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Metabolism > Session 9 > Flashcards

Session 9 Flashcards

0
Q

What are the sections of the kidney that produce hormones?

A
  • Cortex: steroid hormones

- Medulla: amino acid hormone

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1
Q

What hormones are produced by the anterior pituitary gland?

A
  • Thyroid stimulating hormone (produced in thyrotrophs)
  • Adrenocorticotrophic hormone (corticotrophs)
  • Growth hormone (somatotrophs)
  • Follicle stimulating hormone (gonadotrophs)
  • Leuteinizing hormone (gonadotrophs)
  • Prolactin (lactotrophs)
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2
Q

What are the layers of the kidney cortex and what hormones do they produce?

A
  • Zona Glomerulosa: mineralocorticoids (eg aldosterone)
  • Zona Fasiculata: glucocorticoids (eg cortisol and corticosterone)
  • Zona Reticularis: androgens (eg testosterone)
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3
Q

What is secreted by the kidney medulla?

A
  • Adrenaline (Hormone)
  • Noradrenaline (neurotransmitter)
  • Dopamine (neurotransmitter)
    (All are catecholamines - derived from amino acid tyrosine)
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4
Q

What controls the release of cortisol?

A
  • ACTH secretion from tepee anterior pituitary gland

- (which is controlled itself by corticotrophin releasing factor (CRF) produced in the hypothalamus)

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5
Q

What is CRF a secreted in response to?

A
  • Stressors: Physical (temperature, pain); Chemical (hypoglycaemia); Emotional
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6
Q

What is ACTH developed from?

A
  • POMC
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7
Q

Describe the presence of ACTH in the bloodstream

A
  • Has a short half-life (8mins)
  • Released in pulses that follow a circadian rhythm
  • Peak plasma levels are in the morning, lowest levels at night
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8
Q

How does ACTH cause the increase in the synthesis of free cholesterol?

A
  • Is hydrophilic and interacts with high affinity receptors in the surface of cells in the Zona Fasiculata and Zona Reticularis
  • Activates cholesterol esterase
  • Increases conversion of cholesterol esters to free cholesterol
  • Also stimulates conversion of cortisol from cholesterol
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9
Q

What are the clinical consequences of the over-secretion of ACTH?

A
  • Increased pigmentation (effect on tissues)

- Adrenal hyperplasia and over-production of cortisol (effect on a adrenal cortex)

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10
Q

What is are the clinical consequences of under secretion of ACTH?

A
  • Symptoms related to lack of glucocorticoids

- No symptoms related to lack of mineralocorticoids as aldosterone secretion is normal (not controlled by ACTH)

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11
Q

What is the receptor for ACTH and how does it work?

A
  • Melanocortin receptor type 2/MC2/corticoptrophin receptor

- Uses cAMP as a secondary messenger

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12
Q

How is cortisol transported in the blood?

A
  • Is lipophilic so is bound to plasma proteins

- Main transport protein is transcortin/corticosteroid-binding globulin (CBG)

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13
Q

What is the active form of cortisol?

A
  • Free in the plasma
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14
Q

How does cortisol act on its target cells?

A
  • Crosses the plasma membrane and binds to cytoplasmic receptors (as is lipophilic/hydrophobic)
  • Hormone/receptor complex enters nucleus and interacts with specific regions of DNASE
  • This changes the rate of transcription of specific genes
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15
Q

What is cortisol a response to?

A
  • Stress eg starvation
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16
Q

What are the actions of cortisol?

A
  • Increases proteolysis, lipolysis and gluconeogenesis to increase availability of major substrates
  • ⬇️ amino acid uptake; ⬇️ protein synthesis ⬆️ proteolysis (not in liver) -> ⬆️ amino acids
  • ⬆️ hepatic gluconeogenesis and glycogenolysis -> ⬆️glucose
  • ⬆️ lipolysis in adipose tissue -> ⬆️ fatty acids (NB high levels of cortisol increases lipogenesis in adipose tissue)
  • ⬇️ peripheral uptake of glucose (anti-insulin)
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17
Q

What other tissues are directly affected by cortisol?

A
  • Cardiac muscle
  • Bone
  • Immune system
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18
Q

What is the function of aldosterone?

