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EXAM 2 > Pituitary & adrenal glands > Flashcards

Pituitary & adrenal glands Flashcards

1
Q

What are steroid hormones?

A

A lipophilic chemical messenger.
* Easily pass through membranes.
* Bound to carrier proteins in the blood and therefore have longer lasting effects in the circulation.

Example: Estrogen

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2
Q

Non-steroid hormone action

A
  1. Hormone binds to a surface receptor (G-coupled receptor)
  2. Activation and detatchement of Ga stimulatory subunit.
  3. Stimulation of adenylyl cyclase = cAMP synthesis
  4. cAMP causes a cascade of internal reactions.
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3
Q

Steroid action

A

When the steroid hormone passively diffuses through the membrane and either…
* Binds to a receptor protein
* Binds to hormone-receptor complex of which causes a change in gene activity = Increases transcription & mRNA production

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4
Q

Posterior gland hormones

A

Oxytocin, vasopressin

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5
Q

Anterior gland hormones

A

The anterior gland BOTH synthesizes & secretes…
* Adrenocorticotrophic hormone
* GH
* TSH
* Follicle-stimulating hormone
* Prolactin

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6
Q

Vasopressin

A
  • An anti-diuretic hormone that increases the reabsorption of water by binding to V2 receptors at the distal tubule and collecting ducts.
  • Also binds to V1 which causes vasoconstriction
  • Synthetically exists as desmopressin
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7
Q

Oxytocin

A

A hormone that…
* causes the contraction of uterine muscle [Child birth]
* Promotes ‘ejection of milk from mammary glands’ [Breastfeeding]

Can be injected as syntocinon to induce labour and prevent postpartum haemorrhage

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8
Q

Diabetes insipidus

A
  • Cause: Lack of vasopressin effect
  • Symptoms: Polyuria, Polydipsia
  • Left untreated leads to: Hypotension, tachycardia, hypernatremia.

There are two types of DI… Cranial and nephrogenic

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9
Q

Nephrogenic DI

A

When the collecting ducts DO NOT respond to vasopressin.

Urine osmolarity levels should be low after a water deprivation test as the desmopressin should have little to no effect.

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10
Q

What are some of the common causes of nephrogenic DI?

A

Likely causes include…
* Bi-polar disorder medication (contain lithium)
* Genetic mutation at AVPR 2 gene.
* Intrinsic kidney disease
* Hypokalaemia and/or hypercalcaemia

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11
Q

Cranial DI

A

When the hypothalamus DOES NOT PRODUCE vasopressin.

Symptoms: Polydipsia, Postural hypotension, hypernatraemia, dehydration

Urine osmolarity should be HIGH after a Water deprivation test.

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12
Q

What are the existing causes of cranial DI?

x / 7

A

Likely causes include:
* Brain malformation.
* Brain surgery
* Head injuries
* Radiotherapy
* Brain tumors
* Idiopathic - spontaneous or from unknown cause
* Infection - Meningitis, Encephalitis

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13
Q

Primary dipsia

A

The excessive drinking of water that leads to an increase in dilute urine without it being Diabetes insipidus.

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14
Q

What is a water deprivation test?

A

The primary test for diabetes insipidus.
1. The individual undergoes 8 hours inwhich NO fluid intake is allowed.
2. Urine osmolarity check and serum osmolarity check of patients urine.
3. Desmopressin injection is administered.
4. Another 8 hours until the next urine & serum osmolarity test are completed.

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15
Q

What should the urine osmolarity levels look like after a deprivation test to indicate Cranial DI?

A

The osmolarity levels should indicate…
* Before: Low
* After: High

Bc the body still responds to vasopressin.

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16
Q

What should the urine osmolarity levels look like for nephrogenic DI?

A

The osmolarity levels should indicate…
* Before desmopressin: Low
* After desmopressin: Low

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17
Q

What water deprivation test result would indicate primary dipsia and not DI?

A

A high urine osmolarity before desmopressin is administered.

Note that the test should not proceed if HIGH levels are indicated in the first stage of the test.

