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Endocrinology > Pituitary, Adrenal, GH, VP Disorders > Flashcards

Pituitary, Adrenal, GH, VP Disorders Flashcards

1
Q

What is Acromegaly? and what RF (2) are associated with it?

A
  1. Excess GH that causes inc growth of bones and soft tissues (in particular extremities) through inc secretion of IGF-1.
  2. Acromegaly occurs after puberty. If excess GH occurs before puberty (i.e. before epiphyses fuse), this is known as gigantism.
  3. RF = Fx, Multiple endocrine neoplasia type 1 (MEN-1)
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2
Q

Causes of Acromegaly (4)?

A
  1. Pituitary benign adenoma (most common, 95% of cases)
  2. Hypothalamic tumours
  3. Ectopic GH/GRH producing tumours
  4. Congenital Conditions such as Wermer’s Syndrome (MEN1)
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3
Q

Signs and symptoms of Acromegaly (11) due to tumour, excess GH, hypogonadal sx

A

Insidious onset so diagnosis is often delayed:

Due to tumour:

  1. Headache
  2. Bitemporal hemianopia

Due to excess GH

  1. Enlargement of hand, feet, tonuge - Ask if they’ve had to change ring and shoe size, if they have obstructive sleep apnoea?
  2. Growth of jaw (prognathism) and protrusion of forehead
  3. Coarse facial features
  4. Excessive sweating and oily skin
  5. Joints ache and pain
  6. Dental changes: separation, jaw malocclusion, lower dental protruding

Hypogonadal symptoms

  1. Erectile dysfunction
  2. Dec libido
  3. Amenorrhoea
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4
Q

Investigations of Acromegaly (6)

A
  1. Serum IGF1 (1st line Ix), GH
    - If basal serum GH is >0.4mcg/L or there is elevated serum IGF, proceed to OGTT.
  2. 75g OGTT
    - GH is normally inhibited by high glucose levels.
    - if GH levels is below 1.0mcg/L = suppression
    - If glucose fails to suppress GH so that GH is above 1.0mcg/L this confirms acromegaly
  3. MRI
    - Identitfy pituitary tumour
    - or CT to identify ectopic tumours
  4. ECG, ECHO
    - Any cardiac changes such as hypertrophy.
  5. Old photos
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5
Q

Treatment and Management of Acromegaly (4)

A

Goal: reduce GH and IGF to normal levels

  1. Transsphenoidal Surgery (for pituitary adenoma) - 1st line
  2. Radiotherapy and/or Somatostatin (inhibits GH) analogues - 2nd line
  3. GH competitive antagonist
    - Pegvisomant blocks action of GH by binding to its receptor.
  4. Dopamine agonists

Yearly follow up - monitors GH, IGF1, assess visual fields.

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6
Q

Complications of Acromegaly

A
  1. Carpal tunnel syndrome
    - Inc pressure on nerves due to in bone size
  2. Diabetes mellitus
    - Diabetogenic effects on GH
    - ‘Insulin-resistant’ diabetes
  3. Congestive heart failure
    - Enlarged heart
  4. Hypertension
  5. Obstructive sleep apnoea
  6. Anxiety and depression due to self esteem
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7
Q

What is hyperprolactinaemia?

A

Raised levels of prolactin in the blood

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8
Q

Describe feedback mechanism of prolactin

A
  1. TRH (from hypothalamus) stimulates pituitary to produce PL
  2. High PL levels in blood sends negative fb to hypothalamus to inhibit GnRH and releases DA
  3. DA inhibits PL production and this overrides TRH stimulation (in non-pregnant individuals)
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9
Q

What is the importance of prolactin?

A

Prolactin important for breastmilk production (after delivery)

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10
Q

What causes raised prolactin levels (5)?

