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Hematology-Oncology Exam 2 > Pharmacology: Immuno-Modulating Drugs > Flashcards

Pharmacology: Immuno-Modulating Drugs Flashcards

1
Q

RA, SLE, Scleroderma, Sjogren’s Syndrome, Goodpasture Syndrome, Wegener’s Granulomatosis, Polymyalgia Rheumatica, and Guillane-Barree Syndrome are all examples of what?

A

Systemic Autoimmune Diseases

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2
Q

Type I DM, Hasimoto’s Thyroiditis, Graves Disease, Celiac disease, Crohn’s disease, UC, Addison’s disease, Primary biliary cirrhosis, Sclerosine Cholangitis, and autoimmune hepatitis are all examples of what?

A

Localized Autoimmune Diseases

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3
Q

What are 2 branches of the immune system?

A
  1. Innate: Nonspecific (1st line of defense)

2. Adaptive: Specific (2nd line of defense- Protects/Re-Exposure)

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4
Q

Both the innate and adaptive immune system have what 2 types of components?

A

Cellular and Humoral

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5
Q

Name 6 examples of glucocorticoids presented in class.

A
  1. Cortisone
  2. Prednisone
  3. Triamcinolone
  4. Betamethasone
  5. Dexamethasone
  6. Fludrocortisone
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6
Q

What is the MOA of glucocorticoids?

A
  1. Regulate gene expression

2. Inhibits synthesis of eicosanoids

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7
Q

What type of immunity to glucocorticoids interfere with?

A

Cellular

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8
Q

What are the 4 anti-inflammatory effects of corticosteroids?

A
  1. Redistributes components of cellular immunity
  2. Inhibits function and secretions of antigen-presenting cells
  3. Inhibits synthesis of pro-inflammatory eicosanoids
  4. Decrease release of histamines by basophils and mast cells
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9
Q

What types of cells are redistributed by corticosteroids?

A

Neutrophils, lymphocytes (T and B cells), eosinophils, basophils

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10
Q

What pro-inflammatory eicosanoids are inhibited by corticosteroids?

A

Prostaglandins, leukotrienes, and thromboxanes

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11
Q

How do corticosteroids inhibit the synthesis of pro-inflammatory eicosanoids?

A

The decrease the expression of COX

also decrease expression of COX-2

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12
Q

What are the 4 autoimmune conditions corticosteroids are used for?

A
  1. ITP
  2. Autoimmune hemolytic anemia
  3. Acute glomerulonpehritis
  4. Auto-reactive tissue disorders
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13
Q

What types of transplants are corticosteroids used for?

A

Renal, heart, Liver, BM

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14
Q

What are corticosteroids the first line immunosuppressive agents for?

A
  1. Solid organ recipient

2. Hematopoietic stem cell transplant recipients

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15
Q

Corticosteroids have a really long list of toxicities… name them.

A
  • Osteoporosis
  • Glaucoma
  • Hyperglycemia (insulin resistance-steroid diabetes)
  • Hypertension
  • Hypothalamic – pituitary axis (HPA) suppression
  • Adrenal insufficiency (AI) [isolated glucocorticoids deficiency with normal aldosterone secretion]
  • Peptic ulceration
  • Opportunistic infections
  • Retention of Na, H2O (mineralocorticoids)
  • Cataracts
  • Causes muscle weakness on withdrawal
  • Growth hormone inhibition
  • Delayed wound healing
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16
Q

What is the MOA of Cyclosporine or Sandimune?

A

It binds cyclophilin, inhibits T-cell activation, decreases IL-2, IL-3, and IFN-gamma

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17
Q

What are 5 of the main clinical uses for cyclosporine?

A
  1. Immune disorders
  2. Human organ transplant
  3. GVHD (Post-Hematopoietic stem cell transplant)
  4. Dry eye syndrome
  5. Ocular GVHD
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18
Q

True or False: Cyclosporine has an inhaled formula?

A

FALSE… but one is in the works

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19
Q

What types of transplants is cyclosporine used for?

A

Kidney, liver, pancreas, cardiac

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20
Q

What is cyclosporine combined with as standard prophylaxis for GVDH after an allogenic stem cell transplant?

A

Methotrexate

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21
Q

What specific autoimmune diseases is cyclosporine used for?

