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Phase 2a Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Endocrinology definition

A

The study of hormones (and their gland of origin), their receptors, the intracellular signalling pathways and their associated diseases.

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2
Q

What are the major endocrine organs

A 
Pituitary
Thyroid
Parathyroid
Adrenal
Pancreas
Ovary
Testes
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3
Q

What are the 5 hormonal axes?

A 
Posterior pituitary
Growth hormone
Thyroid hormone
Adrenal hormones
Gonadal hormones
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4
Q

What is a hormone?

A

A regulatory substance produced in an organism and transported in tissue fluids such as blood or sap to stimulate specific cells or tissues into action.

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5
Q

What does endocrine mean?

A

(Within/separate) glands pour secretions into the bloodstream (thyroid, adrenal, beta cells of pancreas).

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6
Q

What does exocrine mean?

A

(Outside) glands pour secretions through a duct to site of action (pancreas- amylase, lipase)

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7
Q

What is the hormone action of the endocrine system?

A

Blood-borne, acting at distal sites.

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8
Q

What is the hormone action of the paracrine system?

A

Acting on adjacent cells.

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9
Q

What is the hormone action of autocrine system?

A

Feedback on same cell that secreted the hormone.

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10
Q

How are water soluble hormones transported?

A

Unbound

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11
Q

How are fat-soluble proteins transported?

A

Protein bound

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12
Q

What is the cell interaction of water-soluble proteins?

A

Binds to surface receptor

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13
Q

What is the cell interaction of fat-soluble proteins?

A

Diffuses into the cell.

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14
Q

What is the half-life of water-soluble hormones?

A

Short

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15
Q

What is the half-life of fat-soluble hormones?

A

Long

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16
Q

How quick is the clearance of water-soluble hormones?

A

Fast

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17
Q

How quick is the clearance of fat-soluble hormones?

A

Slow

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18
Q

Examples of water-soluble hormones

A

Peptides, monoamines

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19
Q

Examples of fat-soluble hormones

A

Thyroid hormone, steroids

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20
Q

Where are water soluble hormones stored?

A

In vesicles

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21
Q

Where are fat-soluble hormones stored?

A

They aren’t stored, they are synthesised on demand.

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22
Q

What is the structure of peptide hormones?

A

Varying length, linear or ring structures with 2 chains that may bind to carbohydrates. Are hydrophilic and water soluble.

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23
Q

Where are peptide hormones stored?

A

Secretory granules. They are released in pulses or bursts.

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24
Q

How are peptide hormones cleared?

A

By tissue or circulating enzymes.

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25
Q

Example of peptide hormone

A

Human insulin

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26
Q

What are amine hormones derived from?

A

Amine hormones are derived from the amino acid tyrosine and include adrenaline, thyroxine and triiodothyronine.

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27
Q

What are amine hormones similar to?

A

Both peptide and steroid hormones.

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28
Q

What are iodothyronines?

A

Tyrosine with iodine incorporated.

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29
Q

Where is the hormone receptor location for peptide hormones?

A

Cell membrane

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30
Q

Where is the hormone receptor location for steroid hormones?

A

Cytoplasm

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31
Q

Where is the hormone receptor location for thyroid hormones?

A

Nucleus

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32
Q

Is vitamin D water soluble?

A

No. It is far soluble.

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33
Q

How does vitamin D enter the cell?

A

Enters directly to nucleus transported by vitamin D binding protein to stimulate mRNA production.

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34
Q

Why are 95% of adrenocortical and gonadal steroids protein bound?

A

They are fat soluble.

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35
Q

Where do adrenocortical and gonadal steroids go after entering the cell?

A

They pass through the nucleus, altered to activate metabolite and bind to a cytoplasmic receptor

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36
Q

How are adrenocortical and gonadal steroids cleared?

A

Broken down in the liver and excreted in the kidneys.

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37
Q

When does basal secretion occur?

A

Continuously or pulsatile.

