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Phase 3B > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is secreted by the thyroid gland?

A

-Secretes T3 and T4

>T4 is more abundant. T3 is more active

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2
Q

What is the role of thyroid hormone?

A
  • Metabolism: regulates the use of energy sources
  • Protein synthesis
  • Control of body’s sensitivity to other hormones (particularly adrenaline)
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3
Q

How can thyroid problems be classified?

A

-Hypothryoidism
>Primary
>Secondary
>Congenital

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4
Q

What is the pathology of primary hypothyroidism?

A

-Problem with the thyroid gland itself

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5
Q

What is the pathology of secondary hypothyroidism?

A

-A disorder within the pituitary gland or lesion compressing the pituitary gland

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6
Q

What is the pathology of congenital hypothyroidism?

A

-Due to a proble with thryoid dysgeneiss or thyroid dyshormonogenesis

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7
Q

What is the role of the hypothalamus and pituitary gland in thyroid function?

A

-Hypothalamus secretes thyrotropin-releasing hormone
>causes stimulation of ANTERIOR PITUITARY to secrete TSH
>Stimulates thyroid gland to increase production of: Thyroixine (T4) and Triiodothyronqine (T3)

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8
Q

What is the epidemiology of hypothyroidism?

A

-More common in females than males

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9
Q

What are causes of primary hypothyroidism?

A
  • MOST COMMON: Hashimoto’s thyroiditis
  • Subacute thyroiditis
  • Riedel thyroiditis
  • Iatrogenic
  • Drug therapy: lithium, amiodarone, anti-thyroid drugs
  • Dietary iodine deficiency
  • Congenital hypothyroidism
  • Postpartum thyroiditis
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10
Q

What are the causes of secondary hypothyroidism?

A

-Pituitary failure
-Other ass. conditions:
>Down’s syndrome
>Turner’s syndrome
>Coeliac disease
*Rare

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11
Q

What are the symptoms of hypothyroidism?

A
  • Fatigue
  • Weight gain
  • Anorexia
  • Cold intolerance
  • Poor memory
  • Constipation
  • Goitre
  • Changes to periods (menorrhagia)
  • Puffy/swollen eyes: myxoedema
  • Carpal tunnel syndrome symptoms
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12
Q

What are signs of hypothyroidism?

A
  • Overweight
  • Dry skin
  • Thin hair and eyebrows
  • Mental slowness
  • Ataxia
  • Proximal muscle weakness
  • Slow relaxing reflexes - hyporeflexia
  • Non-pitting oedema (hands and face)
  • Bradycardia and hypotension (Decreased sympathetic stimulation)
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13
Q

What is Hashimoto’s thyroiditis?

A

-Most common cause of hypothyroidism
-Autoimmune disease
-Ass. w/
>T1DM
>Addison’s disease
>Pernicious anaemia
>RA/SLE/Sjorgren’s

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14
Q

Features of Hashimoto’s thyroiditis?

A
  • Normal features of hypo

- Goitre: firm, non-tender

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15
Q

What antibodies will be present in Hashimoto’s thyroiditis?

A
  • Anti-thyroid peroxidase (anti-TPO)

- Anti-Tg

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16
Q

What is subacute thyroiditis also known as?

A

-De Quervain’s thyroiditis

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17
Q

What is subacute thyroiditis?

A
  • 4 phase thyroid dysfunction.

- Typically presents following a viral infection and presents with hyperthyroidism initially

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18
Q

What is phase 1 of subacute thyroiditis?

A

-Phase 1: (3-6 weeks): hyperthyroidism, painful goitre, raised ESR

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19
Q

What is phase 2 of subacute thyroiditis?

A

-Phase 2: (1-3 weeks) of euthryoid

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20
Q

What is phase 3 of subacute thyroiditis?

A

-Phase 3: weeks-months of hypothyroidism

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21
Q

What is phase 4 of subacute thyroiditis?

A

-Thyroid structure and function returns to normal

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22
Q

How is subacute thyroiditis diagnosed and treated?

A

-Investigations: globally reduced uptake of thyroid on iodine-131 scan
-Mx: usually self limiting (most pts don’t require Rx
>Aspirin/NSAIDs for pain
>Severe cases: steroids

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23
Q

What are 3 stages of post-partum thyroiditis?

A
  1. Thyrotoxicosis
  2. Hypothyroidism
  3. Normal thyroid function
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24
Q

Which antibodies are found in post-partum thyroiditis?

A

-Thyroid peroxidase antibodies

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25
Q

How is post-partum thyroiditis managed?

A
  • Propanolol for symptom control of thyrotoxic phase

- Hypothyroid phase: thyroxine

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26
Q

What are features of Riedel’s thyroiditis?

A
  • Rare cause of hypothyroidism
  • Dense firbous tissue replaces normal thyroid parenchyma
  • Middle aged women
  • Ass. w/ retropritoneal fibrosis
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27
Q

What would you find on examination of someone with Riedle’s thyroiditis?

