Endocrine List 2 Flashcards
1
Q
Describe Graves disease
A
Hyperthyroidism due to pathological stimulation of TSH receptor
Autoimmune induced excess production of TH
2
Q
Clinical presentation of Graves disease
A
Rapid Heart beat
Tremor
Diffuse palpable goiter with audible bruit
Eye problems: bulging outwards and lid retraction
Graves’ opthalmopathy
Graves dermopathy (rare)
Thyroid acropachy (clubbing, finger and toe swelling)
3
Q
Pathophysiology of Graves disease
A
TSH receptor stimulating antibodies (TSHR-Ab) recognise and bind to the TSH receptors in thyroid
- > stimulates thyroid hormone production T4 and T3
- > thyroxine (T4) receptors in the pituitary gland are activated by excess hormone
- > reduced release of TSH in a negative feedback look
- > Very high levels of circulating thyroid hormones, with a low TSH
- > as well as excess secretion of thyroid hormones, also results in hyperplasia of thyroid follicular cells resulting in hyperthyroidism and diffuse goitre
4
Q
Aetiology/Risk factors of Graves disease
A
Some genetic element - association with HLA-B8, DR3 & DR2.
Smoking
Stress
High iodine intake
E.coli and other gram-NEGATIVE organisms contain TSH-binding sites so may initiate pathogenesis via ‘molecular mimicry’
Autoimmune disease.
Associated with other autoimmune diseases, such as Vitiligo (pale patches on skin), Addison’s, type 1 DM, pernicious anaemia and myasthenia gravis.
5
Q
Epidemiology of Graves disease
A
Most common cause of hyperthyroidism (2/3 of cases)
More common in females
Typically presents at 40-60 years (appear earlier if maternal family history)
6
Q
Diagnostic of Graves disease
A
High T3 and T4
Lower TSH than normal
Mild neutropenia
*TSH receptor stimulating antibodies (TSHR-Ab) raised
7
Q
Treatment of Graves disease
A
Antithyroid drugs (Carbimazole or Propylthiouracil) with either dose titration or ‘block and replace’.
Thyroidectomy.
Radioactive iodine.
Beta blockers
8
Q
Complications of Graves disease
A
Thyroid storm: treat with Propylthiouracil
Also similar to auto-antigen, can result in retro-orbital inflammation - graves opthalmopathy
9
Q
Describe Hashimotos thyroiditis
A
Hypothyroidism due to aggressive destruction of thyroid cells
(autoimmune hypothyroidism)
10
Q
Clinical Presentation of Hashimotos thyroiditis
A
Thyroid gland may enlarge rapidly, occasionally with dyspnoea or dysphagia from pressure on the neck
Hypothyroidism: Fatigue, cold intolerance, slowed movement, decreased sweating
11
Q
Pathophysiology of Hashimotos thyroiditis
A
Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes.
Antibodies bind and block TSH receptors -> inadequate thyroid hormone production and secretion.
Thyroid peroxidase is essential hormone for production and storage of thyroid hormone: Thyroid peroxidase antibodies (TPO-Ab) are present in high titres
12
Q
Aetiology of Hashimotos thyroiditis
What are triggers?
A
Unknown.
Autoimmune.
Some genetic element.
Triggers; iodine, infection, smoking and possibly stress
13
Q
Epidemiology of Hashimotos thyroiditis
A
12-20 times more frequent in women.
Most common cause of goitrous hypothyroidism.
14
Q
Diagnostic tests of Hashimotos thyroiditis
A
TSH levels, usually raised in hypothyroidism.
Thyroid antibodies.
15
Q
Treatment of Hashimotos thyroiditis
A
Levothyroxine therapy (may shrink the goitre) Thyroid hormone replacement Resection of obstructive goitre.
16
Q
Complications of Hashimotos thyroiditis
A
Hyperlipidemia
17
Q
Define Sequelae
A
condition which is the consequence of a previous disease or injury
18
Q
Sequelae of Hashimotos Thyroiditis
A
Hashimotos encephalopathy
19
Q
Describe hypothyroidism
A
Reduced action/levels of thyroid hormone
20
Q
Types of hypothyroidism (briefly explain each)
A
Primary - disease associated with thyroid
Secondary - disease associated with pituitary or hypothalamus
Transient - disease associated with treatment withdrawal
21
Q
Clinical presentation of Hypothyroidism
A
(same for all 3 types)
Insidious onset.
Tiredness, lethargy, intolerance of cold, goitre, slowing of intellectual activity, constipation, deep hoarse voice.
Puffy face, hands and feet.
Menorrhagia, weight gain, myalgia, dementia, myxoedema (accumulation of mucopolysaccharide in SC tissue)
22
Q
Pathophysiology of Primary Hypothyroidism
A
Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes.
Antibodies bind and block TSH receptors
-> inadequate thyroid hormone production and secretion
23
Q
Pathophysiology of Secondary Hypothyroidism
A
Reduced release or production of TSH by pituitary or hypothalamus (respectively)
-> reduced T3 and T4 release
24
Q
Pathophysiology of Transient Hypothyroidism
A
The thyroid overcompensates until it can reestablish correct concentrations of Thyroid hormone
25
Aetiology of Primary Hypothyroidism
Autoimmune hypothyroidism (Hashimoto's), iodine deficiency, congenital defects
26
Aetiology of Secondary Hypothyroidism
Isolated TSH deficiency, hypopituitarism (due to neoplasm, infection), hypothalamic disorders (neoplasms, trauma)
27
Aetiology of Transient Hypothyroidism
Withdrawal of thyroid suppressive therapy such as radioactive iodine
28
Epidemiology of Primary Hypothyroidism
More common in Japan
29
Diagnostic tests of Hypothyroidism
Thyroid Function Tests (TFTs)
Serum free T4 levels low
Thyroid antibodies may be present
Blood tests:
Raised serum aspartate transferase levels from muscle and/or liver
Increase serum creatinine kinase levels associated with myopathy
Hypercholesterolaemia
Hyponatraemia due to an increase in ADH and impaired free water clearance
30
Treatment of Primary Hypothyroidism
Thyroid hormone replacement (Levothyroxine) - dose is titrated until TSH normalises
Resection of obstructive goitre
31
Treatment of Secondary Hypothyroidism
Thyroid hormone replacement (Levothyroxine). Treat underlying cause
32
Treatment of Transient Hypothyroidism
Remits on its own
33
Complications of Hypothyroidism
```
Myxoedema coma (20-50% mortality)
Reduced level of consciousness, seizures, cardiac failure, hypothermia and hypothyroidism
```
severe hypothyroidism/reduced T4
34
Types of thyroid cancer/malignancies
Papillary (named for papillae among its cells on microscopy)
Follicular
Anaplastic (one of most aggressive cancers in human)
Lymphoma
Medullary
35
What types of thyroid cancers fit this clinical presentation:
Usually asymptomatic thyroid nodule (usually hard and fixed). Possibly enlarged lymph nodes on examination.
