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Phase 2 Metabolic > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

Describe the hypothalamic-pituitary-thyroid axis

A

hypothalamus releases TRH
pituitary releases TSH
TSH stimulates the production of T3 and T4 from the thyroid
T3/T4 negatively feedback on the hypothalamus and pituitary

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2
Q
  1. Out of the thyroid hormones is metabolically active, and which is the pro-hormone?
  2. Which hormone does the thyroid produce more of?
  3. What is the role of peripheral tissues in
A
  1. T3 metabolically active; T4 is prohormone
  2. produces more T4
  3. Converts T4 to active T3
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3
Q
  1. Does thyroid secretion follow a circadian rhythm?

2. What is the implication of this in terms of thyroid function tests?

A
  1. no

2. can be taken at any time.

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4
Q
  1. What is the most common cause of hypothyroidism?
  2. What investigation is useful in its diagnosis?
  3. What is Hashimoto’s thyroiditis?
  4. Name other causes of hypothyroidism (4)
A
  1. autoimmune hypothyroidism
  2. anti-thyroid antibodies
  3. form of autoimmune thyroiditis
  4. postpartum thyroiditis
    thyroidectomy
    radioactive iodine therapy
    external neck irradiation
    drugs - amiodarone, lithium, iodine
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5
Q

Name 4 autoantibodies which are important in the investigation of thyroid disease?

A
  • anti-thyroid peroxidase (anti-TPO)
  • thyroid receptor antibody
  • anti-thyroglobulin antibody
  • TSH receptor IgG (specific for Grave’s disease)
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6
Q

Name some symptoms of thyroid disease

A
  • tiredness/malaise
  • weight gain
  • cold intolerance
  • goitre
  • depression
  • psychosis
  • coma
  • poor memory
  • dry, brittle hair and nails
  • arthralgia and myalgia
  • poor libido
  • anorexia
  • oligo-/amenorrhoea, menorrhagia
  • constipation
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7
Q
  1. In terms of the cardiovascular system, what signs can hypothyroidism cause? (3)
  2. Name 2 signs relating to the hands/wrists which can indicate hypothyroidism
A
  1. hypertension
    heart failure
    bradycardia
  2. cold peripheries
    carpal tunnel syndrome
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8
Q

What are the results of the following if a patient is hypothyroid?

  1. Serum TSH
  2. Free T4
  3. anti-thyroid antibodies
A
  1. high (in primary hypothyroidism)
  2. low
  3. positive if autoimmune thyroiditis
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9
Q

How is hypothyroidism managed?

A

Levothyroixine (T4) - lifelong therapy

- dose adjust to improve clinical state and to normalise but not suppress TSH

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10
Q
  1. What is myxedema Coma?
  2. What are the signs of myxedema coma?
  3. what may patients presenting in myxedema coma have a background of?
A
  1. hypothyroid crisis
  2. look hypothyroid; bradycardic; hypoglycaemic; altered mental state
  3. radioiodine, thyroidectomy or pituitary surgery
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11
Q
  1. What is the most common cause of hyperthyroidism?
  2. What test is specific for this condition?
  3. What sign is a common feature of this condition?
  4. What is the natural hx of this condition?
A
  1. Grave’s disease
  2. TSH-receptor autoantibodies
  3. thyroid eye disease
  4. fluctuating - alternating relapse and remission; many patients eventually become hypothyroid
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12
Q

Other than Grave’s disease, name and describe 4 other causes of hyperthyroidism

A
  1. Toxic Multinodualr goitre - nodules secrete thyroid hormones
  2. solitary toxic adenoma - solitary nodule within the thyroid which produces T3/T4; rest of gland is suppressed
  3. Ectopic thyroid issue - metastatic folicular thyroid cancer; ovarian teratoma with thyroid issue
  4. amiodarone induced or iodine excess
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13
Q

Name symptoms of hyperthyroidism

A
  • weight loss with increased appetite
  • irritability
  • restlessness
  • malaise
  • sweating/heat intolerance
  • breathlessness
  • palpitations
  • tremor
  • thirst
  • diarrhoea
  • oligomenorrhoea
  • gynaecomastia
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14
Q
  1. Name 3 eye signs that are indicative of hyperthyroidism

