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VAP III > Endocrine 3: Adrenal glands, HPA axis, and stress response > Flashcards

Endocrine 3: Adrenal glands, HPA axis, and stress response Flashcards

1
Q

Where are the adrenal glands located?

A
  • Cranial and/or medial to kidneys
  • Morphology/position varies greatly by species usually applied to or closely associated with upper pole of each kidney
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2
Q

What two components is the adrenal gland a composite of?

A
  1. Adrenal cortex
  2. Adrenal medulla
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3
Q

From what tissue type is the adrenal cortex embryollogically derived?

A
  • Intermediate mesoderm
    • Forms towards end of embryonic period
    • Similar embryological origin to gonads
    • Secretes steroid hormones
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4
Q

From what tissue type is the adrenal medulla embryollogically derived?

A
  • Neural crest ectoderm
    • Shares similar origin to sympathetic nervous system
    • Secretes catecholamines
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5
Q

What are the structures labelled (C), (M), and (V) in this histological image of the adrenal gland?

A
  • C = cortex
  • M = medulla
  • V = vein
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6
Q

What are the three zones of the adrenal cortex designated G, F, & R in this histological image?

A
  1. G = zona glomerulosa
  2. F = zona fasciculata
  3. R = zona reticularis
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7
Q

What systems control (1) the adrenal cortex, and (2) the adrenal medulla?

A
  1. Cortex controlled by hypophysis (i.e. pituitary)
  2. Medulla controlled by sympathetic nervous system
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8
Q

What is secreted by cells in the zona glomerulosa of the adrenal cortex?

A

Mineralocorticoid hormones

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9
Q

What is secreted by cells in the zona fasciculata of the adrenal cortex?

A

Glucocorticoid hormones

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10
Q

What is secreted by cells in the zona reticularis of the adrenal cortex?

A

Androgens

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11
Q

What is secreted by cells in the adrenal medulla? What does this tissue look like under H&E stain?

A

Catecholamines (under control of sympathetic NS)

  • Adrenaline (epinephrine)
  • Noradrenaline norepinephrine

There are no distinct histological regions under H&E, just clusters of cells with granular, faintly basophilic cytoplasm and numerous capillaries with larger venous channels (V) draining blood from cortex pass through medulla

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12
Q

What is the term for secretory adrenal medulla cells? What colour do they stain histologically?

A
  • chromaffin cells
  • Colour brown under differential staining - stored catecholamine granules visible
  • Noradrenaline (Na) cells stain more strongly than adrenaline (A) secreting cells
  • cells are homologous to a sympathetic ganglion except no axons
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13
Q

What neurotransmitter released from preganglionic sympathetic neurons stimulates
both synthesis & release of catecholamines from medullary chromaffin cells?

A

Acetycholine (ACh)

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14
Q

Amine hormones (like catecholamines epinephrine & norepinephrine) are synthosised from what precursor?

A

Tyrosine

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15
Q

What are the primary effects of catecholamines (produced by adrenal medulla)?

A
  • Metabolism, especially blood glucose levels
    • e.g. glucose mobilisation from hepatic glycogen stores
  • Effects on other tissues variable depends on receptor types expressed. E.g.
    • Glycogenolysis in skeletal muscle
    • Lipolysis in adipose tissue
    • Increased heart rate & force of contraction
    • Vasodilation in skeletal & cardiac muscle blood vessels
    • Increased sweating
    • Piloerection
    • Excitation of CNS/increased alertness
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16
Q

What are the main factors/physiological conditions that stimulate catecholamine secretion?

A
  • Hypoglycaemia
  • Conditions producing acute stress
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17
Q

What are the two major groups of adrenergic receptors?

A

α (alpha) and β (beta) adrenergic receptors

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18
Q

What are the most common locations and mechanisms of α-adrenergic receptors?

A
  • Most common in target cells for sympathetic neurons (i.e. catecholamines released by adrenals into circulation reinforces sympathetic activity)
  • Responses coupled to G-proteins
  • Activation increases [Ca 2+] in target cells & stimulates activity
  • Common in arteriole & digestive sphincter smooth muscle = increased vascular resistance (vasoconstriction) & slowing of digesta passage
  • Approximately the same affinity for epinephrine & norepinephrine
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19
Q

What does stimulation of β-adrenergic receptors lead to and what are the two types?

