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heme onc pharmacology > the russian > Flashcards

the russian Flashcards

1
Q

glucocorticoid drugs

A

Cortisone, prednisone, triamcinolone,
betamethasone,dexamethasone and
fludrocortisone

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2
Q

glucocorticoid mechanism of action

A

regulates gene expression
inhibits synthesis of eicosinoids
interferes with cellular immunity

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3
Q

corticosteroids anti inflammatory effect

A

1) redistribute the components of cellular immunity(neutrophils,eosinophils,basophils,lymphocytes)
2) inhibits the function and secretion of antigen presenting cells
3) inhibits the synthesis of proinflammatory eicosinoids(prostaglandins, leukotrianes and thromboxanes) - also decreases the expression of cox 2
4) decrease the release of histamine by basophils and mast cells

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4
Q

the clinical uses of corticosteroids

A 
ITP
autoimmune hemo lytic anemia
bone, heart, kidney and liver transplant
acute glomerulonephritis 
auto reactive tissue disorders
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5
Q

first line immunosupressive agents for solid organ and hematopoeitic stem cell transplant recipients

A

corticosteroids

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6
Q

corticosteroid toxicity

A

peptic ulcer
osteoperosis
glaucoma
HTN
hyperglycemia (insulin resistance) (steroid diabetes)
Adrenal Insufficiency(AI) - isolated glucocorticoids deficiency with normal aldosterone secretion
hypothalamic - pituatary(HPA) axis suppression
opportunistic infection
cataracts
growth hormone inhibition
delayed wound healing
causes muscle weakness on withdrawel
retention of NA+, H20 (mineralocorticoids)

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7
Q

cyclosporine mechanism of action

A

binds to cyclophin and inhibits T cell activation and the release of IL-2, IL-3 and IFN

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8
Q

cyclosporine Clinical Indications

A
  • HUMAN ORGAN TRANSPLANT
  • selected immune disorders
  • treatment of graft vs host disease after hematopoeitic stem cell transplant
  • severe dry eye syndrome
  • ocular graft vs host disease
  • cadaveric transplant of KIDNEY, LIVER, PANCREASE, as well as cardiac transplantation

also used for some autoimmune diseases like UVEITIS, rhumatoid arthiritis, psoriasis and asthma

when combined with methotrexate cyclosporine is standart prophylaxis for graft vs host disease following allogentic stem cell transplant

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9
Q

cyclosporine metabolism

A

Oral and IV

Primarily metabolized by the P450 CYP3A4 enzyme system in the liver with resultant multidrug interaction

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10
Q

cyclosporine drugs that diminish the liver enzyme system thus increasing its half

A

drugs that diminish the liver
enzyme system increase the cyclosporine blood levels
Diltiazem, erythromycin, ketoconazole, methyltestosterone and oral contraceptives

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11
Q

cyclosporine drugs that induce the microsomal liver enzyme system

A 
the drugs that reduce the half life and blood levels of cyclosporine include
Carbamazepine
isoniazid 
phenobarbital
phenytoin 
rifampin
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12
Q

cyclosporine toxicity

A

Induces TGF, PROMOTES TUMOR INVASION AND METASTASIS, INCIDENCE OF LYMPHOMAS AND KAPOSIS SARCOMA
also….
nephrotoxicity, seizures, hirsutism, HTN, hyperglycemia, liver dysfunction, hyperkalemia, and altered mental status

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13
Q

tacrolimus drug properties

A

Tacrolimus
(FK 506) is a macrolideantibiotic
•Similar MOA as cyclosporine
•Binds to immunophilin FK-binding protein (FKBP)
•Tacrolimus is more potent than cyclosporin in
inhibiting immune response

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14
Q

tacrolimus clinical indications

A

Same indications as cyclosporine, particularly in
organ and stem cell transplantation
•Effective for preventing rejection in solid organ
transplant patients even after failure of standard
rejection therapy, including anti-T-cell antibodies
•It is now a standard prophylactic agent(usually in combination with MTX or mycophenolatemofitel) for graft-versus-host disease

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15
Q

tacrolimus metabolism

A

Tacrolimus can be administered orally or IV
•Like cyclosporine, tacrolimusis metabolized primarily by P450 enzymes in the liver, with
similar potential for drug interactions

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16
Q

tacrolimus toxicity

A

Renal, neurotoxicity, hyperglycemia,
hypertension, hyperkalemia, and GI disturbances
none of this was highlighted

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17
Q

Sirolimus Mechanism of Action

A

Sirolimus binds to immunophilin(FKBP-12) but does not inhibits calcineurin
•It blocks mTOR (mammalian target of rapamycin) !!