A

-Hard, fixed, painless goitre

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28
Q

How is hypothyroidism investigated?

A 
-TFTs
>Low free T3/T4
>TSH high (primary)
>TSH low (secondary)
-Thyroid antibodies
-FBC: anaemia
-Hyperlipidaemia (decreased metabolism)
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29
Q

What are examples of antibodies that may be present in hypothyroidism?

A
  • Anti-thyroglobulin

- Anti-thyroid peroxidase

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30
Q

How is hypothyroidism treated?

A

-Lifelong levothyroxine

50-100mcg OD

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31
Q

Which pt groups should the dose of levothyroxine be altered?

A
  • Elderly
  • IHD
  • Pregnancy
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32
Q

What are some side effects of thyroxine therapy?

A
  • Hyperthyroidism (overtreatment)
  • Reduced bone mineral density
  • Worsening of angina
  • AF
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33
Q

Which drug interacts with thyroxine?

A

-Iron tablets

>give thyroxine and iron at least 2 hours apart

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34
Q

What is subclinical hypothyroidism?

A
  • TSH raised
  • T3 and T4 normal
  • No obvious symptoms
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35
Q

What is the significance of subclinical hypothyroidism?

A

-Risk of progressing to overt hypothyroidism

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36
Q

What is the most serious complication of hypothyroidism?

A

-Myxoedema coma

>Extreme manifestation of untreated/undertreated hypothyroidism

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37
Q

How does myxoedema coma present?

A
  • History of longstanding hypothyroidism
  • Deterioration in mental state: apathy, low mood, cognitive decline, confusion, coma
  • Hypothermia
  • Hypotension and bradycardia
  • Hypoventilation
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38
Q

What are some factors which maya precipitate myxoedema coma?

A
  • Hypothermia
  • Infections
  • Medications: amiodarone, anaesthetic, beta blockers, lithium, phenytoin
  • Other significant metabolic challenges: hypoglycaemia, Gi bleed, stroke, surgery/trauma
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39
Q

How is myxoedema coma managed?

A

-Admit to ITU
-Supportive Mx:
>ventilation, correction of electrolyte imbalance, monitor CV status, warm hypothermic pts slowly
-Thyroid replacement (IV)
-Abx
-Corticosteroids

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40
Q

What are the causes of hyperthyroidism?

A
  • Grave’s disease
  • Toxic multinodular goitre
  • Solitary toxic nodule/adenoma
  • Acute phase of De Quervain’s thyroiditis
  • Acute phase of post-partum thyroiditis
  • Acute phase of Hashimoto’s
  • Pituitary tumour secreting TSH
  • Drug induced ie amiodarone
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41
Q

What are the symptoms of hyperthyroidism?

A
  • Anxiety/irritability/change in behaviour
  • Sweaty/heat intolerance
  • Diarrhoea
  • Oligomenorrhoea
  • Weight loss
  • Increased appetite
  • Nausea and vomiting
  • Palpitations
  • Loss of labido
  • Eye symptoms in Grave’s
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42
Q

What are signs of hyperthyroidism?

A
  • Tremor
  • Tachycardia and hypertension
  • Warm, vasodilated peripheries
  • Red face/sweating
  • Anxious/manic appearance
  • AF
  • Finger clubbing
  • Goitre
  • Eye signs (Gravea)
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43
Q

What is Graves’ disease?

A
  • Most common cause of thyrotoxicosis

- Typically seen in women aged 30-50

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44
Q

What are the eye signs seen in Graves’ disease?

A
  • Exophthalmos/proptosis
  • Ophthalmoplegia
  • Lidlag
  • Lid retraction
  • Conjunctival oedema
  • Optic disc swelling
  • Blood shot eyes
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45
Q

How often are eye signs seen in Graves’ disease?

A

-30%

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46
Q

What other signs apart from eye signs are seen in Graves’ disease?

A
  • Pretibial myxoedema
  • Thyroid acropachy (soft tissue swelling of the fingers)
  • Other features of hyperthyroidism
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47
Q

What symptoms will pts with Graves’ eye disease complain of?

A
  • Pain or pressure in the eye
  • Gritty sensation
  • Decreased vision
  • Photophobia
  • Dry sore eyes
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48
Q

How may thyroid eye disease be prevented?

A
  • Smoking cessation
  • Avoid radioiodine Rx
  • ?Prednisolone
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49
Q

How is thyroid eye disease managed?

A
  • Thyroid disease Rx
  • Prednisolone
  • Smoking cessation
  • Topical lubricants
  • Radiotherapy
  • Surgery
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50
Q

What are some indications for urgent review by ophthalmology in someone with established thyroid eye disease

A
  • Unexplained deterioration in vision
  • Awareness of change in intensity of quality of colour vision
  • History of eye ‘suddenly popping out’ - globe subluxation
  • Obvious corneal opacity
  • Cornea still visible when eyelids closed
  • Disc swelling
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51
Q

Whats specific antibodies are present in Graves’ disease?