Papillary
Follicular
Anaplastic
36
Clinical presentation of Lymphoma (thyroid malignancy)
Rapidly growing mass in the neck
37
Clinical presentation of Medullary cancer (thyroid malignancy)
Diarrhoea
Flushing episodes (similar to Carcinoid syndrome)
Itching
38
Pathophysiology of papillary thyroid cancer
Tends to spread locally in neck, compressing the trachea
39
Pathophysiology of follicular thyroid cancer
May infiltrate neck, but greater propensity to metastasise to lung and bones relative to papillary
40
Pathophysiology of anaplastic thyroid cancer
Follicular cells of the thyroid, but does not retain original cell features like iodine uptake or synthesis of thyroglobulin
41
Pathophysiology of lymphoma thyroid cancer
Almost always non-hodgkins lymphoma
42
Pathophysiology of medullary thyroid cancer
Parafollicular calcitonin-producing C cells. Produce large amounts of peptide such as calcitonin
43
Aetiology of medullary thyroid cancer
Often familial
44
Epidemiology of papillary thyroid cancer
70% of thyroid cancer.
Young people.
Three times more common in women.
45
Epidemiology of follicular thyroid cancer
20% of thyroid cancer.
Middle age.
Tends to be in areas of low iodine.
46
Epidemiology of anaplastic thyroid cancer
<5% of thyroid cancer
47
Epidemiology of lymphoma thyroid cancer
2% of thyroid cancer.
| Often associated with Hashimoto's thyroiditis.
48
Epidemiology of medullary thyroid cancer
5% of thyroid cancer.
| More sporadic than hereditary.
49
Diagnostic tests of thyroid cancer
Fine needle aspiration.
| Differences: Medullary; elevated serum calcitonin.
50
Treatment of medullary thyroid cancer
Total thyroidectomy and prophylactic central lymph node dissection
51
Which thyroid cancers would you treat via:
| External radiotherapy to provide relief (largely palliative)
Anaplastic
| Lymphoma
52
Treatment of Papillary thyroid cancer
Total thyroidectomy -> ablative radioactive iodine
| same for follicular thyroid cancer
53
Treatment of Follicular thyroid cancer
Total thyroidectomy -> ablative radioactive iodine
| same for papillary thyroid cancer
54
Describe Cushing's syndrome
Persistently and inappropriately elevated circulating glucocorticoid (cortisol)
This is attributed to inappropriate ACTH secretion from the pituitary (due to tumour)
55
Clinical presentation of Cushing's syndrome
(truncal) Obesity (fat distribution central, buffalo hump)
plethoric complexion
Rounded 'moon face', thin skin, bruising, striae, hypertension, pathological fractures
Acne
Cataracts, Ulcers, Skin striae, Hyperglycarmia/hypertension, Increased infection, Necrosis, Glucosuria/gonal dysfunction
56
Pathophysiology of Cushing's syndrome
Excess cortisol can either result from excess ACTH which in turn stimulates excess cortisol release or from neoplasms in the adrenals which in turn stimulate the zona reticularis to release more cortisol.
Excess can also result from ingesting excess glucocorticoid itself e.g. PREDNISOLONE
Many features due to protein-catabolic effects of cortisol; thin skin, easy bruising, striae. Excessive alcohol consumption can mimic the clinical and biochemical signs (Pseudo-Cushings's), but resolves on alcohol recession
57
Aetiology of Cushing's syndrome
ACTH (adrenocortiotropic hormone) dependent disease:
Cushings disease - Bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma (benign).
Ectopic Cushings syndrome - paraneoplastic syndrome (tumour elsewhere in body producing ACTH - especially small cell lung cancer and carcinoid tumours)
ACTH treatment e.g. for asthma
ACTH independent:
Excess oral steroids! (iatrogenic)
Adrenal adenomas,
adrenal carcinomas, excess glucocorticoid administration (most common) e.g. Prednisolone
58
Epidemiology of Cushing's syndrome
10/1,000,000.
Higher incidence in diabetes.
2/3 cases are Cushing's disease.
Most common cause is oral steroids i.e. glucocorticoid therapy.
Spontaneous endogenous causes are rare, but 80% due to raised ACTH, with pituitary adenoma being the most common cause
59
Diagnostic tests of Cushing's syndrome
Confirm raised cortisol: 48 hour low-dose dexamethasone: Fail to suppress cortisol is diagnostic of Cushings.
Urinary free cortisol over 24hrs (normal levels mean Cushings unlikely).
Late night salivary cortisol. Establishing cause: CT and MRI of renal and pituitary
NOT random plasma cortisol test as cortisol levels change through day (stress, illness, morning)
60
Treatment of Cushing's syndrome
Stop steroids if iatrogenic
Transphenoidal removal of pituitary adenoma if Cushings disease
Adrenalectomy or Radiotherapy if Adrenal Adenoma
Ectopic ACTH: Surgical removal of tumour if location known
Cortisol synthesis inhibition: metyrapone, ketoconazole
61
Complications of Cushing's syndrome
Hypertension, obesity, death
62
Describe Acromegaly
Overgrowth of all organ systems due to excess GH
| Increased production of growth hormone occurring in adults after fusion of the epiphyseal plates
63
Clinical Presentation of Acromegaly
Slow onset (old photos). Larger hands/feet. Large tongue, prognathism, interdental separation, spade-like hands.
64
If (acromegaly) tumour arises before fusion of epiphyseal plates (children bones), what condition can result instead/like acromegaly
Gigantism
| worse as don't stop growing as bones not developed
65
Pathophysiology of Acromegaly
GH acts directly on tissues such as liver, muscle bone or fat, as well as indirectly through induction of insulin like growth factor. Excess causes uncontrolled growth of organ systems.
Very slow insidious onset over many years
66
Aetiology of Acromegaly
Usually excessive GH secretion by a pituitary tumour. Other GH releasing tumours possible (hypothalamus, specific lung cancers).
Mainly pituitary adenoma
67
Epidemiology of Acromegaly
3 per million per year
Average 40 yrs.
Same in male and females
68
Diagnostic tests of Acromegaly
Glucose tolerance test: IGF-1 raised. GH raised.
| MRI the pituitary fossa for adenomas
69
Treatment of Acromegaly
```
Transsphenoidal resection surgery.
Dopamine agonists (cabergoline), somatostatin analogues (octreotide) and GH receptor antagonists (pegvisomant)
```
70
Complications of Acromegaly
Hypertension, diabetes.
Untreated adenoma can impact the optic chiasm -> blindness
Colorectal cancer
71
Describe Conn's syndrome
Primary hyperaldosteronism
| High aldosterone levels independent of Renin-Angiotensin system
72
Clinical presentation of Conn's syndrome
```
Hypertension (possibly low urine output)
Hypokalemic:
-Constipation
-Weakness and cramps
-Paraesthesia
-Polyuria and polydipsia
```
73
What is secondary hyperaldosteronism
Hyperaldosteronism due to high renin levels
74
What is another name for Primary Hyperaldosteronism
Conn's syndrome
75
Pathophysiology of Conn's syndrome
Aldosterone causes an exchange of transport of sodium and potassium in the distal renal tubule.