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38
Q

What hormones are released in superadded rhythms (e.g. day-night cycle)

A

ACTH, prolactin, GH and TSH.

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39
Q

What hormones are released in relation to releasing inhibiting factors?

A

Dopamine inhibiting prolactin, sum of positive and negative effects (GHRH and somatostatin on GH).

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40
Q

How is hormone metabolism used to maintain hormones within a normal range?

A

Increased metabolism to reduce function.

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41
Q

How is hormone receptor induction used to maintain hormones within a normal range?

A

Induction of LH receptors by FSH in follicle.

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42
Q

How is hormone receptor down regulation used to maintain hormones within a normal range?

A

Hormone secreted in large quantities causes down regulation of its target receptors.

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43
Q

What is synergism?

A

Combined effects of 2 hormones amplified (glucagon with epinephrine)

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44
Q

What is antagonism?

A

One hormones opposes another hormone (glucagon antagonizes insulin).

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45
Q

Negative and positive feedback

A

Not that tricky to learn realistically

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46
Q

What is vasopressin?

A

Also known as ADH, a hormone that controls

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47
Q

What is oxytocin?

A

A hormone released by the pituitary gland that causes increased contraction of the uterus during labour and stimulates the ejection of milk into the ducts of the breasts.

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48
Q

What are examples of pituitary dysfunction?

A

Tumour mass effects, hormone excess and hormone deficiency

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49
Q

How can you investigate pituitary dysfunction?

A

Hormonal tests. If hormonal tests are abnormal or tumour mass effects performs MRI pituitary.

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50
Q

What do direct actions of growth hormone tend to be?

A

Usually metabolic; stimulates fat breakdown

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51
Q

What are the functions of thyroid hormone?

A

Accelerates food metabolism, increase protein synthesis, stimulation of carbohydrate metabolism, enhances fat metabolism, increase in ventilation rate, increase in cardiac output and heart rate, brain development during foetal life and postnatal development,
growth rate accelerated

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52
Q

What is cortisol?

A

A steroid hormone produced by the adrenal cortex and used medicinally to treat inflammation resulting from eczema and rheumatism.

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53
Q

What are the 2 parts of the adrenal gland?

A

The cortex and the medulla

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54
Q

What are the 3 parts of the cortex of the adrenal gland?

A

The capsule, zona glomerulosa, zona fasciculata

55
Q

What are the 2 parts medulla of the adrenal gland?

A

Zona reticularis and adrenal medulla

56
Q

Where in the adrenal gland is adrenaline produced and secreted?

A

In the adrenal medulla

57
Q

What is the renin-angiotensin system

A

The renin–angiotensin system (RAS), or renin–angiotensin–aldosterone system (RAAS), is a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as systemic vascular resistance.

58
Q

Where is vasopressin and oxytocin made?

A

In the paraventricular nucleus and supraoptic nucleus

59
Q

How is vasopressin and oxytocin transported to the posterior pituitary?

A

In the axoplasm of the neurons.

60
Q

What receptors does ADH bind to?

A

Binds to G-protein coupled 7 transmembrane domain receptors
V1a - vasculature
V2 - renal collecting tubules - reabsorption of water
V1b - pituitary

61
Q

What is the release of ADH controlled by?

A

Osmoreceptors in hypothalamus- day to day

Baroreceptors in brainstem and great vessels in an emergency

62
Q

Water breakdown in the human body

A

Intracellular fluid is 2/3 of total body water (28L), extracellular fluid is 1/3 total body water (14L). Of the extracellular fluid, 1/4 is intravascular fluid (3.5L) and 3/4 is interstitial fluid (10.5L). Total body water is 60% of total body weight (42L)

63
Q

What is the feedback loop for water balance?

A

Water ingested
Plasma, osmolality decreases, cellular hydration increases, causes a decrease in thirst and decrease in vasopressin secretion, you drink less water and increased amount of urine expelled

64
Q

What is the definition of osmolality?

