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PHARMACOLOGY > IMMUNOPHARMACOLOGY IMMUNOSUPPRESSIVE THERAPY > Flashcards

IMMUNOPHARMACOLOGY IMMUNOSUPPRESSIVE THERAPY Flashcards

1
Q

What is immunosuppressive therapy?

A

Tx that lowers the activity of the body’s immune system.
It also reduces the ability of rejection of organ transplant.

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2
Q

STATE THE CLASSIFICATION OF IMMUNOSUPPRESSIVE DRUG.

A
  1. GLUCOCORTICOID
  2. CYTOTOXIC DRUG
    - ANTIMETABOLITES
    - ALKYLATING AGENTS
  3. IMMUNOSUPPRESSIVE ANTIBODIES
    - ALG
    - ATG
    - IGIV
    - RHO (D) IMMUNE GLOBULIN
    - HYPERIMMUNE IMMUNOGLOBULIN
  4. MONOCLONAL ANTIBODIES
  5. IMMMUNOMODULATORS
    - CYTOKINES
    - LEVAMISOLE
    - INTERFERONS
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3
Q

IMMUNOSUPPRESSANT ARE USED IN: (5)

A

ORGAN TRANSPLANT:
1. KIDNEY
2. HEART
3. LIVER
4. PANCREAS
5. BM TRANSPLANT

A/I DISORDER:
1. A/I HAEMOLYTIC ANAEMIA
2. IDIOPATHIC THROMBOCYTOPENIC PURPURA
3. TYPE 1 DM
4. SLE
5. HASHIMOTO’S THYROIDITIS
6. RA
7. SCLERODERMA

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4
Q

MOA OF PREDNISOLONE

A
  • GLUCOCORTICOID BIND TO CYTOSOLIC GLUCOCORTICOID RECEPTOR
  • FORM RECEPTOR LIGAND COMPLEX
    THE COMPLEX TRANSLOCATE INTO THE CELL NUCLEUS
  • THEN BIND TO GRE IN THE PROMOTER REGION OF TARGET GENE
  • IT WILL INHIBIT THE GENE EXPRESSION OF PRO- INFLAMMATORY CYTOKINES AND INCREASE EXPRESSION OF ANTI- INFLAMMATORY CYTOKINES
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5
Q

STATE THE EFFECT THE OCCUR IN CELL MEDIATED IMMUNITY IF GLUCOCORTICOID IS BEING USED.

A
  • INHIBIT GENE THT ENCODE CYTOKINE SUCH AS IL-2
  • REDUCED CYTOKINE PRODUCTION
  • REDUCED T CELL PROLIFERATION
  • REDUCED MACROPHAGE ACTIVITY (INHIBIT ANTIGEN RECOGNITION)
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6
Q

STATE THE EFFECT THE OCCUR IN HUMORAL IMMUNITY IF GLUCOCORTICOID IS BEING USED.

A
  • GLUCOCORTICOID SUPPRESS B CELL F(X)
  • B CELL EXPRESS LOW IL-2 AND IL-2 RECEPTORS
  • DIMINISH B CELL CLONE EXPANSION
  • DIMINISH ANTIBODY SYNTHESIS
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7
Q

STATE THE PK, ADR, AND CLINICAL USE OF GLUCOCORTICOID (PREDNISOLONE).

A

PK: ORAL
ADR:
1. WEIGHT GAIN
2. HPT
3. HYPERLIPIDAEMIA
4. HYPERGLYCAEMIA
5. PEPTIC ULCER
6. MYOPATHY
7. DELAYED WOUND HEALING
CLINICAL USE:
- ORGAN TRANSPLANT -> KIDNEY, HEART, BM
- A/I CONDITION -> ITP, A/I HA, LUPUS NEPHRITIS
- ALLERGIC COND. -> ASTHMA, RA

*** PREDNISOLONE ALWAYS USE TGT WITH OTHER IMMUNOSUPPRESSIVE THERAPY AT INITIAL STAGE.

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8
Q

STATE 2 EXAMPLES OF CALCINEURIN INHIBITOR.

A
  1. CYCLOSPORIN A (PEPTIDE ANTIBIOTIC)
  2. TACROLIMUS
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9
Q

STATE THE MOA OF CYCLOSPORIN A.

