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PBLs > Week 11 - Endocrine > Flashcards

Week 11 - Endocrine Flashcards

1
Q

what is onycholysis?

A

painless detatchment of nail from nailbed

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2
Q

in what endocrine disorder is lid retraction seen? and why?

A

hypertyroidism e.g. Graves Disease
sympathetic hyperactivity causing excessive contraction of the superior tarsal and levator palperbrae superioris muscles

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3
Q

what is exophtalmos?

A

bulging of the eye
graves disease

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4
Q

what is lid lag and what is it most commonly associated with?

A

delay in the descent of the upper eyelid in relation to the eyeball when looking downward

Graves

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5
Q

what happens to thyroid gland masses, lymph nodes and invasive thyroid malignancies during swallowing?

A
  • Thyroid gland masses will move upward with swallowing.
    • Lymph nodes will not move much during swallow
      Invasive thyroid malignancy may not move with swallow
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6
Q

what will move up upon tongue protrusion in the thyroid?

A

thyroglossal cysts

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7
Q

what happens to thyroglossal cysts on tongue protrusion?

A

moves upwards

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8
Q

what will not move in the thyroid with tongue protrusion?

A

thyroid gland masses
lymph nodes

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9
Q

what happens to thyroid gland masses and lymph nodes on tongue protrusion?

A

will not move

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10
Q

what does dullness on percussion of the sternum in a thyroid exam indicate?

A

large thyroid mass that extends posterioinferiorly to the sternum

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11
Q

how many parathyroid glands are there and where are they located?

A

4
small and on posterior surface of thyroid gland

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12
Q

what is the structure of the thyroid?

A

2 lateral lobes → cover the anterolateral surfaces of the trachea, cricoid cartilage and lower part of thyroid cartilage

Isthmus → connects lateral lobes. Crosses anterior surfaces of 2nd and 3rd tracheal cartilages

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13
Q

what is the arterial supply to the thyroid?

A

superior and inferior thyroid arteries

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14
Q

what is the arterial supply to the parathyroid glands?

A

○ Inferior thyroid arteries
Superior thyroid arteries may contribute to supply of superior parathyroid glands

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15
Q

what is the main function of the thyroid?

A
  • Main regulator of metabolism
    • TH3/TH4 act via nuclear receptors in target tissues and initiate a variety of metabolic pathways.
    • Metabolic pathways include →
      ○ Basal metabolic rate
      ○ Gluconeogenesis
      ○ Glycogenolysis
      ○ Protein synthesis
      ○ Lipogenesis
      ○ Thermogenesis
    • Achieve in ways such as →
      ○ Increasing size & number of mitochondria within cells
      ○ Increasing Na-K pump activity
      Increasing the presence of β-adrenergic receptors in tissues such as cardiac muscle
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16
Q

what is released in detection of low plasma conc of thyroid hormone?

A

hypothalamus detects it and releases thyrotopin-releasing hormone
TRH

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17
Q

what is the action of TRH?

A

binds to receptors on thyrotrophic cells of the anterior pituitary gland which causes release of TSH

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18
Q

where is TSH released from?

A

anterior pituitary gland

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19
Q

which cells synthesise and release thyroid hormone?

A

thyroid follicular cells

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20
Q

which structures are able to convert T4 to T3?

A

○ Liver
○ Kidney
○ Muscle
○ Thyroid
○ Pituitary gland
○ Brown adipose tissue
Central nervous system

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21
Q

which of T4 and T3 is inactive?

A

T4

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22
Q

what is the function of T3/T4?

A

○ Regulating the metabolic rate
○ Slowing down or speeding up heart rate
○ Raising or lowering body temperature
○ Influencing the speed at which food moves through digestive tract
○ Affecting brain development
○ Controlling the way your muscles contract
○ Managing skin and bone maintenance by controlling rate at which your body replaces dying cells

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23
Q

how are thyroid hormones found in the circultataion (in what state)?

A

bound to transport proteins
they are lipophillic

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24
Q

what is the location of pathology in primary and secondary hyperthyroidism?