Therefore, hyperaldosteronism causes increased reabsorption of sodium (and water) and excretion of potassium
76
Aetiology of Conn's syndrome
Adrenal adenoma secreting aldosterone in Conn's syndrome (or possibly bilateral adrenal hyperplasia)
77
Diagnostic tests of Conn's syndrome
Plasma Aldosterone (increased) and Renin (decreased)
U and E
Adrenal CT
ECG
78
Treatment of Conn's syndrome
Adenoma: Surgical removal (laparoscopic adrenalectomy)
Hyperplasia: aldosterone antagonist or potassium-sparing diuretic (spironolactone)
79
Describe Adrenal Insufficiency
Hypoadrenalism
| due to destruction or reduced stimulation of adrenal cortex
80
What are types of Adrenal Insufficiency and describe the difference between the two
Primary insufficiency - Destruction of adrenal cortex
| Secondary insufficiency - Reduction of adrenal cortex stimulation
81
What is another name for Primary Adrenal Insufficiency
Addison's disease
82
What is key difference in clinical presentation between Primary and Secondary adrenal insufficiency
Primary - Hyperpigmentation
| Secondary - no pigmentation
83
*Why does Primary Adrenal Insufficiency result in hyper pigmentation but Secondary AI does not?
Primary:
Destruction of adrenal cortex -> Less cortical products. Excess ACTH -> stimulates melanocytes -> hyper pigmentation
Secondary:
Reduction of adrenal cortex stimulation -> Less cortical products. Low ACTH -> less melanocytes stimulation -> no pigmentation
84
Clinical presentation of Addison's disease (primary adrenal insufficiency)
Thin, tanned, tired and tearful.
HYPER-pigmentation.
Insidious. Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue. Postural hypotension. GI: N+V, abdominal pain
85
Clinical presentation of Secondary Adrenal Insufficiency
Insidious. Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue. Postural hypotension. Thin, tanned, tired and tearful.
NO pigmentation
86
Pathophysiology of Addison's disease (primary adrenal insufficiency)
Autoimmune destruction of the entirety adrenal cortex. Associated with other autoimmune conditions.
Loss of cortex -> reduction in ability to produce Cortisol and/or Aldosterone.
Excess ACTH stimulates melanocytes -> pigmentation.
87
Pathophysiology of Secondary Adrenal Insufficiency
Inadequate pituitary or hypothalamic stimulation of the adrenal glands. No pigmentation, since ACTH levels are low.
88
Aetiology of Addison's disease (primary adrenal insufficiency)
Organ specific autoantibodies in 90% of cases. Rarely; adrenal gland tuberculosis, surgical removal or haemorrhage
Addisons is commonest cause in the UK of adrenal insufficiency, TB is most common cause WORLDWIDE
89
Aetiology of Secondary Adrenal Insufficiency
Hypothalamic-pituitary disease or from long term steroid therapy leading to hypothalamic-pituitary-adrenal suppression.
Iatrogenic
90
Epidemiology of Addison's disease (primary adrenal insufficiency)
1/10,000
| Addisons is commonest cause in the UK of adrenal insufficiency, TB is most common cause WORLDWIDE
91
Epidemiology of Secondary Adrenal Insufficiency
200/1,000,000
92
Diagnostic tests of Addison's disease (primary adrenal insufficiency)
Sodium reduction, potassium elevation due to low aldosterone.
Short ACTH stimulation test (Give ACTH (synacthen), then measure cortisol level; in Addison, cortisol remains low after giving ACTH).
test for 21-hydroxylase adrenal autoabs (+ve in 80% Addisons)
93
Diagnostic tests of Secondary Adrenal Insufficiency
Long ACTH test (synacthen test) to distinguish from primary: ACTH raised in primary, lowered in secondary
94
Treatment of Addison's disease (primary adrenal insufficiency)
Cortisol hormone replacement - glucocorticoid (hydrocotisone)
Aldosterone replacement via mineralocorticoid (fludrocortisone) - this also helps treat postural hypotension
95
Treatment of Secondary Adrenal Insufficiency
Hormone replacement (just hydrocortisone). If from steroid therapy; remove steroids very slowly
96
Complications of Addison's
```
Adrenal crisis (patients present with shock, severe hypotension, lost a lot of fluid via vomitting and reduced reabsorption of Na+ -> treat with fluid, hydrocortisone)
Reduced QOL
```
97
Describe Adrenal Hyperplasia
Defective enzymes mediating the production of adrenal cortex products.
Low cortisol, maybe low aldosterone, high androgen
98
Clinical presentation of Adrenal Hyperplasia
In severe forms; salt loss. Female: Ambiguous genitalia with common urogenital sinus. Male: no signs at birth, bar subtle hyperpigmentation and possible penile enlargement.
99
Pathophysiology of Adrenal Hyperplasia
Defective 21-hydroxylase -> disruption of cortisol biosynthesis. This causes cortisol deficiency, with or without aldosterone deficiency and androgen excess. In severe forms, aldosterone deficiency -> salt loss
100
Aetiology of Adrenal Hyperplasia
Genetic 21-hydroxylase deficiency is the cause of about 95% of cases.
101
Diagnostic tests of Adrenal Hyperplasia
Serum 17-hydroxyprogesterone (precursor to cortisol) levels: high
102
Treatment of Adrenal Hyperplasia
Glucocorticoids: Hydrocortisone
Mineralocorticoids: Control electrolytes
If salt loss: Sodium chloride supplement
103
Describe Diabetes Insipidus
Hyposecretion or insensitivity to ADH
104
Types of Diabetes Insipidus and their difference
Cranial - Hyposecretion
| Nephrogenic - Insensitivity
105
Clinical presentation of Diabetes Insipidus
Polyuria
Compensatory polydipsia
Dehydration
106
Pathophysiology of Cranial Diabetes Insipidus
Disease of the hypothalamus, where ADH is produced -> Insufficient ADH production. Interestingly, damage to the Posterior Pituitary gland, does not lead to ADH deficiency, as it can still 'leak' out.
107
Pathophysiology of Nephrogenic Diabetes Insipidus
Depends on the aetiology. Can be due to disruption of the channels, damage to the kidney -> *Lack of response to ADH
108
Aetiology of Cranial Diabetes Insipidus
*trauma, pituitary tumour*
| Neurosurgery,, infiltrative disease, idiopathic Genetic: Mutations in the ADH gene
109
Aetiology of Nephrogenic Diabetes Insipidus
Hypokalaemia, hypercalcaemia, drugs, renal tubular acidosis, sickle cell, prolonged polyuria, chronic kidney disease Genetic: Mutation in ADH receptor
110
Epidemiology of Diabetes Insipidus
1/25,000
111
Diagnostic tests of Diabetes Insipidus
Water deprivation test: Confirm DI
Restrict fluid, measure osmolarity (urine osmolarity low means DI)
Desmospressin (ADH analogues) to differentiate between cranial and nephrogenic
Urine volume: Confirm polyuria.
U&Es (urine and electrolytes): Confirm not a more common cause of polyuria
MRI of hypothalamus: Confirm CDI
112
Treatment of Cranial Diabetes Insipidus
Desmopressin.
Mild cases: thiazide diuretics, carbamazepine and chlorpropramide to sensitise the renal tubules to endogenous vasopressin.
