Modules 3.1-3.3 Flashcards

1
Q

What is the definition of hypo-secretion and causes?

A
  • hormone deficient state, can occur due to glandular tissue inability to synthesize hormones or injured tissue
  • tumour, infection, chronic inflammation are causes
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2
Q

What is the definition of hyper-secretion and examples?

A
  • Over-excretion of hormones
    Ectopic hormone production: another tissue is able to secrete hormone
    Endocrine gland hypertrophy: overstimulated by pituitary gland that creates enlargement
    Impaired negative feedback: impairment in feedback causing increased blood hormone levels
    Medication induced
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3
Q

What is target tissue responsiveness?

A
  • is the number/sensitivity of receptors, can increase or decrease depending on hormone secretion levels
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4
Q

What are ways to diagnose endocrine dysfunction?

A
  • Basal hormone levels (blood or urine sample)
  • Dynamic endocrine test
  • CT, MRI, US
  • Physical examination
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5
Q

What is a dynamic endocrine test?

A
  • based on the feedback loop of hormones to monitor amount and effectiveness of hormones
  • stimulatory test is when hypo. is suspected
  • suppression test is when hyper. is suspected and needs to be differentiated from a tumour
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6
Q

What is the treatment for hyposecretion?

A
  • hormone replacement therapy for deficient hormone (animal and human based)
  • enhancing sensitivity of tissue for poor tissue responsiveness (metformin)
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7
Q

What is the treatment for hypersecretion?

A
  • drug treatment to prevent hormone stimulation
  • Surgical removal/chemical ablation of effected gland
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8
Q

What does the disruption of the hypothalamic-pituitary axis cause?

A
  • Body growth, metabolic and mood disorders due to inc. cortisol in body
  • HPA is a commuincation pathway to maintain hormone and stress levels
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9
Q

What is Growth hormone (GH)?

A
  • GH promotes normal cell growth
  • stimulates protein synthesis by acting as an anabolic agent
  • inc. BGL through anti-insulin activity and affecting IGF-1
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10
Q

What are the effects of hyper/hyposecretion on GH?

A

Hypo: impaired GH secretion, causes pituitary dwarfism
Hyper: excessive GH secretion, causes acromegaly (adults) and gigantism (children)

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11
Q

What is anti-diuretic hormone (ADH)?

A
  • facilitates water resorption from renal system into blood
  • helps balance fluid levels
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12
Q

What are the effects of hyper/hyposecretion on ADH?

A

Hypo: inability to concentration urine and major water loss from body, diabetes insipidus (DI).
- caused by neurogenic (head trauma) or nephrogenic (renal tubules unresponsive)

Hyper: excessive water resorption (SIADHS)
- caused by stress or ectopic causes (tumour)

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13
Q

What is Goitre and the different types?

A

Enlargement of the thyroid gland
Non-toxic: enlarged but no CM
Toxic: CM of thyroid dysfunction present
Diffuse: whole gland is enlarged
Nodular: 1+ parts of gland are enlarged

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14
Q

What are examples of hypothyroidism (insufficient T3 & T4 secretion)?

A

Hashimoto thyroiditis: AI disorder that destroys gland overtime
Myxoedema: non-pitting oedema, can evolve into a coma
Cretinism: due to congenital hypothyroidism, gland may be non-functional or absent

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15
Q

What are examples of hyperthyroidism (excessive T3 & T4 secretion)?

A

Grave’s disease: AI disorder than cannot control secretion, causes optic nerve damage, hypermetabolic state
Thyrotoxic crisis: uncontrolled hyperthyroidism, can be fatal

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16
Q

WHat gland do addison’s and cushings’ disease affect?

A

Adrenal gland, affects the hormone cortisol

17
Q

What is Addison’s disease? (CM, treatment)

A
  • Hypocortisolism
    CM: fatigue, Weight loss, hyperpigmentation salt craving
    low BGL
  • Addison’s crisis can be fatal (tachypnoea/cardia)
  • Treatment is corticosteroids and IV fluids
18
Q

What is Cushing’s syndrome and the causes?

A
  • Hypercortisolism
  • Pituitary or adrenal tumour, causing inc. ACTH release, which triggers cortisol release
  • Prolonged corticosteroid treatment
19
Q

What are symptoms and treatment of Cushing’s syndrome?

A
  • weight gain, muscle weakness, HTN and hyperglycaemia, thin skin
  • Measuring cortisol levels in blood is diagnosis
  • Surgical removal, radiation and medications to control cortisol production
20
Q

What are the 3 types of diabetes?

A

Type 1: hormone hyposecretion due to extensive pancreatic beta islet cell damage
Type 2: hormone insensitivity, insulin that is released is dysfunctional
Gestational: elevated BGL during pregnancy

21
Q

What is the pathophys. of T1DM?

A
  • Beta cell destruction due to antibody production
  • Insulin production decreases, hypergly.
  • Body compensates for beta cell loss until 80-90% are destroyed, and CM appear
  • genetic, 5-10% of all cases
22
Q

What is the pathophys. of T2DM?

A
  • dec. no. of of insulin receptors on beta cells or/and dysfunction in intracellular signalling
  • body compensates by overproduction of insulin initially
  • eventually beta cells cannot sustain hyperinsulinaemia leading to beta cell exhaustion
  • BGL rises, causing hypergly.
  • lifestyle, 90-95% of cases
23
Q

What is the pathophys. of gestational DM?

A
  • insulin resistance due to inc. levels of GH and placental hormones
  • beta cells cannot compensate an inc. in insulin, leading to maternal hyperglycaemia
  • can predispose foetus to T2DM, enhances growth factors of foetus
24
Q

What are complications of hypoglycaemia?

A
  • due to lifestyle imbalances (diet, medications)
  • can lead to brain dysfunction due to glucose imbalance, which triggers SNS activation
  • pale, clammy skin, seizures, headaches
25
Q

What are complications of diabetic ketoacidosis (DKA)?

A
  • due to insufficient insulin, high BGL and mobilisation of lipids, due to infection, stress or poor BGL management, T1DM
  • dehydration
  • ketoacidosis (kussmaul breaths)
  • metabolic acidosis (decreased serum ph and H2CO3)
  • electrolyte imbalances (abdo cramps, lethargy)
26
Q

What is Hyperosmolar Hyperglycaemic Non-ketotic Coma?

A
  • due to excess sugar consumption therefore excess insulin production
  • hyperglycaemia and dehydration develop because of the relative insulin deficit, but there is sufficient insulin to prevent DKA