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Phase1c Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Metabolic ketoacidosis with normal-low glucose is associated with what?

A

Alcoholic ketoacidosis

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2
Q

Which thyroid cells form the colloid?

A

Follicular cells

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3
Q

What mineral is associated with the thyroid colloid?

A

Iodine

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4
Q

What is the function of para-follicular cells (C-cells)?

A

Produce Calcitonin

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5
Q

What is the function of follicular cells?

A

Synthesise T4 and T3

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6
Q

What is the bioactive thyroid hormone?

A

T3

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7
Q

What is the main thyroid hormone produced by the thyroid gland?

A

T4

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8
Q

How is T4 transported int he blood?

A

Thyroid-binding globulin

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9
Q

What are the symptoms of hyperthyroidism?

A 
Tremor
Anxiety
Palpitations
Heat intolerance
Diarrhoea
Oligomenorrhoea
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10
Q

What are the symptoms associated with hypothyroidism?

A 
Lethargy
Cold intolerance
Weight gain
Constipation
Menorrhagia
Decreased deep tendon reflexes
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11
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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12
Q

What are the causes of hyperthyroidism?

A

Grave’s disease
Toxic multi-nodular goitre
Thyroiditis
Drugs (Amiodarone)

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13
Q

Which antibodies are associated with Grave’s disease?

A

Anti-TSH receptor antibodies

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14
Q

Which drug is associated with inducing hyperthyroidism?

A

Amiodarone

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15
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s thyroidits

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16
Q

Which auto-antibody is associated with Hashimoto’s thyroiditis?

A

Anti-TPO antibodies

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17
Q

What are the causes of hypothyroidism?

A

Hashimoto’s thyroiditis
Subacute thyroiditis
Drugs
Iodine deficiency -Common cause in the developing world

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18
Q

Which drugs can induce hypothyroidism (2)?

A

Lithium

Amiodarone

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19
Q

What is the most common cause of hypothyroidism in the developing world?

A

Iodine deficiency

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20
Q

What is the level of TSH in primary hyperthyroidism?

A

Low TSH

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21
Q

What is the level of TSH in primary hypothyroidism?

A

Raised

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22
Q

What is revealed in radio-scintigraphy in Grave’s disease?

A

Homogeneous increased iodine uptake

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23
Q

What is revealed in radio-scintigraphy in a toxic adenoma?

A

Hot nodule - increased iodine uptake in solitary nodule and suppressed uptake in other parts

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24
Q

What is revealed in radio-scintigraphy in a toxic multi-nodular adenoma?

A

Heterogeneous uptake

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25
Q

What is the management of hyperthyroidism?

A

Propranolol - Non cardioselective beta-blocker for symptomatic management

Carbimazole (TPO inhibitor)

Propylthiouracil

Radio-iodine

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26
Q

What are the side effects of carbimazole?

A

Agranulocytosis (No neutrophils)

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27
Q

What is the definitive management for hypothyroidism?

A

Levothyroxine

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28
Q

How common is thyroid eye disease in Grave’s patients?

A

25-50%

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29
Q

What is the most common form of thyroid eye disease in Grave’s?

A

Bilateral exophthalmos

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30
Q

What is the pathophysiology of exophthalmos in Grave’s?

A

Anti-TSH receptor antibodies binding to TSH receptors in the eyes - stimulates growth of tissue

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31
Q

What are the features of Bilateral exophthalmos in Grave’s?

A 
Diplopia 
Conjunctival oedema (chemosis)
Opthalamlgia 
Exposure keratopathy
Optic neuropathy (Blurred vision)
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32
Q

Due to increased sympathetic tone in Grave’s disease what features are seen in the eye?

A

Lid lag and retraction

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33
Q

What are the three specific features in Grave’s disease?

A

Bilateral exophthalmos - lid lag and retraction
Pretibial myxoedema
Thyroid acropachy (Thickening of the extremities)

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34
Q

What are the classic features of thyroid cancer?

