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PHYSIOLOGY IV > LECTURE 4 (Adrenal glands) > Flashcards

LECTURE 4 (Adrenal glands) Flashcards

1
Q

Describe the Adrenal gland

A
  • Adrenal medulla = functionally related to the sympathetic nervous system + secretes epinephrine and norepinephrine
  • Adrenal cortex = secrete corticosteroids (hormones derived from cholesterol)
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2
Q

What are the three distinct layers of the Adrenal cortex?

A
  • ZONA GLOMERULOSA (15%) = secrete aldosterone, contain aldosterone synthase, controlled by extracellular fluid concentrations of ANGIOTENSIN II and K+
  • ZONA FASCICULATA (75%) = secrete glucocorticoids (cortisol + corticosterone) and adrenal androgens + oestrogens, secretion controlled by hypothalamic-pituitary axis via ACTH
  • ZONA RETICULARIS = secrete adrenal androgens (DHEA and androstenedione), small amount of oestrogen’s and glucocorticoids
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3
Q

What causes hypertrophy of zona glomerulosa, zona fasciculata & zona reticularis?

A

zona glomerulosa = angiotensin II

zona fasciculata + zona reticularis = ACTH

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4
Q

Describe how cholesterol is provided by LDLs in the adrenal gland

A

1) LDLs diffuse from plasma into interstitial fluid and attach to specific receptors contained in structures called “coated pits” on adrenocortical cell membranes
2) Coated pits are internalised by endocytosis -> form vesicles that fuse with cell lysosomes + release cholesterol
3) Free cholesterol delivered to mitochondria where it is cleaved by CHOLESTEROL DESMOLASE to form PREGNENOLONE (rate-limiting step!!!!)
4) In three zones, different factors affect cholesterol conversion

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5
Q

Which plasma proteins can adrenocortical hormones bind to?

A
  • Cortisol-binding globulin
  • Transcortin
  • Albumin
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6
Q

Adrenal hormones binding to plasma proteins form a reservoir, what is the importance of this reservoir?

A
  • Lessen rapid fluctuations in free hormone concentrations
  • Ensure a relatively uniform distribution of the adrenal hormones to the tissues
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7
Q

How does the liver metabolise Adrenocortical hormones?

A
  • Conjugated to glucuronic acid or sulfates
  • Some conjugates excreted in bile
  • Some conjugates enter circulation but aren’t bound to plasma proteins -> filtered out by kidneys -> excreted in urine
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8
Q

What is Mineralcorticoid Deficiency?

A

Total loss of mineralcorticoids secretion which causes K+ concentration of extracellular fluid to rise markedly, Na2+ and Cl- to be rapidly lost from body and total extracellular fluid and body volume to greatly reduce

MANIFESTATIONS:
- Diminished cardiac output -> shock -> death

TREATMENT:
- administration of aldosterone/mineralcorticoid
- extensive salt therapy

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9
Q

What is the effect of Aldosterone?

A

Increases reabsorption of sodium and simultaneously increases secretion of potassium by renal tubular epithelial cells -> increases Na+ in extracellular fluid and decreases K+

[IT IS A SODIUM-RETAINING HORMONE]

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10
Q

What happens when there is excess aldosterone?

A

When Na+ is reabsorbed by tubules, there is a simultaneous osmotic absorption of water -> small increase in ECF Na+ concentration stimulate thirst and increased H2O intake -> Rise in arterial pressure increases kidney excretion of both salt and H2O (PRESSURE NATRIURESIS and PRESSURE DIURESIS) -> salt and water concentration go back to normal (ALDOSTERONE ESCAPE)

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11
Q

What happens when aldosterone secretion becomes zero?

A

Large amounts of salt are lost in the urine -> diminishes sodium chloride in ECF and decreases ECF volume -> severe ECF dehydration and low blood volume -> circulatory shock

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12
Q

What does excess aldosterone and too little aldosterone cause?

A
  • Excess aldosterone = Hypokalaemia
    [severe muscle weakness develops due to alteration of the electrical excitability of the nerve and muscle fibre membranes]
  • Too little aldosterone = Hyperkalaemia
    [cardiac toxicity, weakness of heart contraction, development of arrhythmia and heart failure]
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13
Q

How does excess aldosterone cause alkalosis?

A

Aldosterone causes secretion of hydrogen ions in exchange for sodium in the intercalated cells of the cortical collecting tubules -> decreases H+ concentration in ECF causing metabolic alkalosis

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14
Q

What is the effect of aldosterone on other parts of the body?