A
  • Stimulation leads to activation of membrane bound adenylyl cyclase → increased [cAMP] in cytosol
  • β1 and β2 receptors
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20
Q

Where are β1 adrenergic receptors found and what are the major effects of their stimulation?

A
  • almost exclusively found in cardiac muscle
  • approximately equal affinity to epinephrine/norepinephrine
  • increase heart rate & stroke volume
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21
Q

Where are β2 adrenergic receptors found and what are the major effects of their stimulation?

A
  • found in arterioles of skeletal & cardiac muscles, smooth muscle in bronchioles, pancreas, & liver
  • much higher affinity for epinephrine
  • vasodilation in arterioles, dilation of airways, hyperglycaemia
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22
Q

What characterises secretory cells in the adrenal cortex?

A

Cells contain abundant lipid droplets, mitochondria & smooth endoplasmic reticulum → well equipped for steroid hormone synthesis

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23
Q

What hormones are secreted by cells in the zona glomerulosa of the adrenal cortex? How are these synthesised and what are their effects?

A
  • secretes mineracorticoids e.g. aldosterone
  • Synthesised from cholesterol (via pregnenolone)
  • Stimulates Na+ retention & K+ excretion in the kidney
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24
Q

What hormones are secreted by cells in the zona reticularis of the adrenal cortex?

A

Sex hormones - precursor androgens including dehydroepiandrosterone (DHEA) and androstenedione from cholesterol

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25
Q

What hormones are secreted by cells in the zona fasciculata of the adrenal cortex? How are these synthesised and transported?

A
  • secretes glucocorticoids e.g. cortisol , corticosterone , cortisone
  • Synthesised from cholesterol
  • Depend on binding to transport proteins e.g. corticosteroid-binding globulin (aka transcortin)
  • Cortisol transport: 75% bound to transcortin, 15% to albumin, 10% free
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26
Q

What are glucocorticoids?*

*memory aid

A

Glucocorticoids
promote an increase in blood glucose and are steroid hormones
secreted by the adrenal cortex in response to stress

27
Q

How does the hypothalamic-pituitary-adrenal axis (HPA axis)
demonstrate integrated neural & hormonal modulation of endocrine control (three steps)?

A
  1. During stress, neural activity causes a rapid increase in hypothalamic secretion of
    corticotropin releasing hormone (CRH)
  2. Hypothalamo-hypophysial portal system carries CRH directly to the anterior pituitary
    → stimulates adrenocorticotropic hormone (ACTH) secretion
  3. ACTH stimulates glucocorticoid secretion by the adrenal cortex → influence several
    physiological processes

ANY STAGE in this control pathway can be modulated usually negative feedback (i.e. high circulating levels of a hormone suppress its secretion)

28
Q

HPA control

STUDY DIAGRAM

A

HPA control

STUDY DIAGRAM

29
Q

How does anti-diuretic hormone (ADH) play a synergistic role in thhe HPA axis?

A
  • synergistic (i.e. amplifies the effect of another hormone)
  • Some ADH-secreting neurons extend their axons to capillaries in the median eminence rather than the posterior pituitary
  • ADH alone has little effect on ACTH-secreting cells
  • ADH + CRH = much greater secretion of ACTH than with CRH alone
30
Q

What is permissiveness in the context of hormonal control systems?

A
  • presence of one hormone required for another to exert its effect(s)
  • e.g. cortisol permits epinephrine/norepinephrine to cause systemic vasoconstriction → important to maintain blood pressure during haemorrhage
    • “Adrenal insufficiency” sufferers much more likely to die from haemorrhage
    • Addison disease (hypoadrenocorticism; “adrenal insufficiency”), a deficiency in adrenocortical hormones, is seen most commonly in young to middle-aged dogs and occasionally in horses
    • Basal levels of glucocorticoids necessary to maintain blood glucose homeostasis
31
Q

How are insulin & glucagon an antagonistic hormone pair?

A
  • i.e actions oppose each other
  • Glucagon secretion ( α-cells in pancreatic islets) is increased & insulin secretion ( β-cells) is
    decreased during stress
  • Glucagon stimulates release of glucose & fatty acids into blood
  • Synergistic effects of epinephrine & glucagon maintain high blood glucose levels during stress
32
Q

What is stress?