A
  • TSH receptor stimulating antibodies

- Anti-thyroid peroxidase antibodies

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52
Q

What is toxic multimodular goitre ?

A

-Thyroid gland contains a number of autonomously functioning nodules = hyperthyroidism

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53
Q

How should toxic multinodular goitre be investigated and treated?

A
  • Ix: nuclear scintigraphy, reveals patchy uptake

- Rx: radioiodine therapy

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54
Q

How is hyperthyroidism diagnosed?

A
  • T3 and T4: high
  • TSH: low (mainly primary causes)
  • Thyroid autoantibodies
  • Thyroid USS: ddx Graves’ from toxic adenoma
  • Isotope uptake scanning
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55
Q

What medications can be helpful for symptom management in initial diagnosis of thyrotoxicosis?

A

-Propanolol

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56
Q

How is Graves’ disease treated?

A
  • Antithyroid drugs ie carbimazole

- Radioiodine treatment

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57
Q

What are some contraindications for radioiodine Rx for hyperthyroidism?

A
  • Pregnancy
  • Age <16
  • Thyroid eye disease
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58
Q

What are some side effects of antithyroid drugs?

A
  • Rash (most common)
  • Less common: arthralgia, hepatitis, thrombocytopenia, neuritis
  • resovles after stopping drug
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59
Q

What is the major complication to consider in cambimazole therapy?

A

-Agranulocytosis

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60
Q

Which antithyroid drug should be used during pregnancy?

A

-Propylthiouracil

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61
Q

When does surgical management need to be used?

A
  • When medical mx is unsuccessful
  • Solitary toxic nodule/adenoma
  • Partial or total thyroidectomy
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62
Q

What are some poor prognostic factors for hyperthyroidism?

A
  • Severe biochemical hyperthyroidism
  • Large goitre
  • Thyroid antibody +ve
  • Male gender
  • Young at age of onset
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63
Q

What are features of a thyroid storm?

A
  • History of underlying thyroid disease
  • Hyperpyrexia
  • Tachycardia
  • Extreme restlessness
  • Delirium
  • Coma and death (if not treated)
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64
Q

What are some precipitation factors of thyroid storm?

A
  • Infection
  • Stress
  • Surgery
  • Radioactive iodine therapy in unprepared pts (TSH given for a couple days before radioactive iodine therapy to help thyroid cells take in iodine)
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65
Q

How is thyroid storm treated?

A
  • Large doses carbimazole
  • Potassium iodide
  • IV hydrocortisone
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66
Q

What is a goitre?

A
  • Palpable and visible thyroid enlargement
  • Can be euthyroid
  • Common in iodine deficient areas
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67
Q

What are the causes of diffuse goitres?

A
  • Graves’ disease
  • Hashimoto’s
  • Thyroiditis
  • Idodine deficiency
  • Sulfonylureas
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68
Q

What are the causes of nodular goitres?

A
  • Multinodular goitres
  • Solitary nodules
  • Thyroid cysts
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69
Q

What are the types of tumours that can cause goitres?

A
  • Adenoma
  • Carcinoma
  • Lympohomas
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70
Q

What are the physiological causes of goitres?

A
  • Pregnancy

- Puberty

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71
Q

What are some inflammatory causes of a goitre?

A
  • TB

- Sarcoidosis

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72
Q

How should a goitre be investigated?

A
  • USS (fluid vs solid)
  • Fine needle aspiration cytology biopsy
  • TFTs
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73
Q

How does amiodarone affect thyroid function?

A
  • Prevents uptake and organification of iodine
  • Reduces peripheral T4-> T3 conversion
  • TSH raised, T4 high, T3 low
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74
Q

How should amiodarone induced hypothyroidism be treated?

A
  • Levothyroxine

- Continue amiodarone

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75
Q

What are the 2 different types of amiodarone induced thyrotoxicosis?

A

-AIT-1: excessive thyroid hormone synthesis
>treat with carbimazole, stop amiodarone
-AIT-2: amiodarone-related destructive thyroiditis
>treat with corticosteroids, stop amiodarone

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76
Q

What is the relationship between lithium and thyroid function

A

-Hypothyroidism!
>treat with levothyroxine and continue lithium therapy.
-Monitor TFTs every 6/12

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77
Q

What are different types of cancer seen in the thyroid gland?

A
  • Papillary (young females)
  • Follicular
  • Medullary
  • Anaplastic
  • Lymphoma
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78
Q

Features of thyroid cancer?

A
  • Lump
  • Systemic features: fever, night sweats, weight loss
  • Local invasion/pressure symptoms
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79
Q

How are papillary and follicular thyroid cancers treated?

A
  • Thyroidectomy
  • Radioiodine
  • Yearly thyroglobulin levels
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80
Q

What are some complications of thyroid surgery?

