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Phase 3 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Define diabetes.

A

metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with metabolic disturbances leading to defect in secretion and/or action of insulin

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2
Q

What are the symptoms of diabetes?

A
  1. glycosuria (energy source depletion) = tired, weak, weight loss, difficulty concentrating
  2. glycosuria (osmotic diuresis) = polyuria, polydipsia, thirst, dry mucous membranes, postural hypotension
  3. glucose shifts (swollen ocular lenses) = blurred vision
  4. ketone production = N&V, abdo pain, heavy breathing, acetone breath, coma, drowsiness
  5. complications = microvascular, macrovascular, neuropathy, infection
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3
Q

How is diabetes diagnosed?

A 
fasting glucose > 7.0 mmol/L
random > 11.1 mmol/L
HbA1c 6.5% or 48 mmol/mol
one is diagnostic if symptomatic
2 if asymptomatic
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4
Q

Name 3 investigations that you would carry out following diagnosis of diabetes.

A
  1. plasma ketones (>0.6mmol/l = T1DM)
  2. islet autoantibodies e.g. GAD65, IA2 = T1DM
  3. C peptide: secreted in equimolar conc. of insulin, marker of endogenous insulin secretion, useful 3-5 years after diagnosis
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5
Q

Define T1DM and briefly describe its pathogenesis.

A
  • chronic, progressive, metabolic disorder with hyperglycaemic due to absence of insulin secretion
  • autoimmune destruction of Islets of Langerhans insulin-producing beta cells
  • HLA DR3/4 gene
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6
Q

List the genetically susceptible T1DM triggers.

A 
viral infections - enterovirus
immunisations
diet - cow's milk at early age
increased SE status
obesity
vitamin D deficiency
perinatal factors - maternal age, history of preeclampsia
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7
Q

How does T2DM differ from T1?

A

T2 involves insulin resistance rather than absence with relative deficiency as a result

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8
Q

Maturity onset diabetes of the young is an autosomal dominant condition. Name the main gene associated with it and 3 of its main clinical features.

A
  • HNF1-A
  • often <25 years onset
  • runs in families
  • managed by diet, OHAs and insulin
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9
Q

What are the risk factors for development of gestational DM? (3)

A

high BMI, previous GDM, family history of DM

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10
Q

Women with risk factors should have OGTT at 24-28 weeks. Which values are consistent with diagnosis of GDM?

A
  • fasting venous glucose >5.1 mmol/L
  • one hour value > 10 mmol/L
  • 2 hours after OGTT > 8.5 mmol/L
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11
Q

What disorders can lead to secondary diabetes?

A
  • defects in beta-cell function and insulin action
  • disease of exocrine pancreas e.g. pancreatitis
  • endocrinopathies e.g. acromegaly, Cushing’s
  • immune suppressive agents e.g. glucocorticoids
  • antipsychotics
  • genetic syndromes e.g. Downs
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12
Q

Briefly describe the mechanism by which insulin in secreted.

A
  • GLUT2 mediate glucose entry into beta cells
  • ATP production causes ATP-sensitive K+ channels close
  • increases K+ leads to depolarisation of cell
  • Ca2+ enter cell and trigger exocytosis of insulin and C peptide into nearby blood vessels
  • released in 2 phases
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13
Q

Discuss the different types of insulin analogue used in the management of T1DM.

A
  • short/rapid (bolus) e.g. novorapid
  • intermediate/long (basal) e.g. Glargine (Lantus)
  • mixed e.g. novomix 30
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14
Q

What are the benefits of using insulin pens?

A
  • easy to transport and convenient
  • less injection pain
  • can be used without being noticed
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15
Q

What are the benefits of pump therapy?

A
  • continuous SC insulin infusion
  • better glycaemic control
  • infuses insulin at basal rate with patient-activated boosts at meals
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16
Q

What are the disadvantages/complications with using pump therapy?

A
  • expensive with maintenance costs
  • reactions and infections at cannula site
  • tube blockage
  • pump malfunction
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17
Q

What are the 3 components of Whipple’s triad for hypoglycaemia?

