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PHYL2067 > Module 2: Endocrinology > Flashcards

Module 2: Endocrinology Flashcards

1
Q

Contents of Endocrine System

A

= All hormone secreting tissues including:

  • Brain
  • Hypothalamus
  • Pituitary gland
  • Pineal gland
  • Thyroid
  • Parathyroid
  • Adrenal gland
  • Gonads
  • Pancreas
  • Kidneys
  • Liver
  • Thymus
  • Parts of the intestines, heart and skin
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2
Q

Functions of the Endocrine System

A
  • Regulate metabolism, water and electrolyte balance
  • Allow body to cope with stress
  • Regulate growth
  • Control reproduction
  • Regulate circulation and red blood cell production
  • Control digestion and absorption of food
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3
Q

Hydrophilic Hormones: Peptides and Catecholamines

A
  • Most transported in blood dissolved in plasma (some also carried on binding protein)
  • Can’t pass through cell membrane, therefore bind to specific receptors on surface of target cell
  • Elicit response either by changing cell permeability (few) or by activating second messenger system to alter activity of intracellular proteins (most)
  • Vulnerable to metabolic inactivation; so short-term effects
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4
Q

Lipophilic Hormones: Thyroid Hormones and Steroids

A
  • Transported in blood mostly bound to plasma proteins. Small, unbound amount dissolved > only dissolved portion physiologically active
  • Free hormone (unbound) easily passes through cell membrane, binds to specific receptor within target cell (mostly in cell nucleus)
  • Elicit response by activating specific genes within target cell to cause formation of new intracellular proteins
  • Less vulnerable to metabolic inactivation so effects last longer
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5
Q

Catecholamines

a) Solubility
b) Structure
c) Synthesis
d) Storage
e) Secretion
f) Transport in blood
g) Receptor site
h) Mechanism of Action
i) Hormones of this type

A

a) Solubility = hydrophilic
b) Structure = tyrosine derivative
c) Synthesis = in cytosol
d) Storage = in secretory granules
e) Secretion = exocytosis of granules
f) Transport in blood = half bound to plasma proteins
g) Receptor site = surface target cell
h) Mechanism of action = activation of second messenger pathway to alter activity of pre-existing proteins that produce the effect
i) Hormones of this type = hormones from the adrenal medulla, dopamine from hypothalamus

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6
Q

Thyroid Hormones

a) Solubility
b) Structure
c) Synthesis
d) Storage
e) Secretion
f) Transport in blood
g) Receptor site
h) Mechanism of Action
i) Hormones of this type

A

a) Solubility = lipophilic
b) Structure = iodinated tyrosine derivative
c) Synthesis = in colloid within thyroid gland
d) Storage = in colloid
e) Secretion = endocytosis of colloid
f) Transport in blood = mostly bound to plasma proteins
g) Receptor site = inside target cell
h) Mechanism of action = activation of specific genes to make new proteins that produce the effect
i) Hormones of this type = only hormones from the follicular cells of the thyroid

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7
Q

Steroids

a) Solubility
b) Structure
c) Synthesis
d) Storage
e) Secretion
f) Transport in blood
g) Receptor site
h) Mechanism of Action
i) Hormones of this type

A

a) Solubility = lipophilic
b) Structure = cholesterol derivative
c) Synthesis = stepwise modification of cholesterol molecule in various intracellular compartments
d) Storage = not stored; cholesterol precursor stored in lipid droplets
e) Secretion = simple diffusion
f) Transport in blood = mostly bound to plasma proteins
g) Receptor site = inside target cell
h) Mechanism of action = activation of specific genes to make new proteins that produce the effect
i) Hormones of this type = hormones from the adrenal cortex, gonads and some placental hormones

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8
Q

Central Regulation

A
  • Controlled by the brain
  • Affected by negative feedback loops, neuroendocrine reflexes, rhythms (i.e. diurnal)
  • Can be fast, slow or long-term responses
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9
Q

Direct Regulation

A
  • Endocrine cells respond directly to changes in extracellular fluid (especially plasma) levels of substances (e.g. glucose, calcium)
  • Very rapid response to critical needs
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10
Q