A

primary = thyroid pathology
secondary = pathology of hypothalamus or pituitary

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25
Q

what is graves disease?

A

autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism. These TSH receptor antibodies, produced by the immune system, stimulate TSH receptors on the thyroid. This is the most common cause of hyperthyroidism.

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26
Q

what is the most common cause of hyperthyroidism?

A

Graves

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27
Q

what is toxic moltinodular goitre?

A

condition where nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones. It is most common in patients over 50 years.

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28
Q

what is hypothyroidism?

A

insufficient thyroid hormones, triiodothyronine (T3) and thyroxine (T4).

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29
Q

what is primary hypothyroidism?

A

thyroid behaves abnormally and produces inadequate thyroid hormones. Negative feedback is absent, resulting in increased production of TSH. TSH is raised, and T3 and T4 are low.

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30
Q

what is secondary hypothyroidism?

A

where the pituitary behaves abnormally and produces inadequate TSH, resulting in under-stimulation of the thyroid gland and insufficient thyroid hormones. TSH, T3 and T4 will all be low.

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31
Q

patient has low TSH and high T3/T4. what is this?

A

primary hyperthyroidism

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32
Q

a patient has high TSH and high T3/T4. what is this?

A

secondary hyperthyroidism

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33
Q

a patient has high TSH and low T3/T4. what is this?

A

primary hypothyroidism

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34
Q

a patient has low TSH and low T3/T4. what is this?

A

secondary hypothyroidism

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35
Q

where is TRH released?

A

hypothalamus

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36
Q

where does TRH act upon?

A

anterior pituitary

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37
Q

where does TSH act upon?

A

thyroid

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38
Q

how are radioisotope scans used in thyroid disorders?

A

investigate hyperthyroidism and thyroid cancers
○ Radioactive iodine is given orally or IV and travels to thyroid, where it’s taken up by thyroid cells. Iodine needed to produce thyroid hormones.
○ Gamma camera detects gamma rays emitted from radioactive iodine, the greater the rays emitted, the more radioactive iodine has been taken up:

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39
Q

diffuse high uptake of radioactive iodine is seen in a radioisotope scan. what does this suggest?

A

graves

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40
Q

what would be seen in a radioisotope scan of someone with graves disease?

A

diffuse high uptake

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41
Q

focal high uptake of radioactive iodine is seen in a radioisotope scan. what does this suggest?

A

toxic multinodular goitre and adenomas

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42
Q

what is seen on a radioisotope scan in toxic multinodular goitres and adenomas?

A

focal high uptake

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43
Q

cold area e.g. abnormally low uptake of radioactive iodine is seen in a radioisotope scan. what does this suggest?

A

thyroid cancer

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44
Q

what is seen on a radioisotope scan in thyroid cancer?

A

cold area
abnormally low uptake

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45
Q

when are anti-TPO antibodies present?

A

antibodies against thyroid gland – most relevant thyroid autoantibody in autoimmune thyroid disease.

Present in Grave’s disease and Hashimoto’s thyroiditis

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46
Q

when are anti-Tg antibodies seen?

A

antibodies against thyroglobulin – protein produced and present in thyroid gland.

Raised in Grave’s, Hashimoto’s and thyroid cancer.

Can be present in healthy individuals too.

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47
Q

when are TSH receptor antibodies seen?

A

autoantibodies that mimic TSH. Bind to TSH receptor and stimulate thyroid hormone release.

Cause Grave’s disease

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48
Q

what medication is often used to treat hyperthyriodism?

A

carbimazole

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49
Q

what is carbimazole used in?

A

hyperthyroidism

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50
Q

what are the contraindications to carbimazole?

A

severe blood disorders

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51
Q

what side effects can carbimazole cause?

A

neutropenia and agranulocytosis which could cause bone marrow suppression

should always check WBC count

congential malformations - use at risk in pregnancy

ACUTE PANCREATITIS - stop immediately if this occurs

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52
Q

what is the action of carbimazole?

A

blocks the way your body produces iodine .: cannot be used in making thyroid hormones

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53
Q

what medications used to treat hypothyroidism?