A
  1. Symptoms of hypoglycaemia: autonomic/neuroglycopaenic
  2. Measured plasma glucose < 2.8 mmol/L
  3. Relief of symptoms when the glucose is raised to normal
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18
Q

What is the four step treatment for hypoglycaemia?

A
  1. 15-20g quick carbo e.g. dextrosol or lucozade
  2. 1.5-2 tubes of glucose gel
  3. 1mg glucagon IM
  4. IV glucose
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19
Q

What are the DVLA rules regarding patients with hypoglycaemia?

A

BG > 5 mmol/L - carry CHO
BG 4.5, eat before driving
If hypo - wait 1 hour before driving and for BG > 5

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20
Q

What 3 things are seen in diabetic ketoacidosis?

A
  1. METABOLIC ACIDOSIS - venous HCO3- < 18, H+ > 45, pH < 7.3
  2. PLASMA GLUCOSE > 13.9
  3. URINARY/PLASMA KETONES - urinary > 2, plasma > 3
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21
Q

Is DKA more commonly seen in T1DM or T2DM?

A

T1DM

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22
Q

Describe how untreated DKA can cause fatality in the young and in adults.

A
  • young: cerebral oedema

- adults: severe hypokalaemia, ARDS, illness causing decompensation

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23
Q

Briefly describe the pathophysiology of DKA.

A
  • absolute or relative insulin deficiency and increased stress hormones
  • lipolysis: FFAs and ketogenesis
  • gluconeogenesis: severe hyperglycaemia
  • osmotic diuresis and acidosis: dehydration
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24
Q

What are the clinical features of DKA?

A

polyuria, polydipsia, weight loss, breathlessness (Kussmaul’s respiration), abdominal pain, leg cramps, N&V, ketone smell in breath if severe

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25
Q

List precipitating factors of DKA.

A
  • acute illness: MI, trauma, pancreatitis
  • new-onset DM
  • insulin omission: depression, weight management
  • infections
  • others: steroids, pump failure, eating disorders
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26
Q

What is the treatment of DKA?

A
  • IV fluid - 10% dextrose
  • IV insulin
  • IV potassium
  • consider and treat precipitant
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27
Q

Describe the physiological changes seen in hyperglycaemia hyperosmolar state.

A
  • glucose > 30 mmol/L
  • serum osmolality > 320 mOsmol/L
  • HCO3- > 15 mmol/L
  • absence of significant ketones
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28
Q

Briefly discuss the pathogenesis of HHS.

A
  • glycogenolysis and gluconeogenesis
  • hyperglycaemia
  • osmotic diuresis
  • dehydration
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29
Q

What are the 3 main precipitating factors in HHS?

A

infection, poor compliance, drugs

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30
Q

How would you treat HHS?

A
  • treat precipitant
  • 0.9% NaCl - aim for a positive fluid balance of 3-6L by 12 hour
  • insulin
  • LWMH, foot protection
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31
Q

What are the complications of diabetes?

A
  1. retinopathy - annual photographic screening
  2. nephropathy - annual monitoring of renal function
  3. neuropathy/foot disease - foot ulcers, progressive neuropathy, structural change, ischaemia
  4. CVD - stroke, abnormal ECG, MI, claudification, high BP, absent foot pulses, keep BP < 130/80, statins
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32
Q

What drugs are used in the treatment of T2DM?

A
  • metformin
  • sulphonylureas
  • thiazolidinediones
  • SGLT2 inhibitors
  • incretin-based therapy
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33
Q

What is the mechanism of action of metformin?

A

Increase the activity of AMP-dependent protein kinase (AMPK). This inhibits gluconeogenesis and reduces insulin resistance.

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34
Q

What are the benefits of using metformin?

A

weight loss, increased insulin sensitivity, improved glycaemia, improved lipid profile, improved vascular function

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35
Q

What type of T2DM drug is glibenclamide and how does it work?