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18
Q

Three-hormone sequence

A

When the release of hypothalamic hormones cause the release of tropic hormones from the pituary gland that act at endocrine targets. This subsequently causes the release of effector hormones.

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19
Q

TRH hormone sequence

A

1. TRH released from hypothalamus.
2. Release of TSH from the anterior gland.
3. Acts at thyroid gland causing the release of thyroxine (T4) and triodothyronine (T3).

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20
Q

CRH (corticotropin-releasing hormone) sequence

A
  1. CRH released from the hypothalamus
  2. Causes the release of ACTH from the anterior gland.
  3. ACTH acts at the adrenal cortex henceforth causing the release of cortisol.
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21
Q

What are the regulatory factors of the anterior pituary hormones?

A
  • Inhibitory hormones: Dopamine, somastatin
  • Negative feedback loop from target-gland hormones
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22
Q

What does the growth hormone do?

A
  • Lengthening of bones
  • Net synthesis of proteins
  • Increase size & number of cells in soft tissue
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23
Q

What is GH deficiency?

A

Gh deficiency, also known as ‘dwarfism’, is when either the body does not respond to GHRH or when it does not produce it.

Primary: Pituary gland defect
Secondary: Hypothalamic defect

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24
Q

What does GH deficiency lead to?

A

It leads to a short stature due to…
* Reduced skeletal growth
* Reduced muscle protein synthesis
* Increased fat deposition

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25
Q

GH deficiency treatment

A
  • Somatotropin SC injection: recombinant GH
  • Sermorelin/somatorelin SC : recombinant GHRH
  • Mecaserim : recombinant IGF-1

SC: subcutaneous

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26
Q

What is Somatotropin?

A

A synthetic version of GH that is used for GH deficiency, turner’s syndrome , chronic renal insufficiency in children.

  • Ethical considerations regarding therapy as it increases the likelyhood of developing tumors.
  • Requires close monitoring
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27
Q

What is somatorelin/sermorelin?

A

A GHRH recombinant drug that is used as a diagnostic tool for GH secretion {secondary GH deficiency}

28
Q

What is Mecaserim?

A

A recombinant of IGF used as subcutaneous treatment for growth failure in children (lacking IGF-1)

IGF = insulin-like growth factor

29
Q

What is GH excess?

A

When the pituary gland produces and secretes TOO MUCH GH .
* In childhood, this leads to growth in height where there is no distortion of body proportion {gigantism}.

  • In adulthood, it is called acromegaly and it involves the thickening of bones, soft tissue proliferation and possible peripheral nerve disorders as nerves can beocome trapped.
30
Q

GH excess treatments

A
  • Trans-sphenooidal and/or debulking surgery
  • Somatostatin analogue therapy (in adjunction with surgery)
31
Q

What are the Somatostatin analogues used for GH excess therapy?

A
  • Ocreotide
  • Lanreotide
  • Pasireotide
32
Q

What is ocreotide and what is it used for?

A

A somatostatin analogue used as a subcutaneous therapy for…
* Carcinoid syndrome
* Acromegaly (GH excess)

Carcinoid syndrome= A tumor that secretes chemicals into the bloodstream

33
Q

What is Lanreotide and what is it used for?

A

A somatostatin analogue that is subcutantously injected for…
* Carcinoid syndrome (a tumor that secretes chemicals)
* Acromegaly (if first time on somatostatin analogue)
* Thyroid tumors

34
Q

What is Pasireotide and what is it used for?

A

A somatostatin analogue subcutaneously used for…
* Cushing’s disease when surgery is not a viable option.
* Acromegaly when surgery is not a viable option nor is another somatostatin analogue.

It acts at somatostatin receptors in the pituary gland and inhibits the release of ACTH.

35
Q

The adrenal cortex

A

The matrix between the capsule and medulla of the adrenal glands. It consists of…
* Zona glomerulosa : where aldosterone is produced
* Zona fasciculata : where cortisol and corticosteroids are produced.
* Zona reticularis : where androgens are produced.