A

levothyroxine

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54
Q

what is a contraindication of levothyroxine?

A

thyrotoxicosis

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55
Q

what are the side effects of levothyroxine?

A

Angina pectoris, anxiety, arrhythmias, arthralgia, diarrhoea, dyspnoea, fever, flushing, headache (many more)

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56
Q

what is the second line drug treatment of hyperthyroidism?

A

propylthiouracil

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57
Q

what risks does propylthiouracil have?

A

severe liver reactions
including death

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58
Q

patient on carbimazole has a sore throat. what is happening?

A

carbimazole can cause agranulocytosis
they need an urgent FBC and aggressive treatment of any infection

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59
Q

what are the rules for iodine therapy in hyperthyroidism?

A
  • Women must not be pregnant or breastfeeding and must not get pregnant within 6 months of treatment
  • Men must not father children within 4 months of treatment
    Limit contact with people after the dose, particularly children and pregnant women
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60
Q

what is a side effect of radioactive iodine therapy in hyperthyroidism?

A

underactive thyroid
.: may need levothyroxie

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61
Q

what is the role of the parathyroid glands?

A

regulate serum calcium and phosphate levels via the secretion of parathyroid hormone (PTH) from chief cells.

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62
Q

what cells parathyroid hormone?

A

cheif cells

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63
Q

what can cause primary hyperparathyroidism?

A

adenoma (most common)
hyperplasia
carcinoma

64
Q

what are the complications of primary hyperparathyroidism?

A

osteoporosis
renal impairement
pancreatitis
CVD

65
Q

what is primary hyperparathyroidism

A
  • More or one of the parathyroid glands is over-secreting PTH despite normal serum calcium
    • Leads to hypercalcaemia.
66
Q

what is secondary hyperparathyroidism?

A
  • Due to a disorder in calcium-phosphate-bone metabolism
    Causes the parathyroid glands to secrete PTH
67
Q

what are the main causes of secondary hyperparathyroidism?

A

CKD
vit D deficiency

68
Q

what is tertiary hyperparathyroidism?

A
  • Following a prolonged period of hyperparathyroidism.
    • Glands become hyperplastic and secrete PTH autonomously
69
Q

patient shows increased PTH and increased Ca2+. what does this mean?

A

primary hyperparathyroidism

70
Q

patient shows high PTH and low Ca2+. what does this mean?

A

secondary hyperparathyroidism

71
Q

what is the typical presentation of hyperparathyroidism?

A

stones, bones, moans and groans

· Fatigue 
· Polyuria and polydipsia 
· Constipation 
· Abdominal pain 
· Vomiting 
· Confusion 
· Depression 
· Bone pain  Renal stones
72
Q

what imaging can be done in suspected hyperparathyroidism?

A
  • DEXA scan: to assess for reduce bone mineral density - osteoporosis
    • Ultrasound of renal tract: looking for renal stones
    • Ultrasound of the neck: pre-operative planning and to identify adenomas (first-line)
    • Nuclear imaging (eg sestamibi scan): for pre-operative planning and to identify adenomas (first-line)
73
Q

what is the management for acute, severe hypercalcaemia related to hyperparathyroidism?

A
  1. IV fluids
    1. Bisphosphates: preserve bone density and reduce fracture risk
  2. Cinacalcet (a calcium-sensing receptor agonist): reduces PTH secretion and thus serum calcium. Used in primary hyperparathyroidism when surgery isn’t appropriate, declined or unsuccessful
74
Q

what is the management for secondary hyperparathyroidism?

A
  • Treat the underlying cause
    • Cinacalcet if this fails or if patient is on dialysis
    • Phosphate binders and calcium/vit D supplements for those who have chronic kidney disease
75
Q

what is the treatment for tertiary hyperparathyroidism?

A
  • Surgical intervention (partial parathyroidectomy)
    • Residual parathyroid tissue is reimplanted elsewhere in the body - more accessible if future problems arise
76
Q

where is cortisol secreted from?

A

adrenal glands

77
Q

what controls the release of cortisol?