A

sulphonylurea
Stimulates B cells of the pancreas to produce more insulin. Increase cellular glucose uptake and glycogenesis; reduces gluconeogenesis.

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36
Q

How do SGLT2 inhibitors work? Give an example.

A
  • inhibit glucose reabsorption in PCT - decrease blood glucose and increase excretion
  • dapagliflozin
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37
Q

Discuss the mechanism of action of incretin based therapy in T2DM.

A
  • DPP4 inhibitors - inactivation of the inhibition of GLP1 and GIP
  • increased GLP1 causes increased insulin release and decreased glucagon
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38
Q

Describe the symptoms of hypoglycaemia.

A
  • autonomic: sweating, palpitations, pallor, tremor, nausea, irritability, hunger
  • neuroglycopenic: inability to concentrate, confusion, drowsiness, personality change, slurred speech, weakness, dizziness, visual impairment, headache, seizure, coma
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39
Q

List causes of non-diabetes related hypoglycaemia.

A
  • pancreas: insulinoma
  • non-islet cell tumour: mesenchymal tumours, liver carcinomas
  • autoimmune: anti-insulin receptor
  • reactive hypoglycaemia: post-gastric surgery
  • drug induced
  • organ failure
  • endocrine disease: hypopituitarism, adrenal failure, hypothyroidism
  • inborn errors of metabolism
  • sepsis, starvation, anorexia nervosa
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40
Q

What is Conn’s syndrome?

A

primary aldosteronism

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41
Q

What is the commonest secondary cause of hypertension?

A

primary aldosteronism

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42
Q

When is primary aldosteronism suspected and what other investigations need to be carried out?

A
  • aldosterone-renin ratio >35
  • saline suppression tests: 2L saline over 4 hours, aldosterone > 270 pmol/L suspicious
  • stop beta blockers and MR antagonists and replace with a-blockers, verapamil, hydralazine during investigations
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43
Q

How is primary aldosteronism managed?

A
  • unilateral laparoscopic adrenalectomy if unilateral: cure of hypokalaemia and most high BP
  • MR antagonists e.g. spironolactone, eplerenone
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44
Q

What is the most common gene mutation seen in congenital adrenal hyperplasia?

A

CYP21 - 21a hydroxylase

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45
Q

Is congenital adrenal hyperplasia an autosomal dominant or recessive condition?

A

autosomal recessive

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46
Q

What are the different clinical features seen in males and females in CAH?

A

male: low BP, low Na+, early virilisation
female: ambiguous genitalia

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47
Q

How is congenital adrenal hyperplasia treated?

A

mineralocorticoid and glucocorticoid replacement

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48
Q

What are the clinical features of Cushing’s syndrome?

A

proximal myopathy, facial plethora, bruising, striae, hypertension, weight gain, moon face, buffalo hump, hirsutism

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49
Q

What are the different ACTH dependent and ACTH independent causes of Cushing’s syndrome?

A
  • dependent: pituitary adenoma (Cushing’s disease), ectopic ACTH, ectopic CRH
  • independent: adrenal adenoma, adrenal carcinoma, nodular hyperplasia
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50
Q

If cortisol levels are found to be increased, what tests should be carried out?

A

Perform 2 of:

  • 24hr urinary free cortisol
  • urine cortisol: creat. ratio 3x
  • dexamethasone suppression test
  • late night salivary cortisol
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51
Q

What is the management involved in Cushing’s syndrome?

A

short term hydrocortisone replacement

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52
Q

What is a phaeochromocytoma?

A

tumour in adrenal medulla causing increased secretion of catecholamines

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53
Q

What symptoms would make you think of a phaeochromocytoma?

A
  • hypertension (intermittent in 50%)
  • episodes of headache, palpitations, pallor and sweating
  • tremor, anxiety, N&V, chest or abdo pain
  • crises last 15 mins
54
Q

What is the general treatment for a phaeochromocytoma?

A
  • surgical resection

- preoperative treatment: alpha blockade, beta if tachycardic, encourage salt intake

55
Q

What is Addison’s disease?