A
  • CYCLOSPORIN A BIND TO CYCLOPHILIN AND FORM COMPLEX THT INHIBIT PHOSPHATASE ACTIVITY OF CALCINEURIN.
  • PREVENT ACTIVATION OF NFAT AND TRANSCRIPTION OF CYTOKINE (IL-2, IL-3, IFN)

*** CYCLOSPORIN CAN ACTIVATE T CELL SPECIFIC TRANSCRIPTION FACTOR (NFAT)

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10
Q

STATE THE PK, ADR, AND CLINICAL USE OF CYCLOSPORIN A.

A

PK:
- ADMINISTERED VIA IV ROUTE OR ORAL ROUTE
- METABOLISED BY P450 3A IN LIVER
- REQUIRE DOSE ADJUSTMENT (Css)
ADR:
- NEPHROTOXICITY
- HYPERTENSION
- HIRSUTISM
- SEIZURE HYPERGLYCAEMIA
- HYPERK+
- LIVER DYSFUNCTION
CLINICAL USE:
- KIDNEY, PANCREAS, LIVER TRANSPLANT
- PREVENTION GVHD
- RA
- PSORIASIS

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11
Q

STATE THE MOA OF TACROLIMUS.

A

TACROLIMUS BIND TO IMMUNOPHILIN FK- BINDING PROTEIN - THEN THE COMPLEX WILL INHIBIT THE CALCINEURIN - INHIBIT THE GENE TRANSCRIPTION OF CYTOKINES SUCH AS IL2, IL3 AND IFN.

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12
Q

STATE THE PK OF TACROLIMUS.

A

ADMINISTERED ORALLY OR IV
HAVE HALF LIFE OF 9 TO 12 HRS
METABOLISED BY THE CYT 450 ENZYME
DOSE ADJUSTMENT THROUGH LEVEL AT Css.

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13
Q

STATE THE ADR OF TACROLIMUS

A

NEPHROTOXICITY
NEUROTOXICITY
HYPERTENSION
HYPERK+
GI DISORDER

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14
Q

STATE THE CLINICAL USE OF TACROLIMUS.

A

ORGAN TRANSPLANT
STEM CELL TRANSPLANT
AUTO IMMUNE CONDITION - FSGS
PROPHYLAXIS GVHD
DERMATITIS
PSORIASIS

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15
Q

BETWEEN TACROLIMUS AND CYCLOSPORIN, WHICH ONE IS MORE PORTEN AND MORE EFFECTIVE IN PREVENTING ORGAN TRANSPLANT REJECTION.

A

TACROLIMUS

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16
Q

CYCLOSPORIN CAN BE COMBINED WITH IMMUNOSUPPRESSIVE THERAPY TO ___ SUCH AS ___

A

CYCLOSPORIN CAN BE COMBINED WITH IMMUNOSUPPRESSIVE THERAPY TO REDUCE TOXICITY SUCH AS PREDNISOLONE.

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17
Q

STATE AN EXAMPLE OF PROLIFERATION SIGNAL INHIBITOR.

A

SIROLIMUS (RAPAMYCIN)

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18
Q

STATE THE MOA OF A MTOR INHIBITOR (SEROLIMUS)

A

SEROLIMUS WILL BIND TO IMMMUNOPHILIN FK506 BINDING PROTEIN 12 -> THEN IT WILL BLOCK MOLECULAR TARGET OF RAPAMYCIN (MTOR) -> RESULTING IN THE INHIBITION OF THE INTERLEUKIN DRIVEN T CELL PROLIFERATION -> INHIBIT B CELL PROLIFERATION -> REDUCE IMMUNOGLOBULIN PRODUCTION

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19
Q

STATE THE PK OF THE MTOR INHIBITOR.

A

ORALLY ADMINISTERED
HAVE HALF LIFE OF 60 HRS
METABOLISED BY THE CYT450 3A AND P- GLYCOPROTEIN
THE DOSE IS DEPENDS ON THE INDICATION

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20
Q

STATE THE CLINICAL USE OF THE SIROLIMUS.

A
  • ORGAN REJECTION PREVENTION
  • PROPHYLAXIS GVHD IN STEM CELL TRANSPLANT
  • DERMATOLOGIC DISORDER
  • STENT- PREVENT RESTENOSIS
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21
Q

STATE THE ADR OF THE SIROLIMUS.