A

Non-functional (Euthyroid), painless, rapidly growing

Solitary - Irregular (Nodular shape

Palpable nodule, hard and fixed

Hoarse voice - Tumour compression on the recurrent laryngeal nerves

Dysphagia

Haemopotysis

Airway obstruction

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35
Q

Why does a hoarse voice occur in thyroid cancer?

A

Tumour compression on the recurrent laryngeal nerve

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36
Q

What is the most common subtype of thyroid cancer?

A

Papillary carcinoma (70%) - associated with cervical lymphadenopathy

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37
Q

What is the epidemiology of papillary carcinoma?

A

35-year old female with childhood radiation exposure

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38
Q

A circular concentric laminations in papillary carcinoma is known as what?

A

Psammoma body

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39
Q

What thyroid cancer is associated with a Psammoma body?

A

Papillary carcinoma

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40
Q

What is the second most common thyroid cancer?

A

Follicular carcinoma (20%) - associated with low dietary iodine intake

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41
Q

What is a rare variant of follicular carcinoma?

A

Hurthle cell carcinoma

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42
Q

Which MEN types are associated with medullary carcinoma?

A

MEN2a and MEN2B

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43
Q

What are the most aggressive thyroid cancers?

A

Anaplastic carcinomas

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44
Q

What is the definitive investigation for thyroid cancer?

A

Fine needle aspirate biopsy with ultrasound

+TFTs - to exclude functional nodules

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45
Q

What neoplasms are associated with MEN type 1?

A 
3Ps
Pituitary tumours (Prolactinoma)

Pancreatic tumours (Insulinoma, glucagonoma, gastrinomas)

Parathyroid adenomas
(Raised Ca, and HyperPTH)

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46
Q

What are the common pancreatic tumours are associated with MEN1?

A

Insulinoma
Glucagonoma
Gastrinoma

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47
Q

What are the symptoms of hypercalcaemia?

A 
Renal colic
Abdominal pain 
Constipation 
Psychological depression
Bone pain, osteoporosis
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48
Q

What is the onset of symptoms for MEN1?

A

MEN1 mutation has high penetrance and therefore develops early in life.

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49
Q

What investigations are performed for MEN1?

A

CT/MRI (whole-body), genetic testing

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50
Q

What is Zollinger-Ellison syndrome compared with MEN1 gastrinoma?

A

Non-MEN1 gastrinoma

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51
Q

MEN2A and MEN2B is associated with which type of thyroid cancer?

A

Medullary thyroid cancer

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52
Q

Medullary thyroid cancer is associated with which type of cell?

A

Parafollicular C-cell - produce calcitonin

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53
Q

Which tumours are associated with MEN2A?

A

Phaeochromocytoma
Parathyroid adenoma
Medullary thyroid cancer

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54
Q

Which tumours are associated with MEN2B?

A

Phaeochromocytoma
Medullary thyroid cancer
Neuromas (Mucosal) -

Associated with Marfanoid habitus

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55
Q

What is Marfanoid habitus?

A

Including long limbs, with an arm span that is at least 1.03 of the height of the individual, and a crowded oral maxilla, sometimes with a high arch in the palate, arachnodactyly, and hyperlaxity.

Pectus excavatum

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56
Q

A Marfanoid habitus is associated with which type of MEN syndrome?

A

MEN2B

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57
Q

What gene is associated with MEN2A and 2B in genetic testing?

A

RET oncogene

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58
Q

What blood investigation is performed in suspected medullary thyroid carcinoma?

A

Calcitonin

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59
Q

What type of tumour is carcinoid syndrome?

A

Neuroendocrine cell

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60
Q

How does carcinoid syndrome arise to produce a symptomatic presentation?

A

The carcinoid tumour metastasises to the liver

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61
Q

What does serotonin get metabolised into by the liver?

A

5-HIAA (excreted via the urine)

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62
Q

What hormone is raised in carcinoid syndrome?

A

Serotonin
Bradykinin
Histamine

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63
Q

What are the common features of carcinoid syndrome?

A

Flushing (Vasodilation due to bradykinin and histamine)

Diarrhoea (Serotonin induced effect on gut motility)

Shortness of breath

Pulmonary stenosis

Abdominal pain (Serotonin activated fibroblasts)

Itching (Histamine)

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64
Q

What hormone inhibits serotonin release?