113
Treatment of Nephrogenic Diabetes Insipidus
Bendroflumethizide (diuretics) -> cause more Na+ excretion
NSAIDs - reduce GFR
Treatment of the cause.
114
Describe syndrome of inappropriate ADH secretion
Continued ADH secretion in spite of plasma hypotonicity and normal plasma volume
(opposite of DI)
115
Clinical presentation of syndrome of inappropriate ADH secretion
Nausea, anorexia, confusion
Concentrated urine
Irritability and headache with mild dilutional hyponatraemia.
Fits and coma with severe hyponatraemia.
116
Pathophysiology of syndrome of inappropriate ADH secretion
Ectopic (abnormal) production increases the amount of ADH produced, beyond mechanisms of control.
117
Aetiology of syndrome of inappropriate ADH secretion
Disordered hypothalamic-pituitary secretion, or ectopic production of ADH.
Neurological: Tumour, trauma, infection
Pulmonary: Lung small cell cancer (common), mesothelioma, cystic fibrosis
Drugs an CNS disorders also
118
Diagnostic tests of syndrome of inappropriate ADH secretion
(FBC)
| Measure urine and plasma osmolarity
119
Treatment of syndrome of inappropriate ADH secretion
Route: IV
Treat underlying cause
Restrict fluid
Vasopressin receptor antagonists (vaptans)
120
Describe Hyperparathyroidism
Excessive secretion of PTH
121
Types of hyperparathyroidism (describe each briefly)
Primary - One parathyroid gland produces excess PTH
Secondary - Increased secretion of PTH to compensate hypocalcemia
Tertiary - Autonomous secretion of PTH due to CKD (chronic kidney disease)
122
Clinical presentation of primary hyperparathyroidism
70-80% asymptomatic. Bone pain, renal calculi, nausea, neuropsychiatric (Bones, stones, abdominal groans and psychic moans)
Bone resorption causes pain, fracture, osteoporosis. Leads to hypercalcaemia (weak, tired, depressed, thirsty, renal stones)
Hypertension
123
Clinical presentation of secondary hyperparathyroidism
Kidney disease, with skeletal or cardiovascular complications
124
Clinical presentation of tertiary hyperparathyroidism
Bone pain, renal calculi, nausea, neuropsychiatric (Bones, stones, abdominal groans and psychic moans)
125
Pathophysiology of primary hyperparathyroidism
Adenoma or hyperplasia provides additional secretive tissue to provide excess PTH
126
Pathophysiology of secondary hyperparathyroidism
Parathyroid gland becomes hyperplastic in response to chronic hypocalcemia
127
Pathophysiology of tertiary hyperparathyroidism
Glands become autonomous, producing excess of PTH even after the correction of calcium deficiency
128
Aetiology of primary hyperparathyroidism
Single parathyroid adenoma or hyperplasia
80% = solitary adenoma
20% = parathyroid hyperplasia
(parathyroid cancer rare)
129
Aetiology of secondary hyperparathyroidism
CKD (any condition with hypocalcaemia, such as vitamin D deficiency, GI disease such as Crohn's preventing absorption of calcium)
130
Aetiology of tertiary hyperparathyroidism
Develops from secondary hyperparathyroidism
131
Epidemiology of primary hyperparathyroidism
Third most common endocrine disorder
132
Diagnostic tests of primary hyperparathyroidism
Bloods: Hypercalcaemia
↑PTH, ↑Ca, ↓Phosphate
Increased 24hour urinary calcium excretion
DEXA bone scan for osteoporosis
133
Diagnostic tests of secondary hyperparathyroidism
Bloods: low serum calcium
↑PTH, ↓Ca, ↑Phosphate
DEXA bone scan for osteoporosis
134
Diagnostic tests of tertiary hyperparathyroidism
Bloods: Raised calcium, raised PTH
↑PTH, ↑Ca, ↑Phosphate
Increased 24hr urinary calcium excretion
135
Treatment of primary hyperparathyroidism
Surgical removal of adenoma (treat underlying cause).
| Fluids and bisphosphonates.
136
Treatment of secondary hyperparathyroidism
Calcium correction. Treat underlying condition
137
Treatment of tertiary hyperparathyroidism
Calcium mimetic (Cinacalcet), total or subtotal parathyroidectomy
138
Complications of primary hyperparathyroidism
Hypercalcemia
139
Complications of secondary hyperparathyroidism
Development into tertiary hyperparathyroidism
140
Complications of tertiary hyperparathyroidism
Transient hypocalcaemia follows parathyroidectomy
141
Describe hypoparathyroidism
Low levels of PTH
Also:
Hypocalcemia and Hyperphosphataemia
142
Clinical Presentation of hypoparathyroidism
Increased excitability of muscles and nerves.
Numbness around the mouth/extremities, cramps, tetany, convulsions.
Chvostek and Trousseau signs.
143
Pathophysiology of hypoparathyroidism
PTH stimulates the activation of vitamin D, which facilitates intestinal calcium absorption, renal reabsorption of calcium as well as calcium release from bone. Phosphate reabsorption is inhibited by PTH. In disease, these processes do not occur.
144
Aetiology of hypoparathyroidism
May be transient.
Most commonly follows anterior neck surgery (secondary).
VD and/or Magnesium deficiency (Mg used in PTH production)
Genetic: Can be due to defects in PTH gene.
Can be autoimmune destruction of PT glands.
145
Epidemiology of hypoparathyroidism
Rare
146
Diagnostic tests of hypoparathyroidism
Bloods: Calcium and PTH low, phosphate high
| Signs and symptoms of hypocalcaemia
147
Treatment of hypoparathyroidism
Acute: IV calcium
Persistent: Vitamin D analogue (alfacalcidol)
Calcitriol (prevent low calcium levels)
Synthetic PTH
148
Complications of hypoparathyroidism
Over-treatment with vitamin D -> hypercalcaemia
149
Clinical Presentation of Hypercalcaemia
Can be asymptomatic.
More severe: malaise, bone pain, abdominal pain, nausea, constipation, psychiatric moans (affects NS - lethargy, fatigue, memory loss, depression)
Occasionally renal calculi and CKD.
Polyuria and polydipsia
150
On PQRST of an ECG, what interval is affected by hypercalcaemia and what is the change
Shortening of QT interval
| ventricular depolarisation (QRS) and re-polarisation (T)
151
Pathophysiology of Hypercalcaemia
Ectopic secretion of PTH is very rare. Tumour related hypercalcaemia tends to work by a secretion of a peptide with PTH-like activity, direct invasion of bone and production of local factors for calcium mobilisation.
152
Aetiology of Hypercalcaemia
>90% of cases; primary hyperparathyroidism and malignancy. Primary hyperparathyroidism is caused by a single parathyroid gland adenoma, occasionally hyperplasia
153
Epidemiology of Hypercalcaemia
30/100,000
154
Diagnostic tests of Hypercalcaemia
Bloods: Raised calcium
CXR
Malignancy: raised calcium and phosphate in blood
ECG: tented T and short QT interval
155
Treatment of Hypercalcaemia
Give saline drip (NaCl) which will help to dilute the levels of calcium in the blood if you bring the overall body fluids up (or can give Loop diuretic to return calcium to normal)
Bisphosphonate - encourage osteoclasts to undergo apoptosis so there is less bone breakdown
Primary hyperparathyroidism: surgical removal
156
Clinical presentation of Hypocalcemia
Increased excitability of muscles and nerves. Numbness around the mouth/extremities, cramps, tetany, convulsions. Chvostek and Trousseau signs.
