation by irreversibly blocking ADP receptor

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84
Q

What is the effect of clopidogrel with fibrinoge?

A

Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIA from binding to fibrinogen

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85
Q

Clinical use for ADP receptor inhibitors

A

Acute coronary syndrome, coronary stenting

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86
Q

What is a benefit of clopidogrel use?

A

↓ incidense of recurrence of thrombotic stroke

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87
Q

Toxic effect of toclopidine

A

Neutropenia

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88
Q

Possible secondary effect of ADP receptor inhibitors

A

TTP/ HUS may be seen (Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS))

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89
Q

Phosphodiesterase III inhibitor

A

Cilostazol, dipyridamole

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90
Q

What is the mechanism of action of Cilostazol, dipyridamole?

A

Phosphodiesterase III inhibitor; ↑ cAMP in platelets, thus inhibiting platelet aggregation; vasodilators

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91
Q

Clinical use for Cilostazol, dipyridamole

A

Intermitent claudication, coronary vasodilation, prevention of stroke or TIAs (Transient ischaemic attack), angina prophylaxis

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92
Q

Which medicine is combined with Cilostazol, dipyridamole, in Transient ischaemic attack?

A

Aspirin

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93
Q

Toxic effect of Cilostazol, dipyridamole

A

Nausea, headache, facial flushing, hypotension, abdominal pain

94
Q

GP IIb/IIIa inhibitors

A

Abxicimab
Eptifibate
Tirofiban

95
Q

Mechanism of action of Abxicimab

A

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

96
Q

From what is Abxicimab made?

A

From monoclonal antibody Fab fragments

97
Q

Clinical use for GP IIb/IIIa inhibitors

A

Unstable angina, percutaneous transluminal coronary angioplasty

98
Q

Toxic effect og GP IIb/IIIa inhibitors

A

Bleeging, thrombocytopena

99
Q

Which cancer drugs inhibit DNA synthesis (S phase)?

A

Antimetabolites

Etoposide

100
Q

Which cancer drug inhibits both S and G2 phases in cell cycle?

A

Etoposide

101
Q

What is the mechanism of action of Bleomycin as Cancer drug?

A

Inhibits G2 phase of cell cycle

102
Q

What happens in G2 phase of cell cycle?

A

Synthesis of components needed for mitosis

103
Q

Cancer drugs that inhibit M phase in cell cycle

A

Vince alkaloids and taxols

104
Q

What happens in G1 phase of cell cycle?

A

Synthesis of components needed for DNA synthesis

105
Q

Antineoplastic that inhibit nucleotide synthesis

A

Metrotexate
5-FU
6-mercaptopurine

106
Q

Drugs that decrease thymidine synthesis

A

Metrotexate

5-FU

107
Q

Antineoplastic that decreases purine synthesis

A

6-mercaptopurine

108
Q

Drugs that inhibit DNA synthesis

A

Alkylating agents
DNA intercalators
Etoposide

109
Q

Example of Alkylating agent

A

Cisplastin

110
Q

What is the effect of cisplastin?

A

Cross link DNA

111
Q

DNA intercalators

A

Dactinomycin, Doxorrubicin

112
Q

What is the mechanism of action of Etoposide?

A

Inhibits topoisomerase II

113
Q

Antineoplastics that inhibit Cellular division

A

Vinca alkaloids

Paclitaxel

114
Q

What is the effect of Vinca alkaloids?

A

Inhibit microtubule formation

115
Q

What is the mechanism of action of Paclitaxel?

A

Inhibits microtubule disessembly

116
Q

Steps to get to cellular division

A

Nucleotide synthesis → DNA → RNA → Protein → Cellular division

117
Q

Drugs consider antimetabolites

A 
Metrotexate (MTX)
5- fluorouracil (5-FU)
Cytarabine (arabininofuranosyl cytidine)
Azathioprine/ 6 Mercaptopurine
6 thioguanine
118
Q

Mechanism of action of Metotrexate

A

Folic acid analog that inhibits dyhydrofolate reductase

119
Q

What is the result of Metotrexate inhibiting dyhydrofolate reductase?