A

Somatostatin

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65
Q

What investigations are performed on suspected carcinoid syndrome?

A

Urinary 5-HIAA
CT Scan
Octreotide scan - specific

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66
Q

What is octreotide?

A

A somatostatin analogue

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67
Q

What specific scan is performed in carcinoid syndrome?

A

Octreotide scan - binds to neuroendocrine cells

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68
Q

What hormone released by the hypothalamus directly controls LH/FSH secretion?

A

GnRH

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69
Q

Which cells respond to LH in males?

A

Leydig cells

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70
Q

What is the function of Leydig cells?

A

Release testosterone

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71
Q

What is the function of Sertoli cells?

A

Spermatogenesis

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72
Q

Sertoli cells respond to which hormone?

A

FSH

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73
Q

Which hormone is secreted by theca cells?

A

Progesterone

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74
Q

Which hormone is secreted by granulosa cells?

A

Oestrogen

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75
Q

Which gonadotrophin acts on theca cells?

A

LH

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76
Q

What is physiological hypogonadism?

A

Pregnancy

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77
Q

What is primary hypogonadism (Female)?

A

Gonadal dysfunction
-Reduced oestrogen and progesterone production

  • Turner’s syndrome (Gonadal Dysgenesis)
  • Gonadal damage
  • Primary ovarian failure
  • PCOS
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78
Q

What is the karyotype of Turner’s syndrome?

A

45X0

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79
Q

What are the causes of secondary hypogonadism?

A

Kallman syndrome
Pituitary/hypothalamic tumour (Non-functioning or prolactinoma)
Hyperprolactinaemia

Functional - Hypothalamic amenorrhoea
-Low BMI, Excess exercise, stress

Contraceptive pill use - Negative feedback signal to reduce FSH and LH

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80
Q

What symptom is typically associated with Kallman syndrome?

A

Anosmia- Failed development migration of olfactory bundles

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81
Q

What are functional causes of hypothalamic amenorrhoea?

A

Low BMI
Excess exercise
Stress

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82
Q

What are the main causes of primary hypogonadism in Males?

A

Gonadal dysgenesis (Klinefelter’s syndrome, cryptochrodism)

Gonadal damage

Post-orchitis (Mumps)

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83
Q

What is the karyotype for Klinefelter’s syndrome?

A

47XXY

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84
Q

What are the secondary causes of hypogonadism in Males?

A

Kallman Syndrome
Pituitary/hypothalamic tumour
Hyperprolactinaemia

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85
Q

What are the features of hypogonadism?

A

Delayed puberty - Primary amenorrhoea, absent sexual characteristics (absent pubic hair, delayed thelarche, micropenis, high-pitched voice, small undescended testes)

Infertility

Low libido

Female specific - Night sweats/hot flushes
-Amenorrhoea

Erectile dysfunction

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86
Q

What is the first-line investigation in females presenting with symptoms of hypogonadism?

A

Pregnancy test

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87
Q

What investigations are performed in hypogonadism?

A 
Pregnancy test
LH/FSH
Prolactin
Testosterone/Oestradiol
TFTs
Karyotyping 
Pituitary MRI
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88
Q

What is the hormone profile in primary hypogonadism?

A

Hypergonadotrophic hypogonadism
- Raised LH/FSH/GnRH

Low tesosterone/oestrogen

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89
Q

What is the hormone profile in secondary hypogonadism?

A

Hypogonadotropic hypogonadism

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90
Q

What are the effects of growth hormone?

A

Increased blood glucose
Increased insulin resistance
Increased muscle growth
Increased bone thickness

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91
Q

What organs does GH have an effect on?

A

Bone
Muscle
Liver
Kidney

Releases IGF-1

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92
Q

Growth hormone causes the release of what?

A

Insulin-like growth factor-1 (Somatomedin)

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93
Q

What is the most common cause of acromegaly?

A

Pituitary adenoma of somatotrophs

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94
Q

What are the features of Acromegaly?

