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Pharm 413 Drugs > Things To Know > Flashcards

Things To Know Flashcards

1
Q

Do CD4+ Th cells bind to extracellular or intracellular?

A

They bind to Extracellular pathogen-specific peptide epitopes via TCR

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2
Q

Does CD8+ T cells bind to extracellular or intracellular

A

They bind to intracellular pathogen-specific peptide epitopes via TCR

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3
Q

What kind of structure does a TCR bind to?

A

It binds to a peptide antigen which will require processing from an APC in order to bind

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4
Q

What does a BCR bind to in terms of structure?

A

It will bind to a tertiary structure of a protein, carb, lipopolysach, polysaccharide

It does not require processing in order to bind

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5
Q

What is the point of the prevnar vaccine in terms of what it activates?

A

It is a polysaccharide Ag which is conjugated to a protein reactive material (CRM 197) this is important because it allows for Bcell and Tcell cooperation because the Bcell will process the protein and act as an APC to recruit Tcells and cause a larger immune response leading to increased efficacy of the shot.

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6
Q

What does INF-gamma cause for isotype switching?

A

IgM to IgG

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7
Q

What does IL-4 cause in terms of isotype switching

A

IgM to IgE

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8
Q

What does IL-5 cause in terms of isotype switching?

A

IgM to IgA

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9
Q

What is affinity maturation?

A

It’s when you have isotype switching which leads to production of specific antibodies that are able to bind to the pathogen with higher affinity compared to the ones that were originally created

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10
Q

What is CAR t-cell treatment

A

It’s when you pull a patients T-cells out of their peripheral blood and you engineer the T-cell or CAR t-cell to recognize the surface tumor antigens so it can kill them

They CAR T cell has increased signaled so it causes a higher response to the cancer

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11
Q

What is the role of IL-2 in activation of T-cells?

A

It will drive the proliferation and differentiation of activated T-cells

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12
Q

What do Th1 cells secrete?

A

INF-gamma

Which stimulates phagocytosis and killing of microbes by macrophages, inflammation

IgM to IgG

Also IL-2

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13
Q

What do Th2 cells secrete ?

A

IL-4 causes IgM to IgE, big in allergic rxn and eosinophil killing of helminth

IL-5 which changes IgM to IgA

IL-13

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14
Q

What do Th17 cells produce?

A

IL-17

Involved in inflammation and autoimmune diseases MS, IBD

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15
Q

What does the complement system consists of?

A

Serum proteins and cell surface proteins that interact to generate products for elimination of microbes

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16
Q

What part of immunity is our complement system apart of

A

Innate and humoral immunity

People who lack C3 will have a high chance of getting a ton of infections

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17
Q

Which two pathways of the complement system are innate immunity and why?

A

It’s the Alternative pathway and the lectin pathway

the reason is because it does not require and antibody in order to be started

Alternative = activated by the microbe 
Lectin = activate by presence of Mannose

The classical is humoral because you need to have an IgG or IgM bound to the microbe in order to start

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18
Q

What are the steps of T-cell activation?

A

Step 1: binding of peptide Ag with MHC to a TCR

Step 2: Binding of costimulitory factors to increase T-cell proliferation and differentiation

CD28 binds to B7 (CD80/CD86)

CD40L bind to CD40

Also CD3 which is part of TCR which increase stimulating effects

This all increase the amount of NFAT, NFkb and AP1 which are transcription factors to make more and different types of T-cells

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19
Q

What are the central tolerance types of immune tolerance

A

Happens in the bone marrow for Bcells and happens in the thymus for Tcells

Deletion = apoptosis and just kill the cell

Receptor editing = in bcells to change what it does

Development of Tregs = release inhibitory cytokines IL-10 and TGF-Beta to stop the function of Tcells

THESE WORK ON IMMATURE LYMPHOCYTES

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20
Q

What are the types of Peripheral tolerance in immological tolerance?

A

Clinal anergy = do not have function responses (would be like not activating CD28 to bind with B7 so it results in a lower response of Tcell)

Deletion = apoptosis

Suppression - using Tregs to release inhibitory cytokines (IL-10, TGF-Beta) to suppress the action of the lymphocytes

THESE WORK ON MATURE LYMPHOCYTES

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21
Q

What type of lymphocytes is most susceptible to tolerance

A

Immature lymphocytes

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22
Q

What is negative selection when it comes to immune tolerance?