2. What skin condition is a sign of hyperthyroidism?

A
  1. exopthalmos (eye bulging)
    lid lag and stare
    conjunctival oedema
  2. pretibial myxedema
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15
Q

Describe the results of the following investigations into hyperthyroidism

  1. serum TSH
  2. Free T3/T4
  3. TSHr-Ab
A
  1. suppressed (if primary hyperthyroisism(
  2. raised
  3. positive in Graves disease
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16
Q
  1. What is the MOA of carbimazole?
  2. What drug is carbimazole given concurrently with?
  3. What drug is given for symptomatic relief from hyperthyroidism?
  4. Which treatments can be given to treat hyperthyroidism?
A
  1. inhibits thyroid peroxidase enzyme therefore prevents iodination of thyroglobulin
  2. levothyroxine to prevent iatrogenic hypothyroidism
  3. propranolol
  4. radioactive iodine
    thyroidectomy
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17
Q
  1. What is a thyroid crisis?
  2. Name 5 signs of hyperthyroid crisis?
  3. What is a thyroid crisis usually precipitated by?
A
  1. a rapid deterioration of hyperthyroidism
2. hyperpyrexia
    severe tachycardia
    extreme restlessness
    cardiac failure
    liver dysfunction
  1. stress, infection, recent thyroid surgery or radioiodine treatment
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18
Q
  1. Define “Syndrome of Inappropriate Antidiuretic Hormone” (SIADH)
  2. What is the main consequence of SIADH?
A
  1. excessive secretion of Antidiuretic hormone from the posterior pituitary or another source
  2. excessive water retention, which dilutes the blood, leading to reduced concentration of solutes (mainly hyponatraemia)
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19
Q

Describe the abnormal physiology of SIADH, with respect to negative feedback

A

LOSS OF NEGATIVE FEEDBACK

  • Continuous ADH production, despite low serum osmolarity
  • This ultimately leads to low levels of SERUM sodium and osmolality, and high URINARY sodium and osmolality
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20
Q
  1. Name some diseases that can cause SIADH

2. Name some drugs that can cause SIADH

A
  1. primary brain injury
    malignancy
    infections (e.g. pneumonia)
    hypothyroidism
2. anticonvulsants
opiates
chemotherapeutic agents
antipsychotics
SSRI ans TC antidepressants
NSAIDs
ACEi/ARB
PPIs
ADH analogues
Ecstasy
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21
Q

When does SIADH often cause symptoms?

A

if hyponatraemia as a result of SIADH is of acute nature.

Chronically hyponatraemic patients are often asymptomatic

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22
Q

Describe signs and symptoms of hyponatraemia

A

Mild hyponatraemia - nausea, vomiting, headache, anorexia, lethargy

Moderate hyponatraemia - muscle cramps, weakness, confusion, ataxia

Severe hyponatraemia - drowsiness, seizures, coma

  • signs of hypovolaemia - peripheral oedema, raised JVP, pulmonary oedema
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23
Q

Describe important investigations for SIADH, and results that would indicate SIADH

A
  1. Serum sodium - <135mmol/L
  2. serum potassium (if raised in absence of hyponatraemia, consider Addison’s disease)
  3. Plasma Osmolality - reduced
  4. Urine sodium and omsolality - raised
  5. TFTs (possible cause of hyponatraemia)
  6. Serum Cortisol (exclude Addison’s)
  7. Imaging - CT TAP and head (causation)
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24
Q

Name 6 features which must be present for a diagnosis of SIADH

A
  1. hyponatraemia
  2. low serum osmolality
  3. inappropriately elevated urine osmolality
  4. raised urinary sodium
  5. euvolaemia/hypervolaemia
  6. normal thyroid and adrenal function
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25
Q
  1. How is SIADH managed?

2. Describe cautions required in the management of SIADH and why

A
  1. fluid restriction
    sodium replacement
    treat underlying cause
  2. sodium must be replaced gradually - if done too quickly, can result in central pontine myelinolysis
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26
Q

What is the most common cause of pituitary disease?

