Hyperthyroidism Flashcards

1
Q

Symptoms of hyperthyroidism

A
o	Increased basal metabolic rate
o	Tachycardia 
o	Insomnia 
o	Heat intolerance 
o	Diarrhoea 
o	Underweight 
o	Tremors 
o	Amenorrhoea 
o      Pretibial myxoedema
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2
Q

Describe primary hyperthyroidism

A

Pathology is within the thyroid gland

Low TSH, High T4/T3

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3
Q

Describe secondary hyperthyroidism

A

Pathology is within the pituitary gland/hypothalamus

High/normal TSH, High T4/3

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4
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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5
Q

What is Grave’s disease?

A

Autoimmune disorder with TSH receptor autoanitibodies causing diffuse thyroid enlargement/goitre (sometimes with a bruit)

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6
Q

What are the other autoimmune diseases associated with Grave’s disease?

A
  1. Vitiligo
  2. Addisons
  3. T1DM
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7
Q

What is a characteristic symptom of hyperthyroidism?

A

Pretibial myxoedema

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8
Q

Pretibial myxoedema features

A

>

Pink, purple, brown plaques/nodules on anterior shin 
Bilateral 
Shiny
Firm and non-pittng
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9
Q

What eye features are present in hyperthyroidism?

A

Proptosis (Exophthalmos)

Lid lag

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10
Q

Treatment of hyperthyroidism

A
  1. Beta blockers (for symptomatic relief)
  2. Carbimazole (antithyroid drug)
  3. Radio-iodine
  4. Surgery
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11
Q

What drugs are used for the symptomatic relief of hyperthyroidism?

A

Beta blockers

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12
Q

Carbimazole mechanism of action

A

Blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production

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13
Q

Carbimazole side effects

A

> agranulocytosis

> crosses the placenta, but may be used in low doses during pregnancy

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14
Q

What is Toxic multinodular goitre?

A

Refers to one or more nodules (typically benign growths) in the thyroid gland that make thyroid hormone without responding to the signal to keep thyroid hormone balanced.

o Older patients (>60)
o Excess thyroid hormone production
o Multiple overactive nodules/follicles

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15
Q

What is a toxic adenoma?

A

o Secretes T3
o Solitary nodule
o Single hot nodule on isotope scan
o Treat with radioiodine

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16
Q

What is another name for Subacute thyroiditis?

A

De Quervain’s thyroiditis

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17
Q

What is Subacute thyroiditis?

A

Self-limiting viral infection

Thyroid function goes from hyperthyroid to hypothyroid to euthyroid

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18
Q

Features of Subacute thyroiditis

A

o Painful goitre
o Fever
o Increased inflammatory markers (CRP)
o Low isotope uptake on scan

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19
Q

What are the features of the isotope scan in Subacute thyroiditis?

A

Low isotope uptake on scan

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20
Q

What are the features of the isotope scan in Toxic adenoma?

A

Single hot nodule on isotope scan

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21
Q

What is a Thyroid crisis/storm?

A

Acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones (THs) in individuals with thyrotoxicosis.

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22
Q

Thyrotoxicosis

A

Excess thyroid hormones in the tissues due to inappropriately high circulating thyroid hormone concentrations.

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23
Q

Symptoms of Thyroid crisis/storm?

A
>	Temperature >38.5
>	Seizures
>	Vomiting
>	Sweating
>	Extreme restlessness
>	Confusion
>	Jaundice
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24
Q

Treatment of Thyroid crisis/storm?