Target Cell Responsiveness

A
  • Amplification of hormones effects via second messenger cascade
  • Variations in receptor expression on target cell > a cell must have functional receptors specific for the hormone to be able to respond
  • Number and type of cell receptors can vary by down-regulation or up-regulation
  • Permissiveness, synergism and antagonism
  • Presence or absence of one hormone can influence effects of another through receptor regulation, activation or inactivation
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11
Q

Hormones of Anterior Pituitary Gland

A
  • Thyroid Stimulating Hormone (TSH)
  • Adrenocorticotrophic Hormone (ACTH)
  • Growth Hormone (GH)
  • Prolactin
  • Luteinising Hormone (LH)
  • Follicle Stimulating Hormone (FSH)
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12
Q

Two Groups of Action of Anterior Pituitary Hormone

A
  1. “Trophic” hormones control activity of another endocrine gland
    = ACTH, TSH, LH, FSH
  2. Hormones which have a direct effect in their own right
    = Prolactin and GH
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13
Q

“Stalk Section”: Hypothalamo - Pituitary Disconnection

A
  • Prolactin under inhibitory control: needs to be suppressed due to lots being made (will increase if stalk section)
  • All other hormones are under stimulatory control: not readily made and thus need to be stimulated to be released
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14
Q

Function of Thyroid

A
  • Thyroid gland lies over the trachea in the neck
  • Contains follicles, comprised of follicular cells and colloid, that produce the thyroid hormones (TH) T3 and T4 from tyrosine and iodine
  • TH are amines, lipophilic, are transported in plasma bound to carrier proteins, with a balance between bound and free hormone
  • Most TH secreted as T4 which is converted to T3 in tissues > T3 in four times more potent
  • Virtually every tissue in the body is affected by TH
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15
Q

Thyroid Hormone (TH)

A
  • TH is created and stored within the colloid and released when it is needed
  • TH increases basal metabolic rate by increasing fuel metabolism and therefore also increases heat production
  • TH has sympathomimetic effects (increases action of catecholamines) and is permissive for growth
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16
Q

Metabolism

A
  • Refers to all the chemical reactions occurring in the body
  • Includes “external work” (energy used by skeletal muscle to move) and “internal work” (energy used to sustain life)
  • Rate of energy expenditure referred to as metabolic rate (kJ/hr)
  • Two components of metabolic rate:
    1. Energy used at rest: Basal Metabolic Rate (BMR)
    2. Additional energy used for activities
  • BMR determined primarily by thyroid hormones
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17
Q

Hypothyroidism

A
  • Can be primary: thyroid gland failure
  • Or secondary: deficiency of TRH or TSH or inadequate supply of iodine
  • Symptoms: decreased metabolism, poor cold tolerance, excessive weight gain, fatigue, bradycardia, weak pulse, slow reflexes and mental function, slow or slurred speech
  • In adults: myxoedema (puffy especially in face)
  • In neonates: cretinism and dwarfism irreversible unless treated from birth
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18
Q

Hyperthyroidism

A
  • Most common cause is Grave’s Disease
  • Autoimmune production of thyroid-stimulating immunoglobulin (TSI) which activates TSH-R inducing TH release
  • Can also be caused by excess TRH, TSH or TH production (usually from tumour)
  • Symptoms: increased metabolism, excessive sweating, increased appetite but weight loss, muscle weakness, anxiety, palpitations, goitre
  • Grave’s Disease may also result in bulging eyes
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19
Q

Absorptive State

A
  • After a meal: absorption of nutrients from diet

- Excess nutrients are stored in the body

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20
Q

Post-absorptive State

A
  • Between meals

- Stored energy is mobilised for use

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21
Q

Glucose Storage

A
  • Glucose is stored in the liver and skeletal muscle as glycogen (long chains and branches of glucose molecules)
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22
Q

Blood Glucose Control

A
  • Blood glucose levels are maintained between 70-110 mg/100ml of plasma
  • Most tissues can also generate ATP from fats (adipose tissue)
  • During starvation, we can break down proteins (muscle) to make ATP, but, the brain can only get ATP from glucose so blood glucose levels must be maintained
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23
Q