A
  • a physiological state in which homeostasis or safety is threatened or perceived to be threatened
    • → Activation of sympathetic nervous system/adrenal medulla (catecholamines) & adrenal cortex (glucocorticoids)
33
Q

What is a stressor?

A
  • any factor (environmental, pathological, psychological) that has the potential to disrupt homeostasis, e.g.
    • physical injury/haemorrhage
    • cold/heat
    • dehydration
    • prolonged exercise
    • pain
    • psychological strain
    • predation/aggression
34
Q

How does the stress response allows an animal to respond immediately in a generalised way to a threatening situation to improve survival?

A

Ensures survival by:

  • Increasing heart & respiration rates
  • Sharpening cognition & alertness
  • Releasing stored energy
  • Directing oxygen & nutrients where needed (especially CNS)
  • Curtailing feeding, digestion & reproduction

When the stressor is removed, feedback mechanisms ensure that the stress response is turned off. Physiological responses that are adaptive in the short term can be damaging if physical or emotional stress persists in the long term.

35
Q

How do the autonomic nervous system & HPA axis coordinate the stress response to an acute stress like (for a mouse) being chased by a cat?

A
  1. Mouse sees cat & runs → sympathetic nervous system releases epinephrine & norepinephrine (sympathetic nerve terminals & adrenal medulla)
  2. Hypothalamic neurosecretory cells release CRH → anterior pituitary secretes ACTH
  3. CRH also acts as a neurotransmitter → further stimulates sympathetic nervous system
    (i. e. links sympathetic & adrenocortical branches of the stress response)
  4. CRH also modulates function in the hippocampus & amygdala → form memories of emotionally charged events
36
Q

Broadly, what occurs during Phase 1 of the stress response?

A
  • Immediate survival mechanisms come into play rapidly
    (<1)
  • Increased blood flow to skeletal muscle & heart muscle
  • Increased air flow into and out of lungs (& bronchiole airways increase in diameter = reduced resistance to air flow)
  • Metabolic fuel levels maintained in blood
  • Non essential functions curtailed (e.g. digestion)
37
Q

What hormones are involved during Phase 1 of the stress response and what effects do they have?

A
  • Epinephrine stimulates secretion of CRH → ACTH
  • ACTH also facilitates learning learning-probably contributes to recognition of & preparedness for similar future stressors
  • ACTH can be co co-secreted with β-endorphin (endogenous opiate) - may provide analgesia/decrease perception of of pain
    • Both come from the preprohormone POMC (proopiomelanocortin)
38
Q

What happens during phase 2 of the stress response?

A
  • HPA axis stimulates secretion of glucocorticoids by the adrenal cortex
  • These reinforce the actions of sympathetic stimulation and have additional metabolic effects that facilitate energy release to blood
  • & inhibit secretion of gonadotropin & thyrotropin
39
Q
A
40
Q

What happens to heart rate and ventilation during the stress response?

A

They increase

41
Q

What happens to pancreatic hormones during the stress response, and what effect does this have on blood glucose levels?

A

Glucagon increases, insulin decreases

This maintains adequate blood glucose levels as glucose is released from muscle and liver

42
Q

Fat [catabolism/anabolism] increases during the stress response, which leads to increased _________

A

Fat catabolism increases during the stress response free fatty acids and glycerol, which can be used as fuel by all tissues except the brain

43
Q

What are examples of active and passive stress responses?

A

Active - fight or flight

Passive - hiding - passive responses can develop into abnormal behaviour/stereotypies in captive animals

44
Q

How does a stress response cease/turn off?

A
  • Once an animal survives a stressor, the stress response must be turned off
  • Reduced sympathetic stimulation → reduced catecholamine release (adrenal medulla) & reduced heart rate, etc.
  • High circulating levels of glucocorticoids, ACTH & CRH inhibit CRH release by the hypothalamus → return to basal levels
45
Q

How do endocrine responses to severe blood loss maintain blood volume?

A

Endocrine responses to blood loss:

  • Increased vasopressin (ADH; posterior pituitary) → increased water reabsorption at kidney
  • Increased aldosterone (adrenal cortex) → increased Na+ reabsorption at kidney
    • This causes increased fluid retention, blood volume, and blood pressure
  • Catecholamines (epinephrine/norepinephrine) increase cardiac output & cause peripheral vasoconstriction to maintain blood pressure
  • remember cortisol is also important here = permissive effects on vasoconstriction
    • CRH + ADH = greater secretion of ACTH = more cortisol
46
Q

How does the HPA axis modulate the immune system early in the stress response?