A

↓ dTMP → ↓ DNA and ↓ protein synthesis

120
Q

Cancer Clinical use for Metotrexate

A

Leukemias, lymphomas, choriocarcinoma, sarcomas

121
Q

Non neoplastic clinical use for Metotrexate

A

Abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis, inflammatory bowel disease

122
Q

Secondary effects of Metotrexate

A

Myelosuppression
Macrovesicular fatty change in liver
Mucositis
Teratogenic

123
Q

How is reverse the myelosupression caused by Metotrexate?

A

Reversible with Leucovorin (folinic acid) “rescue”

124
Q

Pyrimidine analogs

A

5- FU

Cytarabine

125
Q

How is the activated form of 5-FU?What is its purpose?

A

5F-dUMP, which covalently complexes folic acid

126
Q

What is the effect of 5F-dUMP- Folic acid complex?

A

Inhibtis thymidilate synthase→ ↓ dTMP → ↓DNA and ↓ protein synthesis

127
Q

Clinical use for 5-FU

A

Colon Cancer, pancreatic cancer, basal cell carcinoma (topical)

128
Q

Side effects of 5 FU

A

Myelosuppression

Photosensitivity

129
Q

Myelosuppession caused by 5 FU could it be reverse with leucovorin?

A

NO

130
Q

Which is the “rescue” in case of overdose with 5 FU?

A

Uridine

131
Q

Arabinofuranosyl cytidine

A

Cytarabine

132
Q

Mechanism of action of cytarabine

A

Pyrimidine analog → inhibitions of DNA polymerase

133
Q

When is reccomended the clinical use of Cytarabine?

A

Leukemias, Lymphomas

134
Q

Toxic effects of Cytarabine

A

Leukopenia, thrombocytopenia, megaloblastic anemia

Pancytopenia

135
Q

Purine analogs

A

Azathioprine
6 MP
6 TG (thioguanine)

136
Q

Mechanism of action of Azathioprine, 6 MP?

A

Purine analog → ↓ de novo purine synthesis

137
Q

What activates Purine analogs?

A

HGPRT

138
Q

Clinical use for purine analogs

A

Preventing organ rejection, Rheumatoid Arthritis

Leukemia,

139
Q

Purine analog use for SLE

A

Azathioprine

140
Q

Which purine analogs are used for Inflammatory Bowel disease?

A

6 MP

6 TG

141
Q

Which are the main organs affected by purine inhibitors?

A

Bone marrow, GI, Liver

142
Q

Who metabolizes Azathioprine and 6 MP?

A

Xanthine oxidase

143
Q

What inhibits metabolism of Azathioprine and 6 MP?

A

Allopurinol

144
Q

What is the problem that Azathioprine and 6 MP are metabolized by xanthine oxidase?

A

Increase toxicity with allopurinol, which inhibits their metabolism

145
Q

Antitumor antibiotics

A

Dactinomycin
Doxorubicin
Bleomycin

146
Q

Alternative name Dactinomycin

A

actinomycin D

147
Q

This antitumor antibiotic intercalates in DNA

A

Dactinomycin

148
Q

Clinical use for Dactinomycin

A

Wilms tumor, Ewing sarcoma, rhabdomyosarcoma

149
Q

Antitumor antibiotic used for Childhood tumors

A

Dactinomycin

150
Q

Toxic effect of Dactnimycin

A

Myelosuppression

151
Q

Mechanism of action of Doxorubicin, daunorubicin

A

Generate free radicals

Intercalate in DNA → breaks in DNA → ↓ replication

152
Q

Clinical use of Doxorubicin, daunorubicin

A

Solid tumors, leukemias, lymphomas

153
Q

Toxic effects of Doxorubicin, daunorubicin

A

Cardiotoxocity (dilated cardiomyopathy)
Myelosuppression
Alopecia
Toxic to tissues following extravasation

154
Q

Which drug is used to prevent Cardiotoxicity by Doxorubicin, daunorubicin?

A

Dexrazoxane

155
Q

How is Dexrazonxane consider?

A

Iron chelating

156
Q

Mechanism of action of Bleomycin

A

Induces free radical formation, which caises breaks in DNA strands

157
Q

Clinical use for Bleomycin

A

Testicular cancer, Hodgkin lymphoma

158
Q

Toxic effects cause by bleomycin

A

Pulmonary fibrosis, skin changes, mucositis.