A
  • MYELOSUPPRESSION
  • HEPATOTOXICITY
  • DIARRHOEA
  • HYPERTG
  • PNEUMONITIS
  • HEADACHE
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22
Q

WHEN SIROLIMUS IS BEING USED WITH CYCLOSPORIN, IT WILL

A

INCREASE THE PLASMA LEVEL

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23
Q

STATE 2 EXAMPLES OF CYTOTOXIC AGENTS

A

AZATHIOPRINE
PRODRUG OF MERCAPTOPURINE

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24
Q

STATE THE MOA OF ANTIMETABOLITES.

A

CONVERTED TO 6- MERCAPTOPURINE -> INHIBIT THE SYNTHESIS OF PURINE AND CD28 SIGNALLING -> INCLUDING T CELL APOPTOSIS

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25
Q

STATE THE PK AND THE CLINICAL USE OF AZATHIOPRINE.

A

PK:
- WELL ABSORBED IN GIT
- HAVE HALF LIFE OF 2-5 HRS
- EXCRETED VIA URINE
- WHEN USE WITH ALLOPURINOL, THE DOSE IS REDUCED TO PREVENT TOXICITY.

CLINICAL USE:
- RENAL TRANSPLANT
- ACUTE GLOMERULONEPHRITIS
- RA
- IBD MULTIPLE SCLEROSIS
- A/I HA

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26
Q

STATE THE ADR OF CYTOTOXIC AGENT

A
  • BM SUPPRESSION
  • SKIN RASH
  • FEVER
  • DIARRHOEA
  • INCREASE THE ALKALINE PHOSPHATASE
  • JAUNDICE
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27
Q

WHY AZATHIOPRINE AND ALLOPURINOL CANNOT BE COMBINED?

A

DUE TO XO AND TPMT INHIBITION, THE 6 MERCAPTOPURINE IS SHUNTED DOWN TO FORM METABOLITES THT ARE INCORPORATED INTO THE DNA -> REDUCTION IN WBC REPLICATION/ ACTIVATION AS WELL AS INHIBITION OF THE ACTIVITY OF RAC1 GTP WHICH STIMULATE APOPTOSIS OF THE WBC.

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28
Q

STATE THE DRUG NAME UNDER THE CATEGORY OF CYTOTOXIC AGENT THAT HAVE THE ANALOGUE OF FOLATE.

A

METHOTREXATE

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29
Q

MOA OF METHOTREXATE.

A

METHOTREXATE:
- INHIBIT THE DIHYDROFOLATE REDUCTASE WHICH IS AN ENZYME THAT IS USED TO CONVERT DIHYDROFOLATE TO TETRAHYDROFOLATE
- AS A RESULT, THERE WILL BE NO DNA OR RNA SYNTHESIS
- HENCE, THERE WILL BE NO CELL PROLIFERATION

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30
Q

STATE THE PK OF METHOTREXATE

A

METHOTREXATE IS EXCRETED VIA URINE
IT IS WELL ABSORBED
IT HAS 3-10 HRS OF T1/2
IT CAN BE ADMINISTERED VIA ORAL, IM, IV, INTRATHECAL
IT CANNOT CROSS THE BBB AS IT HAS LOW LIPID SOLUBILITY

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31
Q

CLINICAL USE OF METHOTREXATE.

A
  • BREAST CA
  • LYMPHOID
  • LEUKAEMIA
  • RA
  • CROHN’S DISEASE
  • SLE
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32
Q

ADR OF METHOTREXATE

A
  • MYELOSUPPRESSION
  • GIT EPI. DAMAGE
  • LEUKOPENIA
  • THROMBOCYTOPENIA
  • ANAEMIA
  • PANCYTOPENIA
  • STOMATITIS
  • N & V
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33
Q

STATE THE MOA OF CYCLOPHOSPHAMIDE.

A

CYCLOPHOSPHAMIDE
- TRANSFER THE ALKYL GRP -> COVALENT BOND WITH THE DNA -> DIRECT DNA DAMAGE BY DNA FRAGMENTATION, CROSS BRIDGE FORMATION AND NUCLEOTIDE MISPAIRING -> PREVENT REPLICATION

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34
Q

STATE THE PK OF CYCLOPHOSPHAMIDE.

