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PMP101 - Health, Disease and Patient > Endocrine System - Pituitary Hormone 2 > Flashcards

Endocrine System - Pituitary Hormone 2 Flashcards

1
Q

What is the location, function and hormone of the zona glomerulsa (adrenal cortex)?

A
  • Location: The outermost layer, just beneath the capsule.
  • Function: Produces mineralocorticoids, primarily aldosterone.
  • Hormone: Aldosterone regulates sodium and potassium balance and
    maintains blood pressure.
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2
Q

What is the location, function and hormone of the zona fasciculata (adrenal cortex)?

A
  • Location: The middle layer, which is the thickest of the three cortical zones.
  • Function: Produces glucocorticoids, mainly cortisol.
  • Hormone: Cortisol regulates metabolism, and immune response, and helps
    the body respond to stress.
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3
Q

What is the location, function and hormone of the zona reticularis (adrenal cortex)?

A
  • Location: The innermost layer of the cortex, adjacent to the medulla.
  • Function: Produces androgens, such as dehydroepiandrosterone (DHEA) and
    androstenedione.
  • Hormone: Androgens are precursors to sex hormones and contribute to
    secondary sexual characteristics
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4
Q

What hormones do choffamin cells produce and their function (adrenal medulla)

A
  • Hormones:
  • Adrenaline: Increases heart rate, blood pressure, and energy
    availability.
  • Noradrenaline: Works with adrenaline to enhance the fight-
    or-flight response by constricting blood vessels and increasing
    blood pressure.
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5
Q

What are the functions of aldersterone?

A

Sodium Reabsorption:
* Increases sodium reabsorption in the kidneys, promoting water
retention and increasing blood volume.
* Potassium Excretion:
* Enhances the excretion of potassium in the urine, maintaining proper
potassium levels in the blood.
* Blood Pressure Regulation:
* Increases blood volume and blood pressure by promoting sodium
and water retention.
* Acid-Base Balance:
* Stimulates the secretion of hydrogen ions, helping to maintain the
acid-base balance in the blood.

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6
Q

What is step 1 to stimulation of aldersterone secretion?

A

*Increased Plasma Potassium ([K+]): Directly stimulates aldosterone release to promote potassium excretion

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7
Q

What is step 2 to aldersterone secretion?

A

*Renin-Angiotensin-Aldosterone System (RAAS): Renin release leads to the
formation of angiotensin II, which stimulates aldosterone secretion to increase
sodium reabsorption and blood pressure.

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8
Q

What is step 3 to aldersterone secretion?

A

Independence from Hypothalamus-Pituitary Axis: Aldosterone secretion is
largely independent of ACTH and primarily regulated by plasma potassium levels
and the RAAS system

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9
Q

What is hypoaldersteronism?

A

Hypoaldosteronism is a condition characterised by insufficient production of aldosterone.
This can result from a deficiency in the enzymes required for aldosterone synthesis, which
leads to various electrolyte and fluid imbalances

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10
Q

What are clinical features of hypoaldosteronism?

A

*Hyperkalaemia: High potassium levels.
*Hyponatraemia: Low sodium levels.
*Hypovolemia: Decreased blood volume.
*Hypotension: Low blood pressure.
*Other Symptoms: Metabolic acidosis, fatigue, and weakness

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11
Q

What is hyperaldesteronism?

A

Hyperaldosteronism is a condition characterised by excessive production of aldosterone,
a hormone that regulates sodium and potassium balance. This condition can lead to
hypertension (high blood pressure) and a range of other symptoms due to the imbalance
of electrolytes.

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12
Q

What are the clinical features to hyperaldesteronism?

A

*Hypokalaemia: Low potassium levels.
*Hypernatremia: High sodium levels.
*Hypertension: High blood pressure.
*Other Symptoms: Metabolic alkalosis, polydipsia (excessive thirst) and
polyuria (excessive urination).

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13
Q

What is dehydroepiandrosterone?

A

Dehydroepiandrosterone (DHEA) and its derivatives are steroid hormone that
regulates the development and maintenance of MALE characteristics
(masculinisation)

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14
Q

What is DHEA regulated by +lack of feedback axis?

A

*regulated by ACTH
*lack of feedback axis to ACTH or CRH

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15
Q

What is hypoandrogensim?