36
Q

What is aldosterone and how does it work?

A

Aldosterone is an anti-diuretic hormone that is secreted upon the activation of angiotensin II frm the release of renin.

It binds to receptors at the distal tubule and collecting ducts and increases sodium reabsoprtion and potassium excretion.

37
Q

What is cortisol and how does it work?

A

It is a glucocorticoid hormone that is produced from cholesterol. It..
* Increases blood glucose
* Has immunosuppressive effects (via inhibition of cytokines etc.)
* Allows other actions to take place

38
Q

Cortisol concentration factors

A
  • Cortisol has diurnal rhythm meaning it is at its HIGHEST in the mornning and LOWEST at night.
  • Physical and psycological stress increases secretion of cortisol (e.g. surgery, injury, anxiety etc.)
39
Q

What is Conn’s syndrome and what does it result in?

A

Primary hyperaldosteronism induced by an issue adrenal glands causing oversecretion. This is usually caused by adrenal tumors consisting of aldosterone-secreting cells
* Hypernatraemia
* Hypokalaemia
* High blood pressure

40
Q

What is secondary hyperaldosteronism?

A

Hypersecretion of aldosterone due to the renin-angiotensin aldosterone system. This is bc blood pressure in the kidneys is disproportionately lower than the BP in the rest of the body. This leads to…
* Hypernatraemia
* Hypokalaemia
* High blood pressure

41
Q

What is cushing’s syndrome and what is it caused by?

A

Cushing’s syndrome involves the hypersecretion of cortisol. It can be caused by…
* Excess CRH from the hypothalamus causing overstimulation of the Zona fasciculata.
* Adrenal tumors (secrete excess cortisol)
* ACTH-secreting tumors (in places other than the pituary gland - usually lungs)

CRH = Corticotropin-releasing hormone

42
Q

What does cushing’s syndrome lead to?

A

Cushing’s syndrome can lead to…
* Fat distribution
* Osteoperosis
* Hypertension
* Psychosis
* Depression

43
Q

What is the cushing’s syndrome treatment?

A
  • Surgery or radiotherapy
  • Corticosteroid inhibitors
44
Q

TRUE OR FALSE

HIGH serum renin in hyperaldosteronism indicates primary (conn’s syndrome)

A

FALSE
High serum renin indicates hypersecretion of renin that would lead to hypersecretion of aldosterone. As this is not due to the adrenal glands… it is secondary hyperaldosteronism.

45
Q

What can cause secondary hyperaldosteronism?

In terms of renal defects

A
  • Renal artery stenosis: Patients with atherosclerosis
  • Renal artery obstruction

Renal artery stenosis = narrowing of renal arteries.

46
Q

What are the pharmaceutical treatments for Cushing’s syndrome ?

A
  • Metyrapone
  • Ketoconazole
  • Carbenexone
  • Trilostane (not used in the UK)
  • Aminoglutethimide (not used in the UK)
47
Q

What is Metyrapone and how does it work?

A

Metyrapone is a competitive inhibitor of 11beta-hydroxylase preventing the conversion of deoxycortisol to cortisol.

It is used for the differential diagnosis of ACTH-dependent cushing’s syndrome

Also inhibits the productions of aldosterone.

Aldosterone synthesis includes the same enzyme.

48
Q

What is Ketoconazole and how does it work?

A

Ketoconazole is a competitive inhibitor of the 17a-hydroxylation steps that are involved in the synthesis of aldosterone, cortisol and dihydrotestosterone (DHT).

It is commonly used for endogenous cushing’s syndrome

49
Q

What is Trilostane and how does it work?

A

Trilostane is a competitive inhibitor of 3beta-dehydrogenase steps involved in the synthesis of cortisol, aldosterone and dihydrotestosterone.

It is not used in the UK.

50
Q

What is Aminoglutethimide and how does it work?

A

Aminoglutethimide prevents the conversion of cholesterol to pregnenolone and therefore inhibiting the synthesis of cortisol.

