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Endocrinology Final > HPA Axis > Flashcards

HPA Axis Flashcards

1
Q

Stress

A

Real or perceived threat to homeostasis or well-being

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2
Q

Allostasis

A
  • Maintaining stability through change
  • Continuous process of energy balance by the brain to anticipate and regulate adaptive responses to environmental stressors
  • Dynamic or variable homeostasis (as opposed to steady state)
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3
Q

Allostatic Load

A
  • Cost of adaptation
  • Cumulative wear and tear on the body from chronic stress
  • Allostatic overload (burnout) increases risk for disease
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4
Q

True or False: following a deviation in homeostasis, biological stress systems stimulate adaptive responses to promote survival and well-being.

A

True

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5
Q

Sympatho-Adrenal- Medullary

A
  • Preganglionic neurons target the adrenal medulla
  • Release of acetylcholine activates nicotinic receptors
  • 80% epinephrine and 20% norepinephrine
  • Adrenaline rush
  • Spinal cord -> ventral root -> thoracic splanchnic nerves -> adrenal medulla
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6
Q

Adrenergic Sympathetic Effects

A
  • Epinephrine and norepinephrine signaling through alpha and beta receptors on target organs
  • Mobilize resources to respond to threats
  • Inhibit processes not related to short-term survival
  • Norepinephrine and epinephrine: smooth muscle contraction, inhibition of transmitter release, etc.
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7
Q

What is the primary hormone released by the adrenal medulla?

A

Epinephrine

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8
Q

What is the response of the hypothalamus to a deviation in the internal state (disruption in homeostasis)?

A
  • Autonomic nervous system
  • Neuroendocrine systems
  • Behavioral alterations
  • Regulator of preganglionic neurons (direct input)
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9
Q

Explain the HPA axis.

A
  1. Paraventricular Hypothalamus: corticotropin releasing hormone (CRH)
  2. Portal circulation
  3. Anterior pituitary: (corticotrophs) adrenocorticotropic hormone (ACTH)
  4. Systemic circulation
  5. Adrenal cortex: synthesis of corticosteroids -> cortisol (primary human glucocorticoid)
  6. Systemic circulation
  • Central and peripheral actions
  • Feedback
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10
Q

Corticosteroid Actions

A
  • Primarily cortisol in humans and large mammals
  • Also corticosterone and/or cortisone
  • Catabolic steroids (glucocorticoids)
  • Signal through type I and type II receptors
  • Utilization of glucose, protein, and fat
  • Suppress immune system and reproduction
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11
Q

Which feature best differentiates the HPA axis from the SAM axis?

A

Release of ACTH from the pituitary

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12
Q

How is the stress response triggered?

A
  • Neuronal processing of sensory, homeostatic, emotional, and cognitive information converges on CRH neurons
  • Inputs from brainstem and hypothalamic nuclei transmit homeostatic signals
  • Limbic regions (area of brain involved in emotion and recognition): prefrontal cortex (cognitive, emotional, ability to think), hippocampus (memory), amygdala (emotion, fear, threat recognition); innervate the hypothalamus and brainstem to convey psychosocial influences
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13
Q

True or False: CRH neurons receive direct synaptic inputs from brain regions that mediate memory and cognition.

A

False: not direct input

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14
Q

Corticotropin Releasing Hormone (CRH)

A
  • 41 amino acid peptide synthesized by neurons of the PVN
  • Made by parvocellular (small) neurons that project to the hypophyseal portal veins
  • Transcribed as preproCRH from 2-exon gene
  • Evolutionarily conserved
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15
Q

CRH-R1

A
  • Primary CRH receptor expressed by corticotropes
  • Stimulate HPA axis
  • Knockout reduced HPA axis function
  • G-protein coupled signaling through GalphaS (stimulatory)
  • Protein-kinase A activation = increased intracellular calcium and phosphorylation
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16
Q

CRH-R2

A
  • Low affinity for CRH
  • Reduces stress responses
17
Q

Adrenocorticotropic Hormone (ACTH)

A
  • Synthesized from precursor proopiomelanocortin (POMC)
  • Prohormone convertases (PC) cleave POMC to produce ACTH (pro-ACTH -> ACTH)
  • Stored in vesicles
  • Rise in intracellular calcium leads to exocytosis of ACTH
18
Q

What is the receptor for ACTH?

A
  • Melanocortin-2 receptor (MC2R)
  • Located in all 3 layers of the adrenal cortex
  • GPCR: activates cAMP and PKA
  • In zona fasciculata, PKA signaling leads to the expression and activation of enzymes used for cortisol synthesis
  • All adrenal steroids derived from cortisol
  • Synthetic specificity arises from enzyme expression
19
Q

True or False: Pituitary receptors for CRH (CRH-R1) and adrenal cortex receptors for ACTH (MC2R) both signal through GalphaS- coupled receptors to increase PKA activity.

A

True

20
Q

Steroidogenesis

A
  • All steroids arise from cholesterol
  • Steroids are synthesized on demand, not stored for secretion
  • Lipophilic: readily diffuse through membranes
  • Cholesterol -> pregnenolone -> progesterone -> mitochondria (primary glucocorticoids)
21
Q

Corticosteroid Receptors

A
  • Binary receptor system
  • Act as transcription factors
  • Type I: mineralocorticoid receptors (MR) -> high affinity (bind cortisol at lower concentrations)
  • Type II: glucocorticoid receptors (GR) -> lower affinity (activated by elevated cortisol (stress))
22
Q

Glucocorticoid Response Elements (GRE)

A
  • regulate hundreds of genes
  • transrepression = negative feedback
  • transcriptional activation = positive feedback
23
Q

Explain the structure of the glucocorticoid receptor.

A
  1. LBD: ligand binding domain (hormone binding)
  2. Hinge: allows conformational change
  3. DBD: DNA binding domain (interacts with response element in genome)
  4. N-terminus contains: nuclear localization sequence (covered at rest by chaperone protein -> hormone binds -> conformational change -> open) and dimerization domain (GRalpha or GRbeta)
24
Q

Which domain of the glucocorticoid receptor directly mediates interactions with cortisol?

A

Ligand binding domain

25
Q

Feedback regulation of the HPA axis.

A
  • Feedback to the HPA axis is mediated by GR and MR
  • Negative feedback occurs at hypothalamic CRH neurons and pituitary corticotrophs
  • Cortical and hippocampal GR and MR also provide negative feedback
26
Q

Which process is most likely to contribute to glucocorticoid receptor-dependent negative feedback?

A

Transcriptional repression of POMC in the pituitary

27
Q

Acute actions of glucocorticoids.

A

Liver gluconeogenesis, amino acid mobilization from protein, lipolysis, immune suppression, elevated blood pressure, cognitive enhancing, memory enhancing

28
Q

Chronic actions of glucocorticoids.

A

Insulin resistance, muscle weakness, abdominal obesity, reproductive deficits, hypertension, cognitive dysfunction, impaired negative feedback

29
Q

Cushing Syndrome

A
  • Hypercortisolism (excess glucocorticoids at all times)
  • Excess as a result of ACTH excess (pituitary tumor) or adrenal cortical neoplasm (ACTH independent)
  • Results in cognitive impairment, mood disorders, hypertension, cardiac hypertrophy, obesity, muscle weakness
30
Q

Addison’s Disease

A
  • Hypocortisolism
  • Autoimmune loss of cells in the adrenal cortex
  • High ACTH due to loss of negative feedback
  • Adrenal crisis is a medical emergency, can be fatal if left untreated

Endocrinology Final (13 decks)

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