A
  1. Prolactinoma: excess production of PL from pituitary
  2. Dopamine antagonists: Anti-psychotics, antiemetic drugs
  3. Damage of pituitary stalk (via trauma, surgery)
    - Reduce dopamine release
  4. Stress
    - stress-induced neuroendocrine changes of DA + 5HT will affect PL levels
  5. Hypothyroidism
    - will stimulate inc TSH production and this will increase PL secretion as well TSH
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11
Q

6 Signs and symptoms of hyperprolactinaemia (think tumour signs too)

A

(1. ) Due to tumour: Headache + bitemporal hemianopia
(2. ) Galactorrhoea
(3. ) Amenorrhoea/Oligomenorrhea
(4. ) Infertility
- PL inhibits GnRH so low levels of FSH, LH
(5. ) Loss of libido
(6. ) Erectile dysfunction

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12
Q

Diagnosis of hyperprolactinaemia

A
  1. 0900-1600 Serum prolactin
    - ensure venepuncture taken is stress-free
  2. Pregnancy test, U&E, TFT
  3. MRI
    - visualise pituitary
    - classify prolactinoma size, macro or microadenoma
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13
Q

3 Treatment and management of hyperprolactinaemia

A
  1. DA agonist (1st line)
  2. Trans-sphenoidal surgery
    - for macroadenomas or failed medical therapy
  3. Follow up
    - monitor PL
    - Check if any headaches, visual loss.
    - Dec medication after 2y if possible.
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14
Q

What is Cushing Syndrome? and its RF?

A
  • Elevated cortisol levels in the blood

RF

  • Pituitary or adrenal tumor
  • 25-40y
  • Lung cancer
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15
Q

Describe the feedback mechanism of Cortisol

A

(1. ) Hypothalamus (CRH) -> Anterior pituitary (ACTH) -> Zona fasciculate (cortisol).
(2. ) High cortisol levels causes hypothalamus and pituitary gland to dec CRH + ACTH secretion, thus less cortisol is produced [negative fb].

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16
Q

What is the function of cortisol? (4)

A

Cortisol is a steroid hormone - lipid soluble + hyrdophillic.

(1. ) Cortisol is part of circadian rhythm where levels peak in the morning and drop in the evening
(2. ) Cortisol maintains BP by inc sensitivity of blood vessels to catecholamines –> vasoconstrict
(3. ) Cortisol dampens inflammatory and immune response —> Dec production + release of mediators and inhibits T-lymphocytes

(4. ) In stress, cortisol:
- Inc Gluconeogenesis
- Inc proteolysis
- Inc Lipolysis

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17
Q

Cushing Syndrome Pathology (5)

A

(1.) Muscle, bone, skin breakdown

(2. ) Inc Gluconeogenesis so elevated BGL
- Leads to elevated insulin levels that targets adipocytes in the centre of body –> central obesity

(3. ) HTN
- Amplified effect of catecholamines on blood vessels
- Cortisol is structurally similar to mineralocorticoid so it can bind to mineralcorticoid-receptors in zona glomerulosa
- This inc BP by retaining fluid.

(4. ) Inhibit of GnRH secretion
- affects normal ovarian and testicular function.

(5. ) Dampens the inflammatory and immune response
- individuals more susceptible to infections

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18
Q

Causes of Cushing Syndrome

A

(1) ACTH-dependent disease
- excessive ACTH from the pituitary gland
- ectopic ACTH-producing tumours
- or excess ACTH administration.

(2) Non-ACTH-dependent
- adrenal adenomas
- excess glucocorticoid administration

(3.) Steroid medications over a long period of time

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19
Q

Why may you get an Adrenal gland Shrinkage in a pt that has adrenal adenoma/carcinoma?

A
  • Zona fasciculata divides abnormally and secrete excess cortisol.
  • Excess cortisol supresses CRH and ACTH production.
  • This does not effect zona fasciculata neoplastic cells as they are autonomous
  • zona fasciculata of normal adrenal gland shrinks and produces less than the standard amount of cortisol.
  • The net cortisol result is still abnormally high so Cushing syndrome can develop.
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20
Q

Symptoms of Cushing Syndrome (5.)

A
  1. Muscle breakdown: wasting and thin extremities
  2. Abdominal striae (thin skin, easy bruised)
  3. Bone breakdown: Fractures, osteoporosis
  4. Fat redistribution: moon face, buffalo hump, truncal obesity
  5. Hyperglycaemia
  6. complications: DM, HTN, vulnerability to infections, amenorrhea, psychiatric sx
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21
Q

Examination and 5 Investigations of Cushing Syndrome

A

Physical Ex

(1. ) Striae, oedema, muscle wasting/weakness, excess hair?
(2. ) Visual field defects if pituitary tumour?

