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Pocket MSRA - Book 1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What abnormalities would you expect on TFTs in a patient with Hypothyroidism?

A

High TSH
Low T4

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2
Q

What abnormalities would you expect on TFTs in a patient with Sub-clinical Hypothyroidism?

A

High TSH
Normal T4

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3
Q

What abnormalities would you expect on TFTs in a patient with Hyperthyroidism?

A

Low TSH
High T4/T3

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4
Q

What abnormalities would you expect on TFTs in a patient with Thyrotropinoma?

A

High TSH
High T4

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5
Q

What abnormalities would you expect on TFTs in a patient with Sick Euthyroid/pituitary issues?

A

Low TSH
Low T3/T4

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6
Q

What are the symptoms of thyrotoxicosis?

A

HIGH SYMPATHETIC OUTPUT
Weight loss
Diarrhoea
Weakness
Irritability
Tremor
Heat intolerance
Tachycardia
Brisk reflexes
Proximal weakness

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7
Q

What investigations should be performed in suspected thyrotoxicosis?

A

TFTs - low TSH, high T4/T3
Thyroid autoAb
Isotope scan - if unclear cause

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8
Q

How should thyrotoxicosis be managed?

A

B-blockers for sx
Block
-Carbimazole (1st line)
-Propylthiouracil
Replace
-Levothyroxine

Thyroidectomy/131-Thyroid

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9
Q

What are the side effects of Carbimazole?

A

Rash
Pruritis
Hypothyroidism
TERATOGENESIS - fetal goitre
AGRANULOCYTOSIS

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10
Q

What are the features of Thyroid Storm?

A

SUDDEN ONSET SEVERE HYPERTHYROIDISM
Hyperpyrexia, Dehydration
Tachycardia, Hypotension
Abdo pain, N&V, diarrhoea
Altered mental state

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11
Q

In which patient groups is Thyroid Storm typically seen?

A

Underlying Grave’s/TMN goitre
Precipitated by illness, trauma, emergency surgery, contrast

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12
Q

What is the management of Thyroid Storm?

A

IVI
Carbimazole
Hydrocort/Dex
Digoxin/BB for arrhythmias
Treat underlying cause

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13
Q

What are the features of Grave’s disease?

A

DIFFUSE goitre
Associated w/ autoimmune disease
GAG deposition
-exophthalmos
Pretibial myxoedema
Thyroid acropachy

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14
Q

By what mechanism does Grave’s disease cause hyperthyroidism?

A

Circulating IgG TSHR stimulating autoantibodies

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15
Q

What is the major pregnancy related complication of Grave’s disease and how should it be treated?

A

Fetal thyrotoxicosis
Treat w/ PTU (crosses placenta less)

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16
Q

How should exophthalmos associated w/ Grave’s disease be managed?

A

Stop smoking
Prism (lenses)
High-dose steroids
Decompression
Orbital XRT

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17
Q

What are the features of toxic multinodular goitre?

A

NODULAR goitre
Mass effect (e.g. compression of airway in retrosternal goitre)
Typically euthyroid –> suddenly thyrotoxic as nodules develop

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18
Q

By what mechanism does toxic multinodular goitre cause hyperthyroidism?

A

TSH independent nodules developing

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19
Q

How is toxic multinodular goitre managed?

A

Thyroidectomy

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20
Q

What is a toxic adenoma?

A

Solitary T3/T4 producing nodule
-appears ‘hot’ on isotope scan

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21
Q

What is subacute (de Quervain’s thyroiditis)?

A

Self-limiting PAINFUL goitre post viral illness
-‘cold’ on isotope scan

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22
Q

What is subacute (de Quervain’s thyroiditis) treated?

A

NSAIDs

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23
Q

How should Amiodarone be monitored and why?

A

Can cause hypo/hyperthyroidism
TFTs every 6/12

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24
Q

What are the clinical features of hypothyroidism?

A

LOW SYMPATHETIC OUTPUT + COARSE FACE
-fatigue/lethargy
-cold intolerance
-constipation
-weight gain
-bradycardia
-delayed reflex response
-myxoedema (+/- effusions)
-poor memory/difficulty concentrating

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25
Q

What investigations should be performed in suspected hypothyroidism?

A

TFTs - high TSH, low T4
Thyroid autoAb
FBC - macrocytic anaemia
High cholesterol

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26
Q

What are the common causes of hypothyroidism?

A

PRIMARY
-Deficiency - worldwide most common
-Autoimmune (Hashimoto’s) - UK most common
-Riedel’s fibrosing thyroiditis
-Iatrogenic (post rx, Amiodarone, Lithium)
SECONDARY
-hypopituitarism (rare)

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27
Q

What sort of goitre does Hashimoto’s present with?