157
On PQRST of an ECG, what interval is affected by hypocalcaemia and what is the change
QT prolongation (primarily by prolonging the ST segment/interval between depolarisation and repolarisation)
158
Pathophysiology of Hypocalcemia
CKD -> Increased phosphate -> Microprecipitation of calcium phosphate in tissues -> Low serum level of calcium.
CKD -> Inadequate production of active vitamin D.
159
Aetiology of Hypocalcemia
Increased serum phosphate:
Chronic kidney disease (most common) - poor calcium uptake, Phosphate therapy, Hypoparathyroidism (decreased phosphate excretion)
(Reduced PTH function: Post thyroidectomy and parathyroidectomy)
Low Phosphate:
Osteomalacia - soft bones due to low calcium and vitamin D deficiency, Acute pancreatitis, Vitamin D deficiency (reduced exposure to sunlight) - poor Ca uptake in GI tract and decreased kidney reabsorption
160
Diagnostic tests of Hypocalcemia
History. eGFR to search for CKD. PTH, Vitamin D.
161
Treatment of Hypocalcemia
Acute: IV calcium
Persistent: In vitamin D deficiency, vitamin D supplement. OR Calcium gluconate
(If hypoparathyroidism; alfacalcidol)
Mild - ADCAL
162
Complication of Hypocalcemia
death possible
163
Clinical presentation of Hyperkalemia
Few symptoms until it can cause MI.
| Impaired neuromuscular transmission (muscle weakness and paralysis)
164
On PQRST of an ECG, what interval is affected by hyperkalemia and what is the change
Tall tented T waves
165
Pathophysiology of Hyperkalemia
Renal impairment can lead to retention of potassium in the nephron.
This is possible with potassium sparing diuretic.
Excessive K consumption at a fast rate -IV fluids
166
Aetiology of Hyperkalemia
```
Renal impairment (most common) and drug interference with potassium excretion.
Elevated without either of these may be artifactual.
```
167
Diagnostic tests of hyperkalemia
Bloods: Check potassium. Recheck unexpected result.
ECG: tall tented T waves, (prolonged PR), widened QRS and reduced P
QRS>0.12s
168
Treatment of hyperkalemia
Dietary potassium restriction and loop diuretic.
Non urgent - Polystyrene sulphonate resin= Binds K+ in the gut decreasing uptake
Urgent - Calcium gluconate= decreases VF risk in the heart
Insulin= drives K+ into the cells
169
Complication of hyperkalemia
Myocardial infarction -> Death
170
Clinical presentation of Hypokalemia
Usually asymptomatic, possibly muscle weakness. Increased risk of cardiac arrhythmias. Polyuria.
171
On PQRST of an ECG, what interval is affected by hypokalemia and what is the change
T wave inversion
| possible prominent U wave
172
Pathophysiology of hypokalemia
| and how it leads to decreased mysocyte excitability
Excessive loss of potassium through the kidneys in response to aldosterone or diuretic therapy.
GI fluid loss -> less chloride -> increase in aldosterone -> Decreased potassium reabsorption
Low K+ in the serum (ECF) causes a water concentration gradient out of the cell (ICF)
Increased leakage from the ICF causing hyperpolarisation of the myocyte membrane decreasing myocyte excitability.
173
Aetiology of hypokalemia
Diuretic treatment and hyperaldosteronism.
Possibly due to loss of GI fluids by constant vomiting/diarrhoea.
Fasting and anorexia
174
Diagnostic tests of hypokalemia
Bloods: low magnesium and potassium
ECG: Flat T waves, ST depression, Long PR and prominent U waves
(U have no Pot (K+) & no Tea but a Long PR & a long QT. )
[K+] <3.5 mmol/L
175
Treatment of hypokalemia
Treat underlying cause. Withdraw harmful medication. Normalise magnesium as well as potassium.
Mild hypokalaemia - oral K+
Severe hypokalaemia - IV K+
176
Complication of hypokalemia
Cardiac arrhythmia and sudden death
177
*Describe prolactinoma
Benign adenoma of the pituitary gland producing prolactin
178
Types of Prolactinoma and which is more common
Micro (most common >90%)
| Macro (>10mm)
179
Clinical presentation of prolactinoma
Local effect of the tumour: headache, visual field defect (macroprolacinoma only).
Effects of prolactin (hyperprolactinaemia): menstrual irregularity, infertility, galactorrhoea, hypogonadism
180
Pathophysiology of prolactinoma
Increased release of prolactin can cause galactorrhoea by stimulating milk production from mammary gland, as well as inhibit FSH and LH.
Additionally, it causes secondary hypogonadism, reduced libido and sexual dysfunction in men.
Dopamine has an inhibitory effect on prolactin.
Pituitary tumour is located near to the optic chiasm -> visual field disturbances.
Very rarely malignant.
181
Aetiology of prolactinoma
Prolactinoma: Cause unknown. Some genetic association.
Other causes of Hyperprolactinaemia: Non functioning pituitary tumour; compress pituitary stalk -> no inhibition of prolactin release; Antidopaminergic drugs;
Head injury -> damage to the pituitary stalk
182
Diagnostic tests of prolactinoma
Check prolactin
183
Treatment of prolactinoma
Dopamine agonist (cabergoline). Transphenoidal pituitary resection.
184
*Describe Pheochromocytoma
Catecholamine (adrenaline) secreting tumour
185
Clinical presentation of Pheochromocytoma
Episodic.
Headaches, palpitations, sweating, tremor, anxiety, nausea and weight loss.
Hypertension, tachycardia and pallor.
186
Types of Pheochromocytoma
Familial type: More noradrenaline
| Sporadic: More adrenaline
187
Pathophysiology of Pheochromocytoma
Catecholamine producing tumours of the chromafin cells of the medulla
188
Aetiology of Pheochromocytoma
Inherited or spontaneous. Sometimes associated with multiple endocrine neoplasia.
189
Epidemiology of Pheochromocytoma
10% malignant
190
Diagnostic tests of Pheochromocytoma
24hr urine collection for urinary catecholamines and metabolites (metanephrines). Plasma catecholamines (not as sensitive)
191
Treatment of Pheochromocytoma
Surgery (preceded by alpha and beta blocker to stagger adrenaline loss (alpha first, if beta at all))
192
Complication of Pheochromocytoma
Can stroke out during surgery, due to the rapid effect of adrenaline on the BP
193
*Describe carcinoid tumour
Serotonin secreting tumour.
| Tend to express somatostatin receptors.
194
Types of carcinoid tumours
Foregut
Midgut
Hindgut
195
Clinical presentation of carcinoid tumour
Most clinically silent, can cause pain, weight loss or a palpable mass.
Carcinoid syndrome: Bronchospasm, diarrhoea, skin flushing and right sided heart lesions
196
What is a common place of a carcinoid tumour of lung, bowel or stomach to metastasise to?
