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Pharm II > test 4 part 2 > Flashcards

test 4 part 2 Flashcards

1
Q

Adrenal cortex = Zona glomerulosa releases

A

• Mineralocorticoids -> Aldosterone (main one)

- mainly found in exratory organs

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2
Q

Adrenal cortex = Zona fasciculata releases

A

• Glucocorticoids -> Cortisol (main one)

- located throughout your entire body

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3
Q

Adrenal cortex = Zona reticularis releases

A

• Adrenal androgens -> DHEA (dehydro-epi-angerosterone) goes to turn into other sex hormones

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4
Q

Adrenal medulla secretes

A

• Catecholamines -> Epi and norepi

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5
Q

Corticosteroids

A

• Bind to specific intracellular cytoplasmic receptors in target tissues
– Widely distributed throughout the body
– Glucocorticoid receptors: widely distributed throughout body
– Mineralocorticoid receptors: excretory organs-kidney, colon, salivary & sweat glands
• Receptor-hormone complex recruits coactivator proteins and translocates into cell nucleus where it alters gene transcription
• Attaches to gene promoter elements
• Turns genes on or off

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6
Q

Glucocorticoids Function: 1. Increase resistance to stress

A

– Raise glucose levels and provide the body with energy to combat stress

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7
Q

Glucocorticoids Function: 2. Promote

A

– Gluconeogenesis
– Protein catabolism
– Lipolysis

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8
Q

Glucocorticoids Function: 3. Alter blood cell levels in plasma

A 
• DECREASE:
        – WBC
        – Eosinophils
        – Basophils
        – Monocytes
        – Lymphocytes
• INCREASE:
        – Hemoglobin
        – Erythrocytes
        – Platelets
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9
Q

Glucocorticoids Function: Catabolic vs anabolic

A
  • Catabolic steroids (causing the breakdown of fat and sugar stores)
  • NOT anabolic steroids (building up)
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10
Q

Glucocorticoids Function: Immunosuppressiveness

A

• All glucocorticoids are immunosuppressive even as a single dose (destroying T cells and weakens the immune system)

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11
Q

Glucocorticoids Function: 4. Have POTENT anti-inflammatory and immunosuppressive activity

A

most important therapeutic property
• Decrease circulating lymphocytes
• Inhibit ability of leukocytes and macrophages to respond to antigens
• Decrease production and release of cytokines
• Inhibit the precursor of prostaglandins and leukotrienes (anti-inflammatory action)
• Decrease histamine release

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12
Q

Glucocorticoids Function: 5. Affect other systems at high levels

A
  • Bone density loss (most common)
  • Glaucoma
  • Personality changes
  • Increased appetite
  • Daibetogenic
  • Moon face & humpback
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13
Q

HYPERcortisolism disease

A

Cushing Syndrome

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14
Q

HYPOcortisolism disease

A

Addison’s Disease

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15
Q

Glucocorticoids

A
  • Cause “feedback inhibition” of further glucocorticoid and thyroid stimulating hormone production
  • MUST BE WEANED OFF SLOWLY (if stopped abruptly, you will get symptoms of Addison’s disease)
  • Can induce adrenal insufficiency or even death if not weaned
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16
Q

Therapeutic Use of Glucocorticoids

A 
• Addison’s disease
• Relief of inflammatory symptoms
        – Arthritis
        – Inflammatory skin conditions
        – Asthma
        – Inflammatory bowel disease
• Treatment of allergies
        – Allergic rhinitis
        – Drug, serum & transfusion reactions
• Acceleration of fetal lung maturation helping newborns to breathe 
• Post transplant immunosuppression
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17
Q

Glucocorticoids Pharmacokinetics

A

• Oral, IV, IM, topical, inhalation, intranasal, intra-articulary
• Metabolized by the liver, excreted by kidney
– Liver dysfunction/failure may increase half-life

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18
Q

Glucocorticoids with the most anti-inflammatory effect and no salt-retention effect

A
  • Dexamethasone (Decadron)

- long acting

19
Q

Intermediate length with high anti-inflammatory effect with very little salt-retention effect

A
  • Prednisone
  • Prednisolone
  • Methylprednisolone (Medrol, Solu-Medrol) -> more anti-inflammatory effect and less salt-retention effect
20
Q

Very short acting and even but little amounts of anti-inflammatory effect and salt-retention effect