A

Hypoandrogenism, or androgen deficiency, can occur due to a deficiency in the enzymes
required for the synthesis of DHEA (Dehydroepiandrosterone). DHEA is a precursor to
androgens such as testosterone, and its deficiency can lead to a variety of symptoms
related to reduced androgen levels.

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16
Q

What are the symptoms to hypoandrogenism?

A

Loss of energy, erectile dysfunction, reduced libido, loss of muscle and bone
mass, mood changes, cognitive impairment, and increased body fat.

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17
Q

What is hyperandrogenism?

A

Excessive levels of Dehydroepiandrosterone (DHEA) and its sulphated form (DHEA-S) can
lead to hyperandrogenism, particularly affecting women. Elevated DHEA levels can result
in various symptoms due to the increased production of androgens.

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18
Q

What are the functions of cortisol?

A

*glucose metabolism, protein metabolism, lipid metabolism
*immune response (anti-inflammatory +immune supression
*stress response (fight or flight, adaptation)
*bp regulation, bone health + mood/cognition

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19
Q

What are the symptoms of hyperandrogenism in women?

A

*Excess hair growth (hirsutism), masculinisation (virilisation), acne and oily skin,
menstrual irregularities, hair thinning and baldness.

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20
Q

What is the zona fasciculate of the adrenal cortex responsible for?

A

Zona Fasciculata: The middle layer of the adrenal cortex is responsible for
the production of cortisol.

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21
Q

What hormones does the HPA release and what do they do?

A
  • CRH (Corticotropin-Releasing Hormone): Released from the hypothalamus
    in response to stress and low blood cortisol levels.
  • ACTH (Adrenocorticotropic Hormone): Secreted by the anterior pituitary
    gland in response to CRH, stimulating the adrenal cortex to produce and
    release cortisol.
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22
Q

What type of negative feedback loop is seen in terms of cortisol and CRH, ACTH?

A

Elevated cortisol levels inhibit the release of CRH and ACTH, maintaining
homeostasis

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23
Q

What is the primary cause (10%) of Cushing’s syndrome?

A

Adrenal Carcinoma/Adenoma:
* Adrenal Adenoma: A benign tumour of the adrenal cortex that
autonomously secretes cortisol.
* Adrenal Carcinoma: A malignant tumour of the adrenal cortex that produces
high levels of cortisol.

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24
Q

What are the secondary causes (80%) for Cushing’s syndrome?

A

Pituitary Tumour (Cushing’s Disease):
* Pituitary Adenoma: A benign tumour of the pituitary gland that secretes
excessive Adrenocorticotropic Hormone (ACTH).
* Mechanism: The excess ACTH stimulates the adrenal cortex to produce and
release large amounts of cortisol

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25
Q

What are the ectopic causes (10%) of Cushing’s syndrome?

A

Ectopic ACTH Production (10%)
* Bronchial Tumour: Small cell lung carcinoma or bronchial carcinoid tumours
can produce ACTH.
* Other Ectopic Sources: Tumours in locations such as the thymus or pancreas
may also produce ACTH.
* Mechanism: These tumours secrete ACTH independently of the
hypothalamic-pituitary axis, leading to increased cortisol production by the
adrenal glands.

26
Q

What are the clinical features of Cushing’s syndrome In terms of general appearance?

A

Weight Gain:
* Central obesity with fat accumulation around the abdomen, face,
and neck.
* Thin arms and legs.
* Moon Face:
* Rounded, puffy face due to fat deposition.
* Buffalo Hump:
* Fat accumulation on the upper back and neck.
Skin and Hair Changes
* Skin:
* Thin, fragile skin that bruises easily.
* Purple striae (stretch marks), especially on the abdomen, thighs,
breasts, and arms.
* Slow wound healing.
* Hair:
* Hirsutism: Excessive hair growth on the face, chest, and abdomen in
women.
* Thinning of scalp hair.

27
Q

What are the clinical symptoms of Cushing’s syndrome? (musculoskeletal)

A

Muscle Weakness:
* Proximal muscle weakness, particularly in the thighs and upper arms.
* Osteoporosis:
* Bone pain and increased risk of fractures due to reduced bone
density.