Liver
| only symptomatic with liver metastasises
197
Pathophysiology of carcinoid tumour
Derived from enterochromaffin cells. Can also be in the gallbladder, kidney, liver, pancreas and gonads.
They tend to secrete bioactive compounds, including serotonin and Kallikrein (lead to increase in bradykinin), which cause carcinoid syndrome.
GI carcinoid tumours only cause this if they metastasise to liver, where the products can drain into the heaptic vein.
198
Diagnostic tests of carcinoid tumour
Urine: High volume of 5-hydroxyindoleacetic acid (breakdown product of serotonin).
Liver ultrasound: Confirm metastases
Octreoscan: Radiolabelled ocreotide (somatostatin analogue) hits the somatostatin receptors
199
Treatment of carcinoid tumour
```
Somatostatin analogue (octreotide).
Surgical resection, to reduce tumour mass
```
200
What conditions increase the incidence of carcinoid tumours?
MEN 1 (Multiple Endocrine Neoplasia)
MEN 2
Von-Hippel Lindau
201
Why would a patient be more likely to first approach a dr in later stages of a carcinoid tumour
Only symptomatic with liver metastasises
202
What cells do carcinoid tumours derive from?
Enterochromaffin cells
203
Describe Graves' Opthalmopathy
Presents in most Graves’ and some autoimmune hypothyroidism patients
Results in retro-orbital inflammation and swelling of the extrocular muscles
Eye discomfort, grittiness, increased tear production, photophobia, diplopia, reduced acuity
Exophthalmos - appearance of protruding eye and proptosis - eye protrudes beyond orbit
Conjunctival oedema
Corneal ulceration
Ophthalmoplegia - paralysis of eye muscles
204
Describe treatment of Graves' Opthalmopathy
Conservative treatment includes smoking cessation and sunglasses
Treated with IV METHYLPREDNISOLONE and surgical decompression or eyelid surgery
205
How are eyes examined for Graves' opthalmopathy (except seeing it for yourself)
CT or MRI of orbit
206
Describe Graves' dermopathy
Rare
Pretibial myxoedema
Thyroid acropachy
207
*What is pretibial myxoedema
raised, purple-red symmetrical skin lesions over the anterolateral aspects of the shin
208
What is thyroid acropachy
clubbing, swollen fingers and periosteal bone formation
209
When would you see toxic multi nodular goitre?
Elderly - common older women
Iodine-deficient areas
(drug therapy rarely produces prolonged remission)
210
*What is toxic multi nodular goitre?
nodules that secrete thyroid hormones
| see mind maps hyperthyroidism
211
What % of hyperthyroidism cases are solitary toxic adenoma/nodule
5%
212
What is De Quervain's Thyroiditis
Type of transient hyperthyroidism
| Acute inflammation of the thyroid gland
213
What causes De Quervains Thyroiditis
Acute inflammation of thyroid gland, generally due to viral infection
214
Describe diagnosis of De Quervains Thyroiditis
Typical for there to be globally reduced uptake on technetium thyroidscan
Usually accompanied by fever, malaise and pain in the neck
215
Treatment of De Quervains Thyroiditis
Aspirin
| Prednisolone for severely symptomatic cases
216
What drugs can cause hyperthyroidism?
AMIODARONE (anti-arrhythmic drug) - due to high iodine content
Iodine
Lithium
217
Why can amiodarone also cause hypothyroidism
Inhibits conversion of T4 to T3
218
Clinical presentation of hyperthyroidism specific to elderly
Atrial fibrillation
| Tahcycardias and/or heart failure
219
Clinical presentation of hyperthyroidism specific to young
Excessive height or excessive growth rate
| Behavioural problems like hyperactivity
220
Clinical presentation of Graves disease
```
Palpitations
Diarrhoea
Weight loss and increased appetite
Oligomenorrhoea +/- infertility
Heat intolerance i.e. sweating a lot
Irritability/behavioural change
Tremor
Hyperkinesis
Warm (vasodilator peripheries)
Proximal myopathy and muscle wasting
Anxiety
Lymphadenopathy and Splenomegaly can occur
Diffuse goitre
Lid lag and stare
```
221
What is oligomenorrhoea
infrequent periods
222
What is hyperkinesis
muscle spasm
223
Describe clinical presentation of hyperthyroidism in the hands
Palmar erythema
Warm moist skin
Fine tremor
224
How does differential diagnosis of hyperthyroidism differ to mid anxiety
Eye signs e.g. lid lag & stare
Diffuse goitre
Proximal myopathy and wasting
225
How could you differentiate Graves form toxic adenoma
Ultrasound of thyroid
226
Diagnosis of hyperthyroidism
```
Thyroid function tests (TFTs) (serum TSH is suppressed due to negative feedback, but T4 and T3 raised)
Thyroid peroxidase (TPO) and thyroglobulin antibodies (also presents tin 80% of Graves cases)
```
227
Treatment of hyperthyroidism
Beta-Blockers e.g. propranolol for rapid control of symptoms
Anti-Thyroid drugs e.g. propylthiouracil or oral carbimazole
Radioactive iodine (131)
Surgery (thyroidectomy)
228
What are 2 strategies for treatment of hyperthyroidism using anti-thyroid drugs
Titration e.g. ORAL CARBIMAZOLE for 4 wks then reduce doses according to thyroid function tests (TFTs; TSH, T3 & T4)
Block-replace therapy e.g. ORAL CARBIMAZOLE + THYROXINE (T4) which has less risk of developing hypothyroidism
229
What is main side effect of anti-thyroid drugs like propylathiouracil or carbimazole
Agranulocytosis:
Results in leukopenia
If get sore throat, mouth ulcers and fevers then stop drug asap
230
Side effects of anti-thyroid drugs
```
Agranulocytosis
Rash
Arthralgia
Hepatitis
Vasculitis
```
231
How does anti-thyroid drug Propylthiouracil work?
Stops the conversion of T4 to T3
232
How does anti-thyroid drug Carbimazole (oral) work?