A

hypothalamus

78
Q

what are the normal levels of cortisol throughout the day?

A

diurnal variation

cortisol peaks in the early morning, triggering us to wake up and get going

lowest late in the evening, prompting us to relax and fall asleep.

79
Q

what is the mechanism that leads to cortisol release?

A

hypothalamus releases corticotropin-releasing hormone (CRH)

CRH acts on anterior pituitary to release adrenocorticotropic hormone (ACTH)

ACTH stimulates adrenal gland to release cortisol

80
Q

where is adrenocorticotropic hormone released from?

A

anterior pituitary

81
Q

what stimulates the release of adrenocorticotropic hormone?

A

corticotropin releaseing hormone

82
Q

what is the adrenal axis controled by?

A

negative feedback
keeps cortisol regulated in normal limits

83
Q

what are the actions of cortisol in the body?

A

○ Increases alertness
○ Inhibits the immune system – inhibits the production of several inflammatory cytokines
○ Inhibits bone formation – chronically elevated cortisol can lead to osteoporosis)
○ Raises blood glucose – stimulating gluconeogenesis (synthesis of glucose from non-carbohydrate sources)
○ Increases metabolism – promoting breakdown of proteins which can result in muscle wasting in chronic states of cortisol elevation
○ An initial surge in cortisol levels triggers lipolysis, however, chronically elevated cortisol promotes lipogenesis.

84
Q

what is cushings syndrome?

A

prolonged high levels of glucocorticoids in the body.
cortisol

85
Q

what are the symptoms of cushings syndrome?

A
  • Weakness
    • Facial fullness
    • Weight gain
    • Low mood
    • Decreased libido
    • polydipsia
    • polyuria
      Increased frequency of infection
86
Q

what clinical signs of cushings syndrome?

A
  • Round face (known as a “moon face”)
    • Central (truncal) obesity
    • Abdominal striae (stretch marks)
    • Enlarged fat pad on the upper back (known as a “buffalo hump”)
    • Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
    • Male pattern facial hair in women (hirsutism)
    • Easy bruising and poor skin healing
    • Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)
      ○ ACTH is stimulating melanocytes to produce melanin
      ○ This is absent if the cause is an adrenal adenoma or exogenous steroids
    • Hypertension
    • Signs of tumour in Cushing’s disease e.g. headaches, visual field defects
87
Q

what are the main causes of cushings syndrome?

A
  • C – Cushing’s disease (a pituitary adenoma releasing excessive ACTH)
    • A – Adrenal adenoma (an adrenal tumour secreting excess cortisol)
    • P – Paraneoplastic syndrome – ACTH is released from a tumour somewhere other than the pituitary gland (ectopic ACTH) stimulating excessive cortisol release from the adrenal gland e.g. small cell lung cancer
    • E – Exogenous steroids (patients taking long-term corticosteroids)
88
Q

what are the 2 types of causes of cushings syndrome?

A

endogenous = pituitary adenoma, adrenal adenoma, adrenal carcinoma

exogenous = prolonged use of corticosteroids e.g. prednisolone/dexamethasone

89
Q

what is the main test used in investigating cushings syndrome?

A

dexamethasone suppression test

90
Q

what is the low dose overnight dexamathasone test?

A

dexamethasone (1mg) is given at night (usually 10 or 11 pm), and the cortisol is checked at 9 am the following morning.

* Normal result = cortisol level is suppressed. 
* Failure of the dexamethasone to suppress the morning cortisol could indicate Cushing’s syndrome, and further assessment is required.
91
Q

what is the lowdose 48hr dexamethasone test?

A

dexamethasone (0.5mg) is taken every 6 hours for 8 doses, starting at 9 am on the first day. Cortisol is checked at 9 am on day 1 (before the first dose) and 9 am on day 3 (after the last dose).

* Normal result = cortisol level on day 3 is suppressed.
* Failure of the dexamethasone to suppress the day 3 cortisol could indicate Cushing’s syndrome, and further assessment is required.
92
Q

what is the high dose 48hr dexamethasone test?

