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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
What is immunosuppression caused by according to Marshal 1998 cytokine shift model?
Imbalance in favour of type 2 immunity (humoural) with concurrent suppression of type 1 - ^ cortisol -> v lymphocytes - ^ susceptability to infection - delayed wound healing
26
What model explains the effect of chronic stress on the immune system?
> 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
Give examples of autoimmune disease. Why do they occur?
Immune system over-activation (body tissues mistakenly attacked) Damage associated with inflammation - eg. rheumatoid arthritus, type 1 diabetes
28
What two situations increase the risk of autoimmune diseases?
Phase A without phase B - immune system not down regulated | Multiple transient stressors increasing immune system function until it hits the autoimmune range
29
Outline the pathophysiology and treatment of rheumatoid arthritis
- 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
How is the inflammatory response normally regulated?
Negative feedback | eg. immune system -> IL-12, TNFa (pro-inflam) -> ^ACTH -> ^GC -> v inflamation
31
How does regulation of the inflammatory response differ in RA patients?
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
What is the pathophysiology of type 1 diabetes?
Autoimmune disease - pancreatic cells destroyed | v insulin -> v glucose uptake
33
How has stress been linked with diabetes?
Depression and chornic stress link ^HPA activity and ^ cortisol in diabetic patients Cortisol promotes insulin resistance -> hyperglyceamia
34
How does stress promote insulin resistance?
- ^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
How does Type-2 diabetes occur? What may it lead to?
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
What is diabetes a major catalyst/risk factor for?
Heart disease, kidney disease, blindness and stroke (^ fatty acids and cholesterol in circulation)
37
How does stress increase the risk of myocardial infarction?
``` ^BP, ^HR, ^SV Vasoconstriction (skin, gut, repro) Vasodilation (muscles) Mobilisation of glycogen/FA/lipids -> blood ^ clotting ```
38
How does stress affect clotting?
^ 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
Define hypertension
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
Outline the stages of formation of plaque formation
(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
What are the consequences of atheroscelorosis?
v blood flow -> myocardial ischeamia | Plaque debris and blood clots may break off
42
Give a study demonstrating the effects of stress on atheroscleroisis in animals
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
How is stress associated with asthma?
- 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
How is stress linked to peptic ulcer disease?
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
How can PGs aid healing?
^blood flow
46
How are stress and depression linked?
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
What are the potential hypothesess for the biological cause of depression?
hyperactive HPA axis NT imbalance Cytokine hypotheses of depression - overall dysregulation of the stress response
48
What is evidence for the hyperactive HPA axis hypothesis?
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
What is the evidence for the NT imbalance hypothesis of major depression?
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
What is the evidence towards the cytokine hypothesis of depression?
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
What are the main factors affecting th stress resonse?
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

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