Insulin Effects

A
  • Insulin favours glucose uptake and storage
  • Facilitates glucose transport from blood into body cells (especially skeletal muscle and adipose tissue)
  • Stimulates glycogenesis in liver and skeletal muscle
  • Inhibits glycogendolysis and gluconeogenesis
  • Promotes storage of fats in adipose tissues
  • Stimulates protein synthesis in body cell
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24
Q

Insulin Glucose Uptake

A
  • Insulin binds to a receptor on the surface of the target cell (skeletal muscle, adipose tissue and most other cells of the body)
  • Makes glucose transport molecule (GLUT4) available in cell membrane
  • GLUT4 transports glucose into the cells
  • Some cells do not require insulin for uptake:
  • Neurons, red blood cells, blood vessels, kidney, lens of eye, liver
  • Insulin independent tissues
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25
Q

Glucagon Effects

A
  • Glucagon favours the release of glucose into the blood
  • Breakdown of stored fats
  • Breakdown of proteins in the liver
  • Insulin and glucagon have opposite effects on blood glucose
  • Insulin = released during absorptive state when blood glucose is increased
  • Glucagon = released during post absorptive state when blood glucose is decreased
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26
Q

Hyperglycaemia Process

A

= High blood glucose

  1. Stimulus increases blood glucose levels
  2. Pancreas releases insulin
  3. Insulin stimulates glycogen formation
  4. Insulin stimulates glucose uptake from cells
  5. Blood glucose falls to normal range (90 mg/100ml)
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27
Q

Hypoglycaemia Process

A

= Low blood glucose

  1. Stimulus decreases blood glucose levels
  2. Pancreas releases glucagon
  3. Glucagon stimulates glycogen breakdown
  4. Blood glucose rises to normal range (90 mg/100ml)
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28
Q

Diabetes Mellitus

A

= Impaired ability to utilise blood glucose, characterised by hyperglycaemia

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29
Q

Type 1 Diabetes

A
  • Old Classification: Insulin dependent diabetes mellitus (IDDM), juvenile onset
  • 10-15% of diabetes cases
  • Peak age of onset = <20 years
  • Pathophysiology = autoimmune destruction of beta-cells; inability to produce insulin
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30
Q

Type 2 Diabetes

A
  • Old Classification: Non-insulin dependent diabetes mellitus (NIDDM), adult onset
  • 85-90% of diabetes cases
  • Age of onset = over 35-40
  • Causes: genetics, environmental factors (obesity, poor diet, lack of exercise)
  • Often associated with hypertension and hyperlipidaemia
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31
Q

Three Metabolic Abnormalities of Type 2 Diabetes

A
  1. Insulin Resistance
    - Insulin is produced but insulin receptors are unresponsive or insufficient in number
    - Body compensates by increasing insulin production
  2. Decreased Production of Insulin
    - Beta cells become fatigued
    - Hyperglycaemia
  3. Inappropriate Glucose Production
    - Liver releases glucose when not needed
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32
Q

Diabetes Treatment

A

Type 1 = insulin injections; dietary management; exercise

Type 2 = dietary control and weight reduction; exercise; oral hypoglycaemic drugs

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33
Q

Three Diabetes Diagnosis Methods

A
  1. Fasting plasma glucose = >/= 7 mmol/L
  2. Random plasma glucose = >/= 11.1 mmol/L
  3. Two-hour oral glucose tolerance test (OGTT)
    = plasma glucose >/= 11.1 mmol/L
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34
Q

Acute Consequences of Diabetes

A
  • Glycosuria = glucose in the urine
  • Polyuria = excessive urination
  • Polydipsia = excessive thirst
  • Polyphagia = excessive hunger
  • Weight loss
  • Fatigue
  • Diabetic acidosis = if untreated: coma and death
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35
Q

Chronic Complications of Diabetes

A
  • Chronic complications which are associated with hyperglycaemia > these complication can be prevented/slowed by controlling blood glucose levels
  • Damage to blood vessels:
  • Hyperglycaemia causes endothelial cells of blood vessels take in glucose and form glycoproteins by glycosylation (advanced glycation end products - AGEs)
  • These damage the basement membrane leading to microvascular and macrovascular disease
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36
Q