A
  • Damage to recurrent laryngeal nerve
  • Bleeding
  • Damage to parthyroid glands > hypocalcaemia
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81
Q

What is diabetes mellitus?

A

-Chronic endocrine condition characterised by abnormally raised blood glucose levels

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82
Q

What are the different classifications of DM?

A
  • T1DM
  • T2DM
  • Prediabetes
  • Gestational diabetes
  • Maturity onset diabetes of the young
  • Latent autoimmune diabetes of adults
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83
Q

What medication can result in raised blood glucose levels?

A

-Steroids

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84
Q

What is T1DM?

A
  • Autoimmune disorder
  • Insulin producing beta cells are destroyed by immune system –> absolute deficiency of insulin
  • =Raised blood glucose
  • Usually present in childhood/early adult life
  • May present as DKA
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85
Q

How can bood glucose be checked/monitored?

A
  • Finger prick BM
  • Blood glucose (fasting/non-fasting)
  • HbA1c
  • Glucose tolerance test
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86
Q

What is the diagnostic criteria for diabetes for fasting plasma glucose?

A

> 7.0mmol/L

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87
Q

What is the diagnostic criteria for diabetes for random plasma glucose?

A

->11.0mmol/L

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88
Q

What is the diabetic level cut off for HbA1c?

A

->48mmol/L (6.5%)

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89
Q

What may cause a misleading HbA1c result?

A

-Increased red cell turnover ie
>sickle cell disease
>polycythaemia
>COPD

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90
Q

What are some medical conditions in which HbA1c may not be used for a diagnosis of diabetes?

A
  • Haemaglobinopathies
  • Haemolytic anaemia
  • Untreated iron deficiency
  • Suspected gestational diabetes
  • Children
  • HIV
  • CKD
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91
Q

What does impiared fasting glucose mean?

A

-Fasting glucose of >6.1 but <7.0

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92
Q

What does impaired glucose tolerance mean?

A

-Impaired glucose tolerance:

>plasma glucose <7, >oral glucose tolerance 2 hour value >7.8 but <11.1

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93
Q

What are the main principles of management of diabetes?

A
  • Drug therapy to normalise blood glucose levels
  • Monitor for and treat any diabetic complications
  • Modify any other risk factors for other conditions ie CVD
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94
Q

How is T1DM treated?

A

-Insulin

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95
Q

How is T2DM treated?

A
  • Diet controlled
  • Metformin (1st line)
  • Sulfonylureas, gliptins, pioglitazone (2nd line)
  • Insulin (when meds aren’t sufficient)
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96
Q

How does insulin work?

A

-Direct replacement of endogenous insulin given S/C

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97
Q

How can insulin be classified?

A
  • Source: analogue, human sequencing

- Duration of action: short, immediate, long acting

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98
Q

What are the main side effects of insulin?

A
  • Hypoglycaemia
  • Weight gain
  • Lipodystrophy
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99
Q

How does metformin work?

A
  • Increases insulin sensitivity
  • Decreases hepatic gluconeogenesis
  • Type of biguanide
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100
Q

What is a contraindication for metformin?

A

-Can not be used in patients with eGFR <30ml/min

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101
Q

What are the main side effects of metformin?

A
  • Diarrhoea

- Lactic acidosis

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102
Q

What is the mode of action of sulfonylureas?

A

-Stimulates pancreatic beta cells to secrete insulin

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103
Q

What are examples of sulfonylureas?

A
  • Gliclazide

- Glimepiride

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104
Q

What are the main side effects of sulfonylureas?

A
  • Hypoglycaemia
  • Weight gain
  • Hyponatraemia
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105
Q

What is mode of action of thiazolidinediones?

A

-Activation of PPAR-gamma receptor adipocytes

=promotes apidogenesis and fatty acid uptake

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106
Q

What is an example of thiazolidinediones?

A

-Pioglitazone

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107
Q

What are the main side effects of pioglitazone?

A
  • Weight gain

- Fluid retention

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108
Q

How do DPP-4 inhibitors work?

A

-Increase incretin levels - inhibition of glucagon secretion

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109
Q

What are examples of DPP-4 inhibitors?

A
  • Sitagliptin

- Vildagliptin

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110
Q

What are the side effects of DPP-4 inhibitors?

A

-Increased risk of pancreatitis (generally well tolerated)

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111
Q

How does SGLT2 inhibitors work?

A
  • Inhibitos reabsorption of glucose in the kidney

- commonly cause weight loss

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112
Q

What are examples of SGLT2 inhibitors?

A
  • Canagliflozin

- Dapagliflozin

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113
Q

What is a side effefct of SGLT2 inhibitors?

A

-UTI

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114
Q

How do GLP-1 agonists work?

A

-Inhibits glucagon secretion

ie exenatide, liraglutide

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115
Q

What are side effects of GLP-1 agonists?

A
  • N+V

- Pancreatitis

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116
Q

What should blood glucose targets be during the day?