A
  • Stimulates Na+ reabsorption in the kidney in exchange for K+ or H+
  • Over secretion increases Na+ and water retention and loss of K+ -> hypertension and muscle weakness
  • Under secretion does the opposite -> hypotension
19
Q

What is the function of androgens?

A
  • Stimulates growth and development of male genital tract and male secondary sexual characteristics
  • Over secretion produces effects in females: hair growth (hirsuitism); acne; menstrual problems; increased muscle bulk; deepening voice
20
Q

What is the function of oestrogens?

A
  • Stimulates growth and development of female genital tract, breasts and female secondary characteristics
  • Weakly anabolic and decrease circulating cholesterol levels
21
Q

What is the structure of cortisol?

A
  • Member of C21 steroid family that differs from other steroids in: number of carbon atoms; presence of functional groups; distribution of C=C double bonds
  • Are lipophilic so are transported bound to plasma proteins (~90% transcortin, ~10% free and active)
  • Synthesised from cholesterol via progesterone in a series of enzyme catalysed reactions
22
Q

When is adrenaline secreted?

A
  • As part of fright, flight or fight response

- In response to stress situations

23
Q

What are the effects of adrenaline?

A
  • Cardiovascular system: ⬆️ cardiac output; ⬆️ blood supply to muscle
  • CNS: ⬆️ mental alertness
  • Carbohydrate metabolism: ⬆️ glycogenolysis in liver and muscle
  • Lipid metabolism: ⬆️ lipolysis in adipose tissue
24
Q

What are the clinical consequences of over-secretion of Adrenaline?

A
  • Hypertension
  • Anxiety
  • Palpitations
  • Pallor
  • Sweating
  • Glucose intolerance
    (Usually due to a tumour - phaechromocytoma)
25
Q

How does adrenaline act upon its target cells?

A
  • Cannot cross cell membrane
  • Binds to an adrenoreceptor on the outside of the cell
  • A secondary messenger then affects cell activity
26
Q

What can cause hypoactivity of the adrenal cortex?

A
  • Diseases of the adrenal cortex (autoimmune destruction): reduces glucocorticoids and mineralocorticoids
  • Disorders in pituitary or hypothalamus that lead to decreased secretion of ACTH or CRF: only reduces glucocorticoids
27
Q

What is Addison’s disease?

A
  • Decreased activity (hypoactivity) of adrenal cortex
28
Q

What can cause hyperactivity of adrenal cortex?

A
  • Increased activity of adrenal cortex due to tumour (adenoma)
  • Disoders in the secretion of ACTH caused by pituitary adenoma (Cushing’s disease) or ectopic secretion of ACTH
    (Both cause increased secretion of glucocorticoids)
29
Q

What is Cushing’s syndrome?

A
  • Increased secretion of glucocorticoids
30
Q

What is congenital adrenal hyperplasia?

A
  • Caused by genetic defect in enzymes required for cortisol synthesis
  • Lack of cortisol causes pituitary gland to secrete large amount of ACTH have as cortisol levels don’t feedback
  • ACTH causes adrenal cortex to enlarge (hyperplasia)
  • Severity and consequences depend on which enzymes are affected
31
Q

What abnormal functions of the adrenal cortex can cause clinical problems?

A
  • Hypoactivity
  • Hyperactivity
  • Congenital adrenal hyperplasia
32
Q

What are the clinical effects of excess cortisol secretions?

A
  • Increased proteolysis and hepatic gluconeogenesis may -> hyperglycaemia with associated polyuria and polydipsia (steroid diabetes)
  • Increased proteolysis -> wasting of proximal muscles -> thin arms, legs and muscle weakness
  • Increased lipogenesis in adipose tissue -> deposition of fat in abdomen, neck and face (characteristic body shape, moon-shaped face and weight gain)
  • Purple striae on lower abdomen, upper arms and thighs - caused by catabolic effects on protein structures in skin -> easy bruising because of thinning of skin and subcutaneous tissue
  • Immunosuppresive, anti-inflammatory and anti-allergic reactions of cortisol -> increased susceptibility to bacterial infections and acne
  • Back pain and rib collapse - osteoporosis caused by disturbances in calcium metabolism and loss of bone matrix protein
  • Mineralocorticoid effects of excess cortisol -> hypertension due to sodium and fluid retention
33
Q

Other than Cushing’s disease, in what other situation can patients have symptoms of excess cortisol secretion?