A
  1. Propranolol
  2. High dose digoxin
  3. Carbimazole
  4. Hydrocortisone/dexamethasone
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25
Complications of Thyroid crisis/storm
Shock --> coma --> death
26
Symptoms of hypothyroidism
``` o Decreased basal metabolic rate o Bradycardia o Fatigue o Cold intolerance o Constipation o Overweight o Pale, cold, doughy skin o Menorrhagia o Thin, dry hair o Carpal tunnel syndrome o Hyperlipidaemia o Pitting oedema ```
27
Primary hypothyroidism
Pathology in the thyroid gland | High TSH, Low T4/3
28
Secondary hypothyroidism
Pathology in the hypothalamus/anterior pituitary Low/normal TSH, Low T4/3
29
Most common cause of hypothyroidism
Hashimoto’s thyroiditis
30
Hashimoto’s thyroiditis
Autoimmune disorder with autoantibodies against thyroid peroxidase (TPO) - T-cell mediated
31
Features of Hashimoto’s thyroiditis
``` o Increased levels of TPO antibodies o Gradual thyroid failure o T-cell mediated o Goitre o Commoner in older woman ```
32
Causes of hypothyroidism
* Hashimoto’s thyroiditis * Atrophic thyroiditis * Iodine deficiency * Previous treatment for hyperthyroidism * Sheehan's syndrome * Truama * Pituitary tumours
33
Atrophic thyroiditis
Autoimmune disease, less common than Hashimoto's Diffuse lymphocytic infiltration of the gland leading to Atrophy & Goitre (hypothyroidism)
34
Treatment for hypothyroidism
Levothyroxine – drug form of T4) Monitor TFTs every 2 months since treatment commences
35
Myxoedema coma
Medical emergency of hypothyroidism Unsuspected, untreated or inadequately treated hypothyroidism - Precipitated by illness, drugs
36
Features of Myxoedema coma
``` > Hypothermia > Bradycardia > Hypotension > Hypoglycaemia > Hyponatraemia > Hypoxia > Hypercapnia ```
37
Why are thyroid hormones increased in pregnancy (hyperthyroid)?
HcG is a hormone made by the developing foetus and prevents degeneration of the corpus luteum It mimics TSH and therefore will cause increased T4, which in turn suppresses TSH Therefore normal TFTs in pregnancy are decreased TSH and increased T4
38
What is the treatment of hypothyroidism in pregnancy?
If pre-existing, must increase levels of thyroxine by 25mcg as soon as pregnancy is suspected
39
What effect can untreated hypothyroidism have on the unborn baby in pregnancy?
Can cause cretinism in baby if untreated
40
What is the treatment for hyperthyroidism in pregnancy?
Treat with propranolol in early pregnancy
41
What are thyroid adenomas?
* Benign * Discrete solitary masses * Encapsulated by surrounding collagen cuff
42
What is the name given to a benign mass in the thyroid?
Thyroid adenoma
43
What are the 4 carcinomas of the thyroid?
* Papillary * Follicular * Medullary * Anaplastic
44
What is the most common carcinoma of the thyroid?
Papillary
45
What thyroid carcinoma spreads to the lymph nodes (lymphatic spread)?
Papillary
46
Histological features of papillary carcinoma
Orphan annie nuclei | Psammoma bodies
47
Describe papillary carcinoma
``` o Young adults o Least aggressive o Usually solitary nodule o Good prognosis o Orphan annie nuclei o Psammoma bodies ```
48
What thyroid carcinoma has hematological spread?
Follicular
49
What is the 2nd most common thyroid carcinoma?
Follicular carcinoma
50
Describe Follicular carcinoma
o Usually one nodule o May have surrounding capsule o 30-50s o Haematological spread
51
Where is medullary carcinoma derived from?
Derived by c-cells (calcitonin secretig cells)
52
What is the condition associated with medullary carcinoma?
MEN IIA
53
Describe medullary carcinoma
o Derived by c-cells o Associated with MEN IIA o Amyloid deposition o Aggressive
54
Describe the features of anaplastic carcinoma
o Older patients o Undifferentiated o Rapidly growing - can cause dysphagia and stridor o Very aggressive
55
What is the most aggressive thyroid carcinoma?
Anaplastic
56
What are the functions of GH?
``` o Increased lean body mass o Increased energy substrates, glucose and free fatty acids o Increased protein synthesis in muscles o Decreased fat storage o Acromegaly ```
57
What are the features of GH deficiency in children?
Growth failure
58
What are the features of GH deficiency in adults?
Osteoporosis
59
What are the features of excess GH in adults?
Acromegaly and diabetes
60
What are the features of excess GH in children?
Gigantism
61
Investigations for excess GH & acromegaly?