Obesity

A

= Condition of excessive adipose tissue that prevents a risk to health

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37
Q

Causes of Obesity

A
  • Obesity occurs from positive energy balance: energy from food intake is greater than energy expenditure
  • Reasons for this imbalance are complex
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38
Q

Adipose Cells

A

Increase weight
- Cell size increases (hypertrophy)

Increase weight substantially

  • Cell size increases
  • Cell number increases (hyperplasia)

Lose Weight

  • Cell size decreases
  • Cell number remains
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39
Q

Adipokines: Leptin

A

= Suppresses appetite; dominant long-term regulator of energy balance and body weight

  • Increase adipose tissue causes increase leptin production, which causes decreased appetite
40
Q

Adipokines: Adiponectin

A

= Increases sensitivity to insulin; decreases body weight by increasing energy expenditure. Suppressed in obesity

41
Q

Adipokines: Resistin

A

= Leads to insulin resistance. Released in obesity

42
Q

Short and Long Term Food Intake Control by Hypothalamus

A

Short - Term Control
= controls meals size and frequency

Long - Term Control
= controls satiety and hunger in the long term
- Insulin and leptin act on the hypothalamus to suppress long-term food intake
*Inhibits the appetite stimulant neuropeptide Y (NPY)
*Stimulates the appetite suppressants melanocortins

43
Q

Body Mass Index (BMI)

A
  • Index of weight - for - height measurements
  • Classify healthy, overweight and obesity weights
  • An estimate of body fat

BMI = weight (kg) / height^2 (m^2)

44
Q

Limitations of BMI

A
  • BMI does not distinguish between lean mass and fat mass
  • Overestimates body fat if:
  • body builder
  • broad frame
  • pregnant
  • Underestimates body fat if:
  • elderly
  • muscle wasting
45
Q

Waist Circumference

A
  • Indication of location of body fat
  • May be better indication of health risk than BMI
  • Abdominal fat is higher risk than fat around hips and buttocks
  • Men: greater than 94cm = risk
  • Women: greater than 80cm = risk
46
Q

Android Obesity

A
  • Apple shaped
  • Visceral/abdominal fat
  • Higher risk of obesity-related complications
47
Q

Gynoid Obesity

A
  • Pear shaped
  • Hips and buttocks
  • Lower risk of obesity related complications
48
Q

Prevention and Treatment of Obesity

A

Prevention

  • Increases energy expenditure (exercise)
  • Decrease energy intake

Treatment
- Gastric bypass surgery

49
Q

Growth

A
  • Increased length of long bone (causes an increase in height) and increased size and number of cells in soft tissue
  • Two stages of birth:
    1. Postnatal growth spurt = approx. 20% of total growth and occurs at approx. 1 years of age
    2. Pubertal growth spurt = approx. 70-80% of total growth and occurs at approx. 14-15 years of age
50
Q

Factors that Influence Growth

A
  1. Hormone Levels
    - Primarily controlled by growth hormone
    - Other hormones (e.g. sex hormones during puberty)
  2. Genetics
    - Max height determined by genetics; however, reaching this predetermined height is reliant on environmental factors
  3. Diet
    - Malnourishment stunts growth - may be irreversible
  4. Stress
    - Prolonged secretion cortisol stunts growth
51
Q

Growth Hormone (GH)

A
  • Secreted by anterior pituitary
  • Controlled by hormones from the hypothalamus:
  • Stimulated by growth hormone releasing hormone (GHRH)
  • Inhibited by growth hormone inhibiting hormone (GHIH)
  • Has both metabolic and growth effects
  • Growth effects mediated by insulin like growth factors (IGFs)
  • Growth hormone release is diurnal; higher during deep sleep
  • Growth hormone release also influenced by factors aimed to conserve glucose reserves
  • Exercise, stress, decrease blood glucose
52
Q

Metabolic Effects of Growth Hormone

A
  • Acts on adipose tissue, skeletal muscle and liver to conserve glucose for the brain
  • Lipid metabolism:
  • Breaks down storage gats and releases it into blood
  • Fuel for muscles
  • Increases blood glucose:
  • Increases glucose output from the liver
  • Decreases glucose uptake in skeletal muscle
53
Q