A

Diffuse

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28
Q

By what mechanism does Hashimoto’s cause hypothyroidism?

A

TPO autoAb

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29
Q

What is the potential complication of Hashimoto’s?

A

Conversion to marginal zone B-cell lymphoma

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30
Q

By what mechanism does Riedel’s fibrosing thyroiditis cause hypothyroidism?

A

IgG4 disease
-replaces normal tissue w/ fibrosis

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31
Q

What are the features of Riedel’s fibrosing thyroidits?

A

HARD GOITRE FIXED TO NECK
Chronic
Can mimic anaplastic ca
Signs of other IgG4 disease
-retroperitoneal fibrosis
-liver disease

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32
Q

How is Riedel’s fibrosing thyroiditis managed?

A

Steroids
Thyroidectomy

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33
Q

What is a myxoedematous coma?

A

Extreme presentation of severe hypothyroidism

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34
Q

What are the clinical features of myxoedematous coma?

A

Hypothermia
Hyporeflexia
Hypoglycaemia
Bradycardia
Pancreatitis
Psychosis/seizures –> coma

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35
Q

What are the common precipitants of myxoedematous coma?

A

Recent radioiodine/thyroidectomy/pituitary surgery
Infections
Physiological stressors

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36
Q

What is the management of myxoedematous coma?

A

Ventilation (as required)
Replace (T3, glucose, warm)
Treat underlying cause

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37
Q

What are the distinguishing features of a pharyngeal pouch?

A

Older males
Dysphagia
Halitosis
Regurgitation –> aspiration

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38
Q

What are the distinguishing features of a thyroglossal cyst?

A

Midline b/w thyroid isthmus and hyoid bone
Moves w/ tongue protrusion

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39
Q

What are the distinguishing features of a branchial cyst?

A

TEENS
Oval, mobile cyst b/w SCM and pharynx
Increases in size post URTI

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40
Q

What are the distinguishing features of a cystic hygroma?

A

<2 y/o
LEFT sided
Large
Transilluminates

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41
Q

What are the red flag sx suggestive of thyroid ca?

A

Stridor
Persistent cough
Hoarseness
Haemoptysis
Lymphadenopathy
Rapid growth
Painless
Fixed/hard lump

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42
Q

How should thyroid ca be investigated?

A

Step 1 - TFTs & clinical exam
Step 2 (if euthyroid +/- lymphadenopathy) - FNA (not USS)

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43
Q

What are the different types of thyroid ca?

A

Papillary (60%)
Follicular (~25%)
Medullary (5%)
Lymphoma (5%)
Anaplastic (rare)

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44
Q

In which patients does papillary thyroid ca typically present?

A

Younger patients
-better prognosis if young/female

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45
Q

How does papillary thyroid ca spread?

A

LOCALLY
-LN
-Lung

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46
Q

How is papillary thyroid ca treated?

A

Total thyroidectomy +/- node excision +/- 131-Iodine

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47
Q

What are the features of follicular thyroid ca?

A

Presents in middle age
Spreads early via blood (bone, lungs)
Well differentiated

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48
Q

How is follicular thyroid ca treated?

A

Total thyroidectomy + T4 suppression + radioiodine ablation

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49
Q

In which patients does medullary thyroid ca typically present?

A

Sporadic (80%)
MEN2 syndromes

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50
Q

Which investigations should be performed when ix medullary thyroid ca?

A

Phaeochromocytoma screen
RET genetic screening
Calcitonin
-may be raised as tumour marker
-biopsy to exclude localised amyloidosis

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51
Q

How is medullary thyroid ca treated?

A

Total thyroidectomy + node clearance +/- external beam XRT

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52
Q

In which patients does thyroid lymphoma present?

A

W:M 3:1

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53
Q

How does thyroid lymphoma present?

A

Stridor
Dysphagia

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54
Q

How should thyroid lymphoma be ix?

A

Full lymphoma staging pre-treatment
Assess histology for MALT origin
-medullary associated lymphoma thyroid
-good prognosis

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55
Q

How is thyroid lymphoma treated?

A

ChemoXRT

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56
Q

In which patients does anaplastic thyroid ca present?

A

W:M=3:1
Elderly

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57
Q

What are the features of anaplastic thyroid ca?

A

Rapidly growing, hard, invasive
SOB
Dysphagia
Hoarse voice

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58
Q

How is anaplastic thyroid ca treated?

A

Poor response to ANY treatment
Resection OR excision + XRT to palliate
-protect airway

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59
Q

What are the causes of primary hyperparathyroidism?

A

Adenoma (80%)
Hyperplasia (>19%)
Cancer (<1%)

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60
Q

How does 1o hyperparathyroidism present?