A 
Coarse facial features
Prognathism and large tongue
Spade-like hands and large feet
Excessive sweating
Organomegaly 
Headache
Visual disturbances
Possible: Hyperprolactinaemia, hypopituitarism
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95
Q

Why is gigantism?

A

Growth of long bones (Epiphyseal growth plates have no fused)

96
Q

Why is there hyperprolactinaemia in acromegaly?

A

Pituitary adenoma compression of the pituitary stalk reduces dopamine secretion -Reduces negative regulation of prolactin release from lactotrophs

97
Q

What visual defect is associated with pituitary adenomas?

A

Bitemporal hemianopia

98
Q

What are the common complications of acromegaly?

A 
Diabetes mellitus
Hypertension
Carpal tunnel syndrome
Cardiomyopathy
Colorectal cancer
99
Q

What is seen in an OGTT in acromegaly?

A

Paradoxical rise in Growth hormone

100
Q

What is the first-line investigation in acromegaly?

A

Serum IGF-1

101
Q

What is the diagnostic investigation in confirming acromegaly?

102
Q

What is the first-line definitive management of acromegaly?

A

Trans-sphenoidal surgery

  • Radiotherapy
  • Somatostatin analogues
  • Dopamine receptor agonists (Cabergoline and bromocriptine)
  • GH receptor antagonists
103
Q

What is type 1 diabetes?

A

Pancreatic islet B-cell autoimmune destruction

  • Absolute deficiency in insulin
  • Lipolysis and ketogenesis
104
Q

Which gene is associated with type 1 diabetes mellitus?

105
Q

What is type 2 diabetes mellitus?

A

Reduced peripheral sensitivity to insulin , reduced insulin production over time

106
Q

What is the characteristic presentation of T1DM?

A

<20 years
Polyuria, and polydipsia (osmotic diuresis)

Weight loss and fatigue

DKA signs

FH of autoimmune disease

107
Q

What are DKA signs?

A

Nausea and vomiting
Abdominal pain
Kussmaul breathing (deep hyperventilation)
Sweet-smelling breath (ketonaemia)

108
Q

What is the characteristic features of T2DM?

A

> 40 YEARS
asymptomatic
Polyuria, polydipsia
Examination findings -acanthosis nigricans

109
Q

What are the main risk factors for T2DM?

A

Obesity
Hypertension
South Asian/Afro-Caribbean ethnicity

110
Q

What is the normal random glucose range?

111
Q

What is the cut-off for fasting glucose in diabetes?

112
Q

What is the cut-off for a 2-hour post-prandial glucose?

113
Q

What is the cut-off for HbA1c diabetes diagnosis?

A

> 48 (6.5%)

114
Q

What is the pre-diabetes range for fasting glucose?

115
Q

What confirms the diagnosis of diabetes Mellitus?

A

symptomatic + 1 test

Asymptomatic + 2 different tests on 2 different days

116
Q

What are the specific antibodies involved in type 1 diabetes mellitus?

A

Anti-GA and islet cell antibodies

117
Q

What does a urine dip reveal in T1DM?

A

Urinary Ketones

118
Q

What is the first-line management for T1DM?

A

Basal-bolus

Long-acting and short-acting (Before meals)

119
Q

Example of long-acting insulin

A

Insulin glargine (Subcutaneous injection OD)

120
Q

Example of short-acting insulin

A

Insulin lispro

121
Q

What is basal-bolus insulin?

A

Short-acting and long-acting insulin prior to meals/

122
Q

How is T1DM measured

A

Monitored daily using capillary glucose

Over time using HbA1c

123
Q

What is the first-line management for T2DM?

A

Lifestyle modifications - diet, exercise and education

124
Q

What is step 1 of glycaemic control in T2DM?

A

Metformin if HbA1c >48 despite lifestyle advice

125
Q

What is step 2 in glycaemic control?

A

Add another drug (DPP4i, Pioglitazone, SU, SGLT-2i)

126
Q

What are the indications for starting atorvastatin in lipid management for T2DM?

A

If QRISK >10%

-Atorvastatin 20mg

127
Q

What are the indictions for 80mg OD atorvastatin in T2DM?