A
  • ADMINISTERED VIA IV OR ORAL
  • EXCRETED VIA URINE OR BILE
  • IS A PRODRUG IN WHICH IT IS METABOLISED BY THE CY450
  • HALF LIFE IS 12 HRS
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35
Q

STATE THE CLINICAL USE OF CYCLOPHOSPHAMIDE

A

BREAST CA
LYMPHOMA
NEPHROTIC SYNDROME
CLL
SLE

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36
Q

ADR OF CYCLOPHOSPHAMIDE

A

BONE MARROW SUPPRESSION
HAEMORRHAGIC CYSTITIS
DIARRHOEA

37
Q

MOA OF MMF (MYCOPHENOLATE MOFETIL)

A
  • MMF IS A PRODRUG
  • IT WILL BE CONVERTED INTO MYCOPHENOLIC ACID
  • MYCOPHENOLIC ACID REVERSIBLY INHIBIT THE IMP DEHYDROGENASE.
  • AS A RESULT, THE GUANOSINE MONOPHOSPHATE PRODUCTION IS INHIBITED
  • THEREFORE, THE NUCLEIC ACID SYNTHESIS IS INHIBITED
  • THEREBY, DNA AND RNA SYNTHESIS IS UNABLE TO OCCUR.
  • IT ALSO WILL PREVENT THE PROLIFERATION OF T AND B CELLS.
38
Q

PK OF MMF

A

CAN BE ADMINISTERED VIA PO AND IV
T1/2 OF PO IS 17 HRS
T1/2 OF IV IS 16 HRS
METABOLISED BY THE LIVER
EXCRETED VIA URINE

39
Q

CLINICAL USE OF MMF

A

ORGAN TRANSPLANT - ALTERNATIVE TO CYCLOSPORIN OR TACROLIMUS INTOLERANCE
TX OF GVHD
CARDIAC TRANSPLANT- PREVENT VACULOPATHY
- RA

40
Q

ADR OF MMF

A

HEADACHE
HPT
MYELOSUPPRESSION

41
Q

STATE A DRUG THAT INHIBIT THE PYRIMIDINE SYNTHESIS OTHER THAN 5 FLUOROURACIL

A

LEFLUNOMIDE

42
Q

STATE THE MOA OF LEFLUNOMIDE.

A

LEFLUNOMIDE
- INHIBIT MITOCHONDRIAL ENZYME (DIHYDROOROTATE DEHYDROGENASE) WHICH INVOLVED IN PYRIMIDINE SYNTHESIS
- REDUCTION OF LYMPHOCYTE ACTIVATION

43
Q

PK OF LEFLUNOMIDE

A

PO WELL ABSORBED
;NEED LOADING DOSE DUE TO LONG T1/2 WHICH IS 2 WKS
METABOLISED IN THE LIVER
EXCRETED VIA RENAL OR BILE

44
Q

CLINICAL USE OF LEFLUNOMIDE

A

JUVENILE IDIOPATHIC ARTHRITIS
RA
MULTIPLE SCLEROSIS

45
Q

ADR OF LEFLUNOMIDE

A
  • ELEVATED LIVER ENZYME
  • RENAL IMPAIRMENT
  • TERATOGENIC
  • ANGINA
  • CONTRAINDICATED IN PREGNANCY
46
Q

MOA OF HYDROXYCHLOROQUINE

A
  • HCQ ACCUMULATE IN HUMAN ORGANELLE AND RAISE THE PH
  • INHIBITION OF ANTIGEN PROCESSING, PREVENTION OF A AND B CHAIN OF MHC CLASS 1 FROM DIMERIZING, INHIBIT AG PRESENTATION OF CELL
  • REDUCE INFLAMMATORY RESPONSE
47
Q

PK OF HCQ

A
  • PO (T1/2 3-4 HRS)
  • METABOLISED BY CYP3A4
  • EXCRETED VIA URINE
48
Q

CLINICAL USE OF HYDROCHLOROQUINE

A

RA
MALARIA
DISCOID LUPUS SLE

49
Q

ADR OF HCQ

A

HEADACHE
DROWSINESS
VISUAL DISTURBANCE
CONVULSION
HYPOK+
PROLONGED QT, TORSADES POINTES, VENTRICULAR TACHYCARDIA
VENTRICULAR FIBRILLATION

50
Q

STATE THE MOA AND CLINICAL USE OF ANTILYMPHOCYTE GLOBULIN (ALG) AND ANTI-THYMOCYTE GLOBULIN (ATG).

