Chapter 16 (Adrenal) Flashcards

1
Q

Adrenal Glands

A
  • embedded above each kidney in a capsule of fat

adrenal cortex

  • outer portion
  • secretes steroid hormones (cortisol, DHEA)

adrenal medulla

  • inner portion
  • secretes catecholamines (epinephrine and norepinephrine)
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2
Q

Mineralocorticoids

A
Adrenal cortex
Steroid hormone
Zona glomerulosa
Mineralocorticoids
eg. aldosterone

Functions:

  1. Promotes Na+ retention and enhances K+ elimination during urine formation
  2. Na+ retention by aldosterone induces osmotic retention of H20
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3
Q

Glucocorticoids

A
Adrenal cortex
Steroid Hormone
Zona fasciculata
Glucocorticoids
eg. cortisol 
- Major role in glucose metabolism as well as in protein and lipid metabolism
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4
Q

Sex hormones

A
Adrenal medulla
Catecholamines
Zona reticularis
Sex hormones
eg. estrogen and progesterone
- Most abundant and physiologically important is dehydroepiandrosterone (DHEA) a male sex hormone
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5
Q

Adrenal Cortex

A

3 layers

  1. Zona glomerulosa (outermost)
  2. Zona fasciculata (middle and largest portion)
  3. Zona reticularis (innermost)
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6
Q

Aldosterone (Z. glomerulosa)

A

Secretion of aldosterone is increased by:

  1. The activation of renin-angiotensin- aldosterone system (RAAS) due to a reduction in Na+ and a fall in blood pressure
  2. Direct stimulation of adrenal cortex by a rise in plasma K+ concentration
  3. Angiotensin promotes growth of the zona glomerulosa
    - Regulation of aldosterone secretion is largely independent of anterior pituitary control
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7
Q

Primary Hyperaldosteronism or Conn’s syndrome

A

Caused by the hypersecretion of aldosterone by an adrenal tumour

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8
Q

Secondary Hyperaldosteronism

A

Caused by inappropriately high activity of the renin-angiotensin system

Symptoms:

  • Excessive Na+ retention (hypernatremia) and K+ depletion (hypokalemia)
  • High blood pressure (hypertension) due to excessive Na+ retention
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9
Q

Primary Adrenocortical Insufficiency

A
  • Addison’s disease: all layers are undersecreting
  • Caused by autoimmune disease: destruction of adrenal cortex by adrenal cortex attacking antibodies
  • Both aldosterone and cortisol are deficient
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10
Q

Aldosterone Deficiency

A

Leads to hyperkalemia (high potassium) and hyponatremia (low sodium)
- A part of Primary Adrenocortical Insufficiency

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11
Q

Cortisol Deficiency

A
  • Poor response to stress
  • Hypoglycemia due to reduced gluconeogenic activity
  • Lack of permissive action for many metabolic activities
  • A part of Primary Adrenocortical Insufficiency
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12
Q

Secondary Adrenocortical Insufficiency

A
  • Occurs because of pituitary or hypothalamic abnormality, resulting in insufficient ACTH secretion
  • Only cortisol is deficient as aldosterone secretion does not depend on ACTH stimulation
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13
Q

Addison’s Disease

A

Symptoms:

  • A patient with this condition displays hyperkalemia and hypothermia
  • The hyperkalemia disturbs cardiac rhythms
  • The hyponatremia reduces blood volume, causing hypotension
  • Excessive ACTH secretion causes hyperpigmentation due to rise in melanocyte-stimulating hormone, when blood levels of ACTH are very high (removal of negative feedback)
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14
Q

Functions of Glucocorticoids (Cortisol)

A
  1. Secreted by Zona Fasciculata (middle)
  2. Plays a role in carbohydrate, fat and protein metabolism
  3. Plays a role in permissive actions for other hormonal activites
  4. Helps people cope with stress
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15
Q

Role of Cortisol in CHO Metabolism

A

Glycogen - glucose - blood - brain
fasting - liver -(glycogenolysis)- glucose - blood -brain
- brain and other nervous tissues do not store glycogen
- stimulates hepatic gluconeogenesis (amino acids into glucose)
- inhibits glucose uptake when not needed (except for brain)
- stimulates protein degradation in muscles
- facilitates lipolysis (breaking down fats into fatty acids)
- stress adaption
- pharmacological level: anti-inflammatory and immunosuppressive effects. long-term use can have anti-inflammatory
- displays a characteristic diurnal rhythm
- regulated by negative-feedback loop involving hypothalamic CRH and pituitary ACTH

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16
Q

Control of Cortisol Secretion

A

Stress - Hypothalamus - Corticotropin-releasing hormone (CRH) - anterior pituitary - adrenocorticotropic hormone (ACTH) - adrenal cortex - cortisol