Minimal myelosupression

159
Q

Alkylating agents

A

Cyclophosphamide, ifosfamide
Nitrosoureas
Busulfan

160
Q

Covalently X link (intersrand) DNA at guanine N-7

A

Cyclophosphamide, isofosfamide

161
Q

What do Cyclophosphamide, isofosfamide require?

A

Bioactivation by liver

162
Q

Clinical use for Cyclophosphamide, isofosfamide

A

Solid tumors, leukemia, lymphomas, and some brain cancers

163
Q

Toxic effects of Cyclophosphamide, isofosfamide

A

Myelosuppression

Hemorrhagic cystitis

164
Q

Drug that partially prevents hemorrhagic cystitis caused by cyclophospamide

A

Mesna (bind toxic metabolites)

165
Q

Who are Nitrosoureas?

A

Carmustine
Lomustine
Semustine
Streptozocin

166
Q

What do Nitrofureas need?

A

Bioactivation

167
Q

These Alkylating agents cross blood brain barrier

A

Nitrosoureas

168
Q

Effect of Nitrosureas

A

Cross links DNA

169
Q

Clinical use for Nitrosureas

A

Brain tumors (including glioblastoma multiforme)

170
Q

Alkylating angents that cause CNS toxicity

A

Nitrosureas

171
Q

Effect of Busulfan

A

Cross links DNA

172
Q

Clinical use for Busulfan

A

CML

Also used to ablate patient’s bone marrow transplantation

173
Q

Toxic effect of Busulfan

A

Severe myelosuppression (in almost all cases), pulmonary fibrosis, hyperpigmentation

174
Q

Microtubule inhibitors

A

Vincristine, Vinblastine

Paclitaxel, other taxols

175
Q

How are Vincristine, vinblastine consider?

A

Vinca alkaloids

176
Q

Mechanism of action of Vincristine, vinblastine

A

Bind β tubulin, inhibit its polymerization into microtubules, thereby preventing mitotic spindle formation

177
Q

Which phase of cycle cell do Vincristine, vinblastine intefere with?

A

M phase arrest

178
Q

Clinical use for Vincristine, vinblastine

A

Solid tumors, leukimias and lymphomas

179
Q

Toxic effects caused by Vincristine

A

Neurotoxicity (areflexia, peripheral neuritis)

Paralytic ileus

180
Q

Vinblastine secondary effects

A

Vinblastine blasts bone marrow (suppression)

181
Q

Mechanism of action of paclitaxel, other taxols

A

Hyperstabiliza polymerized microtubules in M phase so that mitotic spindle cannot break down

182
Q

Which phase is inhibited by Paclitaxel and other Taxols?

A

Anaphase cannot occur

183
Q

Which microtubul inhibitors are used for ovarian cancer and breast carcinomas?

A

Paclitaxel and other Taxols

184
Q

Secondary effects of Placlitaxel

A

Myelosuppression, alopecia, hypersensitivity

185
Q

Which is the mechanism of action of Cisplatin, carboplatin?

A

Cross link DNA

186
Q

Clinical use of Cisplatin, carboplatin

A

testicular, bladder, ovary and lung cancer

187
Q

Toxic effect of Cisplatin, carboplatin

A

Nephrotoxicity and acoustic nerve damage

188
Q

How is nephrotoxicity prevented when using cisplatin, carbopatin?

A

With Aminfostine and chloride diuresis

189
Q

What is Amifostine?

A

Free radical scavenger

190
Q

Chemotherapy agent that inhibits topoisomerase II

A

Etoposide, teniposide

191
Q

What is the result of Etoposide inhibiting topoisomerase II?

A

Increases DNA degradation

192
Q

Clinical use for Etoposide

A

Solid tumors (particulary testicular and small cell lung cancer), leukemias, lymphomas

193
Q

Which are secondary effects of Etoposide?

A

Myelosuppression, GI irritation, alopecia

194
Q

Inhibit topisomerasse I and prevent DNA unwinding and replication

A

Irinotecan, topotecan

195
Q

When is recommended the clinical use of Irinotecan?