Too Little Growth Hormone

A
  • Children: Dwarfism
  • Pituitary/hypothalamic defect
  • Abnormal growth hormone (Laron dwarfism)
  • Delayed growth
  • Treatment: growth hormone drugs
54
Q

Too Much Growth Hormone

A
  • Children: Gigantism
  • Excessive growth of long bones
  • Adults: Acromegaly
  • Acro = extremity; mealy = large
  • Thickening of bones
  • Growth of soft tissue (skin and connective tissue)
55
Q

Mechanical Bone Function

A
  • Support
  • Protection
  • Muscle Attachment
  • Facilitate Movement
56
Q

Metabolic Bone Function

A
  • Mineral Storage
  • Calcium Homeostasis
  • Haemotopoiesis
57
Q

Bone Structure

A
  • Composition
  • Cells (2% of mass)
  • Organic osteoid (collagen fibres and other proteins)
  • Inorganic mineral salts
  • High vascularity
  • Types:
  • Trabecular bone tissue: spongy bone
  • Cortical bone tissue: compact bone
58
Q

Chemical Composition of Bone Tissue

A

Mineral 65-70%

  • Inorganic phase
  • Hardness

Matrix (Osteoid) 30-35%

  • Organic phase
  • Collagenous fibres (95%), non-collagenous proteins
  • Flexibility
59
Q

Bone Growth

A
  • Long bones grow at the epiphyseal plate
  • The epiphyseal plate closes during late adolescence (sex hormone dependent)
  • Cartilage of epiphyseal plate increases in length
  • Cartilage calcifies (hardens) and is replaced by bone
60
Q

Osteoblasts

A

= Bone building Cells

  • Produce and secrete osteoid (organic component of bone)
  • Do not calcify/mineralise bone
61
Q

Osteoclasts

A

= Bone resorbing Cells

- Degrade bone matrix to release calcium into blood

62
Q

Osteocytes

A

= Mechanical Sensors in bone

  • Detect changes in mechanical environments to initiate changes in bone matrix
  • Mature osteoblasts
63
Q

Why? Bone Remodelling

A
  • Maintain mineral ion homeostasis (source of calcium ions)
  • Adapt shape and structural organisation to alteration in biomechanics force
  • Maintain structural integrity of skeleton (repair micro damage)
64
Q

How? Bone Remodelling

A
  • Maintaining bone mass requires a balance between osteoclast and osteoblast activity
  • Regulated by the release of chemical messengers by osteoblasts (RANKL and OPG)
65
Q

Hormonal Control of Bone Remodelling

A
  • Parathyroid hormone (PTH)
  • Vitamin D; sources = skin, diet
  • Calcitonin; produced by C-cells in thyroid gland, minor role
  • Stimulus is change in blood calcium
66
Q

Parathyroid Hormone (PTH)

A
  • Secreted when blood calcium drops
  • PTH increases blood calcium by taking it out of bone storage
  • Fast Exchange = immediate calcium ion regulation
  • Slow Exchange = response to chronic hypocalcaemia. Breaks down bone
67
Q

Fast Exchange of Calcium Ions

A
  • Earliest effect of PTH
  • Activates calcium transport carriers in plasma membrane of osteocytes and osteoblasts
  • Transports calcium from bond fluid into cells and then into blood (central canal)
68
Q

Slow Exchange of Calcium Ions

A
  • Prolonged decrease in blood calcium
  • PTH inhibits osteoblasts and causes them to secrete RANKL which stimulates osteoclasts
  • Increases bone resorption
  • Releases calcium and phosphate into blood
69
Q

Osteoporosis

A
  • Reduction in the mass (density) of bone and impairment of spongy bone integrity
  • Weaker bone = prone to fracture
  • Progression from osteopenia to osteoporosis
70
Q

Risk factors of Osteoporosis

A
  • Poor nutrition (particularly calcium)
  • Sedentary lifestyle
  • Low oestrogen levels (menopause)
  • Low testosterone levels
  • Smoking, excessive alcohol and caffeine intake
  • Absence of adequate sunlight exposure (vitamin D deficiency)
  • Corticosteroid use
  • Aortic calcifications
71
Q