A

Uveitis, RA, Psoriasis, Asthma

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22
Q

What are the 2 forms cyclosporine is given in?

A

Oral or IV

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23
Q

What metabolizes cyclosporine and what is the consequence of this?

A 
P450 CYP3A4 (in liver)
-Results in a lot of multidrug interactions
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24
Q

What is the concern with drug interactions and cyclosporine?

A

Drugs that diminish the liver enzyme system will INCREASE cyclosporine blood levels

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25
Q

What are some drugs that will interact with cyclosporine and INCREASE cyclosporine blood levels?

A
  1. Diltiazem
  2. Erythromycin
  3. Ketoconazole
  4. Danazol
  5. Methyltestosterone
  6. Oral Contraceptives
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26
Q

What is another concern with drug interactions and cyclosporine?

A

Worry about drugs that cause induction of the microsomal liver enzyme system and DECREASE the half-life and blood levels of cyclosporine

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27
Q

What are some drugs that interact with cyclosporine and DECREASE cyclosporine blood levels and half-life?

A
  1. Carbamazepine
  2. Isoniazid
  3. Phenobarbital
  4. Phenytoin
  5. Rifampin
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28
Q

Cyclosporine slso has a very long lists of toxicities name them.

A
  • Nephrotoxicity
  • Hypertension
  • Hyperglycemia
  • Liver dysfunction
  • Hyperkalemia
  • Altered mental status
  • Seizures
  • Hirsutism
  • Induces TGF-, promotes tumor invasion and metastasis,  incidence of lymphomas, Kaposi’s sarcoma
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29
Q

What’s the cyclosporine toxicity she noted as important and is in green on our PPT?

A

Induces TGF-, promotes tumor invasion and metastasis,  incidence of lymphomas, Kaposi’s sarcoma

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30
Q

What kind of antibiotic is Tacrolimus (Prograf)?

A

Macrolide antibiotic

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31
Q

What is the MOA of tacrolimus?

A

It binds to immunophilin FK-binding protein (FKBP)

-This is similar to cyclosporine

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32
Q

True or False: Cyclosporin is more potent than tacrolimus in inhibiting immune response

A

FALSE…tacrolimus is more important

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33
Q

What are the clinical uses of tacrolimus?

A

Same as cyclosporine (especially for organ and stem cell tranplants)

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34
Q

Tacrolimus is effective for preventing rejection in solid organ transplant patients even after what?

A

Failure of standard rejection therapy (including anti-T-Cell antibodies)

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35
Q

What is tacrolimus used as a standard prophylactic agent (in combination with MTX or mycophenolate mofitel) for?

A

GVHD

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36
Q

How is tacrolimus administered?

A

Orally or IB

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37
Q

What metabolizes tacrolimus?

A

P450 enzymes in the liver… similar potential for drug interactions like cyclosporine

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38
Q

What are the toxicities associated with tacrolimus?

A
  1. Renal
  2. Neurotoxicity
  3. Hyperglycemia
  4. HTN
  5. Hyperkalemia
  6. GI Disturbances
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39
Q

True or False: Sirolimus binds to immunophilin (FKBP-12) and inhibits calcineurin

A

FALSE

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40
Q

What is the MOA of siromus?

A
  • Sirolimus binds to immunophilin (FKBP-12) but doesn’t inhibit calcineurin
  • It blocks mTOR (mamallian target of rapamycin) which blocks the response of T-cells to cytokines)

“It is serious (SIROLUMIS) if you tear (mTOR) your immune system”

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41
Q

What is sirolimus a potent inhibitor of?

A

B-cell proliferation and immunoglobulin production

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42
Q

How is sirolimus given?

A

As an ORAL drug

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43
Q

What 2 things is sirolimus a substrate for?

A

P450 3A and P-glycoprotein

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44
Q

What are clinical uses of sirolimus?

A

Similar to tacrolimus

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45
Q

What are the toxicity of sirolimus?

A
  • Profound myelosuppression, especially thrombocytopenia
  • Hepatotoxicity
  • Diarrhea
  • Hypertriglyceridemia
  • Headache
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46
Q

Which drug is a inosine monophosphate dehydrogenase (IMPDH) inhibitor?

A

Mycophenolate Mofetil

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47
Q

What is MMF hydrolyzed to in the body?