A

IHD, CVD and PAD

128
Q

What is the BP management in T2DM?

A

ACEi or ARB (In Afro-Caribbean Origin)

129
Q

What is step 2 in BP management?

A

Add CCB or thiazide

130
Q

What step 3 in BP management in T2DM?

A

ACEi/ARB + CCB + Thiazide

131
Q

What are the acute metabolic disturbances associated with DM?

A

Hypoglycaemia
DKA
HHS

132
Q

What glucose parameter is associated with hypoglycaemia?

A

Low plasma glucose <3.6 mmol/L

133
Q

What are the common causes of hypoglycaemia in T2DM?

A

Inappropriate insulin regime
Missed meals
Drugs - SUs

134
Q

What are the signs of Hypoglycaemia?

A 
Palpitations
Tremor
Sweating
Pallor
anxiety
Drowsiness
Confusion
altered behaviour
COMA
135
Q

What is the management for hypoglycaemia in a conscious patient?

A

Oral glucose and complex carbohydrate

Short-acting - glucogel

136
Q

What is the management of hypoglycaemia in impaired consciousness?

A

1mg IM glucagon

137
Q

What is the triad of DKA?

A

Hyperglycaemia
Ketonaemia
Metabolic acidosis

138
Q

What is the main effect of glucose in DKA?

A

Osmotic diuresis (Polyuria) - dehydration

139
Q

What is the main effect of ketones in DKA?

A

Acid induced enzyme dysfunction - coma and death

140
Q

What is the main aim of DKA?

A

IV fluids and insulin

141
Q

What sign is not seen in HHS?

A

Abdominal pain

142
Q

What ketone parameter is indicative of DKA?

A

> 3 mmol/L

pH < 7.3

143
Q

What pH value is associated with DKA?

144
Q

What is the pH value in HHS?

A

Normal (7.35-7.45) and normal ketones <3 mmol/L

145
Q

What is the initial management for HHS and DKS?

A

Fluids (normal saline) and potassium chloride (If K<5.5)

IV insulin after fluids and only when Potassium is not <3.5

146
Q

When is IV insulin administered in HHS?

A

After fluids and when K is not <3.5

147
Q

What is the effect of insulin on potassium?

A

Increase potassium cellular intake- risk of hypokalaemia

148
Q

What type of insulin is given in HHS and DKA?

A

Fixed-rate insulin infusion

149
Q

What signs are seen in background retinopathy on fundoscopy?

A

Blot and dot haemorrhages/hard exudates

150
Q

What is the management of background retionopathy?

A

Improve glycaemic control

151
Q

What is the management of pre-proliferative retionopathy?

A

Pan-retinal laster photocoagulation

152
Q

What fundoscopic signs are seen in pre-proliferative retionopathy?

A

Background + cotton wool spots

153
Q

What is seen in proliferative retinopathy?

A

Neovascularisation

154
Q

What is the management for maculopathy?

A

Intravitreal VEGF inhibitors

155
Q

What are the risks associated with neovascularisation in retinopathy?

A

Associated with retinal detachment and vitreous haemorrhage - visual loss

156
Q

What fundoscopic signs are seen in maculopathy?

A

Hard exudates need the macula

157
Q

What are the signs of diabetic nephropathy?

A

Oedema, polyuria, lethargy and hypertension

158
Q

What is the first-line investigations for diabetic nephropathy?

A

Urinalysis

Albumin:creatinine ratio (Raised) - Microalbuminuria

159
Q

What is the gold standard investigation for diabetic nephropahty?

A

Renal biopsy - revealing Kimmelstiel-Wilson nodules

160
Q

What nodules are seen in a renal biopsy for diabetic nephropathy?

A

Kimmelstiel-wilson nodules

161
Q

What is the definitive management for diabetic nephropathy?

A

ACEi/ARB (renoprotective)

162
Q

What is the aetiology of diabetic neuropathy?

A

Blockage of the vasa nervosum

163
Q

What is the characteristic presentation of peripheral neuropathy?

A

Glove and stocking distribution

  • Loss of sensation
  • Inspect feet

Monofilament on LL exam

Loss of ankle jerk/vibration/sense/fractures (Charcot’s joint)

164
Q

What is mononeuropathy?