A

pituitary tumours - mostly benign adenomas

  • local pressure effects
  • excess hormone secretion
  • inadequate production of hormone by remaining normal pituitary
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27
Q

What are the clinical features of pituitary space-occupying lesions and tumours? (5)

A
  1. visual field defects
  2. CN III, IV and VI lesions (eye movement disturbance)
  3. headache
  4. altered appetite, obesity, thirst, somnolence
  5. hydrocephalus (if infiltrates the ventricles)
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28
Q
  1. What is hypopituitarism
  2. What is usually the cause of multiple pituitary deficiency?
  3. What is panhypopituitarism
  4. What is it commonly caused by?
A
  1. deficiency of hypothalamic releasing hormones or of pituitary trophic hormones
  2. tumour growth or destructive lesions
  3. deficiency of all anterior pituitary hormones
  4. pituitary tumours, surgery, radiotherapy
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29
Q 
HYPOPITUITARISM
What are the clinical features of the following deficiencies:
1. TSH
2. ACTH
3. Gonadotrophins
4. GH
  1. Why does hypopituitarism result in hyperprolactinaemia?
  2. What are the features of hyperprolactinaemia?
A
  1. fatiguability, cold intolerance, weight gain, hair loss
  2. hypotension, hyponatraemia (features similar to addisonian crisis)
  3. loss of libido, amenorrhoea, erectile dysfunction. Females will experience menopausal symptoms but not hot flushes (as these are caused by raised unopposed FSH in the menopause)
  4. growth failure in children; impaired wellbeing in adults
  5. impaired inhibition of prolactin secretion by dopamine
  6. galactorrhoea in women; hypogonadism. amenorrhoea
30
Q
  1. What is acromegaly?
  2. Name 4 key clinical features in acromegaly
  3. What investigations are important for ?acromegaly?
  4. How is it managed?
A
  1. growth hormone excess, leading to excessive skeletal and soft tissue growth
  2. changes in appearance (think of shrek)
    visual defects
    sleep apneoa
    headache
  3. GH levels
    glucose tolerance test (diagnostic if there is no suppression of glucose)
    IGF-1 levels - raised
    MRI
  4. trans sphenoidal surgery
    pituitary radiotherapy
31
Q

How is hyperprolactinaemia managed?

A

dopamine agonists

32
Q

Name 2 spontaneous causes of cushings

A
  1. Increased circulating ACTH from the pituitary or from an ectopic ACTH producing tumour, with consequent glucocorticoid excess - Cushing’s Disease
  2. Primary excess of endogenous cortisol by an adrenal tumour
33
Q

name 3 ways in which cushing’s disease can be distinguished from obesity

A
  1. sarcopenic obesity
  2. dark purple striae (due to raised ACTH which stimulates melanocytes)
  3. thin, bruised skin
34
Q
  1. Under what physiological conditions is ADH secreted?
  2. Name other factors which promote ADH secretion
  3. Name factors which suppress ADH secretion
A
  1. increased plasma osmolality
2. hypovolaemia
    hypotension
    hypothyroidism
    Angiotensin II
    Adrenaline
    Cortisol
    Nicotine
    Antidepressants
  1. Hypervolaemia
    Hypertension
    Alcohol
    Alpha adrenergic stimulation
35
Q
  1. What is the defect in diabetes insipidus?

2. How is it classified?

A
  1. Deficiency in ADH secretion/activity
  2. central DI - deficiency in ADH secretion
    nephrogenic DI - renal tubules insensitive to ADH
36
Q

Name clinical features of Diabetes Insipidus

A
  1. Polyuria
  2. impaired consciousness due to severe dehydration
  3. compensatory increase in thirst
37
Q
  1. What basic investigations are useful for diabetes insipidus?
  2. What specialist investigations are useful for diabetes insipidus?
A
  1. urine osmolarity (low)
    serum osmolarity (high)
    TFTs (if hypothyroidism is sispected cause)
  2. Water deprivation test - deprived of fluid for 8 hours and change in urine and serum osmolarity and urine volume measured hourly. Patients with DI are unable to concentrate their urine in response to dehydration

desmopressin stimulation test - used to distinguish between central and nephrogenic DI; will lead to concentrating ability in central DI but have no effect in nephrogenic DI