A

Asymptomatic
Hypercalcaemic sx - bones, stones, groans, psychic moans
HTN

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61
Q

What clinical syndromes are associated w/ 1o hyperparathyroidism?

A

MEN-1
MEN-2a
Hyperparathyroid-jaw tumour syndrome

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62
Q

Describe MEN-1

A

Autosomal dominant
MEN1 tumour suppressor gene abnormality
Tumours
-parathyroid adenoma/hyperplasia
-pituitary adenoma
-pancreas tumour
-carcinoid/adrenal tumours

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63
Q

Describe MEN-2a

A

Autosomal dominant
RET proto-oncogene mutation
Tumours
-parathyroid hyperplasia (80%)
-thyroid medullary ca (100%)
-phaeochromocytoma (50%)

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64
Q

Describe hyperparathyroid-jaw tumour syndrome?

A

Autosomal dominant
Triad of:
-jaw fibromas
-pituitary adenoma
-GU tumours

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65
Q

Describe MEN-2b

A

Autosomal dominant
RET proto-oncogene mutation
Tumours
-thyroid medullary ca
-phaeochromocytoma
-mucosal neuromas
Marfanoid appearance

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66
Q

What are the causes of 2o hyperparathyroidism?

A

Vitamin D deficiency
CKD

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67
Q

What is the treatment of 2o hyperparathyroidism?

A

Treat underlying cause
PO4 binders
Vit D replacement

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68
Q

What is the management of 2o hyperparathyroidism?

A

Treat underlying cause
PO4 binders
Vit D replacement
Cinacalcet (rarely)
-if high PTH & parathyroidectomy difficult

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69
Q

What are the biochemical findings in 1o hyperparathyroidism?

A

High Ca
Low PO4
High/high normal PTH
High ALP

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70
Q

What are the biochemical findings in 2o hyperparathyroidism?

A

Low/normal Ca
High PO4
High PTH
High ALP

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71
Q

What is the management of 1o hyperparathyroidism?

A

Mild - fluids, avoid thiazides
Mod - excision

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72
Q

What are the complications of parathyroid excision?

A

HypoPTH - can save 1x gland
RLN damage - hoarse voice
Hungry bone syndrome

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73
Q

What is hungry bone syndrome?

A

Rapid hypocalcaemia due to bone remodelling after PTH suddenly suppressed
-check ca for 2/52 post PTH excision

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74
Q

What is the cause of 3o hyperparathyroidism?

A

Adaptation of autonomous parathyroid glands after prolonged 2o hyperparathyroidism
e.g. chronic renal failure AFTER transplant

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75
Q

What are the biochemical findings in 3o hyperparathyroidism?

A

High Ca
Very high PTH

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76
Q

What are the 1o causes of hypoparathyroidism?

A

Reduced PTH scretion from gland failure
-autoimmune
-surgical resection
-hereditary

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77
Q

What are the biochemical findings of hypoparathyroidism?

A

Low Ca
High PO4
Low PTH
NORMAL ALP

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78
Q

What are the presenting features of hypoparathyroidism?

A

Hypocalcaemia (SPASMODIC)
-spasms
-perioral paraesthesia
-anxiety
-seizures
-muscle tone high (colic, wheezing, dysphagia)
-orientation impaired (confusion)
-dermatitis
-impetigo herpetiformis (pustules in pregnancy)
-Chvostek’s/chorea/cataracts/cardiomyopathy/long QTc

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79
Q

What is Trousseau’s sign?

A

Carpopedal spasm on inflating BP cuff
-sign of latent tetany

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80
Q

What is Chvostek’s sign?

A

Facial muscle spasm elicited by tapping CN VII near the tragus

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81
Q

What syndromes are associated w/ 1o hypoparathyroidism?

A

DiGeorge
Autoimmune polyendocrinopathy
-addison’s/hypoPTH
-candidiasis
-ectodermal dysplasia

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82
Q

What are the features of DiGeorge syndrome?

A

CATCH 22
-cardiac
-abnormal facies
-thymic hypoplasia
-cleft palate
-hypoCa
-chromosome 22

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83
Q

What is the treatment for 1o hypoparathyroidism?

A

Alfacalcidol
Ca gluconate if v. low

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84
Q

What is Albright’s osteodystrophy?

A

GNAS1 mutation causing pseudohypoparathyroidism

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85
Q

How does Albright’s osteodystrophy present?

A

SHORT 4th/5th fingers
Round face
Dental hypoplasia
Short height
Low IQ

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86
Q

What are the biochemical findings of Albright’s osteodystrophy?

A

Low Ca
High PO4
High PTH
Normal/high ALP

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87
Q

What is familial hypocalciuric hypercalcaemia?