A

Motor loss

-wrist drop, foot drop, 3rd nerve palsy

165
Q

What is autonomic neuropathy?

A

GI tract: Difficulty swallowing, delayed gastric emptying, bladder dysfunction

Postural hypotension

Cardiac autonomic supply

166
Q

Which neuropathic pain agents are used in DN?

A

Duloxetine
Pregabalin
Gabapentin

167
Q

What is the main symptom of diabetes insipidus?

A

Production of dilute urine (Hypotonic polyuria)

168
Q

What are the two types of diabetes insipidus?

A

Lack of vasopressin release from the posterior pituitary gland

Nephrogenic - Collecting ducts insensitive to vasopressin

169
Q

What are the causes of cranial DI?

A

Pituitary tumour/surgery, TBI, infection (meningitis)
Sarcoidosis/TB
SAH

170
Q

What are the nephrogenic causes of DI?

A 
Lithium therapy
Electrolyte imbalance (HyperCal, hypokal)

Ureteric obstruction
Inherited (AVPV2 gene)

171
Q

What is the presentation of DI?

A

Polyuria, nocturia
Polydipsia
Dehydration: Tachycardia/reduced tissue turgor/dry mucous membranes

Signs of the cause

172
Q

What is the diagnostic test for DI?

A

Water deprivation test

173
Q

How long is a water deprivation test carried out for?

A

8 hours or more than 3% body weight lost

174
Q

After a water deprivation test what drug is adminsitered?

A

Desmopressin

175
Q

What is the urine osmolality in diabetes insipidus during a water deprivation test?

A

Dilute - low

176
Q

What happens to urine osmolality after desmopressin administration in cranial diabetes insipidus?

177
Q

Management for cranial DI?

A

Intranasal desmopressin

178
Q

Management for nephrogenic DI?

A

Thiazide diuretic

179
Q

What is SIADH?

A

Excess ADH

  • Serum sodium decreases
  • Urine osmolality increases
  • Urine sodium increases
180
Q

What are the main CNS causes?

A

SAH, stroke, tumour, TB

Pulmonary: Pneumonia, bronchiectasis

Malignancy - small cell lung cancer

Drugs - Carbamazepine, SSRI

Idiopathic

181
Q

What is the management of SIADH?

A

Treat the underlying cause

Immediate fluid restriction (Hyponatremia)

If ineffective- consider oral demeclocycline (Makes collecting ducts less repsonsive to ADH)

182
Q

What are the three main causes of hypovolaemic hyponatremia?

A

Diarrhoea, vomiting, diuretics

Management is IV fluids, there is low urinary sodium (<20)

183
Q

What is the cause of euvolaemic hyponatremia?

A

SIADH
Hypothyroidism
Adrenal insufficiency

Management is fluid restriction

184
Q

What is the presentation of severe hypervolaemia?

A

Seizures, decreased consciousness

185
Q

What is the complication of administering hypertonic saline in hyponatremia (too fast)?

A

Central pontine myelionlylsis

186
Q

What are the main acquired causes of hypothyroidism?

A

Hashimoto’s thyroidits
Iatrogenic (Post-surgery, radioiodine, medication for hypertyroidism)

Severe iodine deficiency or iodine excess (Wolff-Chaikoff effect)

187
Q

What is the presentation of hypothyroidism?

A 
Cold intolerance
Lethargy
Weight gain
Constipation 
Dry skin 
Hair loss
Hoarse voice
Mental slowness, depression, dementia, cramps, ataxia, paraesthesia

Menstural disturbances (irregular cycles menorrhagia)

Myxoedema coma (severe hypothyroidism)

188
Q

What are the examination findings consistent with hypothyroidism?

A

Bradycardia, cold hands

Pale puffy face, goitre, hair loss, dry skin, vitiligo

Pericardial or pleural effusions

Ascites

Slow relaxation of reflexes

Signs of carpal tunnel syndrome

189
Q

What is subclinical hypothyroidism?

A

Normal serum free-T4 and T3, and increased TSH

190
Q

What is the management for hypothyroidism?