A

The concentration of a solution expressed as the total number of solute particles per kilogram.

65
Q

Why is concentration per kilo slightly different to osmolality?

A

Approx 6% of volume is made up by lipids and proteins.

66
Q

Is the size of the particle important in osmolality?

A

No. one molecule of a larger protein albumin same effect as NA+

67
Q

How do you calculate osmolality?

A

Not sure.

68
Q

What disease is associated with a lack of vasopressin?

A

Cranial diabetes insipidus. Is uncommon but life threatening.

69
Q

What is the disease associated with resistance to action of vasopressin?

A

Nephrogenic diabetes insipidus. Is uncommon but life threatening.

70
Q

What is the disease associated with too much vasopressin when it should not be released?

A

Syndrome of antidiuretic hormone secretion (SIADH). Common but can be life threatening.

71
Q

What is diabetes insipidus?

A

An uncommon disorder that causes an imbalance of fluids in the body.

72
Q

What are the 3 P’s of diabetes insipidus and what do they mean?

A

Polydipsia (increased thirst), polyuria (increased urine production) and polyphagia (extreme hunger)

73
Q

What is glycosuria?

A

The presence of glucose or other sugars in your urine. There is no glycosuria in diabetes insipidus.

74
Q

How do you diagnose diabetes insipidus?

A

Measure urine volume (lots of urine). Check renal function and serum calcium. Biochemistry.

75
Q

What biochemistry is checked in diabetes insipidus?

A

Inappropriately dilute urine for plasma osmolality, serum osmo >300 AND urine osmo<200 consistent with DI, normonatraemia or hypernatraemia,
water deprivation test, hypertonic saline infusion and measurement of AVP.

76
Q

What can the acquired causes of cranial diabetes insipidus be?

A

Idiopathic, tumours, trauma, infections, vascular, inflammatory.

77
Q

What are the primary genetic causes of diabetes insipidus?

A

DIMOAD (wolfdram syndrome), autosomal dominant. Rarely autosomal recessive.

78
Q

What are the primary developmental causes of diabetes insipidus?

A

Septo-optic dysplasia.

79
Q

How do you manage cranial DI?

A

Treat any underlying condition. Desmopressin- high activity at V2 receptors. Try to avoid participating drugs.

80
Q

Definition of hyponatremia?

A

A serum concentration of serum sodium <135mmol/l. Is severe when

81
Q

What are the symptoms of moderate hyponatremia?

A

Headache, irritability, nausea/vomiting, mental slowing, unstable gait/falls, confusion/delirium and disorientation

82
Q

What are the symptoms or severe hyponatremia?

A

Stupor/coma, convulsions, respiratory arrest.

83
Q

What is the general treatment of hyponatremia?

A

Stop hypotonic fluids. Review drug cards.

84
Q

What are the general treatments of hyponatremia?

A

Plasma and urine osmolality, urinary Na+, glucose, TFT’s, +/- assessment of cortisol and an assessment of underlying causes (e.g. chest imaging).

85
Q

What is SIADH (syndrome of antidiuretic hormone secretion)?

A

The body makes too much ADH. Too much water is retained and the urine produced is the wrong concentration.

86
Q

How do you treat SIADH?

A

Ensure correct diagnosis, allow/facilitate increase in serum Na+, treat any underlying condition, identify and stop any causative drug (if possible), in acute setting - daily U+E - hospital, in chronic setting - weekly to monthly U+E - hospital/GP, frequent comorbidity, na+>130 mmol/l - usually no need for urgent intervention.

87
Q

What are the 2 lobes of the pituitary gland?

A

Anterior lobe and posterior lobe.

88
Q

What is tissue of the anterior lobe of the pituitary gland?

A

Glandular tissue. Accounts for 75% of total weight.

89
Q

What is the tissue of the posterior lobe of the pituitary gland?

A

Nerve tissue. Contains axons that originate in the hypothalamus.

90
Q

What are examples of pituitary mass lesions?