A

Autosomal recessive defect in Ca SR
Leads to excess Ca reabsorption –> high serum Ca

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88
Q

What are the biochemical findings of familial hypocalciuric hypercalcaemia?

A

Ca/Cr ratio <1/100
Ca slightly elevated

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89
Q

What is the treatment for familial hypocalciuric hypercalcaemia?

A

No treatment needed

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90
Q

What are the different types of pitutiary tumour, and from what cell line do they arise?

A

Acdiophilic tumours - GHoma, prolactinoma
Basophilic tumours - ACTHoma
Chromophobe tumours - non-secretory

91
Q

What are the pressure effects of pituitary tumours?

A

Headache
Bilateral temporal hemianopia
Diabetes insipidus
Hypothalamic effects - temperature control, sleep, appetite
CSF rhinorrhoea - erosion to sella

92
Q

What is the most common pituitary tumour?

A

Prolactinoma

93
Q

What is the relationship between Dopamine and Prolactin?

A

NEGATIVE FEEDBACK
Prolactin stimulates dopamine release from the hypothalamus
Dopamine inhibits prolactin release

94
Q

What are the causes of hyperprolactinaemia?

A

Physiological - stress, pregnancy, breastfeeding
Dopamine antagonists (metoclopramide, haloperidol, risperidone)
Oestrogen
Prolactinoma
Hypothalamic disease
Trauma/surgery (stalk damage)

95
Q

What are the presenting features of hyperprolactinaemia?

A

Galactorrhoea + amenorrhoea (females)
Erectile dysfunction + reduced facial hair (males)
Late features - mass effects, osteoporosis

96
Q

What investigations should be performed in suspected hyperprolactinaemia?

A

Pregnancy test (ddx amenorrhoea)
Basal prolactin
MRI head

97
Q

How can prolactinomas be classified?

A

Microprolactioma <1cm
Macroprolactinoma >1cm

98
Q

How are microprolactinomas treated?

A

Dopamine agonist (e.g. bromocriptine, carbegoline)

99
Q

What are the s/e of dopamine agonists?

A

Depression
Postural hypotension (give at night)
Nausea
Cause cardiac fibrosis (rarely)

100
Q

How are macroprolactinomas treated?

A

Surgery +/- XRT

101
Q

How does an ACTHoma present?

A

Cushing’s syndrome

102
Q

How does a GHoma present?

A

Acromegaly

103
Q

How does an FSHoma present?

A

Macro-orchidism

104
Q

What is Sheehan syndrome?

A

Pituitary apoplexy/infarct 2o post-partum blood loss

105
Q

What are the sx of hypopituitarism?

A

Addison’s
Hypo’s
SOB (GH loss)
Absent lactation
Amenorrhoea
Infertility + impotence
Hypothyroidism
Osteoporosis (late)

106
Q

What is the treatment for hypopituitarism?

A

Hydrocortisone
Thyroxine
Somatotroping
Testosterone/Oestrogen/Gonadotrophin

107
Q

What is Kallmann syndrome?

A

Congenital hypogonadotrophic hypogonadism + midline defect (anosmia + colour blindness)

108
Q

What are the sx of acromegaly?

A

Acroparaesthesia
Amenorrhoea
Low libido
Headache
Sweating
OSA
Arthralgia/backache
Weight gain
Prognathism, malocclusion
Curly hair

109
Q

What are the clinical signs of acromegaly?

A

Large hands/jaw/feet
Corasened facies
Supraorbital ridges
Macroglossia
Thickened/darkened skin
Acanthosis nigricans
Goitre
Proximal weakness
Carpal tunnel

110
Q

What are the complications of acromgealy?

A

Impaired glucose tolerance (40%, DM in 15%)
Vascular - HTN, LVH, cardiomyopathy, arrhythmias, IHD
Colorectal ca

111
Q

How should suspected acromegaly be investigated?

A

BM
OGTT w/ GH levels (failure to supress)
Ca/PO4 (high)
IGF-1 (gold standard)
GH (serial levels)
MRI
ECG, echo

112
Q

What is the treatment for acroemgaly?

A

1st line - Transphenoidal surgery
2nd line - Somatostatin analogues (octreotide)/XRT

113
Q

How are the causes of hyponatraemia classified?

A

By volume status
-hypovolaemic
-euvolaemic
-hypervolaemic

114
Q

What are the hypovolaemic causes of hyponatraemia?

A

Diuretics
Inherited kidney disorders
GI loss (D/V)
Skin loss (burns/sweat)
Mineralocorticoid deficiencies

115
Q

What are the euvolaemic causes of hyponatraemia?