A

Mycophenolic acid, which is the active immunosuppressive moiety

MMF has enhanced bioavailability

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48
Q

When is mycophenolate mofetil used in solid organ transplant patients?

A

When they have refractory rejection or as an alternative to cyclosporine or tacrolimus in patients who don’t tolerate these drugs

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49
Q

What is mycophenolate mofetil given in combination with?

A

Prednisone

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50
Q

What is mycophenolate mofetil used as prophylaxis for?

A

GVHD

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51
Q

What are 3 other applications of mycophenolate mofetil? (think autoimmune)

A

Lupus nephritis, RA, dermatologic disorders

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52
Q

What are the toxicities with Mycophenolate Mofetil?

A
  • GI: Nausea, vomiting, diarrhea, and abdominal pain
  • Headache
  • HTN
  • Reversible myelosuppression (primarily neutropenia)
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53
Q

Azathioprine, cyclosphosphamide, Leflunomide, Hydroxychloroquine, Vincristine, MTX, Cytarabine, and Pentostatin are all examples of what type of drugs?

A

Cytotoxic Agents

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54
Q

Antilymphocyte, Antithymocyte antibodies, Muromonab-CD3, IVIG, Rho(D) Immune Globulin Micro-Dose, and Hyperimmune Immunoglobulins are all examples of what?

A

Immunosuppressive Antibodies

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55
Q

What are antilymphocyte and antithymocyte antibodies used for?

A

The management of transplant

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56
Q

What 2 settings are muromonab-CD3 is used in?

A

Autoimmune disorders and transplantation settings

57
Q

When is IVIG used for?

A

Autoimmune disorders, HIV, BM transplants

58
Q

What is given to prevent hemolytic disease of newborns?

A

Rh0(D) Immune Globulin Micro-Dose

RHOGAM

59
Q

What do you give for the treatment of RSV, CMV, VZV, Human Herpesvirus 3, HepB, Rabies, Tetanus, Digoxin OD?

A

Hyperimmune Immunoglobulins

60
Q

What are monoclonal antibodies?

A

Humanized and chimeric monoclonal antibodies directed against specific receptors and antigens

61
Q

What do monoclonal antibodies end in?

A

MAB

-Alemtuzumab, bevacizumab, cetuximab, gemtuzumab, rituximab, trastuzumab

62
Q

What is the MOA of alemtuzumab?

A

Humanized IgG1 that binds CD52 on normal and malignant B and T lymphocytes, NK cells, monocytes, and macrophages

63
Q

What are clinical uses of alemtuzumab?

A

Treatment of refractory B cell LL in patients treated with alkylating agents and who have failed fludarabine therapy

64
Q

What are toxicities of alemtuzumab?

A

Lymphopenia, neutropenia, anemia, thrombocytopenia

65
Q

What is the MOA of bevacizumab?

A

Humanized IgG1 monoclonal antibody that binds to vascular endothelial growth factor (VEGF) and inhibits VEGF from binding to its receptor, especially endothelial cells

66
Q

Simple words for the MOA of bevacizumab?

A

It’s an antiangiogenic drug that inhibits growth of blood vessels (or angiogenesis) in tumors

67
Q

What is bevacizumab used for?

A

First-line treatment of patients with metastatic colorectal cancer alone or in combination with 5-FU-based chemotherapy

68
Q

What the toxicities of Bevacizumab?

A

Hemorrhage, GI perforations, Wound healing problems, HTN, proteinuria

69
Q

What type of monoclonal antibody is cetuximab?

A

Human-mouse chimeric MAB

70
Q

What does cetuximab target?

A

Epidermal growth factor receptor (EGFR)

71
Q

What does binding of cetuximab to EGFR do?

A

It inhibits tumor cell growth via:

  1. Decrease in kinase activity
  2. Matrix metalloproteinase activity
  3. Increased apoptosis
72
Q

What are the clinical uses of cetuximab?

A

For patients with metastatic colorectal cancer with a tumor over-expressing EGFR

73
Q

What is the MOA of Gemtuzumab?

A

It is a humanized IgG4 monoclonal antibody with a kappa light chain specific for CD33 found on leukemic blast cells in 80-90% of patients with AML

74
Q

When can you use Gemtuzumab?

A

For relapsed CD33 acute myeloid leukemia (AML)

75
Q

What are associated toxicities of gemtuzumab?

