Psychoneuroimmunology Flashcards

1
Q

What does PNI stand for?

A

psychoneuroimmunology

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2
Q

Give some examples of how psychological stress can affect immunity indirectly?

A
  • Smoking
  • Obesity
  • Lack of exercise
  • Poorer medication compliance
  • Alcohol and drug use
  • Risky sexual practices
  • Poor sleep
  • Caffeine
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3
Q

PNI is the study of ways in which stress ________ affects immunity.

A

directly

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4
Q

Stress directly affects immunity due to alterations in __________ mechanisms that contribute to disease or infection

A

homeostatic

Note: The idea that all stress is just “bad” for immunity is oversimplified… It’s more like “maladaptive under certain circumstances”

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5
Q

How innate immunity works

A
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6
Q

T/F The Autonomonic nervous system sends nerves into tissues that form or store the cells of the immune system and eventually enter the circulation

A

True

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7
Q

T/F Immune System tissue has receptors for all the interesting hormones released by the pituitary (HPA Axis) under the control of the brain

A

True

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8
Q

What is conditioned immunosuppression?

A
  1. Give an animal a drug that suppresses the immune system along with an artificially flavored drink (the conditioned stimulus)
  2. Immune function is suppressed
  3. A few days later present the artificially flavord drink by itself
  4. Immune function is suppressed!
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9
Q

What is the significance of conditioned immunosuppression?

A

Conditioned immunosuppression is the paradigm which was used in the study which most solidified the link between the brain and the immune system

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10
Q

What are the two kinds of immunity?

A
  1. Acquired
  2. Innate
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11
Q

Acquired Immunity involves monocytes (macrophages) which enlist the assistance of lymphocytes (T cells and B cells) in two different types of responses to the presence of an infecious agent.

  1. T-Cells bring about _____________ immunity
  2. B-Cells bring about ________________ immunity
A
  1. T-Cells bring about cell-mediated immunity.
  2. B-Cells bring about antibody-mediated immunity.
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12
Q

The cascade of cell-mediated immunity involves four steps:

  1. An __________ _____ is encountered by a type of monocyte called a ___________.
  2. This stimulates the __________ to present the __________ _____ to a _ ______ ____ and to release __________-_ which stimulates _ ______ ____ activity
  3. The _ ______ ____, as a result, releases __________-_ which triggers _ ____ proliferation.
  4. This eventually causes another type of white blood cell, _________ ______ _____, to proliferate and destroy the infectious agent.
A
  1. An infectious agent** is encountered by a type of monocyte called a **macrophage.
  2. This stimulates the macrophage** to present the **infectious agent to a T helper cell** and to release **interlukin-1 which stimulates T helper cell activity
  3. The T helper cell**, as a result, releases **interlukin-2 which triggers T cell proliferation.
  4. This eventually causes another type of white blood cell, cytotoxic killer cells, to proliferate and destroy the infectious agent.
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13
Q

The cascade of antibody-mediated immunity also involves four steps:

  1. An __________ _____ is encountered by a type of monocyte called a ___________.
  2. This stimulates the __________ to present the __________ _____ to a _ ______ ____ and to release __________-_ which stimulates _ ______ ____ activity
  3. The _ ______ ____, as a result, releases _-____ ______ ______ which triggers differentiation and proliferation of another white blood cell _-_____.
  4. The _-_____ make and release specific __________ that bind to surface proteins of the __________ _____, targeting it for destruction.
A
  1. An infectious agent** is encountered by a type of monocyte called a **macrophage.
  2. This stimulates the macrophage** to present the **infectious agent** to a **T helper cell** and to release **interleukin-1** which stimulates **T helper cell activity
  3. The T helper cell**, as a result, releases **B-cell** **growth factor** which triggers differentiation and proliferation of another white blood cell **B-cells.
  4. The B-cells** make and release specific **antibodies** that bind to surface proteins of the **infectious agent, targeting it for destruction.
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14
Q

In order to sound immune alarms throughout this far-flung system, blood borne chemical messengers that communicate between different cell types, called _________ have evolved

A

Cytokines

Examples of cytokines include interleukin-1 and interleukin-2

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15
Q

Acquired Immunity has three features:

  1. The ability to specifically ______ a pathogen with antibodies and cell-mediated immunity that specifically _________ that pathogen.
  2. I takes ____ to build up that immunity when you are first exposed to a pathogen.
  3. ________ ________ to a pathogen will boost those defenses even further
A
  1. target (imagine a bullet with pathogen-X’s name on it)
  2. time (this involves finding which antibody has the best fit and generating a zillion copies of it)
  3. repeated** **exposure (continues to boost targeted immunity further)
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16
Q

Innate immunity is a ___________ immune response which tends to occur at the beachhead where a pathogen gets its first foodhold, like your skin, or moist mucosal tissue in your mouth or nose.

A

nonspecific

These types of antibodies generically attack any sort of microbe they encounter (i.e. saliva)

These types of antibodies are secreted and coat your mucosal surfaces like an antiseptic paint.

17
Q

One example of innate immunity is a type of response that occurs at the site of an infection causing inflammation. This happens in three stages:

  1. tissue injury accompanied by bacteria triggers the release of ________ _______ such as _________
  2. blood vessels respond with increased dilation and leakiness allowing cells of the innate immune response such as __________ and _____ to slip out of the circulation to infiltrate the immediate area of infection
  3. __________ such as ___________ and __________ along with ______ ______ _____ consume the bacteria and cell debris, followed by healing.
A
  1. tissue injury accompanied by bacteria triggers the release of chemical signals** such as **histamine
  2. blood vessels respond with increased dilation and leakiness allowing cells of the innate immune response such as phagocytes** and **fluid to slip out of the circulation to infiltrate the immediate area of infection
  3. Phagocytes** such as **macrophages** and **neutrophils** along with **natural killer cells consume the bacteria and cell debris, followed by healing.
18
Q

The best documented way in which stress-induced immunosuppression occurs is via _______________.