A

SIADH
Hypothyroidism
Short-term diuretics
2o adrenal insufficiency

116
Q

What are the hypervolaemic causes of hyponatraemia?

A

Heart failure
Renal failure (+ nephrotic syndrome)
Liver failure

117
Q

What is SIADH?

A

Syndrome of ADH excess = concentration of urine
Inappropriately high urine Na >20
High urine Osm >100

118
Q

What are the causes of SIADH?

A

Small cell lung ca
Prostate ca/lymphoma
TB, amyloidosis
Surgery
CNS (stroke, infections)
Drugs - SSRIs, opiates, psychotropics, cytotoxines

119
Q

What is the treatment for SIADH?

A

Fluid restriction
Demelocycline
-tetracycline that inhibits ADH production

120
Q

What is diabetes insipidus?

A

Syndrome of polyuria + polydipsia caused by hyposecretion/insensitivity to ADH

121
Q

What are the three types of diabetes insipidus?

A

Nephrogenic DI
Cranial DI
Psychogenic/primary polydipsia
-1o deficit in regulation of osmoregulation of thirst

122
Q

What are the causes of nephrogenic DI?

A

Impaired ADH response by kidney
-lithium
-democyclcine
-CKD
-low K
-high Ca
-post-obstructive uropathy

123
Q

What are the causes of cranial DI?

A

Reduced ADH secretion from post pituitary gland
-idiopathic (MCC)
-congenital (Wolfram’s)
-brain tumours/bleed/infection
-sarcoidosis

124
Q

How should suspected diabetes insipidus be investigated?

A

BMs (DDx DM)
Water deprivation test (8hr)
Urine Osm (<600 in DI)
Desmopressin IM & repeat
-CDI Urine Osm >600 (kidneys respond)
-NDI (no increase)

125
Q

How should diabetes insipidus be treated?

A

CDI
-IM Desmopressin
NDI
-Thiazides
-NSAIDs
-treat underlying cause

126
Q

What is Cushing’s Syndrome?

A

State of chronic glucocorticoid excess

127
Q

What are the causes of Cushing’s Syndrome?

A

ACTH dependent
-Cushing disease (ACTH secreting pituitary adenoma)
-ectopic ACTH producing tumour
-ectopic CRF producing tumour

ACTH independent
-iatrogenic (steroids)
-adrenal adenoma

128
Q

What are the presenting features of Cushing’s Syndrome?

A

Proximal weakness
Recurrent Achilles tendon rupture
Mood changes
Acne
Sexual dysfunction (hirsutism, irregular menses, virilisation)
Truncal obesity w/ thin limbs
Supraclavicular fat pad, moon facies
Osteoporosis, HTN, insulin resistance

129
Q

How can the ACTH dependent and ACTH independent causes of Cushing’s syndrome be differentiated clinically?

A

ACTH productio ncauses pigmentation

130
Q

What are the electrolyte abnormalities present in untreated Cushing’s syndrome?

A

Low K+
High Na
Hyperglycaemia
Metabolic alkalosis

131
Q

How should Cushing’s Syndrome be investigated?

A

1st line
-overnight Dex suppression test (failure to suppress)
-high 24hr urine cortisol
2nd line
-48hr low-dose Dex (failure to suppress cortisol)
-48hr high-dose Dex (pituitary causes suppressed)
CT adrenals
MRI pituitary

132
Q

What are the investigative findings of Cushing’s Disease?

A

ACTH producing tumour

ACTH - high
Low-dose Dex - not suppressed
High-dose Dex - suppression >50%

CT - bilateral adrenal hyperplasia
MRI - pituitary adenoma

133
Q

What are the investigative findings of an ectopic ACTH producing tumour?

A

Paraneoplastic (small cell lung ca, carcinoid)

ACTH - high
Low-dose Dex - not suppressed
High-dose Dex - not suppressed

CT - bilateral adrenal hyperplasia

134
Q

What are the investigative findings of 1o adrenal adenoma/ca?

A

Cortisol - high
ACTH - high
Low-dose Dex - not suppressed
High-dose Dex - not suppressed

CT - bilateral adrenal atrophy

135
Q

What is the treatment for Cushing’s Disease?

A

Transphenoidal resection of pituitary adenoma
Bilateral adrenalectomy if unable to find source

136
Q

What is the treatment for an ectopic ACTH producing tumour?

A

Resection of tumour
AZOLE drugs/mifepristone if tumour not yet located

137
Q

What is the treatment for a 1o adrenal adenoma/ca?

A

Adrenalectomy

138
Q

What is the treatment for excess exogenous steroids?

A

Taper off steroids

139
Q

What is Nelson’s syndrome?

