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BVetMed - Animal Welfare > Stress and Disease in Humans > Flashcards

Stress and Disease in Humans Flashcards

1
Q

Define a stressor

A

Anything, actual or perceived, that threatens homeostatic balance - physiological/environmental/psychological

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2
Q

Define stress

A

A state of threatened homeostasis - allostatic load

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3
Q

Define stress response

A

The body’s attempt to restore homeostasis

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4
Q

What is another term for distress?

A

Disease

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5
Q

How is stress adaptive? What are sources of stress in wild animals?

A

Predation (acute)
Disease (acute)
Drought/famine (chronic)

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6
Q

How has causes of death changed over time since the 1900s?

A

Hicks and Allen 1999 - Infectious and parasitic disease most common, life expectancy 45
Office for National Statistics 2009 - Heart disease and cancer, life expectancy 80

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7
Q

What stressors affect humans?

A

Traffic jams, work deadlines, dams, relationships, money - anxiety, none are directly life threatening

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8
Q

Give examples of medium-term effects of stress

A

Tension, headaches, insomnia, dizziness, heart palpitations, muscle pain, depression

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9
Q

Give examples of long-term effects of stress

A

Angina, atherosclerosis ,cancer, HIV, shingles, stroke

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10
Q

How does stress affect the immune system?

A

Transiently stimulates the immune system
Immunostimulatory initially, recovery, then immunosupression
IMMUNOMODULATORY

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11
Q

What are the two types of immune disorder linked to stress?

A

Increased susceptibility to infection

Inflammatory or autoimmune disease

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12
Q

What is the evidence for increased susceptibility to infection?

A
  • Healthy volunteers inoculated with a cold virus - ^ stress -> ^ infection and v WBC (Cohen 1991, 1998, 1999)
  • Spousal carers of dementia patients given influenza vaccine - carers v antibody response, ^ rate of infection, v wound healing (Kiecolt-Glaser 1991, 1995, 1996)
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13
Q

How is inflammatory or autoimmune disease affected by stress?

A

Exacerbate inflammatory diseases like asthma (TH2) and autoimmune disease (eg. rheumatoid arthritis TH1)

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14
Q

Where are the humoral and cell-mediated responses effective?

A

Humoral - extracellular

Cell-mediated - intracellular

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15
Q

What are the TH1 nd TH2 calls responsible for?

A

TH1 - Type 1 pathway - cell mediated immunity

TH2 - Type 2 pathway - humoral immunity

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16
Q

What is the cytokine profile of TH1 cells? What is their action?

A

IFN-y, IL-2, IL-12, TNFa
Pro-inflammatory responses (target intracellular pathogens)
Activate macrophages, cytotoxic T cells and NK cells
Trigger autoimmune responses if unbalanced

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17
Q

What is the cytokine profile of TH2 cells? What is their action?

A

IL-4, IL-5, IL-13 (eosinophilic responses) IL-10 (anti-inflammatory responses)
Upregulates Ab production (target extracellular organisms)
Trigger allergic inflammatory responses if unbalanced

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18
Q

How do the TH1 and TH2 immune responses interact?

A

Counter-regulatory by preventing differentiation

eg. IFNy (Th1) suppresses the Th2 response, IL-4 and IL-10 (Th2) suppresses the Th1 response.

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19
Q

How does cytokine directed differentiation from naive T-cells occur?

A

Cytokines = self-specific growth factors (+ feedback)
Each pathway can down regulate the other.
Optimal scenario: balance
- overaction of either pathway can cause unbalance and trigger disease

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20
Q

How do glucocorticoid levels affect cytokine and Th1/Th2 responses?

A

Baseline- low level secretion
> ^ Th2 response inhibits Th1 formation by
- v IL-12 production
- Downregulating IL-12 Receptors on T cells and NK cells
> ^IL-4 and IL-10 production (via ^ Th2 cell formation)

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21
Q

How do cortisol levels vary? What are it’s effect?

A

Diurnal variation

  • circadian rhythm
  • important for immune system regulation
  • v TH1 cytokine production
  • ^ TH2 cytokine production
22
Q

When are type 1 and type 2 immunity most active?

A

Type 1 - nocturnal sleep (low cortisol)

Type 2 - awakening (high cortisol)

23
Q

What model describes how acute stress may affect the immune system?

A

Marshall 1998 - Acute stress eg. exams. [claimed to be too simple]
Cytokine shift model - stress alters the balance of the immune system without changing the overall activation ie. dysregulatino rather than immunosupression.
- describes shifts between Th1 (cellular) and Th2 (humoral) immunity.