A

Glucocorticoids

19
Q

Which are affected more by the effects of glucocorticoids, B-cells or T-Cells?

As a consequence which type of immunity is more disrupted antibody-mediated immunity or cell-mediated immunity?

A

T-cells and cell-mediated immunity is most disrupted by the effects of glucocorticoids.

20
Q

T/F stress causes the active expenditure of energy in order to disasemble the preexisting immune system

A

True

21
Q

Under some circumstances the immune system will ask the body to secrete hormones that will ultimately suppress the immune system, how does this happen?

  1. The immune system releases the cytokine (aka chemical messenger) __________-_
  2. __________-_ stimulates the hypothalamus to release ___
  3. ___ stimulates the pituitary gland to release ____
  4. ____ causes the adrenal release of _____________
  5. _____________ in turn suppress the immune system
A
  1. The immune system releases the cytokine (aka chemical messenger) interleukin-1
  2. interleukin-1** stimulates the hypothalamus to release **CRH
  3. CRH** stimulates the pituitary gland to release **ACTH
  4. ACTH** causes the adrenal release of **glucorticoids
  5. glucorticoids in turn suppress the immune system
22
Q

T/F up to about the first thirty minutes after the onset of a stressor many aspects of immune response is enhanced?

A

True

This is true for all realms of immunity, but in particular for innate immunity.

23
Q

T/F by about an hour after the onset of a stressor sustained glucorcorticoid and sympathetic activation begins to have the opposite effect, namely, suppressing immunity

A

True

24
Q

T/F It is only with major stressors of longer duration, or with really major exposure to glucocorticorticoids, that the immune system does not just return to baseline, but plummets into a range that really does qualify as immunosuppressing

A

True

25
Q

Immune function varies across time in which ways as they relate to which three phases of stress

A
  1. Onset of Stress - Immune function spikes
  2. Moderately prolonged stress- Immune function returns to baseline
  3. Chronic Stress - Immune function plummets below baseline into the immunospuressive range
26
Q

When a persons immune system remains on heightened alert and fails to return to baseline after moderately prolonged stress immune function can rise into the __________ _______ _____

A

autoimmune disease range

27
Q

T/F glucocorticoids prevent immune system response to stress from spiraling into the autoimmune range

A

True

28
Q

While glucocorticoids are know to suppress immune function in massive doses, they can subtly enhance immune function in which two ways?

  1. A subtle rise in glucocorticoid levels for a short time (like in phase B) and the hormones only kill _____ ___________ which don’t work as well, thereby _________ the immune response.
  2. Glucorcorticoids and epipinephrine divert ___________ from circulation and ________ them to the front lines.
A
  1. A subtle rise in glucocorticoid levels for a short time (like in phase B) and the hormones only kill older lymphocytes which don’t work as well, thereby sculpting the immune response.
  2. Glucorcorticoids and epipinephrine divert lymphocytes** from circulation and **reassign them to the front lines.
29
Q

Sapolsky describes two paradoxical facts about autoimmunity, glucocorticoids and stress:

  1. large doses of glucocorticoids make autoimmune diseases ____ ________
  2. at the same time stress can ______ autoimmune diseases
A
  1. large doses of glucocorticoids make autoimmune diseases less damaging
  2. at the same time stress can worsen autoimmune diseases
30
Q

Links between stress and disease can follow two routes _________________ and _________

A

psychoneuroimmune

and

lifestyle

31
Q

The psychoneuroimmune route between stress and disease follows four stages defined by changes in

A
  1. level of stress
  2. glucorcorticoid levels
  3. immune function
  4. disease resistance
32
Q

The lifestyle route between stress and disease follows twp stages defined by changes in

A
  1. stress level
  2. treatment compliance, rates of protective and risk factors
33
Q

Sapolsky tests the four step psychoneuroimmune route model attempting to explain the known relationship between social support (or alternatively isolation) and it’s impact on various diseases. what does he find for each stage?

A
  1. social isolation is a stressor
  2. little evidence for or against chronically over-reactive stress response
  3. social isolation dampens some aspect of immune function
  4. mixed results instudies attempting to prove increase in socially isolated stress caused the disease

Overall pretty good case can be made that soical isolation can impact health through the effects of stress on immunity

34
Q

Sapolsky tests the four step psychoneuroimmune route model attempting to explain the known relationship between stress and the common cold. what does he find?

A

More stress equaled about three times the likelihood of succumbing to a cold after being exposed to the rhinovirus (common cold).

Prolonged stressors more than a month long that were social in nature provided the greatest risk.

35
Q

Sapolsky tests the four step psychoneuroimmune route model attempting to exploring the relationsip between stress and worsening aspects of AIDS. what does he find?

A

psychoneuroimmune aspects could contribute to a link between stress and worsening aspects of AIDS

more research is needed to examine how much stress influences whether people comply with their treatment regimes vs. how well their treatment regimes work.

36
Q

T/F Herpes DNA contains a strand of DNA that is sensitive to glucocorticoid levels, and when levels are up, that DNA sensor activates the genes involved in coming out of latency.

A

True

37
Q

T/F Herpes can trigger neurosystem response further imparing and exploiting your immune system after coming out of latency

A

True

Herpes can cause your hypothalamus to release CRH which releases ACTH which raises glucocorticoid levels which suppress the immune system further while impairing your immune defenses against activated herpes.

38
Q

T/F Stress increases the risk of cancer

A

False

39
Q

T/F Stress increases risk of relapse out of remission from cancer

A

False