Prevention of Osteoporosis

A
  • Increase peak bone mass (good nutrition and weight bearing exercise)
  • Maintain high dietary calcium and adequate vitamin D levels (exposure to UV)
  • Maintain exercise in older age
72
Q

Stress

A
  • In physiology, stress = the physiological responses of the body to stressful stimuli (stressors)
  • May be short - lived “acute” response to a single traumatic event, or can become “chronic” if stressful situation persists or is prolonged
73
Q

Psychological Stressors

A

= Stimuli which lead to fear, anxiety or frustration

  • Includes traumatic events such as death, divorce, conflict, abuse, war and natural disasters
  • Can also include excitement, nervousness
  • Stimuli can be real or imagined
74
Q

Physical Stressors

A

= Stimuli which disrupt normal body function, can be due to internal factors or external environment

  • Hypoxia, hypoglycaemia, infection, physical strain, injury, starvation, dehydration
  • Exposure to heat or cold
75
Q

Acute Stress

A
  • Acute stress response is a normal and beneficial adaptive response
  • Increases alertness and focus, provides energy to respond and cope with stressful situation
  • The extent of the response is dependent on severity of stressor and on the individual
  • Mild stress improves mood, creates new memories, encourages creative thinking, promotes neural growth in brain, facilitates problem solving
  • Severe stress can cause detachment, reduction in awareness, derealisation, depersonalisation, dissociative amnesia
76
Q

Chronic Stress

A
  • When stress is prolonged or persistent, homeostasis is unable to be maintained
  • The body enters an exhausted state, when damage to health can occur, immune suppression, hypertension, gastrointestinal disturbances
  • Can have detrimental psychological effects > anxiety, mental dysfunction, social withdrawal
77
Q

General Adaptation Syndrome

A

= Describes the stages of your bodies response to stress, three phases:

  1. ALARM
    = preparing for fight or flight, heightened alertness, energy mobilised
  2. RESISTANCE
    = stay alter, but keep on with normal functioning (adaptation), homeostasis maintained
  3. EXHAUSTION
    = resources are depleted, burnout sets in, homeostasis cannot be maintained so function is impaired, long term damage occurs
78
Q

Acute Stress Response

A

= The acute response is to ready the body for action:

  • Increased cardiovascular function = heart rate, contractility, mostly vasoconstriction with vasodilation to muscles
  • Increased respiratory function = RR, TV, bronchodilation
  • Liberation of nutrients = increased bloody glucose and fatty acids
  • Skin = paling or flushing, sweating, piloerection
  • Sensory = pupil dilation, auditory exclusion, tunnel vision
  • Muscle tension and shaking
  • Inhibition of gastrointestinal motility, contraction of sphincters
  • Inhibition of the lacrimal gland and salivation
  • Relaxation of bladder, inhibition of erection
79
Q

Sympathetic Nervous System and Stress Response

A
  • Adrenaline from adrenal medulla
  • Noradrenaline from neurones
  • Inhibition of parasympathetic nervous system
80
Q

Endocrine System and Stress Response

A
  • Cortisol and corticosteroids from adrenal cortex
  • Vasopressin (anti-diuretic hormone) from posterior pituitary
  • Activation of Renin-Angiotensin-Aldosterone System (RAAS); involves liver, kidneys, lungs and adrenal cortex
  • Insulin and glucagon from pancreas
81
Q

Adrenal Cortex

A
  • Mineralocorticoids: Aldosterone
  • Produced in response to changes in ECF volume/blood pressure and stress
  • Promoters water retention in kidneys by increasing sodium reabsorption
  • Androgens: DHEA and Androstenedione
  • Produced in both males and females, but in small quantities
82
Q

Glucocorticoids

A
  • e.g. Cortisol and corticosterone
  • Produced in response to stress
  • Actions:
  • Allows body to cope with stress by increasing availability of energy and amino acids
  • Increases vascular reactivity
  • Affects mood and behaviour - improving mood, increases alertness
  • Stimulates brain function - promotes neural growth in brain which improves memory, creative thinking and problem solving ability
  • In chronic stress, may be responsive for immune suppression and other health defects
83
Q