Blocks thyroid hormone biosynthesis and has immunosuppressive effects (which will affect Graves' disease process)
233
Radioactive I (131): contraindications and side effects
CI in pregnancy and breast feeding
SEs indue discomfort in the neck and hyperthyroidism initially
Can be given to all ages
Stop antithyroid drugs 4 days before giving iodine
234
How does radioactive iodine (131) treatment work for hyperthyroidism
Iodine is essential for thyroid hormone production so is readily taken up by the thyroid gland
Here it accumulates and results in local irradiation and tissue damage with return to normal thyroid function over 4-12 weeks
235
When would you undergo surgery for hyperthyroidism
Those with large goitre, poor response to drugs and have drug side-effects
236
When would you undergo a subtotal and when a total thyroidectomy
Subtotal thyroidectomy only in those who have been rendered euthyroid (normal functioning thyroid gland)
Total thyroidectomy only in those with large goitre or suspicion of malignancy (toxic adenoma) in a nodule and also for Graves’
237
Complications of surgery for hyperthyroidism
Hypothyroidism
Tracheal compression from postoperative bleeding
Laryngeal nerve palsy resulting in hoarse voice
Transient hypocalcaemia - due to removal of parathyroid gland too
238
Complications of hyperthyroidism if untreated
Thyroid crisis or thyroid storm
Rare life threatening condition
Rapid deterioration of thyrotoxicosis (rapid T4 increase)
239
Describe features of thyroid crisis or thyroid storm
hyperpyrexia, tachycardia, extreme restlessness
and eventually delirium, coma and death
Usually precipitated by stress, infection, surgery or radioactive iodine therapy in an unprepared patient
240
Treatment of thyroid crisis or thyroid storm or untreated hyperthyroidism
Large doses of:
- ORAL CARBIMAZOLE
- ORAL PROPRANOLOL
- ORAL POTASSIUM IODIDE (to block acutely the release of thyroid hormone from gland)
- IV HYDROCORTISONE (to inhibits peripheral conversion of T4 to T3)
241
Symptoms of hypothyroidism
* Hoarse voice
* Goitre
* Constipation
* Cold intolerant
* Weight gain
* Menorrhagia
* Myalgia, weakness
* Tired, low mood, dementia
* Myxoedema - accumulation of mucopolysaccharide in SC tissue
242
Signs of hypothyroidism
```
BRADYCARDIC:
• Bradycardia
• Reflexes relax slowly
• Ataxia (cerebellar)
• Dry, thin hair/skin
• Yawning/drowsy/coma
• Cold hands +/- temperature drop
• Ascites
• Round puffy face
• Defeated demeanour
• Immobile +/- Ileus (temporary arrest of intestinal peristalsis)
• Congestive cardiac failure
```
243
Primary cause of hypothyroidism
Disease of the thyroid gland
244
Secondary cause of hypothyroidism
Hypothalamic or pituitary disease
| leads to thyroid disease
245
What % of the population is affected by hypothyroidism and what gender is more affected
0.1-0.2%
| females
246
Main cause of primary hypothyroidism
Iodine deficiency
247
What genetic diseases associate with hypothyroidism
Turners*
Downs syndrome
Cystic fibrosis
Others:
Primary biliary cirrhosis
Ovarian hyper-stimulation
248
In Hashimoto's thyroiditis, describe thyroid gland appearance/feel
Gland is usually firm and rubbery but may range from soft to hard
249
In Hashimoto's thyroiditis, what causes goitre
Atrophic changes with regeneration result in GOITRE FORMATION due to lymphocytic and plasma cell infiltration
250
What causes postpartum thyroiditis
Modifications to immune system necessary in pregnancy and histologically is a lymphocytes thyroiditis
251
What can postpartum thyroiditis be misdiagnosed as?
Postpartum depression
| therefore TFTs are essential to confirm diagnosis
252
what is meant by iatrogenic?
caused by treatment or examination
253
What iatrogenic factors can lead to hypothyroidism
Thyroidectomy (for treatment of hyperthyroidism or goitre)
| Radioactive iodine treatment or external neck irradiation for head and neck cancer
254
*What drugs can induce to hypothyroidism
Carbimazole
Lithium
Amiodarone (hyper or hypothyroidism)
Interferon
255
Why can amiodarone cause hyper or hypothyroidism
Hyper - due to high iodine content
| Hypo - as inhibits the conversion of T4 to T3
256
What can result from dietary iodine deficiency?
Goitre
| Patients have are euthyroid or hypothyroid, depending on the severity of iodine deficiency
257
Where is iodine deficiency an issue in the world
```
Netherlands
Western Pacific
India
SE Asia
Russia
some Africa
```
258
*What is myxoedema?
Accumulation of mucopolysaccharide in SC tissue
Swelling of the skin and underlying tissues giving a waxy consistency, typical of patients with underactive thyroid glands
259
Presentation of hypothyroidism in children
Slow growth velocity
Poor school performance
Sometime puberty arrest
may not show classic features
260
Why is diagnosis of hypothyroidism in elderly difficult
Hard to differentiate clinical features from normal ageing
261
Give example of lifelong thyroid hormone replacement drug
Oral Levothyroxine (T4)
262
What would be seen in a blood test of hypothyroidism
Raised serum aspartate transferase levels from muscle and/or liver
Increase serum creatinine kinase levels associated with myopathy Hypercholesterolaemia
Hyponatraemia due to an increase in ADH and impaired free water clearance
263
Complication of Hypothyroidism is Myxoedema coma, what is given in hospital to treat this?
IV/Oral T3
| Glucose infusion
264
In treating hypothyroidism with Levothyroxine, what important things must you bear in mind
Patients with IHD use with caution and start on lower dose
| Don't give too much as completely suppresses TSH as this carries risk of AF and osteoporosis
265
What can occur from Levothyroxine overdose?
Can completely suppress TSH
| Risk of AF and osteoporosis
266
How can you monitor treatment of primary hypothyroidism?
Check T4 levels 6-8 weeks after dose adjustment
267
How can you monitor treatment of secondary hypothyroidism?
TSH will always be low
| T4 is monitored
268
**General treatment of thyroid cancer
Radioactive iodine (will locally irradiate and destroy cancer - providing very little radiation damage to other surrounding structures)
Levothyroxine (T4) to keep TSH reduced as this is a risk factor
Chemotherapy helps reduce risk of spread and treats micro-metastases
269
What is CRH
Corticotropin Releasing hormone
270
Where is CRH released from
Hypothalamus
271
CRH causes the release of what hormone
ACTH
Adrenocorticotrophic hormone
from anterior pituitary
272
What is the function of ACTH
Stimulates cortisol and androgen production by the adrenal cortex
273
Will aldosterone secretion be affected by disease of hypothalamus or pituitary?
No as aldosterone secretion responds to renin release by the juxtaglomerular cells of afferent arterioles kidney
Only pathology of kidney would
274
Are the adrenal glands intra or retro-peritoneal
Retroperitoneal
275
What are the 3 layers of adrenal cortex and what does each secrete
Zona glomerulosa - Mineralocorticoids e.g. aldosterone
Zona fasciculata - Glucocorticoids e.g. cortisol
Zona reticularis - Androgens (sex hormone)
(Makes Good Sex)
276
What are all the layers of adrenal gland in order of most superficial to most deep
```
Capsule
Zona glomerulosa
Zona fasciculata
Zona reticularis
Adrenal medulla
```
277
Androgens released by zone reticularis are converted to what peripherally
Testosterone
| Dihydrotestosterone
278
What does adrenal medulla secrete
Catecholamines e.g. Adrenaline or Noradrenaline
| under sympathetic control
279
Excess of what drug can mimic Cushings Disease?
Alcohol
280
*What are the functions of cortisol
- Increased carbohydrate and protein catabolism (breakdown)
- Increased deposition of fat and glycogen
- Na+ retention
- Increased renal K+ loss
- Diminished host response to infection
281
Describe when corticotrophin and thus cortisol levels are highest and lowest
Released according to a Circadian Rhythm and stress
Highest levels in morning 7/9am
Lowest at midnight
282
Give examples of things that can cause high-cortisol
```
Alcohol pseudo-Cushings syndrome
Depression
Obesity
Pregnancy
(Stress also)
```
283
Why do you get infections in Cushings syndrome more easily?