A

Non-Functioning Pituitary Adenomas
Endocrine active pituitary adenomas
Malignant pituitary tumors: Functional and non-functional pituitary carcinoma
Metastases in the pituitary (breast, lung, stomach, kidney)
Pituitary cysts:Rathke’s cleft cyst, Mucoceles.

91
Q

What are examples of pituitary developmental abnormalities?

A

Craniopharyngioma (occasionally intrasellar location), germinoma

92
Q

What are 2 primary tumours of the central nervous system?

A

Perisellar menigioma and optic glioma.

93
Q

What are craniopharyngiomas?

A

Benign brain tumours

94
Q

Where do craniopharyngiomas arise from?

A

From squamous epithelial cells remnants of Rathke’s pouch
Adamantinous; cyst formation and calcification
Squamous papillary: well circumscribed

95
Q

What are the symptoms of having a craniopharyngioma?

A

Raised ICP, visual disturbances, growth failure, pituitary hormone deficiency, weight increase

96
Q

What is Rathke’s cyst?

A

Single layer of epithelial cells mucoid, cellular, or serous components in cyst fluid derived from the Rathke’s pouch.

97
Q

How does a Rathke’s cyst present?

A

Most are small and asymptomatic, but patient may present with a headache, amenorrhoea, hypopituitarism and hydrocephalus.

98
Q

What are meningioma?

A

Commonest tumour of region after pituitary adenoma. Complication of radiotherapy

99
Q

What are meningioma associated with?

A

Visual disturbance and endocrine dysfunction. Present with loss of visual acuity, endocrine dysfunction and visual field defects.

100
Q

What is lymphocytic hypophysitis?

A

Inflammation of the pituitary gland due to an autoimmune reaction

101
Q

What is non-functioning pituitary adenoma (NFPA)

A

Benign adenohypophysis tumours not associated with clinical evidence of hormonal hypersecretion.

102
Q

How do you find non-functioning tumours?

A

Non specific test but the absence of hormonal secretion. Test normal pituitary function.

103
Q

When and how do you treat non-function tumours?

A

Trans-spheniodal surgery if threatening eyesight or progressively increasing size.

104
Q

How do you test pituitary function?

A

Can be tricky. Many hormones: GH, LH/FSH, ACTH, TSH and ADH. May have deficiency of one or all and may be borderline. Circadian rhythms and pulsatile

105
Q

What is prolactin?

A

A hormone made by the pituitary gland that causes the breasts to grow and make milk during pregnancy and after birth.

106
Q

What may cause raised levels of prolactin?

A

Stress, drugs (antipsychotics), stalk pressure, prolactinoma.

107
Q

What is the preferred method of imaging the pituitary?

A

MRI scan. Is better for visualisation of soft tissues than CT scan.

108
Q

When are CT scans used in pituitary investigations?

A

When looking at bony structures and calcifications within soft tissues.

109
Q

How does thyroxine replacement work?

A

Underactive thyroid treated with levothyroxine to achieve mid to upper levels of thyroxine.

110
Q

How does growth hormone replacement work?

A

Stimulates growth of all bodily tissues. Improves lipid profiles, body composition and bone mineral density.

111
Q

How does testosterone replacement work?

A

Different types of formulation: gels, injections, oral. Improve bone mineral density, libido, function, energy levels and sense of well being, muscle mass and reduced fat.

112
Q

How does oestrogen replacement work>

A

Oral oestrogen or combined oestrogen/progestogen formulations (also transdermal, topical gels, intravaginal creams)
Alleviate flushes and night sweats; improve vaginal atrophy
Reduce risk of cardiovascular disease, osteoporosis and mortality.

113
Q

How does desmopressin work?

A

Used to replace low levels of vasopressin. Different formulations: subcutaneously, orally, intra-nasally, sublingually. Adjusted according to symptoms. Monitor sodium levels.

114
Q

How is CHO regulated in a fasting state?