A

When a lymphocytes has a high affinity for self antigen is will be negatively selected and killed off

They may also become Tregs (CD4+,CD25+), which will release suppressive cytokines (IL-10, TGF-beta) in the peripheral

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23
Q

What is me ant by positive selection of lymphocytes

A

It means it has a low affinity for self Ag meaning it will be saved by TCR receptor and allowed to mature and enter the peripheral system

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24
Q

What is the role of Orencia (abatacept)?

A

it mimics CTLA-4 which is going to cause the blocking of B7 (CD80/86) from binding to CD28 which means there will not be a reaction of the Tcell

It’s an immunosuppressive drug in the use for RA

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25
Q

Where are Tregs created

A

Primarily in the thymus

The IL-10 and TGF-B suppresses activation and effector functions of sel-reactive and pathogenic lymphocytes in periphery

ALSO BLOCKS ACTIVATION OF MACROPHAGES

***if we didn’t have these we would have a lot of autoimmune diseases

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26
Q

What happens to B lymphocytes when it comes to peripheral tolerance

A

When a B-cell reacts to a self antigen it doesn’t cause the activation of Th cells (because it cant package the self antigen into a MCH) this leads to the Bcell to be very ineffective and unresponsive (anergic) and will die by apoptosis

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27
Q

What are the main ways we have central tolerance in Bcells?

A

B cells that target Self antigen in the bone marrow have to fates

1: receptor editing where we change the antigen receptor so that it is no longer self reactive
2: dies by apoptosis with negative selection (deletion)

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28
Q

How can we use immune tolerance to help with allergies?

A

We inject the pt with the allergies or have them eat them (peanuts) this will cause the antigen to seem more like a self antigen and will cause our T and B cells to become desensitized to them and no longer react

We have to start with low amounts and slowly increase the amount we give them

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29
Q

How does autoimmune diseases happen?

A

The self-Ag is not expressed in the thymus or the concentration is way to low. This will allow Tcells that are auto reactive to escape the thymus where they will then start to react with our bodies Self-Ag and cause autoimmune diseases

Type 1 diabetes, SLE (systemic lupus, Type III hypersensitive rxn)

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30
Q

What is a live attenuated vaccine?

A

It’s one that is a mutated form of the bacteria. It does not cause infection but it can replicate and will give a much greater immune response

Can’t not be given to prego, immune compromised pts, or people on steroids more than 2 weeks

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31
Q

Examples of live vaccines

A

BCG TB vaccine

Sabin polo vaccine

MMR

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32
Q

Examples of killed vaccines

A

Flu

Pertussis

Typhoid

Rabies

Cholera

Salk polio vaccine

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33
Q

What is a killed vaccine

A

One that is killed and can not take over host machine so it can not replicate

Will give a much lower response than a live and often requires booster shoots

Safe for immuno compromised pts

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34
Q

What is Provenge (Sipuleicel-T)

A

Approved canner vaccine, DC-mediated prostate cancer immunotherapy

You inject a DC cell with the cancer antigen attached to it and then the body recognizes the cancer antigen and will build antibodies against it so you can fight the cancer if you get it

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35
Q

Why are vaccines short lived in children?

A

The short levied antibody response in children is partially due to the fact that their plasma cells do not survive very long so they cant produce enough antibodies

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36
Q

What kind of Tcells are most likely to occur when a child gets a vaccine?

A

They will usually have Th2 cytokines profiles

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37
Q

Which type of vaccine is the least protective and why?

A

It would be a polysaccharide type of vaccine because it will only result in Bcell activation and no Tcell which means no cytokines release

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38
Q

How long does it take the flu shot to take effect in the body after administration?