A

MOA: SUPPRESS THE T CELL IN THE DONOR MARROW GRAFT
CLINICAL USE:
- INDUCTION OF IMMUNOSUPPRESSION BEFORE ORGAN AND BONE MARROW TRANSPLANT

51
Q

STATE ADR OF ALG AND ATG

A

TYPE III HYPERSENSITIVITY

52
Q

STATE AN EXAMPLE OF ATG AND HOW IT WORKS.

A

ATG: ALEMTUZUMAB
MOA: BIND TO CD52 OF B,T LYMPHOCYTE, NK CELLS, MONOCYTE, MACROPHAGES, GRANULOCYTE AND CAUSE DIRECT ANTIBODY- DEPENDENT LYSIS.

53
Q

IMMUNE GLOBULIN INTRAVENOUS IS ALSO KNOWN AS

A

POLYCLONCAL HUMAN IMMUNOGLOBULIN

54
Q

IGIV IS THE COLLECTIONS OF ___

A

IgG POOLS FROM HEALTHY DONORS

55
Q

STATE THE MOA OF IGIV

A

IGIV REDUCED THE T HELPER CELLS BU INCREASE THE TREG CELLS -> IT DECREASES SPONTANEOUS IG PRODUCTION AND INCREASE THE ANTIBODY CATABOLISM

56
Q

CLINICAL USE OF IGIV

A

IMMUNOGLOBULIN DEFFICIENCY
AUTOIMMUNE DISORDER
HIV
BONE MARROW TRANSPLANT
KAWASAKI DISEASE

57
Q

RHO(D) IS GIVEN VIA __ AT ___ WEEKS OF GESTATIONS.

A

RHO(D) IS GIVEN VIA IM INJECTION AT 26-28 WEEKS OF GESTATIONS.

58
Q

ADR OF RHO(D) IG.

A

LOCAL DISCOMFORT
SLIGHT PYREXIA

59
Q

ROUTE OF ADMINISTRATION OF IVIG.

A

IV

60
Q

CLINICAL USE OF IVIG.

A

IVIG FOR INFX OF CMV, VZV, HBV. TETANUS, RABIES, HERPES VIRUS INFX GIVEN TO IMMUNOSUPPRESSION PT.

61
Q

MOA OF IVIG.

A

IVIG GIVE PASSIVE TRANSFER OF HIGH TITER AB THT CAN REDUCE THE SEVERITY OF INFX.

62
Q

TRUE/FALSE
IVIG IS ANTIVENOM

A

TRUE

63
Q

STATE THE 1ST GENERATION AND 2ND GENERATION OF MONOCLONAL ANTIBODIES.

A

1ST: MURINE MONOCLONAL AB
2ND: CHIMERIC AND HUMANIZED MONOCLONAL AB

64
Q

WHAT IS THE PROBLEM FOUND IN 1ST GEN OF MONOCLONAL AB.

A

SHORT T1/2 IN HUMAN CIRCULATION, AND HAS HIGH IMMUNOGENICITY.
IT ALSO DOES NOT ACTIVATE THE COMPLEMENT SYSTEM.

65
Q

ROUTE FOR MONOCLONAL AB.

A

PARENTERAL, IM, IV, SUBCUTANEOUS

66
Q

ADR OF MONOCLONAL AB.

A

SKIN RASHES
FLU LIKE SYMPTOMS
MYALGIA
GI DISTURBANCE

67
Q

STATE THE DIFFERENCES OF ADALIMUMAB, MUROMONAB, INFLIXIMAB

A

REFER TO LECTURE NOTES PG 42

68
Q

STATE THE DIFFERENCES OF RITUXIMAB, ABCIXIMAB, PALIVIZUMAB

A

REFER TO NOTES PG 43

69
Q

STATE THE DIFFERENCE OF ANAKINRA, ETANERCEPT, AND OMALIZUMAB

A

REFER TO PG 44

70
Q

STATE THE FX OF CYTOKINES

A
  • REGULATE INFLAMMATION
  • BIND TO RECEPTOR AND CAUSE SYNERGISTIC/ ANTAGONISTIC EFFECT
71
Q

BRIEFLY DESC CYTOKINES

A

CYTOKINES:
- FX:
1. REGULATE INFLAMMATION
2. BIND TO RECEPTOR AND CAUSE SYNERGISTIC/ANTAGONISTIC EFFECT
- HAVE ANTI- PROLIFERATIVE, MICROBIAL, NEOPLASTIC EFFECT
- RECOMBINANT CYTOKINES ARE USED AS IMMUNOMODULATORY DRUG IN CLINICAL PRACTISE
- CATEGORIES
1. IL
2. IF
3. CSF