A
  • Early in stress response, catecholamines & glucocorticoids (low concentrations) stimulate the immune system
    • prevents infection from injuries
    • inflammation
47
Q

How does the HPA axis modulate the immune system late in the stress response?

A
  • At higher concentrations (in later stage stress & recovery) high concentrations of glucocorticoids have anti-inflammatory effects
    • prevent damage to healthy tissues
    • speeds healing
48
Q

How do immune cells influence glucocorticoid secretion?

A

Immune cells stimulate recovery by influencing glucocorticoid secretion themselves (independent secretion of ACTH & cytokines stimulating release of CRH)

49
Q

What are the effects of cytokines secreted by cells of the immune system on glucocorticoids?

A

Cytokines are released in response to bacteria, viruses, tumour cells, etc - internal stressors → stimulates CRH secretion → glucocorticoids

  • Mobilisation of energy stores helps fight infection
  • Keep immune system from over-reacting (limits tissue damage from excessive inflammation)

Some immune cells release ACTH directly in the presence of pathogens → glucocorticoid secretion

50
Q

Why does chronic stress cause deleterious effects and what medical issues may result?

A
  • Acute stress is adaptive → allows animals to survive threatening situations, escape predators, etc.
  • Stress can be maladaptive when chronic
    • e.g. continuously constricted peripheral blood vessels & retention of sodium & water when no blood is lost may contribute to hypertension
    • e.g. chronically high glucocorticoids can cause muscle wasting, bone thinning, increased susceptibility to infections (suppressed immune function) & atrophy of neurons in the hippocampus (involved in forming memory)
    • e.g. chronic activation of the HPA axis suppresses reproductive function
    • Also emotional/behavioural issues may arise
51
Q

What is glucocorticoid deficiency also known as?

A

“adrenal insufficiency”

“Addison’s disease”

52
Q

What are the clinical signs and issues with glucocorticoid deficiency?

A
  • Amongst domestic species most common in dogs
  • Usually due to autoimmune destruction of cells in adrenal cortex (slow disease progression)
  • First manifests in humans as dizziness or fainting when standing (reduced ability to maintain BP)
  • Dogs: diminished appetite, weakness, depression, dehydration, prone to vomiting
  • Life-threatening: glucocorticoids assist in maintaining blood pressure, blood glucose homeostasis, dealing with stress, so:
    • Low blood glucose levels
    • Poor recovery from infection & surgery
    • Risk of haemorrhage
    • High ACTH levels (less negative feedback inhibition by plasma cortisol)
    • stimulates pigment secretion by melanocytes
    • Can also be low aldosterone secretion
53
Q

What is glucocorticoid overproduction also called?

A

Cushing’s Disease

54
Q

What are the clinical signs, causes, and issues with glucocorticoid overproduction?

A
  • Amongst domestic species common in dogs, can also occur in cats and horses
  • 85% of canine cases associated with excess production of ACTH by the pituitary → stimulates the adrenal cortex to increase cortisol production (& increased pigmentation) (Pituitary adenoma)
  • Remaining 15% of canine cases → cortisol-producing adrenocortical tumours (low ACTH levels due to negative feedback inhibition- no increased pigmentation)
  • Dogs: increased appetite, polyuria/polydipsia (PU/PD), hair loss, develop thin skin, gradual onset muscle weakness/wasting
  • Reproductive disturbances common (high levels of glucocorticoids suppress LH & FSH production), growth can be reduced (GH also suppressed)
  • Bilateral alopecia (hair loss) occurs in dogs
55
Q

What are some of the flow-on medical issues that can be caused by glucocorticoid overproduction?

A
  • Anti-insulin effects can lead to secondary diabetes mellitus in some patients
  • Anti-inflammatory/anti-immune effects increase risk of infections
  • Bone formation reduced- increased risk of osteoporotic fractures
  • ACTH production inhibited by high cortisol levels → adrenocortical cells become fewer & smaller
  • Similar symptoms from prolonged treatment with cortisol/similar drugs (i.e. iatrogenic Cushing’s-like syndrome)
  • Clinical signs in affected cats & horses similar to dogs
  • Excess hair growth (hirsutism) occurs in horses →
    excessive androgen production by zona reticularis
56
Q

In general, effects of glucocorticoids on carbohydrate, fat and protein metabolism are [opposite/similar to] those of insulin

A

In general, effects of glucocorticoids on carbohydrate, fat and protein metabolism are opposite those of insulin

57
Q

Cushing’s-like syndrome involves low/high plasma cortisol and low/high plasma ACTH. Provide a summary.