A

All glucose comes from the liver through a breakdown of glycogen and glycogenesis. Glucose is delivered to insulin dependent tissues. Insulin levels are low. Muscles use FFA for fuel.

115
Q

How is CHO regulated after feeding?

A

Increased glucose stimulates insulin secretion and suppresses glucagon. 40% of glucose goes to liver and 60% goes to skeletal muscle. Glycogen stores replenished and lipolysis suppressed.

116
Q

How is insulin secreted from the beta-cell?

A

Glucose entry through GLUT2 glucose transporter. . Does some stuff then insulin secretion from insulin secretory granules.

117
Q

What is the action of insulin in muscle and fat cells?

A

Binds to insulin receptor. Does some stuff. Glucose enters the cell via GLUT4 vesicle

118
Q

What does insulin do?

A

Supresses hepatic glucose, increases glucose uptake into insulin sensitive tissues and suppresses lipolysis and breakdown of muscle.

119
Q

What is glucagon?

A

A hormone formed in the pancreas which promotes the breakdown of glycogen to glucose in the liver.

120
Q

What does glucagon do?

A

Increases hepatic glucose output, reduces peripheral glucose uptake, stimulates peripheral release of gluconeogenic precursors (glycerol, AAs).

121
Q

What is diabetes mellitus?

A

A disorder in which the body does not produce enough or respond normally to insulin, causing blood sugar (glucose) levels to be abnormally high.

122
Q

How does diabetes mellitus cause morbidity and mortality?

A

Acute hyperglycaemia left untreated leads to diabetic ketoacidosis (DKA) and hyperosmolar coma (Hyperosmolar Hyperglycaemic State), tissue complications (both macro and microvascular). Side effects of treatment- hypoglycaemia.

123
Q

What are all the types of diabetes?

A

Type 1, type 2 (includes gestational and medication induced diabetes), maturity onset diabetes of youth (MODY), also called monozygotic diabetes, pancreatic diabetes
“Endocrine Diabetes” (acromegaly/Cushings), malnutrition related diabetes.

124
Q

What is the definition of diabetes?

A

Symptoms and random plasma glucose > 11 mmol/l, fasting plasma glucose > 7 mmol/l.

125
Q

What is the pathogenesis of type 1 diabetes?

A

An insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction. Beta cells expressing antigens of the HLA histocompatibility system may be due to an environmental stimulus. Activates a chronic cell mediated immune process leading to chronic ‘insulitis’

126
Q

What does failure of insulin secretion lead to?

A

Continued breakdown of liver glycogen, lots of lipolysis and skeletal muscle breakdown and inappropriate increase in hepatic glucose output and suppression of peripheral glucose uptake.

127
Q

What does failure to treat with insulin lead to?

A

Increase in circulating glucagon further increasing glucose, perceived ‘stress’ leads to increased cortisol and adrenaline, progressive catabolic state and increasing levels of ketones.

128
Q

What does reduced insulin lead to?

A

Fat breakdown and formation of glycerol and FFA.

129
Q

What does FFA do?

A

Impairs glucose uptake. Transported to the liver, providing energy for gluconeogenesis and are oxidised to form ketone bodies.

130
Q

What is ketogenesis sensitive to?

A

Ketogenesis is extremely sensitive to insulin.

131
Q

What is ketoacidosis?

A

A metabolic state caused by controlled production of ketone bodies that cause metabolic acidosis.

132
Q

What does the absence of insulin and rising counterregulatory hormones lead to?

A

Increasing hyperglycaemia and rising ketones.

133
Q

What does glucose and ketone escaping in the urine lead to in ketoacidosis?

A

An osmotic diuresis and falling circulating blood volume.

134
Q

Why is ketoacidosis problematic?

A

Ketones (weak organic acids) cause anorexia and vomiting. Vicious circle of increasing dehydration, hyperglycaemia and increasing acidosis eventually lead to circulatory collapse and death

Phase 2a Medicine (6 decks)

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