28
Q

What are the clinical symptoms of Cushing’s syndrome? (cardiovascular)

A

Hypertension:
* High blood pressure is common due to increased blood volume and
sensitivity to catecholamines.
* Cardiovascular Disease:
* Increased risk of atherosclerosis and other cardiovascular conditions

29
Q

What are the clinical symptoms of Cushing’s syndrome? (metabolic)

A

Hyperglycaemia:
* Elevated blood glucose levels, potentially leading to diabetes
mellitus.
* Dyslipidaemia:
* Abnormal lipid levels, including high cholesterol and triglycerides.

30
Q

What are the clinical symptoms of Cushing’s syndrome? (reproductive)

A
  • Menstrual Irregularities:
  • Amenorrhoea (absence of menstrual periods) or oligomenorrhoea
    (infrequent periods) in women.
  • Infertility:
  • Reduced fertility due to hormonal imbalances.
  • Erectile Dysfunction:
  • Impotence and reduced libido in men.
31
Q

What are some clinical symptoms of Cushing’s syndrome (psychological)?

A
  • Mood Changes:
  • Depression, anxiety, and irritability.
  • Cognitive Impairment:
  • Difficulty concentrating and memory problems.
32
Q

What are some clinical symptoms of Cushing’s syndrome (other features)?

A
  • Immune Suppression:
  • Increased susceptibility to infections due to the immunosuppressive
    effects of cortisol.
  • Peptic Ulcers:
  • Increased risk of developing ulcers in the stomach and duodenum.
  • Fatigue and Weakness:
  • Generalised fatigue and decreased physical stamina
33
Q

What is Addisons disease?

A

Addison’s disease, also known as primary adrenal insufficiency, occurs when the adrenal
glands do not produce sufficient amounts of cortisol, aldosterone, and androgens. This
condition can be life-threatening if not diagnosed and treated properly

34
Q

What are the causes of Addisons disease?

A

1.Autoimmune Disease:
* The most common cause, where the immune system attacks the
adrenal cortex, leading to adrenal gland failure.
2.Infections:
* HIV/AIDS: Can damage the adrenal glands directly or through
opportunistic infections.
* Tuberculosis (TB): Historically a common cause, TB can infect the
adrenal glands and lead to their destruction.
3.Other Causes:
* Genetic disorders, adrenalectomy (surgical removal of the adrenal
glands), and certain medications that affect adrenal function

35
Q

What are the clinical features of Addisons disease?

A
  • Hair Loss:
  • Loss of body hair, particularly in women, due to decreased androgen
    levels.
  • Blurred Vision:
  • Potentially due to hypotension or electrolyte imbalances affecting
    ocular function.
  • Abdominal Pain:
  • Vague, chronic abdominal pain that can be severe during an
    Addisonian crisis.
  • Decreased Appetite:
  • Leading to significant weight loss over time.
  • Darkening of the Skin (Hyperpigmentation):
  • Especially noticeable in areas exposed to friction, such as elbows,
    knees, knuckles, and creases of the hands.
  • Caused by increased production of melanocyte-stimulating hormone
    (MSH) due to high levels of ACTH.
  • Weight Loss:
  • Progressive weight loss due to decreased appetite and chronic illness.
  • Hypoglycaemia:
  • Low blood sugar levels, causing symptoms such as sweating,
    dizziness, and confusion.
  • Postural Hypotension:
  • Low blood pressure, especially when standing up, leading to dizziness
    and fainting.
  • Caused by aldosterone deficiency, leading to sodium loss and
    decreased blood volume
36
Q

Where is ADH stored and what does it do?

A

Antidiuretic Hormone (ADH), also known as Arginine Vasopressin (AVP), is a crucial
hormone produced by the hypothalamus and released by the posterior pituitary gland. It
plays a vital role in regulating water balance, blood pressure, and overall fluid
homeostasis

37
Q

What is ADH secretion (hypovolemia)?

A
  • Decreased blood volume triggers ADH release to conserve water
    and maintain blood volume
37
Q

What is ADH secretion (hypotension)?

A
  • Low blood pressure stimulates baroreceptors, which signal the release of ADH to increase BV and pressure.
38
Q

What is ADH secretion (hyperosmolarity)?

A
  • Increased plasma osmolality (high concentration of solutes in the
    blood) stimulates osmoreceptors in the hypothalamus, leading to
    ADH release.
39
Q

What are the functions of ADH?