Oral glucose tolerance test (OGTT) | MRI pituitary
62
Features of acromegaly
``` > Insidious onset > Growth of hands and feet > Coarsening of facial features > Prominent supra-orbital ridge > Wide spread teeth (because jaw enlarges) > Macroglossia (large tongue) > Headache > Hoarse voice > Obstructive sleep apnoea > Joint pain > Carpal tunnel syndrome > Acroparaesthesia > Loss of libido ```
63
Macroglossia
Large tongue
64
Acroparaesthesia
Tingling, pins-and-needles, burning or numbness or stiffness in the hands and feet, particularly the fingers and toes
65
What hormone suppresses GH?
Somatostatin
66
Treatment for acromegaly
1. Surgery 2. Somatostatin analogue (Octreotide) 3. Dopamine agonists 4. Radiotherapy (if surgery is inappropriate)
67
Examples of somatostatin analogues
Ocreotide
68
Examples of dopamine agonists
Cabergoline or bromocriptine
69
Side effects of Ocreotide (somatostatin analogues)
gastritis, gall stones
70
Prolactinoma
A noncancerous tumor of the pituitary gland. This tumor causes the pituitary to make too much of a hormone called prolactin. The major effect of prolactinoma is decreased levels of some sex hormones — estrogen in women and testosterone in men.
71
Function of prolactin
Causes the breasts to grow and make milk during pregnancy and after birth.
72
Features of Prolactinoma in woman
``` o Amenorrhoea or oligomenorrhoea o Infertility o Galactorrhoea o Loss of libido o Increased weight ```
73
Features of Prolactinoma in men
o Erectile dysfunction o Decreased facial hair o Galactorrhoea
74
Galactorrhoea
Milky nipple discharge
75
Treatment of prolactinoma
Dopamine agonists (cabergoline)
76
Oligomenorrhoea
Infrequent menstrual periods
77
Menorrhagia
Heavy or prolonged menstrual bleeding
78
What is the outer layer of the adrenal gland called?
zona glomerulosa (secrete mineralocorticoids)
79
What is the middle layer of the adrenal gland called?
zona fasciculata (secrete glucocorticoids)
80
What is the inner layer of the adrenal gland called?
zona reticularis (secrete androgens)
81
What is the role of the zona glomerulosa?
secrete mineralocorticoids
82
What is the role of the zona fasciculata?
secrete glucocorticoids e.g. cortisol
83
What is the role of the zona reticularis?
secrete androgens
84
An example of a mineralocorticoid
Aldosterone
85
Aldosterone function
Works on distal convoluted tubule and collecting duct where it increases reabsorption of sodium and increases excretion of potassium
86
What two conditions that arise from the imbalance of aldosterone?
* Conn's disease | * ADDISON’S DISEASE
87
Conn's disease
Excess aldosterone leading to excess sodium and decreased potassum
88
ADDISON’S DISEASE
``` Adrenal insufficiency (hypoadrenalism) Leads to loss of secretion of Cortisol, Aldosterone and Sex hormones ```
89
What hormones does the medulla release?
Adrenaline and noradrenaline in response to increased sympathetic stimulation
90
Presentation of Addison's disease
``` o Fatigue o Hyponatraemia o Hyperkalaemia o Hypotension o Weight loss o Nausea o Vomiting o Skin pigmentation ```
91
Addisonian crisis
Serious medical condition caused by the body's inability to produce a sufficient amount of cortisol. An Addisonian crisis is also known as an acute adrenal crisis.
92
Symptoms of Addisonian crisis
o Severe hypotension (postural hypotension) o Febrile, rapid pulse o Dehydration o Often precipitated by trauma or illness
93
Treatment of Addisonian crisis
1. Immediate fluids 2. IV Hydrocortisone 3. Dextrose
94
Blood profile of Addison's disease
o Hyponatraemia o Kyperkalaemia o High urea
95
Investigations for Addison's disease
Short synacthen test (Synacthen is synthetic ACTH) So if cortisol increases in response to increased ATCH – it is Addison’s - primary adrenal insufficiency If cortisol doesn’t increase in response to increased ACTH – it is secondary adrenal insufficiency
96
What investigations should be done if primary adrenal insufficiency is suspected (after a short synacthen test)?
If primary adrenal insufficiency is suspected, then do CT/MRI to exclude tumour in adrenals. Also do antibodies (because could be autoimmune)
97
What is the treatment for Addison's disease?
Hydrocortisone (replace glucocorticoid) | Fludrocortisone (replace mineralocorticoid)
98
What conditions are associated with Addison's disease?
Hashimoto’s Vitiligo Type 1 DM