Also inhibits the synthesis of aldosterone, DHT and estradiol.

It is not used in the UK.

51
Q

What is carbenexone and what is it used for?

A

Carbenexone is a drug that inhibits the conversion from hydrocortisone to cortisone. Cortisone being the inactive form of cortisol therefore less cortisone results in less cortisol.

52
Q

What is Addison’s disease and what are the symptoms ?

A

Addison’s disease is the atrophy of the adrenal glands that results in cortisol and aldosterone deficiency.
Symptoms:
* Lethargy
* Depression
* Weight loss
* Anorexia

53
Q

What is an Addisonian crisis ?

A

An addisonian crisis is a life-threatening situation that results in LOW BLOOD PRESSURE, LOW BLOOD SUGAR and HYPERKALAEMIA.
Symptoms include vomiting, abdominal pain, weakness, hypotension and coma.

This is a medical emergency.

54
Q

What is the pharmaceutical treatment for Addison’s disease ?

A

Treatment for addison’s disease involves lifelong steroid replacement therapy. This involves taking a glucocorticoid in combination with a mineralocorticoid;
* Hydrocortisone 20-30 mg in 2 divided doses/day
* Fludrocortisone 50-300 mcg /day

55
Q

What is the treatment for Addisonian crisis ?

A

Hydrocortisone IV | 100 mg every 6-8 hours

56
Q

What are steroids commonly used for (include drugs)

A

Steroid replacement therapy
* For addison’s disease
* Hydrocortisone + Fludrocortisone

Anti-inflammatory & immunosuppression {asthma, IBS, Eczema, post-transplant}
* Glucocorticoids: Prednisolone, Hydrocortisone, Betametasone, Dexamethasone

57
Q

What are the topical adverse effects of steroids ?

A
  • Skin thinning
  • Skin infection
  • Folliculitus
  • Stretch marks
  • Acne
58
Q

What are the inhaled adverse effects of steroids ?

A

Side effects can include…
* Hoarseness
* Dysphonia
* Throat irritation
* Candida infection

59
Q

What is Octreotide and what is it used for?

A

A somastatin analogue that is subcutaneously injected for the treatment of Carcinoid syndrome and acromegaly .

60
Q

What is Somatostatin and what does it do?

A

A natural hormone that works as an inhibitor at various receptors.
It inhibits…
* The release of GH (from the anterior pituitary)
* The release of thyrotropin & corticotropin
* Glucagon & insulin (from the pancreas)

61
Q

What is the adrenal suppression issue with taking steroids?

A

Taking steroids over a long-term period {3+ weeks} inhibits the secretion of endogenous steroids (cortisol & aldosterone). Abrupt withdrawal from exogenous steroids will lead to acute adrenal insufficiency .

Therefore, patients should be gradually withdrawn from exogenous steroids

62
Q

What is the role of the pharmacist surrounding steroids?

A

The pharmacist should…
* Ensure patients taking long-term steroids are supplied with a Steroid treatment card
* Where possible, promote low-dose and short period steroid treatment.

  • Ensure gradual withdrawal from steroids.
  • Advize that a higher dose is required surrounding intercurrent illness/trauma/surgery.
63
Q

What is the issue with infection when taking steroids?

A

Steroids are immunosuppressants and therefore your susceptibility of contracting an infection is increased during long-course treatments.

Patients are advised that infection symptoms may present as atypical.

64
Q

What other psychiatric side effects can high doses of steroids also cause ?

A

Psychiatric reactions
* Euphoria
* Insomnia
* Nightmares
* Irritability
* Suicidal thoughts

65
Q

What are the general system adverse effects of taking mineralocorticoids ?

A

These are…
* Hypertension
* Hypernatraemia
* Hypokalaemia
* Hypocalcaemia

66
Q

What are the general adverse effects of taking glucocorticoids ?

x/5

A

These are…
* Glucose intolerance
* Osteoperosis
* Gi disturbances
* Cushing’s syndrome

  • Growth suppression in children
67
Q
A

EXAM 2 (8 decks)

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