A
  • Long-term treatment with glucocorticoids for various chronic inflammatory conditions
34
Q

What is affected by autoimmune destruction of the adrenal gland?
How does this present?

A
  • Decreased cortisol production (glucocorticoid)
  • Loss of mineralocorticoids also
  • Acute emergency (Addisonian crisis) or chronic debilitating disorder (Addison’s disease)
35
Q

What are the clinical effects of too little cortisol secretion?

A
  • Insidious onset with initial non-specific symptoms: tiredness; extreme muscle weakness; anorexia; vague abdominal pain; weight loss; occasionally dizziness
  • Extreme muscle weakness and dehydration
  • Increased pigmentation on: exposed areas of the body; points of friction; buccal mucosa; scars; palmar creases
  • Decreased blood pressure due to sodium and fluid depletion
  • Postural hypotension due to fluid depletion
  • Hypoglycaemic episode especially when fasting
36
Q

What exacerbates the effects of low cortisol secretion and what does this cause?

A
  • Stress eg trauma or severe infection

- Leads to nausea; vomiting; extreme dehydration; hypotension; confusion; fever; coma (Addisonial crisis )

37
Q

How would an Addisonian crisis be treated?

A
  • Intravenous cortisol

- Fluid replacement (dextrose in normal saline)

38
Q

What is important to measure when investigating suspected adrenocortical disease?

A
  • Plasma cortisol
  • Plasma ACTH
  • 24hr urinary exertion of cortisol and breakdown products (17-hydroxysteroids)
39
Q

What tests are used in the differential diagnosis of adrenocortical disease?

A
  • Dexamethasone suppression tests

- ACTH stimulation test

40
Q

What is Dexamethasone and why is it used in diagnosing adrenocortical disease?

A
  • A potent synthetic steroid
  • When given orally it normally suppresses (by feedback inhibition) the secretion of ACTH and therefore cortisol
  • In Cushing’s disease, it causes suppression of cortisol by ~50% (although diseased pituitary is relatively insensitive to cortisol, it remains sensitive to potent synthetic steroids)
  • Suppression does not occur when cortisol is too high due to adrenal tumours or ectopic ACTH production
41
Q

What is Synacthen and why is it used in diagnosing adrenocortical disease?

A
  • Is a synthetic analogue of ACTH
  • When given intramuscularly, it normally increases plasma cortisol by >200 mmol/L
  • A normal response usually excludes Addison’s disease
42
Q

What are steroid receptors?

A
  • Part of a family of nuclear DNA-binding proteins that include thyroid and vitamin D receptors
  • Have 3 main regions: hydrophobic hormone-binding region; DNA-binding region (rich in cysteine and basic amino acids); variable region
43
Q

Why can cortisol act as a mineralocorticoid in high concentrations?

A
  • There is homology in the hormone binding regions of the steroid receptors
  • Cortisol can bind to the mineralocorticoid and androgen receptors with low affinity
44
Q

How can ACTH lead to increased pigmentation?

A
  • Precursor of ACTH is pro-opiomelanocortin (POMC)
  • Post-translational processing of POMC at different sites produces biologically active peptides eg ACTH, MSH (melanocyte stimulating hormone) and endorphins
  • MSH sequence is contained within the ACTH a sequence in POMC
  • This gives ACTH some MSH-link activity when present in excess
45
Q

What are the clinical consequences of over-secretion of ACTH?

A
  • Occur with little/no negative feedback from cortisol to anterior pituitary- Addison’s disease
  • ACTH has effects on the adrenal cortex and on tissues (increased pigmentation due to partial MSH activity)
46
Q

What are the key consequences of excess and deficiency of cortisol?

A
  • Deficiency: - Excess:
    ~ Low glucose ~ High glucose
    ~ Weight loss ~ Weight gain
    ~ Nausea ~ Increased appetite
    ~ Hypotension ~ Hypertension
    ~ Cushingoid fat distribution

Metabolism (11 decks)

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