99
What is primary conn's disease?
Due to a problem of the adrenal glands themselves, which causes them to release too much aldosterone.
100
What are the causes of primary conn's disease?
Solitary benign adenoma | Bilateral cortical adrenal hyperplasia
101
What is secondary conn's disease?
A problem elsewhere in the body causes the adrenal glands to release too much aldosterone.
102
What are the causes of secondary conn's disease?
Volume depletion | Renal artery stenosis
103
Symptoms in Conn's disease
``` o Hypertension o Hypokalaemia o Hypernatraemia o Alkalosis o Polyuria o Polydipsia o Muscle weakness and cramps o Headaches o Non-oedematous ```
104
What is another name given to Conn's disease?
Hyperaldosteronism
105
Diagnostic test for Conn's disease
Step 1: confirm aldosterone excess > Measure plasma aldosterone and renin and express as ratio (ARR-aldosterone to renin ratio) > If ratio raised (assay dependent) then investigate further with saline suppression test > Failure of plasma aldosterone to suppress by > 50% with 2 litres of normal saline confirms PA Step 2: confirm subtype > Adrenal CT to demonstrate adenoma > Sometimes adrenal vein sampling to confirm adenoma is true source of aldosterone excess
106
Treatment for Conn's disease
Surgical > Unilateral laparoscopic adrenalectomy > Only if adrenal adenoma (and excess confirmed in adrenal vein sampling) > Cure of hypokalaemia Medical > In bilateral adrenal hyperplasia > Use MR antagonists (spironolactone or eplerenone)
107
Cushing's disease
A serious condition of an excess of the steroid hormone cortisol in the blood level caused by a pituitary tumor secreting adrenocorticotropic hormone (ACTH).
108
Causes of Cushing's dsease
Exogenous steroids Pituitary adenoma (secreting ACTH) Ectopic ACTH secretion
109
Symptoms of Cushing's disease
``` o Central obesity o Purple striae on abdomen o Hirsuitism and acne (in females) o Frontal balding (in females) o Menstrual dysfunction o Moon face o Buffalo hump o Easy bruising o Proximal myopathy o Osteoporosis and fractures o Depression o Cardiomyopathy o “Lemon on sticks appearance” ```
110
Investigations for Cushing's disease
Dexamethasone suppression test > Give oral dexamethasone > Measure cortisol levels at 0 and 48 hours > If cortisol remains high, diagnosis is Cushing’s > If cortisol levels drop, normal response o 24 hour urinary free cortisol o Late night salivary cortisol o Low dose dexamethasone suppression test o MRI/CT
111
Treatment for Cushing's disease
Trans-sphenoidal removal of the tumour External pituitary irradiation Medical therapy Bilateral adrenalectomy
112
Congenital Adrenal Hyperplasia
A group of rare inherited autosomal recessive disorders characterized by a deficiency of 21a hydroxylase deficiency
113
Phaeochromocytoma
* Rare tumour of adrenal medulla | * From chromaffin cells, which secrete Adrenaline and Noradrenaline
114
What is 10% rule of Phaeochromocytoma?
o 10% bilateral o 10% familial o 10% malignant o 10% extra adrenal
115
What condition is associated with phaeochromocytoma?
MEN II
116
Symptoms of Phaeochromocytoma
``` Usually young patients o Sweating o Hypertension o Headache o Palpitations o Flushing o Breathlessness ```
117
Investigations of Phaeochromocytoma
3x 24hour urine collections for catecholamines Abdominal CT/MRI
118
Treatment for Phaeochromocytoma
Alpha blockers (phenoxybenzamine – 1st line treatment) Beta blockers Surgery Chemotherapy
119
What is the 1st line drug given in Phaeochromocytoma?
Alpha blockers (phenoxybenzamine – 1st line treatment then beta blocker)
120
Why are alpha blockers given before beta blockers in Phaeochromocytoma?
Can cause hypertensive crisis
121
Hyperparathyroidism
A condition in which one or more of your parathyroid glands become overactive and release (secrete) too much parathyroid hormone (PTH). This causes the levels of calcium in your blood to rise, a condition known as hypercalcemia.
122
Primary Hyperparathyroidism causes
Solitary parathyroid adenoma Carcinoma Parathyroid hyperplasia
123
Symptoms of Hyperparathyroidism
1. Muscle weakness 2. Arthralgia 3. Abdominal pain 4. Constipation 5. Renal calculi 6. Tiredness 7. Dehydration 8 Polyuria. 9/ Polydipsia 10. Renal stones 11. Osteoporosis and fractures 12. Moans, bones, stones and abdominal groans
124
Polyuria
excessive urination.
125
Polydipsia
extreme thirstiness