Investigations
(1.) Blood: hypokalaemia, elevated WBC (in 40%)

(2. ) Cortisol (urine and blood)
- Normal levels = high in morning, low at night
- Cushings = high throughout

(3. ) Dexamethasone suppression test 1st line
- dexamethasone: exogenous steroid that suppresses ACTH production
- Normal = decrease in serum cortisol levels
- Cushing syndrome caused by endogenous cortisol production = serum cortisol levels remain unchanged.

(4. ) Plasma ACTH (determine cause)
- Normal = highest at 8am and lowest at night
- Low ACTH = adrenal adenoma, carcinoma
- High ACTH = Cushing disease, ectopic acth production

(5.) MRI/CT: ectopic tumours

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22
Q

Treatment and Management of Cushing’s

A
  1. Referral when suspecting Cushing syndrome.
  2. Stopping/weaning off steroid medications
  3. Adrenal steroid inhibitors (not for long-term)
    - lowers cortisol by directly inhibiting synthesis and secretion in the adrenal gland
  4. Trans-sphenoidal surgery if pituitary adenoma
23
Q

What is adrenal insufficiency?

A

Adrenal gland does not produce enough hormones needed, particularly aldosterone and cortisol.

24
Q

Describe the hypothalamic-pituitary-adrenal axis

A

CRH (hypothalamus) –> ACTH (pituitary) –> adrenal steroids (adrenal gland)

Adrenal Gland hormones

  • ZG - aldosterone
  • ZF - cortisol
  • ZR - androgens
25
Q

What is primary, secondary, tertiary adrenal insufficiency?

A
  1. Primary AI
    - problems producing cortisol from adrenal glands
    - Addison’s disease
  2. Secondary AI
    - PITUITARY GLAND IMPAIRMENT
    - lack of ACTH
    - steroid use and hypopituitarism
  3. Tertiary AI
    - HYPOTHALAMUS IMPAIRMENT/DISEASE
    - dec in CRH
    - brain tumours
    - sudden withdrawal from long-term steroid use
26
Q

What does aldosterone do?

A

(1.) Part of RAAS = dec K, inc Na, inc BP.

MoA:
(2.) Aldosterone is secreted in response to renin levels

(3. ) Binds to Na/K so K is excreted and Na resorbed, water follows. This inc BP.
(4. ) Stimulates ATPase so more protons excreted causing an increase in pH.

27
Q

What does cortisol do?

A

(1. ) Zona fasciculata secretes cortisol. It is lipid soluble so able to diffuse across plasma mb
(2. ) Cortisol is needed in times of emotional and physical stress

(3. ) Function of Cortisol
- Inc Gluconeogenesis
- Break down of muscles
- Break down of adipose tissue

28
Q

What does androgens do?

A

(1. ) Zona reticularis secretes androgens
(2. ) Dehydroepiandrosterone (Androgen) is a precursor of testosterone
(3. ) Androgens are important for testosterone levels in both male (hi levels) and women (low levels).
(4. ) Androgen production is stimulated by ACTH (although mechanism not well understood)

29
Q

What is Primary Adrenal Insufficiency and causes

A

(1. ) Adrenal cortex is damaged. This can be acute or chronic.
(2. ) Acute causes= Waterhouse-Friderichsen syndrome (inc BP–>vessel rupture–>adrenal ischaemia)
(3. ) Chronic causes= Addison’s/Autoimmune disease, tuberculosis, metastatic cancer

30
Q

What is RF for Addisons?

A
  • Autoimmune disease,
  • Infection (e.g Tuberculosis),
  • Exogenous steroids,
  • Surgery (pituitary or adrenal),
  • Radiotherapy,
  • Malignancy
31
Q

What Sx would be seen in destruction of ZG, ZF, ZR?

A

If ZG destroyed so Aldosterone levels fall:

  • Hyperkalaemia, Hyponatremia, Hypovolemia, Acidosis
  • Craving for salty food
  • Nausea, vomiting, fatigue, dizziness

If ZF destroyed, cortisol levels fall:

  • Low BGL levels in times of stress
  • Hyperpigmentation as low cortisol levels causes inc ACTH and aMSH (responsible for melatonin)

If ZR destroyed, androgen falls

  • Male are not as affected as their main androgen source is the testes
  • Women experience loss of pubic and armpit hair, dec sex drive
32
Q

What is Adrenal Crisis?