A

Bilateral adrenalectomy performed before treating pituitary adenoma
-leads to disinhibition of that tumour
-aggressive ACTH secretion
-hyperpigmentation, VF defect/opthalmoplegia
-Paradoxical worsening Cushing’s

140
Q

What is Addison’s disease?

A

State of low mineralocorticoid and glucocorticoid

141
Q

What are the causes of Addison’s disease?

A

Primary (destruction of cortex)
-autoimmune (80%)
-secondary (TB, lymphoma, mets, haemorrhage)
Secondary
-iatrogenic due to acute steroid withdrawal

142
Q

What is Waterhouse-Friderichsen Syndrome?

A

Addison’s syndrome 2o haemorrhagic destruction of adrenal cortex

143
Q

How does Addison’s Syndrome present?

A

Vague constitutional sx
Unexplained N&V + abdo pain + diarrhoea + dizziness
Acute vascular collapse/coma (crisis)
Hyperpigmentation
Psych - depression, psychosis, anorexia

144
Q

What are the electrolyte abnormalities of Addison’s Syndrome?

A

High K
Low Na
Metabolic acidosis
Hypoglycaemia
(Hypotension)

145
Q

How should suspected Addison’s Syndrome be investigated?

A

Short synACTHen stimulation test
9am plasma cortisol w/ serial measurements
-no rise in Addison’s
AutoAb
CT adrenals

146
Q

How should Addison’s Syndrome be treated?

A

ACUTE crisis - glucose, IVF, hydrocort +/- fludrocort
Non-acute - steroid replacement +/- mineralocrticoid if postural hypotension

147
Q

What is Conn’s syndrome?

A

1o hyperaldosteronism
-2/3 due to aldosterone producing adrenal adenoma
-1/3 due to bilateral hyperplasia

148
Q

How does Conn’s syndrome present?

A

Triad of
-hypokalaemia
-metabolic acidosis
-HTN

149
Q

How should suspected Conn’s syndrome be investigated?

A

Renin (low)
Aldosterone (high)
CT/MRI - localisation
-if unilateral adenoma seen –> adrenal vv sampling

150
Q

How should Conn’s Syndrome be treated?

A

Lap adrenalectomy + spironolactone

151
Q

What is a phaeochromocytoma?

A

A catecholamine secreting tumour derived from chromaffin cells in the adrenal cortex

152
Q

How do phaeochromocytomas present?

A

Triad of
-headache
-sweating
-tachycardia (sense of impending doom)

153
Q

Where are phaeochromocytomas found?

A

Rule of 10s
-10% extra-adrenal
-10% malignant
-10% bilateral
-10% FHx

154
Q

What conditions are commonly associated with phaeochromocytoma?

A

MEN2A/2B
NF1
Von Hippel Lindau
Sturge-Weber Syndrome

155
Q

What investigations are indicated in suspected phaeochromocytoma?

A

24hr urinary metanephrines
Localisation - CT/MRI, isotope scan

156
Q

How should phaeochromocytoma be treated?

A

Surgery
Pre-op blockade
-alpha block THEN b-block

157
Q

How does T1DM typically present?

A

Symptomatic younger pts
Sudden polyuria/polydipsia
Recurrent UTIs
Thrush
Weight loss
DKA

158
Q

How does T2DM typically present?

A

Asymptomatic
Gradual onset
Older pts

159
Q

What is the underling mechanism of T1DM?

A

Insulin-dependent autoimmune disease
Low C-peptide

160
Q

What is the underlying mechanism of T2DM?

A

Non-insulin dependent due to end-organ insulin resistance
Initially normal C-peptide

161
Q

What are the diagnostic criteria for DM?

A

HbA1c >47
OGTT 2hr >11.1
Fasting BM >7.0
Random BM >11.1

Symptomatic pts need 1x abnormal reading
Asymptomatic pts need 2x abnormal readings

162
Q

What are the two pre-diabetic conditions?

A

Impaired glucose tolerance
-7.8-11.1 and normal fasting glucose
Impaired fasting glucose
-5.5-7.0 and normal OGTT

163
Q

What investigations can be performed when there is diagnostic uncertainty in DM?

A

GADA
B-islet cell Ab
Low C-peptide
high Ketones - Type 1

164
Q

What is LADA?

A

Latent autoimmune diabetes in adult
-T1DM that presents in adults
-C-peptide undetectable

165
Q

What is MODY?

A

Maturity onset diabetes of young
-autosomal dominant T2DM
-presents <25 y/o
-C-peptide detectable

166
Q

What is Wolfram Syndrome?

A

DIDMOAD
-diabetes insipidus
-diabetes mellitus
-optic atrophy
-deafness (sensorineural)
-<16 y/o
-urogenital tract malformations
-neurology (ataxia, seizures, neuropathies)

167
Q

What is DKA?