Blocks the response of T cells to cytokines!!!!

  • It is a potent inhibitor of B-cell proliferation and immunoglobulin production
  • Available only as an oral drug
  • Substrate for P450 3A and P-glycoprotein
  • Similar clinical use as tacrolimus!!!
18
Q

Sirulimis Toxicity

A 
Profound myelosuppression, especially 
thrombocytopenia
•Hepatotoxicity
•Diarrhea
•Hypertriglyceridemia
•Headache
non of this was highlighted
19
Q

mycophenolate mofetil MOA

A

Inosinemonophosphate dehydrogenase (IMPDH) inhibitor!!!!!!!
•MMF is hydrolized to mycophenolic acid, the
active immunosuppressive moiety (MMF –enhanced bioavailability)

20
Q

mycophenolate mofetil Clinical Indications

A

Used for solid organ transplant patients for
refractory rejection!!!!!
•In combination with prednisone
•As an alternative to cyclosporine or tacrolimusin
patients who do not tolerate these drugs!!!!
•For prophylaxis to prevent graft-
versus-host disease!!!!.
•Other applications
•Lupus nephritis
•RA
•Dermatologic disorders

21
Q

mycophenolate mofetil Toxicity

A

GI (N/V/D and abdominal pain)
Headache
Hypertension
Reversible myelosuppression (primarily neutropenia)

22
Q

Cytotoxic Agents

A 
Azathioprine
Cyclosphosphamide
Leflunomide
Hydroxychloroquine
Other agents
•Vincristine
•MTX
•Cytarabine
•Pentostatin
23
Q

Immuno Suppressive Antibodies

A

Antilymphocyte & Antithymocyte antibodies
•Indication: management of transplant

Muromonab-CD3
•Indications: autoimmune disorders and transplantation settings

Immune Globulin Intravenous (IVIG)
•Indications: autoimmune disorders, HIV, bone
marrow transplants

Rh0(D) Immune Globulin Micro-Dose
•Indication: prevention of hemolytic disease of
newborns

Hyperimmune Immunoglobulins
•Indications: treatment of respiratory syncytial
virus, cytomegalovirus, varicella zoster, human
herpesvirus 3, hepatitis B, rabies, tetanus,
digoxin overdose

24
Q

Monoclonal Antibodies

A

Humanized and chimeric monoclonal antibodies
directed against specific receptors/antigens

  • Members
  • Alemtuzumab
  • Bevacizumab
  • Cetuximab
  • Gemtuzumab
  • Rituximab
  • Trastuzumab
25
Q

Alemtuzumab

A

Mechanism of action
•Humanized IgG 1 that binds to
CD52!!! on normal and malignant B and T lymphocytes, NK cells, monocytes and macrophages
•Clinical uses
•Treatment of (refractory!!!) B cell LL in patients
treated with alkylating agents and who have failed
fludarabine therapy
•Toxicity
•Lymphopenia, neutropenia, anemia,
thrombocytopenia

26
Q

Bevacizumab

A

-MOA - Humanized IgG1 antibody that binds to vascular endothelial growth factor (VEGF) and prevents it from binding to its receptor especially on endothelial cells. Is a new drug which inhibits the formation of blood vessels in Tumors.
-Clinical Indications - Is first line treatment in patients with metastatic colorectal cancer!!! alone or in combination with 5 FU based chemotherapy
Toxicity - GI perf. hemohragge, wound healing problems, HTN and proteinuria

27
Q

Cetuximab

A

Mechanism of action
•A human
-mouse chimeric monoclonal antibody
•Targets epidermal growth factor receptor (EGFR)!!
•Binds EGFR and inhibits tumor cell growth via:
•Decrease in kinase activity
•Matrix metalloproteinase activity
•Increased apoptosis
•Clinical uses
•In patients with metastatic colorectal cancer!!(tumor over-expressing EGFR)

28
Q

Gemtuzumab

A

•Mechanism of action
•A humanized IgG 4 monoclonal antibody with a
kappa light chain specific for CD33found on leukemic blast cells in 80-90% of pts with AML!!!