Adrenal Medulla

A
  • Adrenal Medulla is part of the sympathetic nervous system:
  • Medullary “chromaffin” cells are modified post-ganglionic neurones
  • Produce the catecholamines adrenaline and noradrenaline in response to direct stimulation by sympathetic pre-ganglionic neurones from the splanchnic nerve
  • Hormones are released directly into the bloodstream and act on distant target tissues including heart, blood vessels, bronchioles, GIT
84
Q

Adrenaline and Noradrenaline

A
  • Elicits acute physical reactions of body to prepare for fight or flight
  • Increases cardiac and respiratory function, slows digestion/kidney function, tenses muscles, increases sweating
  • Vasoconstriction to skin and organs (including kidneys), vasodilation to skeletal muscles
  • Inhibits parasympathetic nervous system
  • Act on pancreas to reduce insulin secretion, increase glucagon secretion to increase blood glucose
85
Q

RAAS/ Vasopressin

A

Maintain blood volume and blood pressure

86
Q

Responses to Chronic Stress

A

Chronic Stress can cause:

  • Immune suppression through excess glucocorticoid production, increasing risk of infection
  • Hypertension and sodium and water retention - through excess glucocorticoid exposure, activation of RAAS and vasopressin
  • Disruption of body weight - weight loss or obesity, redistribution of body fat
  • Poor growth in children through suppression of growth hormone production
  • Inhibition of parasympathetic nervous system can result in reproductive failure, poor digestion
  • Psychological disorders such as anxiety, depression, social withdrawal, substance abuse
87
Q

Effects of Chronic Stress on Immune System

A
  • Chronic stress worsens diseases which are inflammatory in origin
  • Increased allergic response can worsen conditions such as eczema and asthma
  • Immune suppression through decreased lymphocyte and natural killer cell function > increased risk of cancer and infection
  • Increased antibody response but less new antibodies made, so autoimmune diseases worsened but increased risk of new infections
88
Q

Effects of Chronic Stress on Cardiovascular System

A
  • Hypertension a possible result of chronic stress

- Atherosclerosis and coronary artery disease as a result of chronic stress

89
Q

Hippocampus

A
  • Chronic stress causes continued excitation of neurones via high glucocorticoid levels
  • Leads to dendrite atrophy, spine loss and reduction in cell number
  • Hippocampus becomes reduced in volume
  • Impairment in explicit/spatial memory
  • Impaired regulation of endocrine response to stress
  • Effects are reversible if stress desists
90
Q

Pre-Frontal Cortex (PFC)

A
  • Chronic stress leads to decreases in dendrite length, branding and spine density in PFC
  • Disrupts the plastic relationship between the PFC and the hippocampus (loss of flexible memory consolidation)
  • PFC becomes reduced in volume
  • Impairment in working memory
  • Effects are reversible if stress desists
91
Q

Amygdala

A
  • Chronic stress causes hyperactivity of the amygdala
  • Hypertrophy of neuronal cells with increased dendritic branching
  • Amygdala becomes increased in volume
  • Leads to exaggerated responses to stress
  • Increased fear and anxiety, altered recall of emotional memories
  • Effects are persistent even if stress desists
92
Q

Chronic Stress and Psychiatric Illness

A
  • Loss of explicit memory and depression via hippocampus
  • Increased emotional memory, response and anxiety via amygdala
  • Loss of working memory via prefrontal cortex
93
Q

Acute Stress Disorder (ASD)

A
  • Occurs after 2 days and within 4 weeks of original stressful event
  • Dissociation, re-living of event (nightmares), hyperarousal (including panic attacks), avoidance of reminders, impaired social functioning
94
Q

Post Traumatic Stress Disorder (PTSD)

A
  • Occurs after 4 weeks of original stressful event

- as for ASD

95
Q

Risk Factors for Developing ASD/PTSD

A
  • Exposure to severe life threatening trauma
  • Their responses involved intense fear, feelings of helplessness or horror
  • Lack of social supports and other stressful life events
  • A past history of trauma and/or previous psychiatric disorder

PHYL2067 (5 decks)

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