A

carried out the same way as the low-dose test, other than using 2mg per dose (rather than 0.5mg).

* higher dose is enough to suppress the cortisol in Cushing’s syndrome caused by a pituitary adenoma (Cushing’s disease), 
* not when it is caused by an adrenal adenoma or ectopic ACTH.
93
Q

what is the test when ACTH is measured directly in the dexamethasone test?

A
  • ACTH is suppressed due to negative feedback on the pituitary when excess cortisol comes from an adrenal tumour (or endogenous steroids)
    ACTH is high when produced by a pituitary tumour or ectopic ACTH (e.g., small cell lung cancer
94
Q

dexamethasone test shows these results:
low dose test = low cortisol
high dose test = low cortisol
ACTH = normal
what does this show?

A

normal

95
Q

dexamethasone test shows these results:
low dose test = cortisol not supressed
high dose test = cortisol not supressed
ACTH = low
what does this show?

A

adrenal adenoma causing cushing

96
Q

dexamethasone test shows these results:
low dose test = cortisol not suppressed
high dose test = low cortisol
ACTH = high
what does this show?

A

pituitary adenoma causing cushings

97
Q

dexamethasone test shows these results:
low dose test = cortisol not suppressed
high dose test = cortisol not suppressed
ACTH = high
what does this show?

A

ectopic ACTH causing cushings

98
Q

what is the 24hr urinary free cortisol test?

A

used in cushings
* An alternative to the dexamethasone suppression test.
* cumbersome to carry out and does not indicate the underlying cause
Cortisol excretion of more than 3 times the upper limit of normal is strongly suggestive of Cushing’s syndrome

99
Q

what is the late night salivary cortisol measurement test?

A
  • Simple and reliable test
    • Normal = level of cortisol decreases in the evening compared to morning
      Cushing’s syndrome = normal diurnal variation is absent
100
Q

what is inferior petrosal sinus sampling and why is it used in cushings?

A
  • Invasive procedure where ACTH levels are sampled from veins that drain the pituitary gland
    • These ACTH levels are compared to peripheral ACTH levels to determine whether a pituitary tumour is the cause
      Used when neuroimaging and previous investigations has not reached a diagnosis
101
Q

what is the management of cushings syndrome?

A

(C) Pituitary adenoma
Trans-sphenoidal (through the nose) removal of the tumour
May also require adjunct radiotherapy

(A) Adrenal tumour
Surgical removal – laparoscopic excision

(P) Ectopic ACTH
Surgical removal of the tumour (e.g. small cell lung cancer) if possible

(E) Exogenous steroids
Review patients current glucocorticoid treatments and reduce doses where possible

  • could surgically remove both adrenal glands and then give lifelong steroid replacement
    • Metyrapone, ketoconazole + mitotane all reduce the production of cortisol in the adrenals (inhibit glucocorticoid synthesis) and is occasionally used in treating of Cushing’s.
      Either used as long term treatment if patient is unfit to have surgery or short term before surgery
102
Q

what are the complications of cushings syndrome?

A
  • hypertension
    • diabetes
    • obesity
    • Metabolic syndrome
      Osteoporosis
103
Q

what is addisons disease?

A

primary adrenal insufficiency

when adrenal glands are damaged -> reduced cortisol and aldosterone secretion, most common cause is autoimmune.

104
Q

what is adrenal insufficiency?

A

where the adrenal glands do not produce enough steroid hormones, particularly cortisol and aldosterone. Steroids are essential for life. Therefore, the condition is life-threatening unless the hormones are replaced.

105
Q

what is secondary adrenal sufficiency?

A

inadequate adrenocorticotropic hormone (ACTH) and a lack of stimulation of the adrenal glands, leading to low cortisol.

This is the result of loss or damage to the pituitary gland.

106
Q

What are some causes of secondary adrenal insufficiency?

A

▪ Tumours (e.g., pituitary adenomas)
▪ Surgery to the pituitary
▪ Radiotherapy
▪ Sheehan’s syndrome = where major post-partum haemorrhage causes avascular necrosis of the pituitary gland
Trauma

107
Q

what is tertiary adrenal insufficiency?