38
Q
  1. how is Central DI managed?

2. How is nephrogenic DI managed?

A
  1. desmopressin

2. treat cause; low salt, low protein diet; NSAIDs; thiazides (alleviates polyuria)

39
Q
  1. What type of hormones are produced by the adrenal cortex?

2. What type of hormones are produced by the adrenal medulla?

A
  1. steroid

2. catecholamines

40
Q

Which hormones are produced in the following adrenal cortex zones

  1. zona glomerulosa
  2. zona fasiculata
  3. zona reticularis
A
  1. aldosterone (under the control of raas)
  2. glucocorticoids (under the control of HPA axis)
  3. androgens (under control of HPA)
  • use GFR and salt sweet sex to remember this!
41
Q

Name 7 actions of glucocorticoids

A
  • increased expression of anti-inflammatory proteins
  • gluconeogenesis
  • protein metabolism
  • fat deposition
  • sodium retention and potassium secretion
  • uric acid production
  • decreased protein synthesis
42
Q

How is inactive cortisone metabolised to active cortisol?

A

via IIBHSD type 1 enzymes (and type 2 enzymes convert cortisol to cortisone)

43
Q

what is the main action of mineralocorticoids

A

increase sodium reabsorption and potassium secretion from the distal renal tubule

44
Q

What is mineralocorticoid escape?

A

high cortisol concentrations can overload 11BHSD enzymes. Due to similarities in structure, cortisol can also bind to the mineralocorticoid receptor

45
Q
  1. When are ACTH and cortisol levels highest?

2. What is the clinical relevance of this?

A
  1. morning and periodically in response to stress

2. serum cortisol levels should be taken between 8 and 9am

46
Q
  1. What adrenal disease are dexamethasone suppression tests used to investigate?
  2. What adrenal disease are ACTH stimulation tests used to investigate
A
  1. Cushing’s

2. Adrenal insufficiency

47
Q

Describe the pathophysiology of Addison’s disease

A

destruction of the adrenal cortex → glucocorticoid, mineralocorticoid and androgen insufficiency

48
Q
  1. What is the most common cause of addison’s disease?

2. Name other causes of Addison’s disease

A
  1. Autoimmune destruction (f > m; association with other autoimmune conditions)
  2. tuberculosis
    adrenectomy
    haemorrhage/infarction
    infiltration - malignant/amyloid
49
Q

In primary adrenal insufficiency (addison’s), what are the levels of CRH and ACTH and why?

A

both are raised due to reduced negative feedback from steroid hormines

50
Q
  1. What is the mechanism surrounding skin hyperpigmentation in Addison’s disease?
  2. Why do patients with Addison’s disease commonly present with Postural hypotension?
A
  1. ACTH stimulates melanocytes to produce melanin

2. mineralocorticoid deficiency - no stimulation of sodium and water retention

51
Q

Describe clinical features of Addison’s disease

A
  • confusiom
  • bronze pigmentation of the skin/buccal pigmentation
  • viteligo (changes in hair pattern)
  • depression
  • postural hypotension
  • GI disturbance
  • weight loss
  • impotence/amenorrhoea
  • weakness
  • myalgia/arthralgia
52
Q

Which investigations are useful for ?Addison’s disease

A
  • random cortisol
  • 9am plasma ACTH (high ACTH + low cortisol confirms primary adrenal insufficiency)
  • ACTH stimulation test
  • U+E - hyponatraemia, hypercalaemia, high urea
  • VBG - patients often acidotic
  • blood glucose - low
  • Adrenal antibodies
53
Q

How is Addison’s disease managed?