24
Q

What is immunostimulation caused by according to Marshal 1998 cytokine shift model?

A

Imbalance in favour of type 1 immunity (cell mediated) with concurrent suppression of type 2

  • v cortisol -> immune systme hyperactivity and ^ phagocytosis
  • ^ pro-inflammatory responses -> ^ tissue damage
  • ^ risk of inflammatory/autoimmune disease eg. RA, type 1 diabetes
25
Q

What is immunosuppression caused by according to Marshal 1998 cytokine shift model?

A

Imbalance in favour of type 2 immunity (humoural) with concurrent suppression of type 1

  • ^ cortisol -> v lymphocytes
  • ^ susceptability to infection
  • delayed wound healing
26
Q

What model explains the effect of chronic stress on the immune system?

A

> GC-ressitance model Miller 2002
- Type 1 pro-inflammatory response
- chronic stress alters GC ability to regulate the immune system
- ^GC -> vGC recepetors
- vGC sensitivity -> v suppression of inflammation
- continued stress -> ^^ IL-6 pro-inflammatory cytokine levels
OR extreme prolonged stress -> complete dysregulation
- vTH1 vTH2 -> immunosupression

27
Q

Give examples of autoimmune disease. Why do they occur?

A

Immune system over-activation (body tissues mistakenly attacked)
Damage associated with inflammation
- eg. rheumatoid arthritus, type 1 diabetes

28
Q

What two situations increase the risk of autoimmune diseases?

A

Phase A without phase B - immune system not down regulated

Multiple transient stressors increasing immune system function until it hits the autoimmune range

29
Q

Outline the pathophysiology and treatment of rheumatoid arthritis

A
  • Chronic inflammatory (Th1 dominant) disorder
  • Risk factor gene
  • Stress associated with RA
    > major life events eg. death of a spouse and chronic stressors -> ^ disease activity and pain [counterintuitive, GCs should suppress this]
    > acute stressors -> transient v disease activity and pain
  • treatment = anti-inflammatory steroids
30
Q

How is the inflammatory response normally regulated?

A

Negative feedback

eg. immune system -> IL-12, TNFa (pro-inflam) -> ^ACTH -> ^GC -> v inflamation

31
Q

How does regulation of the inflammatory response differ in RA patients?

A
  1. hypo functional HPA axis -> vGC production and ^ACTH production to compensate
  2. Immune cell GC resistance (vGC-R expression/sensitivity)
  3. Th1 rheumatoid inflammation - excess IL-12 and TNFa, LACK of IL-10
    Hypothesis - following exposure to a stressor, blunted GC response and immune cell resistance prevents TH1/TH2 axis being shifted away from TH1 dominant profile -> TH2 dominant
32
Q

What is the pathophysiology of type 1 diabetes?

A

Autoimmune disease - pancreatic cells destroyed

v insulin -> v glucose uptake

33
Q

How has stress been linked with diabetes?

A

Depression and chornic stress link
^HPA activity and ^ cortisol in diabetic patients
Cortisol promotes insulin resistance -> hyperglyceamia

34
Q

How does stress promote insulin resistance?

A
  • ^SNS -> v insulin secretion (v PNS)
  • ^GCs -> v fat cells sensitivity to insulin, blocking glucose storage
  • fat cells secrete hormones to prevent muscle/liver responding to insulin
    > Require larger insulin injection
35
Q

How does Type-2 diabetes occur? What may it lead to?

A

Failure of cells to respond to insulin

  • meals -> insulin release (even when fat cells full)
  • full fat cells = less responsive.
  • release hormones == cortisol triggering other cells to become insulin resistant
  • ^ blood sugar -> ^ insulin from the pancreas
  • eventually insulin secreting cells “wear out” and TYPE 1 DIABETES results
36
Q

What is diabetes a major catalyst/risk factor for?

A

Heart disease, kidney disease, blindness and stroke (^ fatty acids and cholesterol in circulation)

37
Q

How does stress increase the risk of myocardial infarction?

A 
^BP, ^HR, ^SV
Vasoconstriction (skin, gut, repro)
Vasodilation (muscles) 
Mobilisation of glycogen/FA/lipids -> blood
^ clotting
38
Q

How does stress affect clotting?