A
  • Sweat glands = conserve body salt in hot environments
  • Salivary glands = conserve salt when excessive quantities of saliva are lost
  • Colon = prevent loss of sodium in stools (loss will lead to diarrhoea)
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15
Q

Describe sodium reabsorption

A

1) Aldosterone diffuses readily to the interior of the tubular epithelial cells
2) In the cytoplasm of the tubular cells, aldosterone combines with a highly specific cytoplasmic MINERALCORTICOID RECEPTOR
3) Aldosterone-receptor complex diffuses into the nucleus, inducing one or more specific portions of DNA to form one or more types of mRNA related to sodium and potassium transport
4) mRNA diffuses back into cytoplasm to ribosome to form proteins
- enzymes
- membrane transport proteins

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16
Q

What are the four factors known to play essential roles in the regulation of aldosterone?

A
  • Increased K+ concentration in the extracellular fluid greatly increases aldosterone secretion
  • Increased angiotensin II concentration in the ECF increases aldosterone secretion
  • Increased Na+ concentration in the extracellular fluid very slightly decreases aldosterone secretion
  • ACTH from the pituitary gland is necessary for aldosterone secretion but has little effect in controlling the rate of secretion in most conditions

[the strongest in factors in regulating aldosterone secretion are POTASSIUM ION CONCENTRATION and RENIN-ANGIOTENSIN SYSTEM]

17
Q

How does aldosterone act on the kidneys?

A
  • To help them excrete the excess potassium ions
  • To increase the blood volume and arterial pressure -> returning the renin-angiotensin system towards its normal level of activity
18
Q

How does Cortisol stimulate gluconeogenesis?

A
  • Increases the enzymes required to convert amino acids into glucose in the liver cells (by activating DNA transcription in the liver cell nuclei to form enzymes)
  • Causes mobilisation of amino acids from the extrahepatic tissues (more amino acids available in plasma to enter into gluconeogenesis)
19
Q

How does cortisol decrease the rate of glucose utilisation in most cells of the body?

A

Glucocorticoids (e.g cortisol) depress the oxidation of NADH to form NAD+ which must be oxidised to allow for glycolysis

20
Q

What happens to the blood glucose concentrations because of cortisol?

A

Blood glucose concentrations rise

Explanation: Due to increased rate of gluconeogenesis and the moderate reduction in the rate of glucose utilisation. If the concentration is great enough it is called “Adrenal diabetes”

21
Q

How does Cortisol cause a reduction in cellular protein?

A
  • Decreased protein synthesis
  • Increased catabolism of protein already in the cells

CAUSES:
- decreased amino acid transport into extra hepatic tissues
- depressed formation of RNA and subsequent protein synthesis in many extra hepatic tissues

[This happens to everywhere in the body APART FROM THE LIVER!!!! IT ENHANCES LIVER PROTEINS]

22
Q

What effects does cortisol have on the liver proteins?

A
  • Increased rate of deamination of amino acids by the liver
  • Increased protein synthesis in the liver
  • Increased formation of plasma proteins by the liver
  • Increased conversion of amino acids to glucose (gluconeogenesis)
23
Q

How does cortisol cause mobilisation of free fatty acids?

A

There is a diminished transport of glucose into fat cells -> alpha-glycerophosphate derived from glucose is required for maintenance of triglycerides -> absence causes fatty acid release -> increased mobilisation of fats + increased oxidation of fatty acids, shifts metabolic systems to utilisation of fatty acids

24
Q

What type of Obesity is caused by excess cortisol?

A

Excess deposition of fat in the chest and head regions giving a buffalo-like torso and a rounded “moon face”

CAUSE: fat is generated in some tissues of the body more rapidly than it is mobilised and oxidised

25
Q

What are the different cortisol effects in preventing inflammation?

A
  • stabilises lysosomal membranes (decreased amount of proteolytic enzymes released that cause inflammation)
  • decreases permeability of capillaries (prevents loss of plasma into the tissues)
  • decreases both migration of WBCs into the inflamed area + phagocytosis of the damaged cells (cortisol decreases formation of prostaglandins and leukotrienes)
  • suppresses the immune system causing lymphocyte reproduction to decrease
  • reduces fever by reducing release of IL-1 from WBCs
26
Q

When excess cortisol is secreted by the adrenal glands, __________ often results

A

Polycythemia

27
Q

What is the cellular mechanism of cortisol action?