A

Diabetic Ketoacidosis
-acidaemia (pH <7.3/HCO3- <15)
-hyperglycaemia (BM >11 or known DM)
-ketonaemia >3 or ketonuria > ++

168
Q

How does DKA present?

A

Acute onset in T1DM
Vomiting
Abdo pain
Dehydration
Polyuria/polydipsia
Fatigue/drowsiness/coma
Ketone breath
Kussmaul resp

169
Q

How should DKA be treated?

A

Fixed rate insulin (0.1 unit/kg/hr)
IVI
-including K/dextrose

170
Q

What is HHS?

A

Hyperglycaemic Hyperosmolar State
-hypovolaemia
-marked hyperglycaemia >30
-no ketonaemia (<3) or acidosis
-Osm >320

171
Q

How does HHS present?

A

Insidious onset
Precipitant (infection/cardiovascular)
Polyuria/polydipsia over weeks - dehydration
Neurological signs
-FND
-visual acuity changes
-confusion –> coma

172
Q

How should HHS be treated?

A

Fixed rate insulin (0.05 units/kg/hr)
IVI
-including K+/dextrose

173
Q

What are the potential complications of DKA/HHS?

A

Cerebral oedema (replace fluid deficit slowly)
Aspiration pneumonia
VTE
Dehydration
Hypo K/Mg/Po4

174
Q

How do hypoglycaemic episodes present?

A

BM <4
Autonomic sx - sweating, anxiety/agitation, tremor, palpitations, dizziness, hunger
Neuroglycopenic sx - drowsy/confusion, visual issues, seizure, coma

175
Q

How should hypoglycaemic episodes be treated?

A

Conscious - oral replacement
Drowsy/uncooperative - buccal glucose gel
Unconscious/refractory - 10% dextrose/glucagon gel

176
Q

What is the DVLA advice for hypoglycaemic episodes?

A

Stop car safely & switch engine off
Fast-acting carbohydrate
Wait 45mins before resuming
Snack regularly

177
Q

What are the cardiovascular complications of DM?

A

Atherosclerosis –> higher MI risk (silent)
Peripheral neuropathy
Retinopathy
Nephropathy

178
Q

How should blood pressure be managed in DM?

A

Lower BP target
-T1DM <135/85
-T2DM <140/80
-if end organ damage <130/80
ACEi preferable (except afro-carribean)

179
Q

How does diabetic Amyotrophy present?

A

Aymotrophy
-proximal motor neuropathy
-painful progressive weakness w/ wasting
-usually unilateral
-absent knee reflexes

180
Q

How does diabetic polyneuropathy present?

A

Glove/stocking distribution of paraesthesia

181
Q

How does mononeuritis multiplex present?

A

Acute mononeuropathy (sensory AND motor loss) of non-contiguous nerves
-asymmetrical

182
Q

How does autonomic neuropathy present?

A

Postural sx
Gustatory sweating
Impotence
Visual blurring
Gastroparesis

183
Q

Which antiemetic is first line for gastroparesis?

A

Metoclopramide (prokinetic)

184
Q

Which skin changes can present in diabetes?

A

Lipidoca diabeticorum
-shiny, yellowish area on shin w/ vessel growth
Acanthosis nigricnas
Granuloma annulare

185
Q

What are the treatment aims for diabetes?

A

HbA1c <48
HbA1c <53 if hypoglycaemic risk (Sulphonylurea)

186
Q

What is the first line treatment for T2DM?

A

Metformin (biguanide)

187
Q

What are the key features of Metformin?

A

Stops weight gain
No hypoglycaemic risk
Held/stopped if eGFR <30/Cr>150

188
Q

What are the s/e of Metformin?

A

GI upset (try MR)
Lactic acidosis (v. rare)

189
Q

What is the method of action of Gliclazide?

A

KATP channel inhibitor = increase insulin secretion

190
Q

What are the s/e of Gliclazide?

A

Hepatic cholestasis
Blood dyscrasias
Allergic skin reactions
Weight gain/hypos

191
Q

What is the method of action of Gliptins?

A

DPP4 inhibitors increase insulin secretion

192
Q

What is the method of action of Metformin?

A

Insulin sensitisation
-only effective if residual islet cells left

193
Q

What are the s/e of Gliptins?

A

Headaches
N&V
Heart failure
Pancreatitis/pancreatic ca risk
Arthralgia

194
Q

What is the method of action of Glitazones?

A

PPAR-gamma activator –> increase insulin secretion + sensitivity

195
Q

What are the key features of Glitazones?

A

Weight gain
Use if insulin resistant/NAFLD

196
Q

What are the s/e of Glitazones?