A

it can take around 2 weeks and it will last around a year

Make sure to get the shot in September or October since flu season runs Nov-May

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39
Q

What is the Coombs and tell classification of a type 1 hypersensitivity rxn

A

Allergic or immediate: due to allergen triggering the response IgE is responsible

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40
Q

What is the Coombs and tell classification of a type II hypersensitivity rxn

A

IgM/IgG binding to cell surface self-Ag developing cytotoxic rxn

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41
Q

What is the Coombs and tell classification of a type III hypersensitivity rxn

A

Immune complex rxn involving non-clearance of immune complex

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42
Q

What is the Coombs and tell classification of a type IV hypersensitivity rxn

A

T Cell mediated: also known as delayed Type hypersensitivity (DTH)

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43
Q

How is anaphylaxis defined?

A

Anaphylactic shock due to vasodilation and smooth muscle contraction

Can lead to cardio vascular collapse

44
Q

What is Atopy?

A

Presence of high levels of IgE in serum, which can be inherited (HLA gene issue) or genetic predisposition to having more Th2 bias (this will produce more IgE which will stay in the serum)

45
Q

What are the basic mechanisms for developing a type I rxn?

A

First exposure will lead to B cells to produce IgE plasma cells. This IgE will have a high affinity for Fc receptors which are found on basophils and mast cells.

Second exposure will lead to the allergen binding to the IgE which is bound to the mast cell and basophils. This will cause a release of vasoactive amines from those cells which will result in the rxn

Also cytokines will be released and cause inflammation

46
Q

What does a mast cell release when it get active and degranulared?

A

Pre formed mediators: give you the first large rxn

New synthesized mediators: created and will cause the late phase rxn

47
Q

What are the pre formed mediators of a type I rxn?

A

Histamine: leads to bronchoconstricton, vasodilation, increased permeability, increased mucus production
Breathing issues and problems with swelling and redness

Neutrophil and eosinophils chemotaxtic factor

Platelet activation factor

48
Q

What are the newly synthesized mediators?

A

Leukotrienes: same effect as histamine

Prostaglandin D2: bronchoconstriction and vasodilation

Cytokines: will be big in inflammation

49
Q

How do drugs cause a type I rxn?

A

Drug will covalently bind to a protein in the body, this will cause the body to see it as a foreign entity and will cause the body to react to it and try to kill it

Penicillin and the beta lactam is the most common type of drug allergy

Does not have cross sensitivity with cephalosporins

50
Q

What are the in Vivo skin tests for find a type I rxn?

A

Prick test: use a needle and inject a bit of the allergen and see if you get a reaction

Intradermal: more sensitive
You have a control and measure the effect that happens when you inject and look to see what kind of rxn the person has

51
Q

What are the in vitro tests for a type I rxn?

A

Looking to see how much IgE is in the serum

RAST test: uses a radio marked anti-IgE and see how much it bind to see how much IgE is in the serum

ELSIA: uses an assay to see how much IgE is in the serum

These are quantitative and looks for IgE in the serum

52
Q

How does Fasenra work?

A

It binds to eosinophils to help treat pts with asthma

Eosinophils express IgE and IL-5, this drug binds to IL-5 receptor on the eosinophil, this then shows Fc which causes an NK cell with an Fc receptor to come along and kill the eosinophil

53
Q

What is Xolair (omalizumab)

A

It’s a drug used to treat asthma

It works by binding to an IgE after it is created by a B-cell. This will prevent the IgE from bind and activating mast cells, so you do not get any degranulation of the mast cell

Lowers the amt of circulating IgE

Used in persistent asthma or chronic idiopathic urticaria

54
Q

What does the pathogenic role of autoantibodies depend on?

A

Concentration and charge of the auto-antigen (Anti-DNA Ab have weak postive charge and they will bind to negative charge to glomerular in kidney causing SLE)

Affinity and charge of the autoantibody (higher affinity means more likely pathogenic, will form immune complexes and activate complement system)

55
Q

What is Graves diseases?

A

When you have hyperthyroidism, this is due to autoantibodies bind to thyroid peroxidase and the TSH receptor, this cause an increase in thyroid hormone that is produced and gives hyperthyroidism

56
Q

How does Humira (adalimumab) and Infliximab work?

A

These are anti-TNF-a meaning they bind to TNF-a and block its interaction with cell surface TNF receptors

TNF-a = inflammatory cytokine

57
Q

How does Abatacept (Orenica) work?

A

It’s a CTLA4Ig fusion protein. It binds to CD80/86 (B7), this blocks Tcell activation (by stoping costimulitory action)

Used in RA

58
Q

How does Tocilizumab (actemra) work?