A

> 5-7mmol/l on waking
4-7mmol/L before meals at other times of day
-Monitor >4 times a day

117
Q

When should BMs be taken more fequently?

A
  • During periods of illness
  • Bfore/during/after sport
  • Trying to conceive
  • During pregnancy
  • breastfeeding
118
Q

What are the different types of insulin that can be given?

A
  • Mutliple daily basal-bolus insulin

- Rapid acting insulin analogues before meals

119
Q

What medication can be offered to T1DM if BMI >25?

A

-Metformin

120
Q

How quickly does rapid acting insulin analogues work?

A

-5 minutes

>Peaks at 1 hour

121
Q

How quickly does short acting insulin analogues work?

A

-30 mins

>Peaks at 3 hours

122
Q

How quickly does immediate acting insulin analogues work?

A

-2 hours

>Peaks at 5-8 hours

123
Q

How quickly does long acting insulin analogues work?

A

1-2 hours
-Flat profile
Lasts 24 hours

124
Q

Examples of rapid acting insulin?

A
  • Novorapid

- Humalog

125
Q

Examples of short acting insulin?

A
  • Actrapid

- Humulin S

126
Q

Examples of intermiediate acting insulins?

A

-Isophane insulin

127
Q

Long acting insulin examples?

A
  • Insulin detemir (Levemir)

- Isulin glargine (lantus)

128
Q

Examples of premiexed insulin preparations?

A

-Novomix 30
-Humalog Mix25
HumalogMix 50

129
Q

What type of diet should someone with T2Dm receive?

A
  • High fibre, low glycaemic index source of carbs
  • Low fat dairy products and oily fish
  • Control intake of foods containing saturated fats
  • Aim for weight loss by 5-10%
130
Q

What are examples of triple therapy for T2DM if HbA1c rises >55mmol/L?

A
  • Metformin + glyptin + sulfonylurea
  • Metformin + pioglitazone + sulfonylurea
  • Metformin + sulfonylurea + flozin
  • Metformin + pioglitazone + flozin
131
Q

What is the target blood pressure for someone with T2DM?

A
  • <140/80 or <130/80 if end-organ damage is present
  • > ACEi
  • Antiplatelets if CVD present
  • Statins if Q risk >10%
132
Q

What are the sick day rules for a diabetic pt?

A
  • Increase frequency of BM monitoring
  • Encourage fluid intake
  • Sugary drinks if struggling to eat
  • Sick day supplies
133
Q

Advice for pts taking oral hypoglycaemic meds if they are unwell?

A
  • Continue taking even if not eating much

- Stress response to illness ^^ cortisol levels = ^^BM

134
Q

When does an unwell diabetic require admission?

A
  • Suspicion of underlying illness
  • Inability to maintain fluid intake
  • Persistent diarrhoea
  • Significant ketosis
  • BM persistently >20
  • Pt unable to manage adjustment
  • Lack of support at home
135
Q

What are DVLA criteria for diabetics and their medication use?

A
  • No severe hypoglycaemic event in 12 months
  • Driver must have full hypo awareness
  • Regular Bm monitoring
  • Driver must understand risks of a hypo
  • No other complications
  • Inform DVLA if on sulfonylureas
136
Q

What is the definition of hypoglycaemia?

A

-Blood glucose <3.0mmol/L

137
Q

How is hypoglycaemia diagnosed?

A
  • Plasma hypoglycaemia
  • Symptoms attritutable to low blood sugar
  • Resolution of symptoms with correction of the hypoglycaemia
138
Q

Risk factors for hypoglycaemia?

A
  • Tigh glycaemic control
  • Malabsorption
  • Injection into lipohypertrophy sites
  • Alcohol
  • Insulin prescription error
  • Poor oral intake
  • Hypo-unawareness
  • Sepsis/infection
139
Q

Presentation of hypoglycaemia?

A
  • Coma
  • Convulstions
  • Transient hemiparesis
  • Reduced consciousness and cognitive dysfunction
  • Precipitation of CV events ie arrhythmias, ischaemia, cardiac failure
140
Q

Treatment for hypoglycaemia in conscious pt?

A
  • Glucose 10-20g PO

- Glucogel

141
Q

Treatment for hypoglycaemia in unconscious or uncooperative pt?

A
  • IV 10/20% glucose

- IM glucoagon 1mg

142
Q

What is pre-diabetes?

A
  • Impaired glucose levels but not high enough for diagnosis of DM?
  • Fasting plasma glucose: 6.1-6.9mmol/L
143
Q

What are the main factors that cause diabetic foot disease?

A

-Neuropathy
>Lack of protective sensation, dry skin, Charcot’s athropathy
-Peripheral arterial disease

144
Q

How does diabetic foot disease present?

A
  • Neuropathy
  • Ischaemia
  • Calluses
  • Ulceration
  • Charcot’s foot
  • Cellulitis
  • Osteomyelitis
  • Gangrene
145
Q

What are the most common precipitating factors for DKA?