A

1) Cortisol diffuses through the cell membrane and binds with its protein receptor and GLUCOCORTICOID RESPONSE ELEMENTS to induce or repress gene transcription
2) Alter mRNA synthesis for proteins that mediate their multiple physiological effects

28
Q

What stimulates cortisol secretion?

A

ACTH secreted by the anterior pituitary gland

[also called “corticotropin” or “adrenocorticotropin”]

29
Q

What is ACTH secretion controlled by?

A

Corticotropin-Releasing factor (CRF)

Explanation: CRF is secreted into the primary capillary plexus of the hypophyseal portal system in the median eminence of the hypothalamus and then carried to the anterior pituitary gland where it induces ACTH

30
Q

What does Cortisol have a direct negative feedback on?

A
  • The hypothalamus to decrease the formation of CRF
  • The anterior pituitary gland to decrease the formation of ACTH
31
Q

What is Addison’s disease?

A

Also called “Hypoadrenalism” or “Primary adrenal insufficiency” results from an inability of the adrenal cortices to produce sufficient adrenocortical hormones

CAUSES:
- primary atrophy/injury of adrenal cortices
- invasion by cancer
- secondary to impaired pituitary gland function (ACTH output is too low -> cortisol and aldosterone production decrease -> adrenal glands atrophy due to lack of ACTH stimulation)

MANIFESTATIONS:
- Mineralcorticoid deficiency
- Glucocorticoid deficiency
- Melanin in thin skin areas

TREATMENT:
an untreated person can die in a few days/weeks due to weakness + circulatory shock but a person can live for years if given mineralocorticoids and glucocorticoids daily

32
Q

What does Mineralcorticoid deficiency cause?

A
  • decrease in renal tubular sodium reabsorption (allows Na+, Cl- and water to be lost in urine)
  • decrease ECF volume
  • hyponatremia, hypokalaemia and mild acidosis (failure of K+ and H+ to be secreted in exchange of sodium reabsorption)
  • RBC concentration increase
  • plasma volume falls, cardiac output and blood pressure decrease -> SHOCK + DEATH
33
Q

What does Glucocorticoid deficiency cause?

A
  • impossible to maintain normal blood glucose concentrations between meals (no glucose by gluconeogenesis)
  • sluggish energy mobilisation
  • patient highly susceptible to deteriorating effects of different types of stress
34
Q

What is addisonian crisis?

A

The critical need for extra glucocorticoids and the associated severe debility in times of stress

35
Q

What is Cushing’s syndrome?

A

Cushing’s syndrome is a disorder that occurs when your body makes too much of the hormone cortisol over a long period of time

CAUSES:
- Adenomas of the anterior pituitary that secrete large amounts of ACTH which causes adrenal hyperplasia and excess cortisol secretion
- Abnormal function of the hypothalamus that causes high levels of CRH (stimulates excess ACTH release)
- Ectopic secretion of ACTH by a tumour elsewhere in the body
- Adenomas of the adrenal cortex

TREATMENT:
- Adrenal tumour is surgically removed or destroyed by radiation
- Drugs that block steroid genesis (e.g ketoconazole)
- Drugs that inhibit ACTH secretion (e.g serotonin antagonists)

LAB FINDINGS:
- increased blood cortisol
- increased blood ACTH

36
Q

What is Conn’s syndrome?

A

Also called “Primary Aldosteronism” is a small tumour of the zona glomerulosa cells and secretes large amounts of aldosterone

MANIFESTATIONS:
- hypokalemia
- mild metabolic alkalosis
- increase in ECF and blood volume
- increase in plasma Na+ concentration
- hypertension

DIAGNOSIS:
- decreased plasma renin concentration (from feedback suppression of renin secretion caused by excess aldosterone or by excess ECF volume and arterial pressure)

TREATMENT:
- surgical removal of tumour
- pharmacological antagonism of mineralocorticoid receptor with SPIRONOLACTONE or EPLERENONE

37
Q

What is Adrenogenital syndrome?

A

An occasional adrenocortical tumour that secretes excessive amounts of androgens that cause intense masculinising effects throughout the body

DIAGNOSIS:
17-ketosteroids in the urine might be 10-15 times than normal

SYMPTOMS:
- female will develop male characteristics: beard, deeper voice, baldness, growth of clitoris to resemble penis, deposition of proteins into muscles
- young male will develop manly characteristics

PHYSIOLOGY IV (14 decks)

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