A

^ catecholamines -> pro-thrombotic state
^ clotting factors
^ fibrinogen
^ platelet count and aggregation
Abnormal heamostasis -> ^ risk of thrombus formation or haemorrhage
Black and Garbutt 2002, Thrall 2007

39
Q

Define hypertension

A

Consistently high Bp at rest -> damage of arterial walls and organs (esp kidneys)
Triggered by consistently high catecholamines due to SNS hyper-reactivity
Flaa 2008

40
Q

Outline the stages of formation of plaque formation

A

(deposition of fatty substances, calcium and cholesterol)
- hypertension damages endothelia
- WBCs congregate - chronic inflammation -> further damage
- LDL cholesterol penetrates arterial wall
- WBCs ingest cholesterol and produce initial plaque deposits
Plaque calcifies -> v arterial diamter and flexibility

41
Q

What are the consequences of atheroscelorosis?

A

v blood flow -> myocardial ischeamia

Plaque debris and blood clots may break off

42
Q

Give a study demonstrating the effects of stress on atheroscleroisis in animals

A

In stable social groups, subordinate female monkeys develop greater atheroscelrosis than dominants - Kaplan 1996
Social disruption causes heater atheroscelrosis in male monkeys - Manuck 1995

43
Q

How is stress associated with asthma?

A
  • Common, chronic, inflammatory disease
  • Triggers - allergens, irritants, infections, stress
  • Stress -> Th2 dominant, enhanes susceptability to bronchiole inflammation (th2 linked to allergic disease swell)
    > Liu 2002
44
Q

How is stress linked to peptic ulcer disease?

A

Helicobacter pylori and psychological stress two main factors
Stress
- v blood flow to gut altering stomach acid secretion
- v stomach wall thickness
- v mucous/bicarbonate excretion
- v prostaglandins (v cellular repair)
- type 1 immune supression
Basically - ^ cortisol -> TH2 biased response -> TH1 suppression, alongside gastric hyperacidity ->. H pylori ulcer formation
Stress also ^risk of 2dry infection and ^ susceptibility by behaviour (less sleep, NSAIDs)

45
Q

How can PGs aid healing?

A

^blood flow

46
Q

How are stress and depression linked?

A

major depression ranks 5th among leading causes of global disease burden due to link with ^morbidity/mortality from other medical conditions
complex aetiology/pathology - genetic, neurological, endocrinological, immunological components
- Numer/severity of major stressful life events associated with risk of developing MD, and the course of the disease.

47
Q

What are the potential hypothesess for the biological cause of depression?

A

hyperactive HPA axis
NT imbalance
Cytokine hypotheses of depression
- overall dysregulation of the stress response

48
Q

What is evidence for the hyperactive HPA axis hypothesis?

A

Lee 2002; Chrousos 2009
MD patients
- ^ plasma cortisol due to CRH hypoersecretion
- a defective feedback system
> constant anxiety, over-reaction to stimulation -> learned helplessness and loss of motivation
- excessive GC down-regulates GC receptors in the hippocampus
- prolonged cortisol hyper secretion may lead to neuronal death and hippocampal atrophy, which is associated with ^no/duration depressive episodes.

49
Q

What is the evidence for the NT imbalance hypothesis of major depression?

A

Inhibitory NTs
-Serotonin v with stress, low levels associated with depression
-Many antidepressants ^ serotinergic transmission
-Serotonin receptor abnomalities in MD patients
Excitatory NTs
-DA responsible for motivation and interest. Low levels - v concentration and v energy. High levels = smoke/drug dependance
-NA - high levels linked to anxiety, stress, ^BP, low levels linked to lack of energy, focus (Seen in depression)

50
Q

What is the evidence towards the cytokine hypothesis of depression?

A

Symptoms of sickness behaviour in animals == depression
Hypothesis = ^pro-inflamatory cytokines and v anti-inflam act upon the brain
Evidence
- depressed patients have immune abnormalities
- depression common side effect of cytokine therapy
- antidepressant medication v pro-inflammmatory cytokine secretion
- IL-1 -> sickness behaviour in animals and actuates both SAM and HPA
- IL-1, IL-6 and TNFa affect 5-HT transmissino in the brain
BUT
> little evidence for ^IL-1 in depressed patients
> ^IL-6 linked to depression/infection/stress but not sickness behaviour

51
Q

What are the main factors affecting th stress resonse?

A
  1. Mediating processes
    - appraisal
    - coping strategies (problem-focused or emotion-focused coping)
  2. Vulnerability factors
    - personality types (Friedman and Rosenmn 1974 - type A [aggressive, impatient] v type B[alm, laid back] behaviour)
    - health habits
    - social support
    - genetics
    - experience
    - demongraphic
    - pre-existing stressors

BVetMed - Animal Welfare (19 decks)

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