A

Blocks IL-6 receptor to stop inflammation

Used for RA

59
Q

How does Stelara (Ustekinumab) work?

A

Binds to p40 subunit of both IL-12 and IL-23 cytokines which bocks IL-12 and IL-23.

Used for plaque psoriasis, psoriatic arthritis and Crohn’s disease

60
Q

What are the three methods for cytotoxicity?

A

Complement-mediated lysis of cells

Cell injury by inflammatory cells

Phagocytosis of antibody coated cell

61
Q

What is RhoGAM?

A

It is used for suppressing the immune response of individuals exposed to RhD+ blood

Only used for Rh- mothers who have no created anti-RhD Abs. infant must also be Rh+

Given before birth 26-28 weeks, also given 72 hours after birth

62
Q

How do you get type II blood rxns that are drug-induced?

A

The drug gets absorbed into the red blood cell. This then causes the Abs that go after the drug to bind to the RBC which will activate the complement system and to will lysis the RBC

Also immune complexes from the drug will be absorbed into the RBC and activate complement lysis

Also drugs in the RBC can cause the formation of Abs to other blood group Ag on cell surface

63
Q

What is Rituximab?

A

Anti-CD20 that treat non-Hodgkins lymphomas

It will eliminate host autoreactive Bcells by type II cytotoxic rxn

64
Q

What is the Arthur’s reaction?

A

When an antigen combines with an Ab to form an immune complex

This takes place at a local site in and around small blood vessels

The picture of it is a large red area that has undefined edges and covers a large area of the arm

65
Q

What are some side effects that happen with glomerulonephritis?

A

Blood and protein leakage in urine

Hypertension

Acute renal failure

It’s causes when autoantibodies to DNA bind to places in the kidney and cause type III HS rxn

66
Q

What is the cellular basis of type IV hypersensitivity rxn?

A

1: Macrophages and DCs (APCs) recognize and present antigen to Th1 CD4 T cells
2. CD4 Tcells secrete cytokines: INF-gamma
3. This will recruit monocytes and macrophages to the area and activate them
4. Activated phagocytes will produce TNF-a and IL-1 to act on blood vessels
5. Phagocytes will also release lytic enzymes and cause tissue dmg
6. usually takes 48-72 hours to happen
7. Late stage prostaglandins E will help in down regulation of the inflammation

67
Q

What is chronic granulmoa?

A

When your immune system fails to kill and clear the replicating pathogen causing persistent antigenic stimulation which produces chronic DTH reactions

It’s your body trying to wall off the invader

68
Q

How does contact dermatitis caused by small molecule sensitization work?

A
  1. The small molecule is usually to small to be antgentic
  2. It’s often lipophilic and will conjugate with self proteins
  3. This creates neo-antigen (hapten)
  4. The hapten then binds to a langerhan’s cell which presents the antigen for a Th cell and activates the type IV pathway for DTH
69
Q

What are primary immunodeficiency?

A

They are ones that are genetic defects

Leads to a defect in the immune system and leads to serious disorders. Most likely an increase in getting an infection

70
Q

What are acquired immunodeficiency?

A

These are secondary due to an infection, or drugs that are immosppressive. This can also be due to malnutrition

71
Q

What is transient hypogammglobulinemia of infancy?

A

Primary

This is a normal thing, what happens is the baby get IgG from the mother this can lead to a delay in B-lymphocyte production meaning less Ab for the baby. This does usually need a treatment but in time the baby will be able to develop their immune system in about 9 months

Have to watch for increased risk of bacterial infection

72
Q

What is Bruton’s Agammaglobulinemia?

A

Primary, X-linked

B cell deficiency which leads to B cells not maturing in the bone marrow.