A

primary adrenal insufficiency due to autoimmune destruction

56
Q

List the clinical features of Addison’s disease.

A

anorexia/weight loss, fatigue, abdominal pain, vomiting, diarrhoea, dizziness, low BP, skin pigmentation

57
Q

How is Addison’s disease diagnosed?

A
  • biochemistry: low Na, high K, hypoglycaemia
  • short synACTHen test: measure plasma cortisol before and 30min after IV ACTH injection - normal baseline > 250 nmol/L, post > 480
  • ACTH levels - very high -> skin pigmentation
  • high renin, low aldosterone
  • adrenal autoantibodies
58
Q

What are the primary and secondary causes of adrenal insufficiency?

A
  • primary: autoimmune, infection (TB), metastatic cancer, adrenal haemorrhage, drugs
  • secondary: panhypopituitarism, isolated ACTH deficiency
  • tertiary suppression: chronic high-dose glucocorticoid therapy, after cure of Cushing’s
59
Q

What causes secondary aldosteronism? Name 3 processes that affect this.

A

defect in RAAS

heart failure, liver cirrhosis, nephrotic syndrome

60
Q

Discuss the release products of the hypothalamus and how they affect the anterior pituitary.

A
  • GHRH: release of GH from somatotrophs to multiple organs
  • GnRH: release of FSH and LH from gonadotrophs to ovaries/testes
  • CRH: release of ACTH from corticotrophs to adrenal cortex
  • TRH: release of TSH from thyrotrophs to thyroid
  • dopamine: negative feedback to prolactin from lactotrophs to breast/uterus
61
Q

What does the posterior pituitary release?

A
  • ADH - decreases water excretion

- oxytocin

62
Q

What causes hypopituitarism and how is it treated?

A
  • failure of anterior pituitary function
  • multiple hormone replacement: hydrocortisone (first for cortisol), thyroxine, testosterone and oestrogen, growth hormone
  • no replacement for prolactin
63
Q

What leads to failure of anterior pituitary function?

A

tumours, radiotherapy, infarction/haemorrhage, infiltration (sarcoid), trauma

64
Q

List some causes of high prolactin levels.

A
  • prolactinomas
  • lactation/pregnancy
  • drugs that block dopamine e.g. antiemetics, tricyclics
  • ‘stalk effect’ - due to loss of inhibitory dopamine
65
Q

Discuss the different types of pituitary tumours.

A
  1. Non-functioning - commonest
  2. Prolactinomas
  3. TSHoma
66
Q

What are the clinical features, investigations and treatment of non-functioning pituitary tumours?

A
  • CF: visual field defects, headache, eye movement problems
  • investigations: imaging, visual field assessment, prolactin, other pituitary hormones
  • treatment: surgery, RT
67
Q

What are the clinical features, investigations and treatment of prolactinomas?

A
  • galactorrhoea, headaches, mass effect, visual field defect, amenorrhoea/erectile dysfunction
  • serum prolactin > 6000, MRI pituitary
  • dopamine agonists e.g. cabergoline, surgery
68
Q

Discuss the impact of pregnancy in prolactinoma.

A
  • gets bigger
  • dopamine agonists are contraindicated
  • monitor visual fields in macro
69
Q

What causes agromegaly?

A

pituitary tumour secreting GH post puberty

70
Q

What are the features seen in agromegaly?

A

sweats and headaches, alteration of facial features, increased hand and feet size, visual impairment, cardiomyopathy, increased inter-dental space

71
Q

How is agromegaly diagnosed?

A
  • glucose tolerance test: should suppress GH, agromegaly stays > 2ug/L
  • measure IGF1
  • MRI
72
Q

Discuss the treatment of agromegaly.

A
  • surgery
  • somatostatin analogue, dopamine agonist, GH receptor agonist
  • radiotherapy if residual tumour or ongoing symptoms
73
Q

What are the risks associated with long exposure to increased growth hormone?