A

(1. ) Usually happens when majority of zona glomerulosa and fasciculata are destroyed.
(2. ) It is until a major stressor, like a serious injury, surgery, or infection, that symptoms become severe due to body’s inc demand for aldosterone, cortisol, and the failing adrenal cortex simply can’t deliver.
(3. ) Sx = lower back or leg pain, vomiting, diarrhea, dehydration, low BP, loss of consciousness.
(4. ) Left untreated, it can be fatal.

33
Q

Management of Adrenal Crisis?

A
  • If suspected, arrange emergency admission to hospital.
  • 100mg IV hydrocortisone (if not already self-administered)
  • IV saline infusion
34
Q

Sx and Hx of Addison’s

A
  • Fatigue, weight loss, poor recovery from illness, headache, hyperpigmentation, postural hypotension, salt craving
  • LEAN TANNED TIRED TEARFUL
  • Past Hx - TB, post partum bleed, cancer
  • Fx - Autoimmunity, congenital disease
  • Mx - Any steroids use, etomidate, ketoconazole
35
Q

Investigations for Primary and Secondary AI (5)

A

(1.) 8-9am Serum Cortisol: This would be reduced in AI

(2. ) Serum ACTH
- high = primary/addison’s
- low = secondary (pituitary dysfunction)

(3. ) Plasma Renin/aldosterone
- Primary/Addisons = elevated renin and low aldosterone [renin is released due to low blood Na, as low aldo causes salt loss]
- Secondary AI = RAAS function normally

(4.) U&E: Low Na levels, High K levels in Addison’s disease

(5. ) ACTH stimulation test/Synacthen test
- Administration of synthetic ACTH and then measurement of serum cortisol
- No cortisol inc is seen in AI

36
Q

Treatment of AI

A

(1. ) Glucocorticoid replacement: hydrocortisone OR oral prednisolone
- 2-3 divided doses (waking, midday, 1700h)
- lowest doses should be given for best QoL.

(2.) Mineralocorticoid replacement: fludrocortisone

(3. ) Androgen replacement: DHEA
- in women with low libido & low energy

(4. ) Pt Education and monitoring
- Ensure family, carers are aware of lifelong steroid therapy and life-threatening complications
- Ensure pt is carrying emergency information such as steroid treatment card and understands sick day rule

37
Q

What is Addison’s Disease? Dx?

A

(1. ) Autoimmune destruction of adrenal gland causing primary AI.
(2. ) Sx = postural hypotension (due to reduced aldosterone), inc pigmentation, new scars, wt loss, fatigue, GI upset

Remember -> LEAN, TANNED, TIRED, TEARFUL

(3.) Dx of adrenal insufficiency = Synacthen Test (ACTH stimulation test)

(4. ) Results:
- Normal adrenals: synthetic ACTH would stimulate cortisol production = cortisol levels increase
- In Addison’s: giving synthetic ACTH would NOT lead to cortisol rise

38
Q

What is Diabetes Insipidus?

A

(1. ) Disorder caused by hyposecretion and/or insensitivity to ADH
(2. ) This leads to polydipsia and polyuria (>3L in 24hrs)
(3. ) DI differs to diabetes mellitus as it is ‘tasteless urine’ rather than ‘sweet’

39
Q

Action and mechanism of ADH/VP

A

(1. ) ADH and oxytocin are made in the PVN and SON nucleus within the hypothalamus.
(2. ) It is then transported to the posterior pituitary - where it would be secreted into the blood.
(3. ) Osmoreceptors within the hypothalamus detect changes within blood osmolarity
(4. ) An increase in blood osmolarity causes ADH production and secretion
(5. ) ADH binds to AVP-R2 in the kidney, this initiates a signalling cascade where AQP2 are inserted onto the lumen/apical mb.
(6. ) This allows for water to enter the cell and then the blood and ultimately dilutes the blood so it returns to normal osmolarity levels

40
Q

What is VP and its function?

A
  1. VP decreases water excretion within the kidneys by increasing water reabsorption in the collecting ducts (hence why it is also referred to as ADH)
  2. VP effects how much urine is excreted and how concentrated it is
  3. It is secreted in response to elevated blood osmolarity
  4. It also causes vasoconstriction of blood vessel’s smooth muscle
41
Q

Why is polyuria and polydipsia seen in Diabetes Insipidus in relation to ADH/VP?