A

Cushing’s-like syndrome involves high plasma cortisol and low plasma ACTH.

Glucocorticoid over-production independent of ACTH

Adrenocortical tumours (adenoma or carcinoma)

Also caused by chronic high levels of exogenous glucocorticoids (iatrogenic)

58
Q

Tests on a dog returned high levels of plasma cortisol but low levels of plasma ACTH. The dog shows no increased pigmentation but shows increased appetite and polyuria/polydipsia (PU/PD).

What is a likely diagnosis and cause? What else could also cause these symptoms?

A

Cushings-like syndrome (glucocorticoid overproduction) caused by cortisol-producing adrenocortical tumour (low ACTH levels due to negative feedback inhibition - no increased pigmentation).

~15% canine cases of glucocorticoid overproduction have this etiology

Similar symptoms from prolonged treatment with cortisol/similar drugs (i.e. iatrogenic Cushing’s-like syndrome)

59
Q

Pituitary-dependent hyperadrenocortism (PDH; “Cushing’s disease”) involves low/high plasma cortisol and low/high plasma ACTH. Provide a summary.

A

Pituitary-dependent hyperadrenocortism (PDH; “Cushing’s disease”) involves high plasma cortisol and high plasma ACTH.

Glucocorticoid over-production stimulated by excess ACTH

Pituitary adenoma → eventual adrenocortical hyperplasia

Cutaneous pigmentation

60
Q

Tests on a dog returned high levels of plasma cortisol and high levels of plasma ACTH. The dog shows increased pigmentation, increased appetite and polyuria/polydipsia (PU/PD), bilateral alopecia, and has developed secondary diabetes mellitus.

What is a likely diagnosis and cause?

A

Pituitary-dependednt hyperadrenocorticism (PDH)“Cushing’s Disease” - glucocorticoid over-production stimulated by excess ACTH

Usually caused by pituitary adenoma

~85% of cases have this etiology

Anti-insulin effects can lead to secondary diabetes mellitus in some patients

61
Q

Primary hypoadrenocortism (“Addison’s disease”) involves low/high plasma cortisol and low/high plasma ACTH. Provide a summary.

A

Primary hypoadrenocortism involves low plasma cortisol and high plasma ACTH.

lack of glucocorticoid production → no negative feedback on ACTH production

Adrenal cortex failure (autoimmune destruction)

cutaneous hyperpigmentation & mineralcorticoid deficiency

62
Q

Tests on a dog returned low levels of plasma cortisol and high levels of plasma ACTH. The dog is also sluggish, with diminismed appetite, and shows hyperpigmentation.

What is a likely diagnosis and cause?

A

Primary hypoadrenocortism (‘adrenal insufficiency’) “Addison’s disease”

Usually due to autoimmune destruction of cells in adrenal cortex (slow disease progression) → glucogocricoid deficiency

High ACTH levels (less negative feedback inhibition by plasma cortisol) - stimulates pigment secretion by melanocytes

Can be life threatening, and amongst domestic species is most common in dogs

63
Q

Secondary hypoadrenocortism involves low/high plasma cortisol and low/high plasma ACTH. Provide a summary.

A

Secondary hypoadrenocortism involves low plasma cortisol and low plasma ACTH.

lack of adrenal stimulation by ACTH

pituitary or hypothalamic failure (tumours, trauma or inflammation, congenital)

no hyperpigmentation

64
Q

Tests on a dog returned low levels of plasma cortisol and low levels of plasma ACTH. The dog is also sluggish, with diminismed appetite, but shows no hyperpigmentation.

What is a likely diagnosis and cause?

A

Secondary hypoadrenocortism ‘adrenal insufficiency’ ⇒ lack of adrenal stimulation by ACTH

pituitary or hypothalamic failure (tumours, trauma or inflammation, congenital)

Low ACTH levels = no extra pigment secretion by melanocytes

VAP III (11 decks)

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