A
  • arthropathy (reversible)
  • neuropathy (intermittent anaesthesias - irreversible)
  • CV disease - LV dysfunction, arrhythmias
  • hypertension
  • reversible upper airway obstruction
  • malignancy - colonic polyps
  • diabetes mellitus - reversible
74
Q

What are the clinical features of diabetes insipidus and what are the differential diagnosis?

A
  • polydipsia, polyuria

- nephrogenic diabetes insipidus or psychogenic polydipsia

75
Q

What causes central diabetes insipidus?

A

ADH deficiency - idiopathic, trauma, pituitary tumour, pituitary surgery, pregnancy, familial

76
Q

How would you diagnose diabetes insipidus?

A
  • water deprivation test - suppress ADH release

- assess ability to concentrate urine with ADH

77
Q

How is diabetes insipidus treated?

A
  • treat underlying cause

- DDavP - synthetic ADH as spray, tablets or injection

78
Q

What are the 3 component of the autoimmune polyendocrine syndrome type 2?

A
  • addisons
  • AI thyroiditis
  • T1DM
79
Q

What is the gene mutation associated with APS type 2?

A

HLA DR 3/4

80
Q

List 6 conditions that are associated with APS type 2?

A
  • pernicious anaemia
  • coeliac disease
  • primary hypogonadism
  • alopecia
  • myosthenia gravis
  • stiff man syndrome
81
Q

How does PCOS present?

A

polycystic ovarian syndrome

  • anovulation - amenorrhoea, oligomenorrhoea, irregular cycles
  • hyperandrogen - hirsutism, alopecia, acne
  • adolescence
  • metabolic abnormalities and T2DM
  • increased testosterone and LH
82
Q

What is primary amenorrhoea and what causes it?

A
  • never had a period
  • GU absence
  • Turner’s syndrome
  • secondary hypogonadism
83
Q

Name some causes of secondary amenorrhoea.

A
  • uterine - Ashermans syndrome
  • ovarian - PCOS, failure
  • pituitary - prolactinoma, tumour
  • hypothalamus - weight, stress, drugs
84
Q

Define hirsutism.

A

excess hair growth in a male pattern due to increased androgens and increased skin sensitivity to androgens

85
Q

What are the causes of hirsutism?

A

PCOS, androgen secreting tumour, CAH, idiopathic

86
Q

Discuss the pathophysiology of PCOS.

A

GONADOTROPHINS
- high LH - more LH receptors in PCOS ovaries, more theca cells, increased androgens
- low FSH - leads to continuous stimulation of follicles without ovulation, decreased conversion of androgens to oestrogens
ANDROGENS
- increased due to LH
- disordered action of enzymes
- decreased SHBG - more free testosterone
INSULIN
- increased insulin resistance

87
Q

How is PCOS managed?

A
  • lifestyle changes
  • metformin: improves insulin sensitivity, decreased LH and increased testosterone, may regulate ovulatory function and hence menstruation BUT ineffective for fertility/hirsutism
  • COCP: ovarian androgen suppression
  • corticosteroids: adrenal androgen suppression
  • spironolactone: MR antagonist
  • finasteride: 5 alpha reductase inhibitor
88
Q

Discuss the action of parathyroid hormone.

A
  • to raise blood calcium
  • kidneys: reabsorption of Ca from DCT
  • bone: increased osteoclasts leading to Ca resorption
  • gut: increased Ca absorption and stimulate vit D synthesis
89
Q

What causes familial hypocalciuric hypercalcaemia?

A

loss of function mutation of calcium sensing receptor

90
Q

Where are calcium sensing receptors found?

A

parathyroid gland, kidneys, thyroid (calcitonin)

91
Q

Briefly describe the process by which vitamin D is produced.

A
  • 7-dehydrocholesterol is converted to cholecalciferol in the skin by IV light
  • converted to 25-hydroxycholecalciferol (storage form of vit D) in the liver
  • converted to 1,25-dihydroxycholecalciferol (active form) in the kidneys
92
Q

List some symptoms of hypercalcaemia.