126
Investigations for hyperparathyroidism
* Increased parathyroid hormone * Increased calcium * Decreased phosphate
127
Treatment for primary hyperparathyroidism
Surgery
128
Causes of secondary hyperparathyroidism
1. Chronic renal failure 2. Vitamin D deficiency 3. Insufficiency calcium in the diet 4. Excessive magnesium in the diet
129
Blood results in hyperparathyroidism
1. Increased calcium 2. decreased phosphate 3. Increased parathyroid hormone
130
Treatment for hyperparathyroidism
Increase calcium with supplements
131
Tertiary hyperparathyroidism
o Parathyroid glands develop autonomous function o Keep on producing massive amounts of PTH o This happens in patients with long term secondary hyperparathyroidism o So, although calcium levels are increased, PTH is still released
132
Blood results in Tertiary hyperparathyroidism
Greatly increased PTH | Increased calcium
133
Treatment for Tertiary hyperparathyroidism
Surgery
134
Malignant hyperparathyroidism
Parathyroid related protein PTHrP is produced by malignant squamous cell carcinomas - Non-small cell lung cancer, Breast & Renal cancer. PTHrP mimics PTH resulting in decreased PTH, increased calcium and increased phosphate
135
Primary hypoparathyroidism
Decreased PTH secretion due to gland failure. PTH roles is to keep blood calcium level stable
136
Causes of Primary hypoparathyroidism
Autoimmune | Digeorge syndrome
137
Blood results in Primary hypoparathyroidism
1. Decreased PTH 2. Decreased calcium 3. Increased/normal phosphate
138
Digeorge syndrome
Congenital absence of parathyroid glands. Autosomal dominant
139
Treatment for Primary hypoparathyroidism
Vitamin d supplements | Calcium supplements
140
Secondary hypoparathyroidism causes
Radiation Post thyroidectomy Severe hypomagnesaemia
141
Blood results in secondary hypoparathyroidism
Low PTH | Increased calcium
142
Pseudohypoparathyroidism
A genetic disorder in which the body fails to respond to parathyroid hormone (resistance)
143
Blood results in Pseudohypoparathyroidism
Decreased calcium | Increased PTH
144
Features in Pseudohypoparathyroidism
``` > Short 4th metacarpals > Round face > Short stature > Mental retardation > Obesity ```
145
Treatment for Pseudohypoparathyroidism
Vitamin D supplements | Calcium supplements
146
Causes of SiADH
``` o Cancer (ectopic production of ADH) o Meningitis o Pneumonia o TB o Alcohol withdrawal  Opiates  Carbamazepine ```
147
Drugs that cause SiADH
Opiates | Carbamazepine
148
Clinical features of SiADH
``` o Nausea o Dizziness o Light headedness o Irritability o Collapse ```
149
Investigations in SiADH
Hyponatraemia Decreased serum osmolarity Increased urine Osmolarity Normal renal function
150
Treatment for SiADH
Water restriction | Demeclocycline (inhibits action of ADH in kidney)
151
Osmolarity
Concentration - e.g increased urine osmolarity is increased urine concentration.
152
Demeclocycline
inhibits action of ADH in kidney - used in SiADH
153
Nephrogenic Diabetes insipidus
Is an uncommon disorder that causes an imbalance of fluids in the body. This imbalance leads you to produce large amounts of urine. Due to impaired water re-absorption by the kidneys
154
Causes of cranial Diabetes insipidus
Decreased secretion of ADH from posterior pituitary - Trauma - “DIDMOAD syndrome
155
Causes of nephrogenic Diabetes insipidus
Impaired response to ADH in the kidneys - Inherited - Lithium - Chronic renal disease
156
DIDMOAD
(DI+DM+optic atrophy+deafness)
157
The two types of Diabetes insipidus
Cranial and nephrogenic
158
Clinical features of Diabetes insipidus
o Polyuria o Polydipsea o Dehydration o Hypernatraemia
159
Investigations for Diabetes insipidus
o Increased sodium o Increased serum Osmolarity o Decreased urine Osmolarity (because the kidneys aren’t able to concentrate the urine by reabsorbing the water in nephrogenic)
160
Diagnosis of Diabetes insipidus
Water deprivation test - the normal response to deprivation is to increase the action of ADH and produce more concentrated urine Give desmopressin (synthetic ADH) then measure urine Osmolarity to differentiate between cranial and nephrogenic DI.
161
How to differentiate between cranial and nephrogenic DI?
Give desmopressin (synthetic ADH) then measure urine Osmolarity > If urine Osmolarity fails to increase its nephrogenic DI > If urine Osmolarity increases then its cranial DI