This leads to absence of Ab in the blood and you can get infections systems when the material IgG wares off

Therapy for this is:

  1. Prevention of diseases thro vaccines
  2. treat infections extremely aggressively with antibiotics
  3. Monthly injects of IVIgG in order to provide protect to this person
73
Q

What is hyper-IgM syndrome

A

X-linked, primary

B-lymphocytes cannot undergo isotype switching die to absence of CD40L on Th cells

You need the CD40L on the Th cells to bind with the CD40 on B cells to cause the Tcell to become active and create cytokines which cause class switch over

Hyper-IgM pts will have a lack of or very low IgG, IgE and IgA. Meaning they will be at a high risk for bacterial infections and reoccurring infections

Treat with monthly IVIg

74
Q

What is selective immunoglobulin isotype deficiency

A

Primary

Most common type. It’s when you have very low levels of IgA

It may be asymptomatic or you can get respiratory infections and diarrhea

Celiac disease is more common in pats with IgA

You are more likely to have oral mucosal infections

75
Q

What is common variable immunodeficiency (CVID)?

A

It’s when you have B-cells present but you lack Ab secreting plasma cells .

This leads to impaired Ab response to infections or vaccinations

You will have low levels of IgG and IgA but normal or reduced IgM

High chance of getting malignant tumors, you can live a normal life but might be shorter and you need monthly IVIg.

76
Q

What is DiGeorge syndrome?

A

Primary

Defect in T lymphocyte maturation. You have very little T cells or they are absent

Still have normal B-cells

Usually due to an issue with malformation of the thymus (where Tcells mature)

You will get lots of viral infections and they treatment is to transplant with a fetal thymus

77
Q

What is severe, combined immunodeficiency (SCID)

A

Primary

Boy in plastic bubble

You have issues with cell-mediated and humoral immunity deficient

Leads to reduced B and T lymphocytes, X-linked and EXTREMELY infection prone

Treatment is a bone marrow transplant

78
Q

What is a Host vs graft response?

A

This is a rejection when the host cell attacks the donor cells due to major differences in HLA antigens (allotypes) where the host Tcells recognize the HLA and attack them

79
Q

What is a graft vs host rxn?

A

It’s when the donor lymphocytes attack the host cells. This usually happens in a bone marrow transplant and will require removal of Tcells from the graft

80
Q

Do you have to worry about RhD matching when it comes to organ transplants?

A

No, RhD is only expressed on the RBC and not on the organ.

Important to note that ABO antigens are expressed on the organ so blood typing must be done for a transplant

81
Q

What is the point of tissue cross-matching when it comes to organ transplants?

A

It means you want to closely get HLAs to be as close as possible to one another to ensure the transplant is a success.

What you do is take the recipients serum and mix it with the donors leukocytes. This is to seee if the recipient has IgG Abs to the donor leukocytes antigen

If you get a positive rxn (clumping will form) or cross-match that means the transplantation in contra indicated

82
Q

What the is MOA action for Calcineurin inhibitors?

A

They will inhibit activation of transcription factor NFAT

this will block transcription of IL-2 genes and IL-2 production

Without IL-2 growth and differentiation of T lymphocytes is blocked

Cyclosporine and tacrolimus

83
Q

How does Sirolimus (Rapamune) or Rapamycin work?

A

It’s a MTOR inhibitor

Inhibits the enzyme mTOR which causes inhibition of IL-2 driven proliferation of T lymphocytes

**does not block production of IL-2, just stop IL-2 driven proliferation

84
Q

How does Antithymocyte Globulin (Atgam) work?

A

It’s non-specific and binds not only to T cells but also B cells and platelets and other leukocytes and causes them to not function

85
Q

How do the drugs Daclizumab (zenapax) and Basiliximab (simulect) work?

A

They are IL-2 receptor antagonists

They bind to IL-2 receptor on the surface of activated T-lymphocytes

This means secreted IL-2 can not bind to the IL-2 receptor and there is no T cell proliferation

86
Q

How do the drugs Azathioprine (Imuran) and Mycophenolate mofetil (cellcept) work?

A

These work to block both T and B cell function

They block the purine synthesis in lymphocytes which block proliferation and prevents cell division

Purine analogs

87
Q

How are steroids used in immunosuppressive treatments?

A

They inhibit PLA2 which means less prostaglandins and leukotrienes

Less prostaglandins = decreased inflammation and T-cell migration

Less leukotrienes = less inflammation, chemotaxis and degranulation of PMN and CTL proliferation

88
Q

What is the difference between small molecule drugs and biological?