A
  • Infectino
  • Missed insulin dose
  • MI
146
Q

What are the symptoms of DKA?

A
  • Occurs over a few days
  • Polydypsia
  • Polyuria
  • Dehydration
  • N+V
  • Weakness
  • Abdo pain
  • Visual disturbance
  • Drowsiness/confusion
147
Q

Signs of a DKA?

A
  • Hyperventilation (Kussmaul breathing)
  • Dehydration
  • Hypotension
  • Tachycardia
  • Coma
  • ‘Pear drop breath’
  • Ketouria
  • Hyperglycaemia and ketosis
148
Q

What are the key points for diagnosis of DKA?

A
  • Glucose >11mmo/L or known T1DM
  • pH <7.3
  • Bicarbonate <15mmol/L
  • Ketones >3mol/L or urinary ketones ++
149
Q

How is DKA managed?

A
  • Fluid resuscitation
  • Insulin (0.1units/kg/hour) + 5% dextrose infusion once BM <15
  • Correct hypokalaemia
150
Q

What are the complications of DKA?

A
  • Gastric stasis
  • Thromboembolism
  • Arrhythmias/death due to hyperkalaemia
  • ARDS
  • AKI
  • Iatrogenic: cerebral oedema, hypokalaemia, hypoglycaemia
151
Q

What is hyperosmolar hyperglycaemic state?

A
  • Complications of T2Dm
  • Extremely high BM
  • Can develop insidiously due to illness, infection, dehydration
152
Q

What is the diagnostic criteria for hyperosmolar hyperglycaemic state?

A

-Dehydration (+hypovolaemia)
-Osmolality >320osmol/kg
-Hyperglycaemia >30 with:
>pH 7.3
>Bicarb >15mmol/L
>No ketones in blood or urine

153
Q

Risk factors for HHS?

A
  • Increasing age
  • Nursing home resident
  • Lives alone
  • Dementia
  • Sedative drugs
  • Heat waves
  • Immunosuppressed or steroids
  • Children with long term steroid use +gastroenteritis
154
Q

Symptoms of HHS?

A
  • Frequent urination
  • Thirst
  • Nausea
  • Dry skin
  • Disorientation
  • Sensory disturbance and neuro signs
  • Coma
  • Weakness, leg cramps
  • Visual disturbance
  • *can present like stroke**
155
Q

Causes of HHS?

A
  • Co-existing illness ie stroke, MI, infection, endocrine, AKI
  • Medication induced ie diuretics, metformin, steroids
  • Diabetes related: first presentation, poor control
156
Q

How is HHS investigated?

A
  • BM >30
  • Urinalysis - raised glucose
  • Serum osmolarity >320
  • U&es deranged
  • FBC< CRP
  • Blood cultures
  • ABG
  • CK and trop: Mi and rhabdo
  • ECG and CXR
157
Q

Treatment of HHS?

A
  • ABCDE and fluids
  • Treat underlying cause
  • Safely normalise osmolarity
  • Replace fluids and electrolytes
  • Normalise BM
  • Prevent complications
158
Q

Whast are the microvascular complications of DM?

A
  • Retinopathy
  • Nephropathy
  • Peripheral neuropathy
159
Q

What are the macrovascular complications of DM?

A
  • Ischaemic heart disease
  • Peripheral vascular disease
  • Renal artery stenosis
160
Q

What is the role of the anterior pituitary?

A
  • Production of hormones
  • Lactotroph cells produce prolactin
  • Somatotrophs produce growth hormone
  • Gonadotroph cells produce LH and FSH
  • Corticotrophs produce ACTH
  • Thyrotrophs produce TSH
161
Q

What is the role of the posterior pituitary?

A
  • Receives hormones from the hypothalamus

- Stores hormones and secretes them when they are needed

162
Q

What hormones are released from the posterior pituitary?

A
  • Oxytocin

- Vasopressin

163
Q

What are some diseases that affect the pituitary gland?

A
  • Benign pituitary adenoma
  • Craniopharyngioma
  • Trauma
  • Apoplexy
  • Sarcoidosis, TB
164
Q

How does benign pituitary adenoma present?

A
  • Visual field loss
  • If large, raised ICP and headaches
  • Pituitary dysfunction
165
Q

What is a craniopharyngioma?

A
  • Common childhood tumour which presents with signs of raised ICP and visual field defects
  • Can cause pituitary hormone deficiencies
  • Detected by calcification on CT
166
Q

What are some clinical features that can occur with pituitary tumours?

A
  • Pressure on local structures
  • Pressure on normal pituitary > hypopituitarism
  • Functioning tumour producing hormones
167
Q

Which structures may be compressed by a pituitary tumour?

A
  • Optic nerve: bitemporal hemianopia, headaches from ^ICP

- Cavernous sinus syndrome if expands laterally > CN 3,4,5i, 6 defects

168
Q

What signs may be present if there is pressure on normal pituitary?