Anti-inflammatory effect of cortisol and poor healing
284
Differential diagnosis of Cushings syndrome
Pseudo-Cushing’s syndrome - caused by alcohol excess, resolves after 1-3 weeks of alcohol abstinence
285
Diagnosis of Cushings
Drug history - oral steroids?
Random plasma cortisol
1st line test: Dexamethasone overnight suppression test (normally causes cortisol depression but this is not the case in cushings) or Urine free cortisol test over 24 hours
2nd line test:
if no suppression
48 hour
286
Aetiology of hyperthyroidism
2/3 cases are Graves Disease
Toxic multi nodular goitre
Toxic thyroid adenoma
Iodine excess congenital (less common)
287
Symptoms of hyperthyroidism
```
(like how you feel before an exam)
Diarrhoea
Weight loss
Sweats
Heat intolerance
Palpitations
Tremor
Anxiety
Menstrual disturbance
```
288
Signs of hyperthyroidism
```
Tachycardia
Thin hair
Lid lag
Lid retraction
Onycholysis
Exophthalmos
```
289
Investigations of hyperthyoridism
```
TFTs (thyroid function test)
Thyroid autoantibodies (Thyroid peroxidase, thyroglobulin, TSH receptor antibody)
Radioactive iodine isotope uptake scan
```
290
What would a TFT show in primary hyperthyroidism
Low TSH
| High T3/T4
291
What would a TFT show in secondary hyperthyroidism
High TSH
| High T3/T4
292
Describe Graves Ophthalmology appearance
Extraocular muscle swelling
Eye discomfort
Lacrimation
Diplopia
293
Define gigantism
Increased production of GH occurring in children
294
Symptoms of acromegaly
Acroparaesthesia, Arthralgia, Sweating, Decreased libido, Headache
295
Signs of acromegaly
```
Massive growth of the hands, feet and jaw
Big tongue with widely spaced teeth
Puffy lips, eyelids and skin
Darkening skin
Obstructive sleep apnoea
Deep voice
```
296
What is acroparaesthesia
pins and needles in extremities
297
Why do you not do a growth hormone measurement to investigate if patient has acromegaly
GH is a pulsatile protein and levels vary throughout day
| Do oral glucose tolerance test
298
Describe ECG of Conns syndrome
Flat T
Long PR
Long QT
U waves
299
What is pseudohypoparathyroidism
Decreased response to PTH
Bloodwork shows low Ca, high PTH
Treat as normal hypoparathyroid
300
What hormone stimulates the secretion of potassium in the kidney?
Aldosterone
301
Is hypokalaemia a result of high or low aldosterone
High aldosterone
More K excretion
Less K in body
302
Hyperkalemia is a result of low aldosterone. What can therefore cause hyperkalemia
Low aldosterone - adrenal insufficiency
ACE inhibitors - block the binding of aldosterone to receptor
AKI - decreased fibrillation rate so more K+is maintained in the blood
303
What is the role of K in the body
Charged and Helps maintain the resting potential of all muscles in the body
304
Hypokalaemia - describe effects on muscles
Everything slows
Smooth - constipation
Skeletal - Weakness/cramps
Cardiac - Arrhythmias and palpitations
305
Hyperkalaemia - describe effects on muscles
```
Everything speeds up
Smooth - cramping
Skeletal - Weakness/ flaccid paralysis
Due to over contraction muscles become totally drained of energy
Cardiac - Arrhythmias and arrest
```
306
How does insulin affect potassium balance
Excess insulin -> Hypokalaemia
too much K+ follows insulin into cell
Insulin deficient -> Hyperkalemia
Not enough K+ follows into the cell
307
**How does pH change with potassium balance
Alkalosis (high pH) -> H+ out of cell and K+ in -> hypokalaemia
Acidosis (low pH) -> H+ into cell and K+ out ->Hyperkalemia
(decrease K+ by replacing with H+)
308
How do drugs acting on the Beta 2 receptor affect potassium balance
B2 agonists (SABA/LABA) -> increase B2 pumping of K+ into cell -> Hypokalaemia
Beta blocker -> inhibits pumping of K+ into cell -> Hyperkalemia
309
How does cell lysis cause potassium balance issues
Intracellular contents released as get Hyperkalaemia
| Severe burns or tumour lysis syndrome for example
310
Symptoms of hypocalcaemia
```
SPASM
Spasms
Peripheral paraesthesia
Anxious
Seizures
Muscle tone increase
```
311
Signs of hypocalcaemia
```
CATS
Convulsion
Arrhythmias
Tetany
Spasm and Stridor
```
312
ECG of hypocalcaemia
Long QT interval
313
What malignancies cause hypercalcaemia?
Myeloma
| Non-hodgkin lymphoma
314
What is difference between Cushings syndrome and disease?
Both involve:
Excess cortisol
Loss of hypothalamic pituitary axis feedback
Loss of circadian rhythm
C Disease also caused by pituitary adenoma
315
How can an Adrenalectomy lead to Nelson's syndrome
If you remove the adrenal glands then no cortisol will be produced in response to ACTH produced by the pituitary gland.
If no cortisol is produced then there is no negative feedback on ACTH levels which can cause ACTH to build up in the body tissues.
This can cause a bronze pigmentation of the skin, visual disturbances and headaches.
316
a 16yr old female, presents to A&E with her mother after feeling vey weak and experiencing some palpitations. Her mother is concerned that her daughter is very skinny, you check her BMI and it is 16.What is the most likely cause of her condition?
Hypokalaemia
Hyperkalaemia
Hypocalcaemia
Hypercalcemia
Hypokalemia
| anorexic BMI
317
a 73 year old gentleman presents to his GP for some routine tests following a recent diagnosis of secondary hyperparathyroidism. All the results get mixed up in the pile which one is Jims?
A) Calcium high, Phosphate high, ALP high
B) Calcium low, phosphate low, ALP low
C) Calcium low, Phosphate high, ALP high
D) Calcium low, phosphate low, ALP high
A- tertiary
B Nothing
*C- secondary
D- primary
318
A 29yo man presents with 4-week history of polyuria and extreme thirst. The urine is very dilute. The patient does not have any weight loss and maintains a good diet. No findings are found on urine dipstick. The most appropriate invevstigation is:
```
Serum osmolality
Fasting plasma glucose
Urinary electrolytes
MRI head
Water deprivation test
```
*Water deprivation test = Diagnostic for DI
319
The initial treatment for somebody having a thyrotoxic storm (hyperthyroid crisis) is:
```
IV 0.9% saline
Propanolol
Salbutamol
Carbimazole
Omeprazole
```
Propanolol
(Carbimazole long term)
saline would probably be given but isn’t going to have much of an effect, salbutamol is for asthma / respiratory disease, carbimazole is an antithyroid treatment and would probably be given too but does not help immediately with symptoms, and omeprazole is a PPI. Therefore the best initial treatment is propanolol, a beta blocker
320
Hypocalcaemia
Chvostek's sign is the twitching of the facial muscles in response to tapping over the area of the facial nerve.
Trousseau's sign is carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes.