A

*water reabsorption in the kidneys
*stimulation of ACTH release
*vasconstriction of blood vessels

40
Q

Describe ADH’s water reabsorption function

A
  • Increased Permeability: ADH increases the permeability of the distal
    convoluted tubule (DCT) and the collecting ducts in the kidneys.
  • Water Reabsorption: This allows more water to be reabsorbed back into the
    bloodstream, concentrating the urine and reducing urine volume.
  • Mechanism: ADH binds to V2 receptors on the cells of the renal tubules,
    triggering the insertion of aquaporin-2 water channels into the cell
    membranes, facilitating water reabsorption.
41
Q

Describe ADH’s stimulation of ACTH release function

A
  • ADH can stimulate the release of Adrenocorticotropic Hormone (ACTH) from
    the anterior pituitary.
  • Effect: ACTH stimulates the adrenal cortex to produce cortisol, which helps
    the body respond to stress and maintain blood pressure and glucose levels
42
Q

Describe ADH’s vasoconstriction of bv function

A
  • Higher Concentrations of ADH: At higher levels, ADH causes vasoconstriction
    (narrowing of blood vessels).
  • Mechanism: ADH binds to V1 receptors on vascular smooth muscle cells,
    causing the muscles to contract and the blood vessels to narrow.
  • Effect: Vasoconstriction increases peripheral resistance, raising blood
    pressure.
43
Q

What is diabetes insipidus?

A

Diabetes Insipidus (DI) is a condition characterised by excessive urination (polyuria) and
excessive thirst (polydipsia) due to the body’s inability to regulate water balance
effectively. There are two main types of DI: Pituitary DI (Central DI) and Nephrogenic DI

44
Q

What are the clinical features of diabetes insipidus?

A

1.Polyuria:
* Excessive production of dilute urine.
* Patients may produce large volumes of urine, often more than 3
litres per day.
2.Polydipsia:
* Excessive thirst and increased fluid intake.
* Patients may drink large amounts of water to compensate for fluid
loss

45
Q

What are the types of DI?

A

*pituitary diabetes insipidus (central DI)
*nephrogenic diabetes insipidus

46
Q

What are the the cause, mechanism and effect of central DI?

A
  • Cause: Inadequate release of Antidiuretic Hormone (ADH) from the pituitary
    gland.
  • Mechanism: Damage to the hypothalamus or pituitary gland due to trauma,
    surgery, tumours, infections, or genetic disorders leads to insufficient ADH
    production.
  • Effect: Low levels of ADH result in decreased water reabsorption in the
    kidneys, leading to excessive urine output and thirst
47
Q

What are the cause, mechanism and effect leading to nephrogenic DI

A
  • Cause: Dysfunction of ADH receptors in the collecting ducts of the kidneys.
  • Mechanism: The kidneys are unable to respond to ADH, despite its normal or
    elevated levels. This can be due to genetic mutations, certain medications
    (like lithium), chronic kidney disease, or electrolyte imbalances (such as
    hypercalcaemia or hypokalaemia).
  • Effect: The inability of the kidneys to respond to ADH results in reduced
    water reabsorption, causing excessive urine output and thirst
48
Q

What is syndrome of inappropriate antidiuretic hormone secretion (SIADH)?

A

is a condition
characterised by excessive release of antidiuretic hormone (ADH), leading to water
retention, highly concentrated urine, and hyponatraemia. Unlike other forms of
hyponatraemia, the low sodium levels in SIADH are due to dilution rather than actual
sodium loss.

49
Q

What are the causes of SIADH?

A

1.CNS Pathologies: Conditions such as head injury, infections (e.g., meningitis,
encephalitis), strokes, and brain surgery can lead to excessive ADH release.
2.Malignancy: Certain cancers, particularly small cell lung carcinoma, can produce
and secrete ADH ectopically.
3.CNS Drugs: Medications affecting the central nervous system, such as
antidepressants, antipsychotics, and anticonvulsants, can trigger SIADH

50
Q

What are the clinical features of SIADH?

A
  • Retention of Water:
  • Excessive ADH causes the kidneys to reabsorb more water, leading to
    water retention in the body.
  • Highly Concentrated Urine:
  • Despite the body retaining water, the urine remains highly
    concentrated due to the reabsorption process.
  • Hyponatraemia:
  • The retained water dilutes the sodium in the bloodstream, leading to
    low serum sodium levels (hyponatraemia) due to a dilution effect
    rather than a direct loss of sodium.
51
Q

What are the primary functions of oxytocin?