A

Fluid retention (CCF)
Hepatotoxic
Osteoporosis/#
Bladder ca
Drug interactions

197
Q

What monitoring is required for Glitazones?

A

LFTs every 2/12 for 1 year
Monitor and stop in 3-6/12 if ineffective

198
Q

What is the method of action of Gliflozins?

A

SGLT2 inhibitor –> blocks glucose reabsorption by kidneys –> excess glycosuria
-only effective if eGFR <60

199
Q

What are the key features of Gliflozins?

A

Reduced mortality in patients w/ CVD/heart failure
Weight loss

200
Q

What are the s/e of Gliflozins?

A

Normoglycaemic DKA
UTIs/thrush/diuresis (glycosuria)
Hyperkalaemia

201
Q

What is the method of action of Exenatide/Liraglutide?

A

GLP analogues/mimetics –> augment insulin release/slow gastric emptying

202
Q

What are the key features of Exenatide/Liraglutide?

A

Weight loss
No hypos when used alone

203
Q

What are the indications for Exenatide/Liraglutide?

A

BMI >35 + psych/medical problems associated w/ obesity OR
BMI <35 + insulin posing occupational implication OR
weight loss may benefit obesity comorbidities

204
Q

What are the s/e of Exenatide/Liraglutide?

A

TDS injections
GI s/e
Pancreatitis/pancreatic ca risk
Worsens gastroparesis
C/i if eGFR <30

205
Q

What is the method of action of Repaglinide/Nateglinide?

A

Secretogogues/sulphonylurea receptor binders –> increase insulin release

206
Q

What are the s/e of Repaglinide/Nateglinide?

A

Rash
GI upset
Hypos
Hepatptoxic

207
Q

What is the method of action of Acarbose?

A

Intestinal a-glucosidase inhibitor = less absorption of glucose

208
Q

What are the key features of Acarbose?

A

Weight neutral
Reduces post-prandial hyperglycaemia
Used in DUMPING SYNDROME

209
Q

What are the s/e of Acarbose?

A

Flatulence + abdo discomfort
Osmotic diarrhoea

210
Q

What is the method of action of Orlistat?

A

Inhibits pancreatic/gastric lipases –> steatorrhoea and weight loss

211
Q

What are the common types of Insulin?

A

Ultra-fast acting - Novorapid, Humalog
Short-acting soluble - Actrapid, Humulin S
Intermediate-acting - Humulin I, Insulatard
Long-acting - Lantus, Levemir
Tuojeo - v. concentrated
Degludec - v. long acting
Pre-mixed - NovoMix

212
Q

What insulin regimens are commonly prescribed?

A

Biphasic
-good for T2DM
Basal-bolus
-QDS insulin

213
Q

What is the Dawn phenomenon?

A

Physiologically high BM in the early am
No nocturnal hypos

214
Q

How should insulin generally be titrated?

A

Increase dose prior to high BMs by 10%

215
Q

What is the Somogyi effect?

A

High rebound BM in the morning due to insufficient night-time insulin delivery in T1DM

216
Q

What are the sick day rules?

A

Check BM QDS
Check Ketonuria
Increase insulin dose if BM rising
GP to consider ultra-fast acting insulin
Admit if vomiting, dehydrated, ketotic, children or pregnant

217
Q

What is the DVLA advice re. diabetic medications?

A

Notify if on insulin/sulphonylureas AND >1 hypo in last 1/12
HGV drivers
-no hypos last 1/12
-full hypo awareness
-self monitoring at least BD/times of driving

218
Q

What are the indications for bariatric surgery?

A

BMI >35 + 1x comorbidity responding to weight loss
BMI 30-34.9 and recent onset T2DM
Consider for Asian pts w/ recent onset T2DM and BM <30

219
Q

What is Dumping Syndrome and how does it present?

A

Excess insulin secretion post fundoplication
Presents with
-flushing
-dizziness
-post-prandial hypos

220
Q

What are the indications for islet cell transplant?

A

T1DM + >2 severe hypos in 2 years + impaired hypo awareness

221
Q

What are the contraindications to islet cell transplant?

A

Obesity
>50U insulin/day
Poor renal function

222
Q

What is a glucagonoma and how does it present?

A

Glucagon secreting pancreatic tumour
Presents with
-flushes + diarrhoea
-diabetes
-DVT
-depression
-NME rash
-hyperglycaemia
-weight loss

223
Q

What is hypoglycaemic hyperinsulinaemia and what are its causes?

A

Excess insulin causing low BM
Causes
-insulinoma
-fictitious disease/exogenous insulin poisoning/sulphonylurea overdose

Pocket MSRA - Book 1 (7 decks)

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