A

-Hydrocortisone

21
Q

Allograft Rejection types

A
  • Hyperacute
  • Acute
  • Chronic
22
Q

direct and indirect allorecognition

A
  • direct- using the MHC complex from the donor

- indirect- using the MHC from the recipients body

23
Q

Hyperacute Rejection

A
  • Minutes to hours
  • Thrombotic occlusion of graft vasculature
  • Mediated by pre-existing antibodies in host (multiple transfusions, past transplant)
24
Q

Acute Rejection

A

• After first week
• Vascular and parenchymal injury
• Mediated by T cells and antibodies
- damage to inside the cell causing occlusion

25
Q

Chronic Rejection

A
  • Occurs during a prolonged period
  • Fibrosis and vascular abnormalities
  • Pathogenesis less understood – T cells, macrophages
26
Q

Immunosuppressants: Induction Drugs

A

• used at the time of transplantation

27
Q

Immunosuppressants: Maintenance Drugs

A

• required for long term immunosuppression

28
Q

5 Major Classes of Immunosuppressants

A
  1. Glucocorticoids
  2. Calcineurin Inhibitors
  3. mTOR Inhibitors
  4. Antiproliferative Agents
  5. Antibodies
29
Q

Glucocorticoids

A

• A standard component of induction and maintenance
– Initial high doses that taper over time
• D.O.C. for moderate rejection episodes
• Complex mechanism
– Profoundly suppresses T-lymphocytes
- Have the most side effects of any immunosuppressive category when given at high doses over the long term

30
Q

Calcineurin

A

• the major T-cell activator

31
Q

Calcineurin Inhibitors: Cyclosporine

A

• The “break-through” drug that allowed transplants
• Used in combination therapy to reduce dosage and side effects
– Nephrotoxicity
– Immune suppression
– Hepatotoxicity
– Lymphoma
• Levels must be monitored closely

32
Q

Calcineurin Inhibitors: Tacrolimus

A

• More potent & efficacious than Cyclosporine
• More nephrotoxic than Cyclosporine
- can be more toxic to kidneys
• Less cardiovascular toxicities than Cyclosporine
– Hypertension
– Hyperlipidemia

33
Q

mTOR Inhibitors

A

• Block mTOR (an intracellular serine/threonine kinase)
– TOR proteins are essential for cellular functions
• Binding to mTOR blocks the maturation of activated T cells and their proliferation

34
Q

Sirolimus (Rapamune)

A 
- mTOR Inhibitors
• Oral
• Nephrotoxic (w/ Cyclosporine) = additive effects cause kidney toxicities
• Hyperlipidemia
• Delayed wound healing
35
Q

Antiproliferative Agents

A

• Prevent proliferation of rapidly dividing cells
– B lymphocytes
– T lymphocytes
- often used in combination with corticosteroids and Calcineurin Inhibitors
- prevent the transcription of the DNA in the nucleus

36
Q

Antiproliferative Agents -Azothioprine

A

• First agent to achieve widespread use in organ transplantation
• Works better on acute rather than chronic responses
– Because cells are rapidly dividing
• Numerous & severe side effects have limited its use
– Bone marrow suppression

37
Q

Antiproliferative Agents -Mycophenolate mofetil

A 
• Less severe side effects than Azothioprine
• Side effects are GI related
        – Diarrhea
        – Nausea
        – Vomiting
        – Abdominal pain
38
Q

Antiproliferative Agents -Mycophenolate sodium

A

• Designed to be a slower releasing and more enterically pleasing form of mycophenolate mofetil
– Enteric coating
– Releases drug in small intestine
• No real evidence that it is more effective or safer

39
Q

Antibodies

A
  • React with T cell surface structures and deplete or inhibit T cells
  • Used to treat acute rejection episodes
40
Q

Antibodies - Monoclonal

A

• Monoclonal antibodies: contain ONLY one type of antibody that is derived from a single cloned B-lymphocyte

  • most common
  • more specific and less variable on where they work
  • more expensive
41
Q

Basiliximab (Simulect)

A
  • Monoclonal antibody
    – Binds to the IL-2 receptor on activated T cells and interferes with proliferation (doesn’t activate it)
    – Blocks the ability of antigens to activate the T cell response system
42
Q

Antibodies - Polyclonal

A

• Polyclonal antibodies: contain multiple antibodies

  • cheaper
  • less specific and more variable on where they work
43
Q

Antithymocyte Antibodies

A
  • Used at time of transplant OR for episodes of severe rejection
  • Bind to circulating T lymphocytes and inactivate them

Pharm II (37 decks)

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