A

inadequate corticotropin-releasing hormone (CRH) release by the hypothalamus.

	○ Usually the result of patients taking long-term oral steroids (for more than 3 weeks), causing suppression of the hypothalamus (via negative feedback)
	○ When the exogenous steroids (originating outside the body) are suddenly withdrawn, the hypothalamus does not “wake up” fast enough, and endogenous steroids (originating inside the body) are not adequately produced Long-term steroids must be tapered slowly to allow the adrenal axis to regain normal function.
108
Q

what are the symptoms of addisons disease?

A
  • Fatigue
    • Muscle weakness
    • Muscle cramps
    • Dizziness and fainting
    • Thirst and craving salt
    • Weight loss
    • Abdominal pain
    • Depression
    • Reduced libido (mainly in women)
      Loss of hair in axillary/pubic regions (mainly in women)
109
Q

what are the clinical signs of addisons disease?

A
  • Bronze hyperpigmentation of the skin (particularly in creases, scars, lips and buccal mucosa) = excessive ACTH stimulates melanocytes to produce melanin
    Hypotension (particularly postural hypotension – with a drop of more than 20 mmHg on standing)
110
Q

what endocrine disorder commonly presents with bronze hyperpigmentation of the skin?

A

addisons disease

111
Q

what blood results are seen in addisons disease?

A
  • Hyponatraemia (low sodium) is a key biochemical finding. This may be the only presenting feature.
    Other potential biochemical findings may occur. Normal results do not exclude the diagnosis:
    ○ Hyperkalaemia (high potassium)
    ○ Hypoglycaemia (low glucose)
    ○ Raised creatinine and urea due to dehydration
    Hypercalcaemia (high calcium)
112
Q

what is the key biochemical finding in addisons disease?

A

hyponatraemia

113
Q

what does the early morning cortisol test show in adrenal insufficeincy?

A

(8 – 9 am) has a role but is often falsely normal and does not distinguish between the types of adrenal insufficiency

  • < 100 nmol/L: adrenal insufficiency very likely
    • 100–500 nmol/L: adrenal insufficiency possible
      > 500 nmol/L: adrenal insufficiency unlikely
114
Q

what do the levels of ACTH show in the types of adrenal insufficiency?

A

ACTH level high = primary adrenal insufficiency, as the pituitary is producing lots of ACTH without negative feedback in the absence of cortisol.

ACTH level low = secondary/tertiary adrenal failure.

115
Q

what is the gold standard investigation in addisons disease and what results are shown?

A

Short Synacthen Test
* Also known as the ACTH stimulation test. It is the test of choice for diagnosing adrenal insufficiency.

It is ideally performed in the morning.
The test involves giving a dose of Synacthen (synthetic ACTH)/ IV administration of 250mcg of tetracosactide (synthetic ACTH).
The blood cortisol is checked before and 30 and 60 minutes after the dose.

	○ Normal = cortisol level should at least doubel,synacthen will stimulate healthy adrenal glands to produce cortisol. 

	○ Failure of cortisol to double indicates either:
		▪ Primary adrenal insufficiency (Addison’s disease)
		▪ Very significant adrenal atrophy after a prolonged absence of ACTH in secondary adrenal insufficiency
116
Q

what is the management of adrenal insuffiency?

A
  • Hydrocortisone 15-30mg/day divided into doses(a glucocorticoid) is used to replace cortisol.
    • Fludrocortisone 50-300mcg/day (a mineralocorticoid) is used to replace aldosterone, if aldosterone is also insufficient.
117
Q

what is done to steroid doses in acute illness?

A

doubled

118
Q

what is an adrenal crisis?

A

Adrenal crisis, also known as Addisonian crisis, describes an acute presentation of severe adrenal insufficiency, where the absence of steroid hormones leads to a life-threatening emergency

119
Q

what is the presentation of an adrenal crisis?

A
  • Reduced consciousness
    • Hypotension
    • Hypoglycaemia
      Hyponatraemia and hyperkalaemia
120
Q

what is the management of an adrenal crisis?