Cortisol:

  • increases blood glucose by stimulating gluconeogenesis and inhibits glucose uptake
  • increases blood amino acids by stimulating protein degradation
  • increases blood fatty acids by stimulated lipolysis
17
Q

Role of Cortisol in Protein Metabolism

A
  • cortisol stimulates protein degradation. it converts muscle proteins into amino acids
  • mobilized amino acids are made available for use in gluconeogenesis for repairment of damaged tissue or synthesis of new cellular structures
      cortisol
           | protein - amino acids - glucose
18
Q

Role of Cortisol in Fat Metabolism

A

cortisol
|
Fats/lipids -(lipolysis)- fatty acids - glucose

  • cortisol facilitates lipolysis in adipose tissue, releasing fatty acids into the blood
  • fatty acids are then available for converting into glucose
19
Q

Role of Cortisol in Adaption to Stress

A
  • cortisol is the generalized, non-specific response of the body to any factor that threatens the body’s compensatory abilities to maintain homeostasis
  • physical, chemical, physiologic, emotional, and social triggers stimulate the adrenal cortex to produce cortisol. cortisol then stimulates CHO, protein, and fat metabolism that converts glucose, amino acids, and fatty acids to be used by the body
20
Q

Permissive Actions of Cortisol

A
  • cortisol must be present in adequate amounts to permit the catecholamine to induce vasoconstriction to prevent circulatory shock in a stressful situation
  • a person lacking cortisol and if left untreated, enter into circulatory shock during a stressful situation when it demands immediate widespread vasoconstriction.
21
Q

Role of Anti-Inflammatory and Immunosuppressive Effects

A
  • glucocorticoids suppress antibody production, prevents allergic reactions and organ transplants
  • a large amount of glucocorticoids inhibit every step of the inflammatory response. makes it effective for treating rheumatoid arthritis
  • prolonged exposure to high concentrations of glucocorticoids induce: gastric ulcers, high blood pressure, atherosclerosis, menstrual irregularities and bone thinning
  • someone being treated by glucocorticoids has a limited ability to resist infections
22
Q

Cushing’s Syndrome

A
  • caused by cortisol hypersecretion
  • overstimulation of adreanl cortex by excessive amounts of CRH and ACTH
  • adrenal tumours that uncontrollably secrete cortisol independent of ACTH
  • ACTH secreting tumour located in places other than the pituitary

symptoms

  • hyperglycemia and glycosuria (adrenal diabetes)
  • excessive gluconeogenesis causes hyperglycemia
  • abnormal fat distributions cause: buffalo hump and moon face (face edema)
23
Q

Dehydroepiandrosterone (DHEA)

A
  • adrenal cortex produces sex hormones in both sexes in the zona reticularis
  • androgen (sex steroid)
  • only adrenal sex hormone that has any biological importance
  • overpowered by testicular testosterone in males
  • physiologically significant in females with:
    a. growth of pubic and axillary hair
    b. enhancement of pubertal growth spurt
    c. development and maintenance of female sex drive
24
Q

Adrenogenital Syndrome

A
  • effects genitalia and sexual characteristics

Adult Females:

  • androgen exerts masculinizing effects
  • hirsutism: male pattern of body hair
  • deepening of voice, muscular arms and legs
  • breasts become smaller and menstruation may cease because androgen may suppress the woman’s hypothalamo-pituitary-ovarian axis (HPO). this impacts her own female sex hormone secretion

Newborn Females:

  • have male type external genitalia (pseudohermaphroditism)
  • clitoris is equivalent to the male penis

Prepubertal males: (precocious pseudopuberty)
- excessive androgen secretion in boys causes premature development of secondary male sex characteristics. deep voice, beard, longer penis, and longer sex drive)

Adult Male:
- overactivity of adrenal androgens have no apparent effect as any masculinizing effects are induced by weak DHEA

25
Q

Hormonal Interrelationship in the Adrenogenital Syndrome

A
  • adrenocortical cells that should produce cortisol produce androgens because a lack of cortisol synthesis.
  • because cortisol isn’t present to act in the negative feedback loop, CRH and ACTH levels are elevated
  • increased ACTH stimulated the adrenal cortex to produce more androgen secretion
  • excess androgen produces virilization and inhibits the gonadotropin pathway
  • gonads stop producing sex hormones and gametes.
26
Q

Adrenal Medulla

A
  • primary stimulus for increased adrenomedullary secretion activation of sympathetic nervous system by stress
  • releases epinephrine and norepinephrine. secreted into the blood by exocytosis of the chromaffin granules.
  • epinephrine. reinforces sympathetic system in mounting flight or fight response. maintenance of arterial blood pressure. increased blood glucose and blood fatty acids.