A
  • Signs of hormone deficiencies that are usually produced
  • Pale
  • Lack of body and facial hair
  • Central obesity
  • Amenorrhoea
  • Low cortisol
169
Q

What hormones are commonly raised in functioning pituitary tumours?

A
  • Prolactin
  • Growth hormone excess > gigantism in children, acromegaly in adults
  • Cushing’s disease
170
Q

How should a pituitary tumour be investigated?

A
  • MRI pituitary

- Visual field tests

171
Q

What is the most common type of pituitary tumour?

A

-Prolactinoma

172
Q

What are other examples of pituitary tumours?

A
  • Non functioning
  • Growth hormone
  • Cushing’s disease (ACTH)
173
Q

How are pituitary tumours treated?

A

-Trans-sphenoidal surgery

174
Q

How are prolactinomas treated?

A
  • Cabergoline

- Surgery if doesn’t respond to treatment

175
Q

What’s the difference between Cushing’s disease and Cushing’s syndrome?

A

Cushing’s disease is caused by the pituitary tumour and not by exogenous cortisol (syndrome)

176
Q

What are the clinical features of a prolactinoma?

A
  • Galactorrhoea
  • Gynaecomastia
  • Oligomenorrhoea
  • Decreased labido
  • ED
  • Pressure effects: visual fields, ^ICP
177
Q

Investigations for a prolactinoma?

A
  • Prolactin levels
  • Pituitary function tests: GH, prolactin, ACTH, FSH, LH and TFTs
  • MRI pituitary
  • Visual field testing
178
Q

How are prolactinomas treated?

A

-Dopamine agonists

179
Q

What are examples of dopamine agonists?

A
  • Cabergoline

- Bromocriptine

180
Q

What are the symptoms of acromegaly?

A
  • Rings and shoes don’t fit
  • Excruciating headache
  • Increased sweating
  • Arthralgia
  • Amenorrhoea
  • Backache
  • Snoring
181
Q

What are signs of acromegaly?

A
  • Spade like hands, big feet
  • Prognathism (protrusion of the jaw)
  • Coarse facial features
  • Macroglossia
  • Carpal tunnel syndrome
  • Bitemporal hemianopia
182
Q

Investigations for acromegaly?

A
  • Oral glucose tolerance test (gold standard)
  • Serum IGF-1 level
  • Serum GH level
  • Mri pituitary
183
Q

What should happen to glucose levels in someone with acromegaly when given the oral glucose tolerance test?

A

-GH levels should not become suppressed

>in a normal pt, GH levels would become suppressed by the glucose load

184
Q

What are some complications of acromegaly?

A
  • Impaired glucose tolerance
  • Hypertension
  • Cardiac failure
  • Colon cancer
185
Q

Treatment for acromegaly?

A

-Trans-spenoidal surgery to remove the whole adenoma.
-Medical treatments:
>somatostain analogues ie octreotide, lanreotide
>Gh antagonists ie Pegvisomant

186
Q

What are the layers of the adrenal glands?

A 
-Cortex:
>Zona glomerulosa
>Zona fasiculata
>Zona reticularis
-Medulla
187
Q

What does the zona glomerulosa produce?

A

-Mineralocorticoids

188
Q

What does the zona fasiculata produce?

A

-Glucocorticoid

189
Q

What does the zona reticularis produce?

A

-Androgens

190
Q

What generally does the adrenal cortex do?

A
  • Helps control
  • GFR
  • Salt
  • Sugar
  • Sex
191
Q

What does the medulla produce?

A

-Catecholamines

192
Q

What disease is associated with the zona glomerulosa?

A

-Conn’s syndrome

>Hyperaldosteronism

193
Q

What disease is associated with the zona fasiculata?

A

-Cushing’s syndrome

194
Q

What disease is associated with the entire adrenal cortex?

A

-Addison’s disease
>Insufficiency of mineralocorticoids and glucocorticoids
-Congenital adrenal hyperplasia
>21-hydroxylase deficiency causing insufficient mineralocorticoids and glucocorticoids but ^^ testosterone

195
Q

Which diseases are associated with the adrenal medulla?

A

-Phaeochromacytoma

>excess catecholamine

196
Q

What is Cushing’s syndrome?

A

-Too much steroids

197
Q

What are the causes of Cushing’s syndrome?

A

-Exogenous causes - Corticosteroid meds)(most common)
-Endogenous causes:
>Pituitary (Cushing’s disease)
>Adrenal (adenoma or carcinoma)
>Ectopic (small cell lung cancer producing ACTH)

198
Q

What are some symptoms of Cushing’s syndrome?

A
  • Depression
  • Central weight gain
  • Acne
  • Muscle weakness (proximal pattern)
  • Amenorrhoea
  • Easy bruising
  • Thin skin
199
Q

Signs of Cushing’s syndrome?