A
  1. Hydrocortisone - 10mg:5mg:5mg
  2. fludrocortisone
  3. Androgen replacement
54
Q

What advice do patients need to be given regarding management of Addison’s disease

A
  • sick days - double dose
  • carry steroid card
  • wear medic alert bracelet with details of condition
  • keep an up to date ampoule of hydrocortisone at home in case oral therapy is impossible
55
Q
  1. Describe signs and symptoms of an addisonian crisis

2. Name 4 precipitating factors of an addisonian crisis

A
    • shock
    • dehydration
    • profound fatigue
    • hypoglycaemic
  2. infection/countercurrent illness
    trauma
    surgery
    missed medication
56
Q
  1. Name 2 causes of secondary hypoadrenalism
  2. Why is postural hypotension not common in secondary hypoadrenalism?
  3. Why is skin pigmentation in secondary hypoaldosteronism?
A
  1. hypothalamic pituitary disease
    long term steroid therapy leading to adrenal suppression
  2. mineralocorticoid production remains intact (under control of RAAS)
  3. ACTH is low - no melanocyte stimulation
57
Q
  1. What is the pathogenesis of congenital adrenal hyperplasia?
  2. What is the classical presentation of congenital adrenal hyperplasia?
  3. What is the non-classical presentation of congenital adrenal hyperplasia?
A
  1. autosomal recessive deficiency of an enzyme in the cortisol synthetic pathways, resulting in reduced cortsol secretion
    - increased ACTH to maintain adequate cortisol, resulting in adrenal hyperplasia
    - diversion of steroid precursors to androgenic pathways (raised testosterone)
  2. addisonian crisis in young
  3. signs of androgen excess in mid-teens
58
Q

Name endogenous causes of Cushing’s syndrome (3)

A
  1. ACTH secreting pituitary tumours
  2. Ectopic ACTH production (SCLC and carcinoid tumours)
  3. Adrenal adenoma
59
Q

Describe the clinical presentation of Cushing’s Syndrome

A
  • weight gain
  • mood change - depression, irritability, psychosis
  • proximal weakness
  • gonadal dysfunction
  • acne
  • virilization
  • hypertension
  • hyperglycaemia
  • purple abdominal striae
  • osteoporosis
  • poor healing
  • infection prone
  • central obesity
  • moon face
  • buffalo hump
60
Q

Name 3 investigations for cushing’s syndrome

A
  1. plasma cortisol
  2. overnight/48dexamethasone suppression test
  3. Plasma ACTH
61
Q

What does hyperaldosteronism result in?

A
  • hypertension

- hyperkalaemia

62
Q

In which patients should primary hyperaldosteronism be considered in?

A
  • hypertensive people under 35 without a fam hx of hypertension
  • malignant hypertension
  • hypertension + hyperkalaemia before diuretic therapy
  • hypertension resistent to conventional antihypertensives
63
Q

Name 2 causes of primary hyperaldosteronism

A
  1. Conn syndrome - adrenal adenomas

2. bilateral adrenal hyperplasia

64
Q

What are the clinical features of primary hyperaldosteronism?

A
  • often asymptomatic
  • signs of hyperkalaemia - muscle weakness, ECG changes, palpitations
  • Hypertension
  • alkalosis
65
Q

Name 4 investigations for primary hyperaldosteronism

A
  1. plasma aldosterone:renin
  2. saline infusion test (should normally suppress aldosterone by raising BP)
  3. fludrocortisone suppression test
  4. serum potassium
66
Q

Name 5 causes of secondary hyperaldosteronism

A
  1. renal artery stenosis
  2. accelerated hypertension
  3. diuretics
  4. heart failure
  5. hepatorenal syndrome
  • all are associated with decreased renal perfusion leading to elevated renin
67
Q

What is phaeochromocytoma?

A

very rare tumour of the sympathetic nervous system (usually adrenal medulla) which secrete catecholamines

68
Q

Name clinical features of phaeochromocytoma

A
  • anxiety/panic attacks
  • palpitations
  • tremor
  • sweating
  • headache
  • flushing
  • nausea and/or vomiting
  • weight loss
  • constipation or diarrhoea
  • reynaud’s
  • chest pain
  • polyuria/nocturia
69
Q

Name 3 investigations for phaeochromocytoma

A
  1. urinary catecholamines and metabolites
  2. clonidine suppression tests
  3. CT/MRI
70
Q

How is phaeochromocytoma managed?

A
  1. alpha blockers and beta blockers (give alpha first)

2. surgical removal of the tumour

Phase 2 Metabolic (12 decks)

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