72
Q

IL REGULATE THE ACTIVITY OF

A

LEUKOCYTE

73
Q

WHAT IS IL?

A

IL:
- IS A PROTEIN THT REGULATE THE ACTIVITY OF LEUKOCYTE
- IS A POTENT ANTI INFLAMMATORY EFFECT SUCH AS TGF-B, IL4, IL10, IL13
- WILL INHIBI CHEMOKINE PRODUCTION AND TH1 RESPONSE
- IS USED IN:
1. RCC
2. MELANOMA
3. HYPOTENSION

74
Q

WHAT IS IFNS.

A
  • IFN SUCH AS IFN-a, IFN - B, IFN -y
  • IT WILL INTERACT WITH CELL OR RECEPTOR AND PRODUCE EFFECT SUCH AS
    1. ANTIPROLIFERATIVE EFFECT
    2. INCREASE EXP. OF MHC ON CELL SURFACES, INCREASE ACTIVITY OF NK CELLS AND CYTOTOXIC T CELLS
    3. ANTI NEOPLASTIC EFFECT
    4. ANTIVIRAL ACTIVITY
75
Q

STATE THE PK OF IFN.

A

SUBCUTANEOUS INJ OR IV
T1/2 IFN-a 16 hrs
T1/2 IFN-B 1-2 hrs
T1/2 IFN-y 25 mins

76
Q

CLINICAL USE OF IFN-a

A

CHRONIC HEPATITIS B AND C
CML
MULTIPLE MYELOMA
MALIGNANT MYELOMA

77
Q

CLINICAL USE OF IFN-B

A

MULTIPLE SCLEROSIS

78
Q

CLINICAL USE OF IFN-y

A

CGD

79
Q

ADR OF IFN

A

FLU LIKE SYMPTOMS
HEADACHE
HYPOTENSION
FATIGUE
JT PAIN
ANOREXIA
CNS DEPRESSION
CONFUSION

80
Q

CSF IS GIVEN VIA

A

SUBCUTANEOUS AND IV

81
Q

EXAMPLE OF CSF

A

FILGRASTIM
LENOGRASTIM
PEGFILGRASTIM

82
Q

CLINICAL USE OF CSF

A
  • NEUTROPENIA INDUCED BY CYTOTOXIC DRUG
  • APLASTIC ANAEMIA
  • PERSISTENT NEUTROPENIA
83
Q

ADR OF CSF

A
  • FEVER
  • BONE PAIN
  • MYALGIA
  • RASH
  • GI EFFECT
  • HEPATOSPLEENOMEGALY
84
Q

LEVAMISOLE IS USED IN

A

ANTIHELMINTH AND IMMUNOMODULATING EFFECT

85
Q

MOA OF LEVAMISOLE

A
  • STIMULATE THE FORMATION OF AB TO VARIOUS AG
  • ENHANCE THE T CELL RESPONSES BY STIMULATING T CELL ACTIVATION AND PROLIFERATION
  • POTENTIATE MONOCUTE AND MACROPHAGES FUNCTIONS INCLUDING PHAGOCYTOSIS AND CHEMOTAXIS
  • INCREASED NEUTROPHILS MOBILITY, ADHERENCE AND CHEMOTAXIS
86
Q

PK OF LEVAMISOLE

A

METABOLISED IN LIVER
T1/2 5 HRS

87
Q

CLINICAL USE OF LEVAMISOLE

A

ADJUVANT THERAPY IN COLON CA
RA

88
Q

ADR OF LEVAMISOLE

A

AGRANULOCYTOSIS
NAUSE
TASTE IMPAIRMENT
STOMATITIS
BONE PAIN
GI DISTURBANCE

PHARMACOLOGY (9 decks)

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