A
  • “stones, bones, abdominal groans, thrones and psychiatric overtones”
  • confusion, depression, fatigue, coma
  • shortening of QTc, bradycardia, hypertension
  • polyuria, nephrogenic DI, stones, nephrocalcinosis
  • muscle weakness, bone pain, osteoporosis
  • anorexia, nausea, constipation, pancreatitis
93
Q

Discuss the aetiology of hypercalcaemia

A

PTH MEDIATED

  • primary hyperparathyroidism
  • familial syndromes e.g. MEN1
  • familial hypocalciuric hypercalcaemia

PTH INDEPENDENT

  • malignancy
  • granulomatous disorders
  • vit D toxicity
  • drugs e.g. thiazides, lithium
  • adrenal insufficiency
94
Q

Give 3 mechanism by which malignancy can cause hypercalcaemia.

A
  • osteolytic metastases and myeloma
  • tumour secretion of PTHrP: binds to PTH receptor - bone resorption and renal reabsorption e.g. squamous cell lung cancer, oesophageal cancer, renal cell carcinoma, breast cancer
  • tumour cell production of vit D: activated macrophages e.g. lymphoma
95
Q

What is the management strategy of hypercalcaemia?

A

Underlying cause, intravenous fluids (saline), furosemide (diuretic), calcitonin, pamidronate (bisphosphonate)

96
Q

What are the causes of primary hyperparathyroidism?

A

isolated PT adenoma, PT hyperplasia, PT carcinoma

97
Q

What conditions are associated with primary hyperparathyroidism?

A
  • bone: osteoporosis, bony cysts
  • kidneys: renal calculi, nephrocalcinosis, renal impairment
  • pancreatitis
98
Q

What investigations would you carry out if you suspected primary hyperparathyroidism?

A
  • drugs, U&Es, PTH, urine Ca:creat ratio, vit D
  • DEXA, renal US
  • consider MEN1 or MEN2 if <40 or 1st degree relative of highPTH
99
Q

Discuss the management plan for primary hyperparathyroidism.

A
  • parathyroidectomy: if Ca >3 mmol/L, hypercalciuria, osteoporosis, <50, renal stones
  • observation: if no end damage/unfit for surgery
  • medicine: if not surgery e.g bisphosphonates, CaSR agonists (cinacalcet)
100
Q

Give 4 causes of vitamin D deficiency.

A
  • poor sunlight exposure: elderly, housebound, Northernisation
  • malabsorption
  • gastroectomy
  • renal disease
101
Q

What is osteomalacia and briefly describe how it develops.

A
  • failure to ossify bones in adulthood as a result of vit D deficiency
  • hypomineralisation of cortical and trabecular bone
102
Q

How does osteomalacia present?

A

insidiously with bone pain, proximal myopathy, hypocalcaemia

103
Q

What metabolic abnormalities are seen in osteomalacia?

A

low Ca, low P, high ALP, low vit D, high PTH

104
Q

Discuss the treatment for osteomalacia.

A
  1. cholecalciferol
    - restore body stores, correct metabolic disturbances, heal bone abnormalities
  2. alfacalcidol
    - i.e. active vit D
    - in renal impairment and hypoparathyroidism
    - higher risk of hypercalcaemia
105
Q

Discuss the differences in clinical features between male hypogonadism in children and adults.

A

CHILD

  • slow growth in teens
  • no pubertal growth spurt
  • small testes and phallus

ADULT

  • depression/low mood/low energy
  • poor libido and erectile problems
  • poor muscle bulk
  • sparse hair, gynaecomastia, small testes and phallus
106
Q

What is hypogonadotrophic hypogonadism?

A

secondary hypogonadism is due to problems with either the hypothalamus or pituitary gland - deficiency in GnRH or LH/FSH

107
Q

What are the causes of secondary hypogonadism?

A

tumour genetic syndromes, injury, cerebellar ataxia, surgery, RTx, Kallmann’s syndrome

108
Q

What are the hormonal features seen in secondary hypogonadism?

A

low testosterone, low LH+/-FSH+/-prolactin

109
Q

What is Kallmann’s syndrome?