A
  • ABCDE approach to initial assessment and arrange transfer to hospital
    • Intramuscular or intravenous hydrocortisone (the initial dose is 100mg, followed by an infusion or 6 hourly doses)
    • Intravenous fluids
    • Correct hypoglycaemia (e.g., IV dextrose)
      Careful monitoring of electrolytes and fluid balance
121
Q

list the hormones produced in the anterior pituitary?

A

ACTH
FSH
GH
LH
prolactin
TSH

122
Q

list the hormones produced the posterior pituitary?

A

ADH
oxytocin

123
Q

what is the difference between the anterior and posterior pituitary?

A

anterior = makes and releases hormones

posterior = stores and releases hormones rhat the hypothalamus has made

124
Q

what is hypopituitarism?

A

Hypopituitarism happens when the pituitary gland is not active enough. It does not make enough hormones. Hypopituitarism can directly affect the pituitary gland. Or it can indirectly affect the gland through changes in the hypothalamus. Symptoms depend on which hormones the pituitary gland is not making enough of.

125
Q

what is seen in someone with a growth hormone deficiency?

A
  • Fatigue
    • Muscle weakness
    • Changes in body fat composition
    • Lack of ambition
      Social isolation

in children it may cause growth problems and short statures

126
Q

what symptoms are seen when women have gonadotropin deficiencies?

A

○ Hot flashes
○ Irregular or no periods
○ Loss of pubic hair
An inability to produce milk for breast-feeding

127
Q

what symptoms are seen when men have gonadotrophin deficiencies?

A

§ Erectile dysfunction
§ Decreased facial or body hair
Mood changes

128
Q

what symptoms are seen in ACTH deficiency?

A

® Severe fatigue
® Low blood pressure, which may lead to fainting
® Frequent and prolonged infections
® Nausea, vomiting or abdominal pain
Confusion

129
Q

what symptoms are seen in diabetes insipidus?

A

◊ Excessive urination
◊ Extreme thirst
Electrolyte imbalances

130
Q

what is an ADH deficiency known as?

A

diabetes insipidus

131
Q

what is the main cause of prolactin deficiency?

A

pituitary tumor - prolactinoma

132
Q

what are the signs and symptoms of prolactinomas?

A

women:
Irregular or no periods (as prolactin decreases FSH/LH)
Reduced fertility
Reduced sex drive
Galactorrhea
Increased hair growth on face and body

men
Reduced fertility
Erectile dysfunction
Reduced sex drive
Breast enlargement
Galactorrhea

children
Reduced growth
Delayed puberty

133
Q

what is the management of prolactinomas?

A

not treating - if its small and symptoms arent troublesome

dopamine agonists e.g. bromocriptine, cabergoline, quinagolide - shrink tumour and reduce prolactin released

surgery = trans-sphenoidal

134
Q

what is acromegaly?

A

hypersecretion of pituitary growth hormone, usually as a result of a pituitary tumour, which leads to an abnormal increase in size of the skeletal extremities.

135
Q

what are the symptoms of acromegaly?

A

· Onset often slow and insiduous, most often diagnosed in middle age. Men and women are equally affected.
· Growth of hands and feet
· Change in facial features – widening bridge of nose, thick lips, protruding jaw and brow, macroglossia, teeth seperation

· Headaches and visual disturbance due to tumour
· Deeper voice
· Skin tags, excessive sweating. Mild hirsuitism in women.
· Joint pain and carpal tunnel syndrome.
· Hypertension and diabetes
· Organomegaly (liver/spleen/goitre)

136
Q

what is the gold standard invesitgation for acromegaly?

A

oral glucose tolerence test
glucose should supress GH

normal = normal IGF1
acromegaly = raised IGF1

137
Q

what is the first line treatment of acromegaly? and what is the first line drug treatment?

A

endoscopic trans-sphenoidal surgery
radiotherapy as an adjuvent

somatostatin analogues e.g. octreotide
sometimes dopamine agonists e.g. bromocriptine

138
Q

what is diabetes insipidus?