A
  1. In DI, little water is absorbed from lumen, resulting in production of lots of urine (polyuria)
  2. There is little water in blood so osmolarity is high this makes a person thirsty (polydipsia)
42
Q

Signs and Symptoms of DI?

A
  1. Polyuria (>3L per day)
  2. Polydipsia
  3. No glycosuria
  4. Nocturia - wake up during night to urinate
  5. fatigue, nausea, poor concentration, or confusion - due to inc in plasma osmolarity
43
Q

Investigations of DI?

A
  1. High blood osmolarity
  2. Water deprivation test
  3. 24 hour urine + monitor urine volume, is it >3L ?

Determining the cause:

  1. MRI of pituitary or hypothalamus
  2. Renal tract ultrasound or intravenous pyelogram
  3. Copeptin (new)
44
Q

What is the Water deprivation test?

A

(1. ) Individual doesn’t drink water for up to 8hrs, then hourly measurements of urine volume and osmolality are done.
(2. ) After desmopressin (ADH-analogue) if urine osmolality increases + returns to normal levels, this is suggestive of low ADH. This would be Central DI.
(3. ) After desmopressin if urine osmolality increases slightly or not at all - then kidneys are not responding to the ADH, indicating Nephrogenic DI

45
Q

Treatment and Management of DI.

A

(1. ) Rehydration and correct any metabolic abnormality
(2. ) Stop any offending drugs e.g. lithium (causes kidney to unresponsive to ADH)
(3. ) Low-solute diet: help dec urine output

(4. ) Cranial DI = Desmopressin
(5. ) Nephrogenic DI = Thiazide diuretic

46
Q

How do thiazide diuretics helps with DI?

A
  1. Increase urine excretion of sodium
  2. Since sodium contributes to blood osmolality, getting rid of sodium reduces blood osmolality and stops the hypothalamus from stimulating thirst.
47
Q

What causes Central DI?

A

Hypothalamus or pituitary gland preventing ADH production or release

Causes (can be genetic or spontaneous)

(1. ) damage to hypothalamus osmoreceptors, the supraoptic nucleus, or the supraoptico-hypophysial tract
(2. ) any condition which impairs the production, transportation or release of ADH

48
Q

What is Nephrogenic DI? Causes?

A
  1. Problem with kidneys themselves, which makes them unresponsive to ADH.
  2. Causes:
    - Genetic Defect: abnormal VP-R or AQP that are unresponsive to ADH
    - Lithium: dec AQP production
    - Polycystic kidney disease
49
Q

4 Causes of SIADH?

A
  1. CNS: head injury, meningitis, cerebral haemorrhage
  2. Malignancy: tumours, small cell carcinoma
  3. Resp: pneumonia, TB, severe asthma
  4. Drugs: thiazide diuretics, SSRIs, PPI, ACEi
50
Q

What is Syndrome of Antidiuretic hormone secretion, SIADH?

A

Inappropriate ADH secretion from posterior pituitary or ectopic source, despite low serum osmolality.

51
Q

Symptoms of SIADH

A

Linked to low Na levels (hyponatremia):

  • Dehydration, N+V, Headaches, Muscle cramps, Tremors
  • Cerebral oedema: Confusion, mood swings, hallucinations, Seizures, coma, death
52
Q

Treatment and Management of SIADH

A
  1. Identify and stop any causative drug (if possible)
  2. Restrict fluid intake <1L/24hr
  3. High salt and protein diet –> Help replace loss of Na
  4. Demeclocycline - inhibit ADH secretion
  5. Tolvaptan - Selective V2-R oral antagonist h/e expensive
  6. Hypertonic IV fluid (1st line for severe)
53
Q

Diagnostic features of SIADH

A
  • Low plasma osmolarity & Na

- High urine osmolality & Na

54
Q

Causes and Sx of Secondary AI?

A

(1. ) Due to corticosteroid withdrawal
(2. ) Long-term corticosteroid leads to suppression of the adrenal glands.
(3. ) With prolonged suppression, the adrenal glands atrophy, which means that they can’t produce enough corticosteroids if exogenous corticosteroids are stopped abruptly it will lead to Sx of adrenal insufficiency
(4. ) Sx = fatigue, loss of appetite, postural hypotension

Endocrinology (9 decks)

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