A

failure of cell migration of GnRH cells to hypothalamus from olfactory placode

110
Q

Describe the inheritance of Kallmann’s syndrome.

A

familial with variable penetration

  • X linked = absence of KAL1 gene
  • AD = KAL2
  • AR = KAL3
111
Q

List the clinical features that are associated with Kallmann’s syndrome.

A
  • deafness (hypoplasia of olfactory lobes)
  • renal agenesis
  • cleft lip +/- palate
  • micropenis +/- cryptorchidism
112
Q

Give examples of causes of primary hypogonadism.

A
  • complex genetic syndromes
  • cryptorchidism
  • adult Leydig and semineferous tubule failure e.g. trauma, chemotherapy, RTx, multisystem failure
  • Klinefelter’s syndrome
113
Q

What are the hormonal features of primary gonadal disease?

A

low testosterone, normal/high FSH/LH, normal prolactin

114
Q

What is Klinefelter’s syndrome?

A
  • commonest genetic cause of hypogonadism
  • XXY sex chromosomes
  • high LH and TSH - but semineferous tubules regress and Leydig cells do not function normally
115
Q

Discuss the variation in phenotype in Klinefelter’s syndrome.

A

due to hormonal response to LH surges during puberty

  • delayed puberty
  • suboptimal genital development
  • decreased male sexual characteristics
  • persistent gynaecomastia
  • azospermia
  • behaviour/learning difficulties
116
Q

How is Klinefelter’s syndrome managed?

A

androgen replacement, psychological support, fertility counselling

117
Q

Discuss the management plan of male hypogonadism.

A
  • androgen replacement e.g. oral, IM, topical

- fertility treatment e.g. HCG, recombinant LH and FSH, GnRH pumps

118
Q

What are the side effects associated with androgen replacement therapy?

A

mood issues, libido issues, increased haemocrit, possible prostate effects, acne, sweating, gynaecomastia

119
Q

List the causes of hypothyroidism.

A

hypopituitarism, thyroidectomy, Hastimoto’s thyroiditis, congenital

120
Q

What is the treatment for hypothyroidism?

A

levothyroxine (T4)

121
Q

What are some of the symptoms of neonatal hypothyroidism?

A

coarse facial features, macroglossia, umbilical hernia, dry skin, developmental delay, pallor, myxoedema, goitre

122
Q

What are the causes of congenital hypothyroidism?

A

thyroid dysgenesis, dyshormonogenesis

123
Q

What is the standard treatment for hyperthyroidism?

A

beta blockers, carbimazole, or radioactive iodine

124
Q

Discuss the aetiology of Grave’s disease.

A

autoimmune, genetics (HLA, TG, thyroid receptor), environmental, immune modulating treatment

125
Q

What are the causes of hyperthyroidism?

A

pituitary adenoma, autoimmune, thyroid adenoma, toxic multinodular goitre

126
Q

What is the name given to iodine induced hyperthyroidism?

A

Jod Basedow phenomenon

127
Q

What is the name given to iodine induced hypothyroidism?

A

Wolff Chaikoff effect

128
Q

What are the two types of amiodarone thyroid disease and how are they treated??

A
  1. Autoimmune thyrotoxicosis - high dose carbimazole

2. Destructive thyroiditis - glucocorticoids

129
Q

How are thyroid carcinomas managed?

A
  • FNA of nodules
  • surgery and therapeutic radioiodine
  • monitoring of thyroidglobulin
130
Q

List three associations of the RET proto-oncogene.

A
  • familial medullary thyroid cancer
  • multiple endocrine neoplasia 2 and 3
  • Hirschprungs (nerves missing from intestine, constipation)
131
Q

Describe the clinical manifestations of hyperthyroidism.

A

weight loss, tremor, heat intolerance, diarrhoea, tachycardia, hypertension, palpitations, sweating

132
Q

Describe the clinical manifestations of hypothyroidism.

A

weight gain, constipation, cold intolerance, depression, lethargy, concentration, hoarseness, menorrhagia

Phase 3 (10 decks)

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