A

Diabetes Insipidus (DI) is a disorder caused by hyposecretion or insensitivity to ADH which leads to polydipsia, polyuria and large amounts of dilute urine.

139
Q

what are the 2 types of diabetes insipidus?

A
  1. Cranial DI – caused by any condition which impairs the production, transportation or release of ADH which in turn reduces the process involved in the concentration of urine leading to polyuria and polydipsia.
    1. Nephrogenic DI – decreased inability to concentrate urine due to conditions within the renal collecting duct causing a resistance to ADH. There are also two minor forms of DI
140
Q

what is suggested by impaired production, transportation or release of ADH leading tp increased conc of urine?

A

cranial diabetes insipidus

141
Q

what is suggested by renal collecting duct having a resistance to ADH?

A

nephrotic diabetes insipidus

142
Q

what are some symptoms of diabetes insipidus?

A

Polyuria
Large dilute vol of urine
Polydispsia

143
Q

what are some causes of diabetes insipidus?

A

· Idiopathic
· Tumour of the brain- craniopharyngioma, germinoma, lymphoma
· Intracranial surgery
· Head injury
· Infection- encephalitis, meningitis
· Vascular disorder- aneurysms, sickle cell disease
Radiotherapy

144
Q

what is the gold standard investigation for diabetes insipidus?

A

Record 24 hr urine = looking for >3L within 24hrs

145
Q

what is the management of diabetes insipidus?

A

· Oral fluids encouraged
· Metabolic abnormalities are corrected if present
· Medication review for possible causes/worsening drugs
· If symptoms are mild (<4L urine per day) intervention is not usually advised
· Moderate cases – treated with Desmopressin.
· Can consider combination treatment involving thiazide diuretic and NSAID
In severe cases may require intermittent catheterization

146
Q

what is an androgen secreting tumor?

A

make too much testosterone and can cause a virilizing (i.e. masculinizing) syndrome.

147
Q

what are the symptoms of a woman with an androgen secreting tumour?

A

excessive facial and body hair growth, a receding hairline, acne, irregular menstrual periods, deepening of their voice (hirsutism) and ambiguous genitalia.

148
Q

how is an androgen secreting tumour diagnosed?

A

high blood testosterone + DHEA-s levels + urine 17 ketosteroids

149
Q

what surgery option is available for androgen secreting tumours?

A

open adrenalectomy with lymph node dissection ( these tumours have a high risk of spreading to lymph nodes.

150
Q

what are some drugs that destroy adrenal tissue in an androgen secreting tumor?

A

mitotane
ketoconazole

151
Q

what is a phaeochromocytoma?

A

rare, usually benign tumor that develops in an adrenal gland

152
Q

what type of hormones are released from phaeochromocytomas? where are they released from?

A

catecholamines e.g. adrenaline and noradrenaline

usually from sympathetic preganglion cells in the adrenal medulla

153
Q

what symptoms can be seen in a phaeochromocytoma?

A
  • High blood pressure
    • Headache
    • Heavy sweating
    • Rapid heartbeat
    • Tremors
    • Pallor
    • Shortness of breath
    • Panic attack-type symptoms
154
Q

what complications are seen with a phaeochromocytoma?

A

High blood pressure can damage organs, particularly tissues of the heart and blood vessel (cardiovascular) system, brain and kidneys. This damage can cause several critical conditions, including:

* Heart disease
* Stroke
* Kidney failure
* Problems with the nerves of the eye
155
Q

when should a diagnosis of phaeochromocytoma be suspected most?

A

patient simultaneously presents with hypertension and the classic triad of heart palpitations, headaches, and profuse sweating.

156
Q

what investigations are carried out in a suspected phaeochromocytoma?

A

Plasma + 3x24hr urinary metadrenaline and normetadrenaline

Abdominal CT or MRI (to detect adrenal tumours)

157
Q

what is the management of a phaeochromocytoma?

A

Alpha blockade and beta blockade

Surgery, if malignant then chemotherapy and radiotherapy may be helpful

PBLs (19 decks)

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