A
  1. Severe myelosuppression (especially neutropenia)
  2. Significant hepatotoxicity
  3. Hypersensitivity reactions
76
Q

What is the MOA of rituximab?

A

It is a chimeric murine-himan monoclonal IgG1 that binds to CD20 molecule on malignant B lymphocytes

77
Q

What does rituximab cause?

A
  1. Induction of apoptosis
  2. Complement-mediated lysis
  3. ADCC
78
Q

What are the clinical uses for rituximab?

A

Relapsed or refractory low-grade or follicular, B-cell non-Hodgkin’s lymphoma

79
Q

Which drug is a recombinant DNA-derived, human monoclonal antibody that binds to the extracellular domain of the human epidermal growth factor receptor HER-2/neu?

A

Trastzumab

80
Q

When do you give trastuzumab?

A

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

81
Q

What type of HS is characterized by the immune system detecting a drug-hapten conjugate and responding by generating IgE antibodies specific for the drug-hapten complex?

A

TYPE I

82
Q

What is given to treat a Type I HS?

A

Prednisone or desensitization to drugs

83
Q

When can allergy to certain drugs occur?

A

When the drug can’t induce an immune response by itself and it covalently binds to a host carrier protein (hapten)

84
Q

What is associated with autoimmune syndromes?

A

Type II HS

85
Q

What is characteristic of a Type II HS?

A

IgG antibodies binding to drug-modified tissue that are destroyed by complement or phagocytic cells with Fc receptors

86
Q

What is used for severe cases of Type II HS?

A

Immunosuppressive therapy

87
Q

What are some examples of type II HS?

A
  1. SLE following hydralazine or procainamide

2. Autoimmune hemolytic anemia resulting from methyldopa

88
Q

What are serum sickness and vasculitic reactions examples of?

A

Type III HS

89
Q

What are the clinical features of Type III HS reactions?

A
  1. Urticarial and erythematous skin reuptions
  2. Arthralgia or arthritis
  3. Lymphadenopathy
  4. Glomerulonephritis
  5. Peripheral edema and fever
90
Q

What are some drugs that can induce immune vasculitis?

A
  1. Sulfonamides
  2. Penicillin
  3. Thiouracil
  4. Anticonvulsants
  5. Iodides
91
Q

How long do type III HS reactions usually last?

A

6-12 days

92
Q

What antibodies are involved in type III HS reactions?

A

IgM and IgG

93
Q

What is useful for treatment of type III HS?

A

Glucocorticosteroids

94
Q

What can be done in severe cases of Type III HS to remove the offending drug from circulation?

A

Plasmapheresis

95
Q

What is inflammation of the blood vessels?

A

Vasculitis

96
Q

What 4 things are used to treat vasculitis?

A
  1. Steroids
  2. Cyclophosphamide
  3. Azathiprine
  4. Plasma exchange
97
Q

What does Goodpasture’s Disease cause?

A

Rapid destruction of the kidneys and bleeding into the lung

98
Q

What 3 things are done to treat Goodpasture’s Disease?

A
  1. Prednisolone
  2. Cyclophosphamide
  3. Plasma exchange
99
Q

What is plasma exchange?

A

A mechanical procedure to remove antibodies from the blood by filtering or spinning to remove plasma

100
Q

What kind of antibodies are found in the glomerular basement membrane in Good pastures disease?

A

Anti-GBM

101
Q

What is a chronic disease with many manifestations including dermatologic and renal which is an autoimmune disease where the body’s own immune system is directed against the body’s own tissues?

A

SLE

102
Q

What is the treatment for SLE?

A
  1. Steroids: Prednisolone tabs, methylpredisolon IV
  2. Cyclophosphamide
  3. Azathioprine
103
Q

What kind of antibodies are seen in immunoflouresence in SLE?

A

Antinuclear antibodies

104
Q 
Which disease has manifestations that include:
Dry eyes 
Dry mouth 
Dental cavities 
Fatigue 
Enlarged parotid glands 
Difficulty swallowing or chewing 
Change in sense of taste 
Hoarseness 
Oral yeast infections (eg candidiasis) 
Skin rashes or dry skin 
Vaginal dryness 
Dry cough that doesn't produce sputum 
Joint pain, swelling and stiffness
A

Sjogren’s Syndrome

105
Q

What are some of the first things that Sjogren’s syndrome attacks?