A

Colon cancer

196
Q

In these cancers Topotecan could be used

A

Ovarian and small cell lung cancer

197
Q

Toxic effect caused by Irinotecan, topotecan

A

Severe myelosuppression, diarrhea

198
Q

Mechanism of action of Hydroxyurea

A

Inhibits ribonucleotide reductase → ↓ DNA Synthesis

199
Q

In which phase of Cell Cylce does Hydroxyurea works?

A

S phase specific

200
Q

Which is the clinical use for Hydroxyurea?

A

Melanoma, CML, sickle cell disease (↑ HbF)

201
Q

Secondary effects of Hydroxyurea

A

Bone marrow suppresion, GI upset

202
Q

Mechanism of action of Prednisone, predinisolone as drugs for cancer

A

MAy trigger apoptosis. May even work on nondividing cells

203
Q

Most commonly used glucocoricoids in cancer chemotherapy

A

Prednisone, predinisolon

204
Q

When is recommended the clinical use of Prednisone, predinisolone as cancer chemotherapy?

A

Used in CLL, non Hodgkin Lymphomas (part of combination chemotherapy regimen)
Also used as immunosuppressants (eg. autoimmune disease)

205
Q

Toxic effects caused by Prednisone, predinisolone

A

Cushing like symptoms; weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis

206
Q

Selective estrogen receptor modulators (SERMs)

A

Tamoxifen, raloxifene

207
Q

Mechanism of action of Tamoxifen, raloxifene

A

Receptor antagonists in breast and agonists in bone

Block the binding of estrogen to ER + cells

208
Q

Which is the clinical use of Tamoxifen?

A

Breast cancer treatment and prevention

209
Q

Clinical use for Raloxifene

A

Useful to prevent osteoporosis

210
Q

Toxic effect cause by Tamoxifen

A

Partial agonist in endometrium, which ↑ risk of endometrial cancer, “hot flashes”

211
Q

Why Raloxifene does not increase the risl of Endometrial cancer?

A

Because it is an endometrial antagonist

212
Q

Commercial name for Trastuzumab

A

Herceptin

213
Q

Monoclonal antibody against HER-2 (c-erbB2)

A

Trastuzumab

214
Q

Which kind of receptor does Monoclonal antibody against HER-2 (c-erbB2) has?

A

A tyrosine kinase kinase receptor

215
Q

What is the effect of Trastuzumab?

A

Helps kill breast cancer cells that overexpress HER-2, through inhibition of HER-2 initiated cellular signanling and antibody dependent cytotoxicity

216
Q

Clinical use of Trastuzumab

A

HER-2 + breast cancer and gastric cancer

217
Q

Toxic effect of Trastuzumab

A

Cardiotoxicity

218
Q

Commercial name for Imatinib

A

Gleevec

219
Q

Mechanism of action of Imatinib

A

Turosine kinase inhibitor of bcr- abl (Philadelphia chromosome fusion gene in CML) and c-Kit (common in GI stromal tumors)

220
Q

Clinical use for Imatinib

A

CML, GI stromal tumors

221
Q

Toxic effect of Imatinib

A

Fluid Retention

222
Q

Monoclonal antibody against CD 20

A

Rituximab

223
Q

Where is Monoclonal antibody against CD 20 found?

A

On most B cell neoplasms

224
Q

Clinical use for Rituximab

A

Non Hodgkin lymphoma, rheumatoid arthtitis (with MTX), ITP (Immune thrombocytopenic purpura)

225
Q

Side effects of Rituximab

A

Increase risk of progressive multifocal leukoencephalopathy

226
Q

Which is the mechanism of action of Vemurafenib?

A

Small moleculr inhibitor of forms of the B-Raf kinase with the V600E mutation

227
Q

Clinical use for Vermurafenid

A

Metastatic Melanoma

228
Q

Monoclonal antibody against VEGF

A

Bevacizumab

229
Q

What is the effect of Bevacizumab?

A

Inhibits angiogenesis

230
Q

Clinical use for Bevacizumab

A

Solid tumors (colorectal cancer, renal cell carcinoma)

231
Q

Toxic effect of Bevacizumab

A

Hemorrhage and impaired wound healing

HEMATOLOGY AND ONCOLOGY (4 decks)

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