A
  • Milk Let-Down Reflex:
  • Stimulation of Milk Ejection:
  • Oxytocin stimulates the contraction of myoepithelial cells
    surrounding the alveoli in the mammary glands.
  • This contraction forces milk into the ducts, facilitating its
    expression from the nipple during breastfeeding.
  • Uterine Contraction:
  • Labour and Delivery:
  • Oxytocin causes the smooth muscle of the uterus to contract,
    helping to initiate and sustain labour.
  • These contractions are essential for childbirth, assisting in the
    delivery of the baby
52
Q

What is the role of oxytocin in maternal behaviour, sexual behaviour and social bonding?

A
  • Maternal Behaviour:
  • Bonding with Offspring:
  • Oxytocin is involved in the establishment of maternal
    behaviours, such as nurturing and protecting the offspring.
  • It strengthens the bond between the mother and her baby,
    enhancing maternal care.
  • Sexual Behaviour:
  • Role in Sexual Activity:
  • Oxytocin is released during sexual activity and is thought to
    contribute to the feeling of pleasure and emotional bonding
    between partners.
  • It enhances sexual arousal and satisfaction.
  • Social Bonding:
  • Social Interactions:
  • Oxytocin is often referred to as the “love hormone” due to its
    role in promoting social interactions and bonding.
  • It facilitates trust, empathy, and social recognition, playing a
    key role in forming social relationships.
53
Q

What are the pancreatic hormones?

A

*insulin
*glucagon
*somatostatin
*pancreatic polypeptide

54
Q

What are the sources and functions of insulin, glucagon, somatostatin and pancreatic polypeptide?

A

*Insulin:
* Source: Beta (β) cells.
* Function: Lowers blood glucose, promotes glucose uptake and storage, and
inhibits fat and protein breakdown.
*Glucagon:
* Source: Alpha (α) cells.
* Function: Raises blood glucose by stimulating gluconeogenesis and
glycogenolysis.
*Somatostatin:
* Source: Delta (δ) cells.
* Function: Inhibits insulin and glucagon release, and regulates digestion
* Source: PP cells (F cells).
* Function: Regulates pancreatic functions, gastric motility, and enzyme
secretion.
* Relevance: Pancreatic tumours, other disorders

55
Q

What is glucose homeostasis?

A

Glucose homeostasis is the balance of insulin and counter-regulatory hormones to
maintain blood glucose levels within a narrow range, typically between 4-8 mmol/L. This
balance is crucial for providing a steady supply of glucose to the body, particularly the
brain, which relies on glucose as its primary energy source

55
Q

What are the functions of insulin?

A

*regulation of blood glucose
*fat metabolism
*protein metabolism
*overall anabolic effects (promotes storage of energy and build up of tissues)

56
Q

How is hyperglycaemia balanced?

A
  • Insulin is released to promote the uptake and storage of glucose, lowering
    blood glucose levels.
  • Insulin’s effects counteract those of glucagon, adrenaline, growth hormone,
    and cortisol.
57
Q

How is hypoglycaemia balanced?

A
  • Glucagon, adrenaline, growth hormone, and cortisol are released to
    increase blood glucose levels.
  • These hormones promote the production and release of glucose into the bloodstream.
58
Q

What is diabetes mellitus?

A

Diabetes mellitus is a chronic metabolic disorder characterised by hyperglycaemia (high
blood glucose levels). It results from defects in insulin production, insulin action, or both.
There are two primary types of diabetes mellitus: Type 1 and Type 2.

59
Q

Describe features of Type 1 diabetes mellitus

A
  • Insulin Deficiency: Autoimmune destruction of pancreatic beta cells.
  • Onset: Typically in children and young adults.
  • Symptoms: Hyperglycaemia, polyuria, polydipsia, polyphagia, weight loss
60
Q

Describe features of Type 2 diabetes mellitus

A
  • Impaired Beta-Cell Function and Insulin Resistance:
  • Insulin Resistance: Cells are resistant to insulin’s effects.
  • Beta-Cell Dysfunction: Pancreas produces insufficient insulin.
  • Onset: Typically in adults over 45, but increasingly in younger individuals.
  • Symptoms: Hyperglycaemia, polyuria, polydipsia, polyphagia, fatigue, blurred
    vision, slow healing of wounds

PMP101 - Health, Disease and Patient (21 decks)

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