  • Clinical uses
  • Approved for relapsed CD33 acute myeloid leukemia (AML)!!!!
  • Toxicity
  • Severe myelosuppression, especially neutropenia
  • Significant hepatotoxicity
  • Hypersensitivity reactions
29
Q

Rituximab

A

Mechanism of action
•Chimeric murine-human monoclonal IgG1that binds to CD20 molecule on malignant B lymphocytes-

-Causes
1 Induction of apoptosis
2 Complement-mediated lysis
3 Antibody-dependent cellular cytotoxicity

•Clinical uses
Approved for the therapy of patients with relapsed or refractory low-grade or follicular, B-cell non-Hodgkin’s lymphoma

30
Q

Trastuzumab

A

A recombinant DNA-derived, human monoclonal antibody that binds to the extracellular domain of the human epidermal growth factor receptor HER-2/neu

•Indication: treatment of metastatic breast cancer in patients whose tumors over-express HER-2/
neu

31
Q

Type 1 Sensitivity

A

•Allergy to certain drugs occurs when the drug
not capable of inducing an immune response by
itself covalently binds to a host carrier protein
(hapten)

•The immune system detects the drug-hapten conjugate and responds by generating IgE antibodies specific for drug-hapten complex

•Treatment include: prednisone or
desensitization to drugs

32
Q

Type II Sensitivity

A

•Autoimmune syndrome

•IgG antibodies bind to drug-modified tissue and
are destroyed by complement system or by
phagocytic cells with Fc receptors

•Immunosuppressive therapy used for severe cases

•Examples: Systemic lupus erythematosus
following hydralazine or procainamide,
autoimmune hemolytic anemia resulting from
methyldopa

33
Q

Type III sensitivity

A

–Serum Sickness & Vasculitic Reactions:
•Clinical features: urticarial and erythematous skin
eruptions, arthralgia or arthritis, lymphadenopathy,
glomerulonephritis, peripheral edema and fever

•Immune vasculitis can be induced by different
drugs eg. sulfonamides, penicillin, thiouracil,
anticonvulsants, iodides

•Usually last 6-12 days
•IgM and IgG antibodies involved
•Glucocorticosteroids are useful for treatment
•In severe cases plasmapheresis can be used to
remove offending drug from circulation

34
Q

Whats used to treat Vasculitis

A

Vasculitis- inflammation of the blood vessels

  1. Steroids
  2. Cyclophosphamide
  3. Azathioprine
  4. Plasma exchange
35
Q

what is goodpastures disease and how to you treat it?

A

goodpastures disease is an autoimmune disease which causes rapid destruction of the kidneys and bleeding into the lungs.
*anti GBM antibodies which illuminate yellow
Treatment:
1.Prednisolone
2.Cyclophosphamide
3.Plasma exchange

(a mechanical procedure to
remove antibodies from theblood by filtering or
spinning to remove the plasma

36
Q

what is SLE and how do you treat?

A

a disease where the bodies own immune system is attacking itself. Has many manifestations. dont forget the ANA immunoflurescence

Treatment:

  1. Steroids(Prednisolone tabs,methylprednisoloneIV)
  2. Cyclophosphamide
  3. Azathioprin
37
Q

what are the symptoms of sjogrens syndrome and how do you treat?

A 
the moisture secreting glands are amount the first mucous membranes which SS attacks
1.Dry eyes 
2.Dry mouth 
3.Dental cavities 
4.Fatigue 
5.Enlarged parotid glands 
6.Difficulty swallowing or chewing 
7.Change in sense of taste 
8.Hoarseness 
9.Oral yeast infections (eg candidiasis) 
10.Skin rashes or dry skin 
11.Vaginal dryness 
12.Dry cough that doesn't produce sputum 
13.Joint pain, swelling and stiffness 
TX=HYDROXYCHLOROQUINE
38
Q

Dermatomyositis

A

is a connective-tissue disease related to polymyositis characterized by inflammation of the muscles and the skin

Most frequently affects the skin and muscles

May also affect joints, esophagus, lungs, and less
commonly heart

39
Q

dermatomyositis treatment options

A 
prednisone
methotrexate
azothioprine
mycophenolate
hydroxychloroquine
chloroquine
40
Q

how do you treat psoriasis?

A

betamethasone .05% cream

cyclosporine

heme onc pharmacology (1 decks)

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