A

Levothyroxine

191
Q

What is the management of myxoedema coma?

A 
Oxygen
Rewarming
Rehydration
IV T4/T3
IV hydrocortisone
192
Q

What is thyrotoxicosis?

A

A syndrome resulting from an excess of circulating free thyroxine (T4) and/or free triiodothyronine (T3).
-Due to increased thyroid hormone synthesis

193
Q

What autoantibodies are associated with Hashimoto’s thyroiditis?

A

Anti-thyroid peroxidase

194
Q

What auto-antibodies are associated with Grave’s disease?

A

TSH-receptor antibodies

195
Q

What are the features of Grave’s disease?

A

-eye signs (30% of patients)
-exophthalmos
-ophthalmoplegia
-pretibial myxoedema
-thyroid acropachy, a triad of:
digital clubbing
-soft tissue swelling of the -hands and feet
periosteal new bone formation

Symptoms of thyrotoxicosis

  • Heat intolerance
  • Sweating
  • Palpitations
  • Anxiety and irritability
  • Weight loss (Despite good appetite)
  • Diarrhoea, pruritus
  • Exertional dyspnoea
  • Menstural irregularities
196
Q

What is Graves opthalmopathy?

A

Blurred vision, double vision, eye grittiness, eye protrusion (Exophtalmos)

197
Q

What is the presentation of subacute thyroiditis?

A

neck pain radiating to the jaw or to the ear, inability to the swallow

  • Fever
  • Palpitations
  • Malaise
  • Tremor
  • Heat intolerance
198
Q

What is the TFT picture in subacute thyroidits?

A

Low TSH

Raised T3 and T4 due to release of pre-formed thyroid hormone in the colloid.

199
Q

What is the first-line management for subacute thyroiditis?

A

Corticosteroid

Analgesia - Ibuprofen

200
Q

What is the first-line management for controlling symptoms of thyrotoxicosis?

A

Propanolol (Beta-blockers)

201
Q

What are the symptoms of thyrotoxicosis?

A

General: Underweight, restless, irritable, sweating.
• Signs of associated autoimmune conditions – vitiligo.
• Hands: tremor, warm, moist, rapid, or irregular pulse, onycholysis, acropachy, palmar erythema.
• BP: Wide pulse pressure
• Eyes: Lid retraction and lid lag (due to increased catecholamine sensitivity of levator palpebrae superioris)

202
Q

What does a radioisotope uptake scan reveal in Grave’s disease?

A

Homogenous uptake

203
Q

What does a radioisotope uptake scan reveal in Toxic multinodular goitre?

A

Heterogenous activity - multiple areas of increased activity with suppression of uptake of the gland

204
Q

What is the first-line management of an acute thyroid crisis?

A

Beta-blockade - atenolol, propanolol

205
Q

What is the pharmacological management for thyrotoxicosis?

A

Carbimazole

Propylthiouracil

206
Q

What is a toxic multi-nodular goitre?

A

Excess production of thyroid hormones from a functionally autonomous thyroid nodules which do not require stimulation from TSH.

207
Q

What is the management of a toxic multi-nodular goitre?

A

Radioiodine therapy

208
Q

What is the presentation of thyroid storm?

A
  • Medical emergency: 50% mortality untreated.
  • Hyperpyrexia > 41 oC
  • Accelerated tachycardia/arrhythmia
  • Cardiac failure
  • Delirium/frank psychosis
  • Hepatocellular dysfunction – jaundice
209
Q

What is the management of a thyroid storm?

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

210
Q

What is the surgical management of a thyroid storm?

A

Thyroidectomy

Radiodine

211
Q

What are the side effects of thioamides?

A

Agranulocytosis (Reduction in neutrophil - neutropenia)

  • Increased sepsis risk
  • Rashes
212
Q

What is the pre-operative preparation for thyroidectomy?

A

Potassium iodide

213
Q

What effect is observed by the administration of iodine therapy in hyperthyroidism?

A

Wolff-Chaikoff effect - inhibition of thyroid hormone synthesis and secretion

214
Q

What are the main causes of Addison’s disease?