A

The moisture-secreting glands

106
Q

What is a treatment option for Sjogren’s Syndrome?

A

Hydroxychloroquine (plaquenil)

107
Q

What are 2 things that can be seen in dermatomyositis?

A
  1. Diffuse alopecia

2. Poikiloderma in a photodistribution

108
Q

What is dermatomyositis?

A

A CT disease related to polymyositis characterized by inflammation of the muscles and the skin

109
Q

What does dermatomyositis most frequently affect?

A

Skin and muscles

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

110
Q

What are the treatment options for dermatomyositis?

A 
-Prednisone (Deltasone®, Meticorten®, 
   Orasone®)
 -Methotrexate (Folex®, Rheumatrex®) 
- Azathioprine (Imuran®) 
- Mycophenolate (CellCept®)
- Hydroxychloroquine (Plaquenil®)
 -Chloroquine (Aralen®)
111
Q

What are 2 characteristics of plaque psoriasis?

A

It is raised and roughened

112
Q

What are 2 treatment options for psoriasis?

A

-Betamethasone (dipropionate )
(Diprolene®, Diprosone®),
0.05% cream
-Cyclosporin

113
Q

What is the major difference between the different glucocorticoids?

A

Potency

114
Q

True or False: Dexamathasone is 10 times more potent than prednisone

A

TRUE

115
Q

Glucocorticoids interfere with what type of immunity?

A

CELLULAR MEDIATED

116
Q

What kind of immunosuppression do patients with solid organ transplant require?

A

Lifelong

117
Q

Patient who get a BM transplant need immunosuppression for how long?

A

6 months to 2 years

-You re-establish hematopoiesis with “new” T-cells, so its like it’s brand new

118
Q

Long term use of glucocorticoids refers to usage how long?

A

Months to years

119
Q

Short term use of glucocorticoids refers to usage how long?

A

Days to weeks

120
Q

What is a long term SE of glucorticoids?

A

Osteoporosis

121
Q

Why do you have to be careful giving glucocorticoids to a diabetic?

A

Because it increases glucose levels (might have to adjust diabetes meds accordingly)

122
Q

Why is there delayed wound healing seen with glucocorticoids?

A

Because of the increased glucose levels

123
Q

What drug is it super important to check levels of daily to prevent organ rejection?

A

Cyclosporine (because of all the drug-drug interactions that can affect it’s levels)

124
Q

What drug is a second line agent for prevention of organ rejection?

A

Tacrolimus

125
Q

Which drug taught is actually a pro-drug?

A

Mycophenolate mofetil

126
Q

In using any type of antibody drug, what is required for it to work?

A

Either the antigen or receptor for the antibody has to be present in the disease for the drug to function

127
Q

When is Rhogam given?

A

Within 72 hours of delivery

-Also at 28 weeks

128
Q

What does it mean to be a targeted therapy?

A

It targets something specific to the disease… aka you have to do expression testing for the receptor to see if the drug even has the potential to work… this is seen with monoclonal antibodies

129
Q

True or False: Bevacizumab is given with other drugs?

A

YES

-This drug is cytotoxic to CA cells and good cells

130
Q

What BP is Bevacizumab contraindicated in?

A

Anyone with a systolic over 160

131
Q

What level of proteinuria is bevacizumab contraindicated in?

A

2+ or more on dipstick

132
Q

Generally, when is bevacizumab contraindicated?

A

28 days before and after surgery

133
Q

What is an off label use for cetuximab?

A

Head and neck cancer

134
Q

Why do some monoclonal antibodies have increased risk for HS reaction?

A

Because the have the mouse component… with increased % of the mouse component, there can be an increased risk of reaction

135
Q

What do you give before MAB to reduce the issues of a potential HS reaction?

A

Tylenol or benedryl

136
Q

How are MAB given?

A

Start at a low infusion rate and slowly increase once you see they aren’t reacting

137
Q

When is drug desensitization done for Type I HS?

A

When there are no other alternatives

-Example was a CF patient who became resistant to all antibiotics except one they were allergic too

138
Q

What is drug desensitization?

A

You give a small concentration of the drug and increase it slowly over time to diminish the response and slowly increase IgG level

Hematology-Oncology Exam 2 (15 decks)

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