A

Small molecule = smaller, less complex and are chemically synthesized

Biologics = larger and more complex and are created from living cells (little drug interactions from pharmaceutical standpoint )

89
Q

What is a biosimilar drug?

A

ITs a drug that looks very much alike in function and actual results of use to another drug that is already FDA approved

Has only minor differences in clinically inactive components

90
Q

What is acute inflammation?

A

Immune response to eliminate pathogen/infection

Has high number of PMN and Th cells

Disappearance of leukocytes and you get full function of the tissue back and is good for healing

91
Q

What is chronic inflammation?

A

Incomplete clearance of infection and persistent antigenic stimulation

Has high numbers of macrophages, CTLS and B cells

Chronic inflammation leads to changes in the cell and you do not restore full function leading to issues

92
Q

What are the Pharmacological mediators of inflammation?

A

Trigger by arachidonic acid metabolites

Prostacyclin: vasodilator

Prostaglandins: vasodilation and increased permeability

Leukotrienes: increased vascular permeability

93
Q

What are the immunological mediators for inflammation?

A

Trigged by chemokines and inflammation cytokines
Chemokines= endothelium
Cytokines = WBC

TNF-a
IL-1
IFN-gamma
IL-6

94
Q

What are Interferons (INF)?

A

Create resistance by interferometer the spread of viral infections : INF-a and INF-gamma

95
Q

What are interleukins?

A

For cell signaling, communication

IL-1, IL-2 and IL-12

96
Q

What are tumor necrosis factors (TNF)

A

Induces necrosis in tumor; enhances inflammation and cytotoxic reactions
TNF-a

97
Q

What are Transforming growth factor (TGF)?

A

Suppresses inflammation and cytotoxic reactions by transformation of other cell functions

TGF-b (Tregs)

98
Q

How does B cell targeting by biological drugs work?

A

B cells have specific antigens on their surface and mABs against these B cell antigen coat and bind to these antigens

B cell antigens are= CD20, CD52 and BLyS

What the mABs do is coat the cancerous auto reactive B cell which triggers its destruction

Activates ADCC from NK and CLL cells to kill it

99
Q

How does Alemtuzumab work?

A

Targets CD52 antigen on B cell chronic lympcytic leukemia (CLL) and marks it to be killed

100
Q

How does Belimumab work?

A

Binds to “b-lymphocyte stimulator” (BLyS) and inhibits B cell survival/differentiation

Used in SLE patients

Trigger ADCC to kill the infected cell

101
Q

How does Infliximab (remicade) work?

A

It blocks TNF-a binding to its receptor and reduces inflammation

Can get TB, fungal infections, Hep B

Can’t give with live vaccines

This has a higher rate of clearance so it has reduced efficacy

102
Q

How does Canakinumab (Ilaris) work?

A

IL-1 antagonist, and anti-IL-1 Beta

Binds only to IL-1 beta and has anti-inflammatory effect

Good for arthritis and gout

103
Q

How does Anakinra (kineret) work?

A

Inhibits activities of IL-1, IL-1B by blocking the interaction between IL-1B and the cell surface receptor

Used for RA and gout and AS

ALL BIOLOGICS INCREASE RISK OF INFECTION
DO NOT USE LIVE VACCINE WHEN GIVING A BIOLOGIC

104
Q

How does Tociliumab (Actemra) work?

A

IL-6 receptor antagonist, blocks binding of IL-6

So this blocks monocyte activation, PMN recruitment, thrombocytosis and B cell differentiation

Used in RA, and juvenile idiopathic arthritis

105
Q

How do Opdivo (nivolumab) and Keytruda (pembrolizumab) work?

A

They are anti-PD-1 and Anti-PD-L1 respectively

Blocks binding of PD-1 on T lymphocytes with PD-L1 expressed on APCs and tumor cells. We do this because if those two bind together it suppresses the ability of the T-lymphocytes to recognize and destroy tumor cells.

106
Q

How does Yervoy (ipilimumab) work?

A

An anti CTLA-4

We want to block CTLA-4 because it is expressed highly on tumors and when it binds to T lymphocytes they become inactive

This drug allows T lymphocytes to interact with B7 which is found on APCs to allow them to become active and will allow it to kill the cancer cell

Pharm 413 Drugs (4 decks)

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