A
  • Primary - Autoimmune >70%
  • Infections: Tuberculosis, meningococcal septicaemia, CMV, histoplasmosis.
  • Infiltration: Metastasis (lung, breast, melanoma), lymphomas, amyloidosis.
  • Infarction: Secondary to thrombophilia.
  • Inherited: Adrenoleukodystrophy, ACTH receptor mutation.
  • Iatrogenic: Sudden cessation of long-term steroid therapy.
215
Q

What is the presentation of Addison’s disease?

A

Dizziness, anorexia, weight loss, diarrhoea, vomiting, abdominal pain

Lethargy, and weakness

Depression

Postural hypotension

216
Q

What are the examination findings associated with Addison’s disease?

A

Increased pigmentation - palmar creases, buccal mucosa

Loss of body hair in women

217
Q

What are the signs of an Addisonian crisis?

A 
Hypotensive shock
Tachycardia
Pale
Cold
Clammy 
Oliguria
218
Q

What are the consequences of adrenocortical failure?

A 
Hyponatremia
Hyperkalaemia
Hypotension
Hypoglycaemia fatigue
Hyperpigmentation
Weight loss
219
Q

What is the first-line investigation for Addison’s disease?

A

9 am cortisol - low (Diurnal rhythms exhibited by cortisol secretion)
<100

High ACTH

220
Q

What is the diagnostic investigation to confirming primary adrenal insufficiency?

A

Short synacthen test - 250ug

-There is reduced cortisol secretion - unresponsive to ACTH stimulation

221
Q

What is Waterhouse-Friderichsen syndrome?

A

Meningococcal infection precipitating adrenal haemorrhage and Addisonian crisis

222
Q

What are the precipitating factors for an Addisonian crisis?

A

Steroid withdrawal

Waterhouse-Fridericshen syndrome

Sepsis/Acute exacerbation of chronic insufficiency

223
Q

What is the first-line management of an Addisonian crisis?

A

Rapid IV infusion rehydration (0.9% saline, 1L over 30-60 minutes, 2-4L)

IV 200mg hydrocortisone bolus

224
Q

Which corticosteroid is administered first in Addison’s

A

Hydrocortisone

225
Q

What is the definitive management for Addison’s disease?

A

Hydrocortisone and fludrocortisone

226
Q

What is Cushing’s syndrome?

A

Syndrome associated with chronic inappropriate elevation of free circulating cortisol

227
Q

What are the ACTH-dependent causes of Cushings?

A

Excess ACTH secretion from a pituitary adenoma (Cushing’s disease)- Responds to High-dose dexamethasone suppression test

228
Q

What are the ACTH independent causes of Cushing’s?

A

Benign adrenal adenoma
Adrenal carcinoma
Adrenal nodular hyperplasia
Oral steroids - main cause

229
Q

Which lung is the associated?

A

Small cell lung cancer

230
Q

What is the presentation of Cushing’s?

A 
Weight gain 
Fatigue
Muscle weakness- Proximal myopathy 
Myalgia
Thin skin 
Easy bruising
Poor wound healing
Fractures
Frontal balding
Recurrent Achilles tendon rupture
231
Q

What are the examination findings are associating with Cushing’s?

A 
Moon face
Facial plethora
Interscapular fat pad- buffalo neck hump
Supraclavicular fat distribution 
Thin skin
Myopathy
Bruises
Central obesity
Striae
Kyphosis
Hypertension, ankle oedema
Pigmentation in ACTH dependent cases
232
Q

What is the first-line investigation for Cushing’s?

A

24-hour urine collection of urinary free cortisol

Late-night salivary cortisol

233
Q

What is the diagnostic investigation to differentiate between Cushing’s disease and syndrome?

A

Low-dose dexamethasone test

High-dose dexamethasone test

234
Q

What does a high-dose dexamethasone test reveal ACTH-independent Cushing’s?

A

No suppression- indicates adrenal hyperplasia

235
Q

What investigations are performed in ACTH-independent Cushing’s?

A

Low plasma ACTH

CT or MRI of adrenals

Phase1c Medicine (11 decks)

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