A
  • ‘Moon face’
  • Acne
  • Hirutism
  • Thin skin
  • Bruising
  • HTN
  • Osteoporosis
  • Pathological fractures
  • Purple striae
  • Proximal myopathy
  • Buffalo hump of fat and central obesity
200
Q

What does it mean by ACTH dependent Cushing’s?

A

-Cushing’s due to increased ACTH production

201
Q

What does it mean by ACTH independent Cushing’s?

A

-Cushing’s due to increased cortisol production

>doesn’t matter what ACTH levels are doing

202
Q

What are the causes of ACTH dependent Cushing’s?

A
  • Pituitary tumour (Cushing’s disease) - secretes ACTH

- Ectopic (Small cell lung cancer) - secretes ACTH

203
Q

What are the causes of Cushing’s that are ACTH independent?

A
  • Adrenal adenoma
  • Adrenal carcinoma
  • *both originate in the adrenal medulla and produce cortisol without any stimulation from ACTH
204
Q

How is Cushing’s investigated?

A
  • Drug history
  • Low dose dexamethasone suppression test > no suppression will occur
  • 24hr urinary free cortisol levels
  • ACTH levels: High in dependent disease, low in independent disease
205
Q

If ACTH is high in someone with suspected Cushing’s, what does this indicate and what should be done next?

A
  • ACTH dependent disease ie piuitary tumour or ectopic
  • High dose dexamethasone suppression test
  • Imaging: MRI pituitary, CT thorax and abdo
206
Q

What will happen when the high dose dexamethasone suppression test is given to someone who’s Cushing’s is caused by a piuitary tumour?

A

-Suppression will occur as the high dose causes the high functioning pituitary to stop through negative feedback

207
Q

What will happen when the high dose dexamethasone suppression test is given to someone who’s Cushing’s is caused by an ectopic?

A

-No suppression as there is no axis for negative feedback. will keep overproducing ACTH

208
Q

If the ACTH level is low in a pt with Cushing’s syndrome, what investigation should be done?

A

-Indicates ACTH independent disease = adrenals!

>CT abdomen

209
Q

How is Cushing’s sndrome treated?

A
  • Exogenous: stop steroids
  • Cushing’s disease: trans-sphenoidal surgery and radiotherapy
  • Adrenal adenoma: adrenalectomy
210
Q

What is Addison’s disease?

A

-Destruction of the adrenal cortex
>deficiency of cortisol and aldosterone
(glucorticoid and mineralocorticoid)

211
Q

What are the causes of Addison’s disease?

A
  • Autoimmune
  • Adrenal mets
  • Infiltration: amyloid, sarcoidosis
  • Infection: TB, fungal
  • Adrenal haemorrhage: anticoagualants
  • Infarction
  • Iatrogenic: surgery, meds
212
Q

What are the risk factors/associations with Addison’s disease?

A 
-Other autoimmune diseases
>Vitilgo
>T1Dm
>Hypothyroidisim
>Hyperthyroidism
213
Q

Clinical features of Addison’s disease?

A

-Non-specific features: thin, tanned, tired, tearful
-Hyperpigmentation
-Fatigue
Lethargy
-Depression
-Anorexia
-Polyuria and polydipsia
-Hypotension
-Nausea and vomiting
-Diarrhoea and constipation

214
Q

Why is someonle likely to be hyperpigmented if they have Addison’s disease?

A

Increased ACTH which reacts with melanin receptors

215
Q

What is the gold standard Ix for Addison’s disease?

A

-Short synacthen test

>synthetic ACTH given but failure to increase cortisol

216
Q

What other investigations would be needed to investigate someone with suspected Addisons?

A
  • U&E: aldosterone deficiency = hyponatraemia and hyperkalaemia
  • Low glucose
  • 21-hydroxylase adrenal autoantibodies
  • Plasma renin increased
  • Plasma aldosterone decreased
  • Abdo XR ?prev. TB
  • Adrenal CT
217
Q

How is Addison’s treated?

A
  • Hydrocortisone
  • Fludrocortisone
  • Steroid card nad medical alert bracelet
  • Sick day rules: increase steroids in febrile ilness, injury, stress
  • Emergency steroid pack: IM hydrocortisone
218
Q

What are the features of an Addisonian crisis?

A
  • Malaise
  • Fatigue
  • Nausea and vomiting
  • Abdo pain
  • Low grade fever
  • Muscle cramps and pain
  • Dehydration
  • Confusion
  • Loss of consciousness and coma
219
Q

What are the causes of an Addisonian crisis?

A
  • Sepsis or surgery causing an acute exacerbation of chronic insufficiency ie Addisons, hypopituitarism
  • Adrenal haemorrhage
  • Steroid withdrawal
220
Q

How is Addisonian crisis managed?

A
  • Hydrocortisone 100mg IM or IV over 30mins-1hr)
  • 1L normal saline (w/ dextrose if hypoglycaemic)
  • Continue hydrocortisone 6hrly until pt stable
221
Q

What are the causes of primary hyperadlodsteronism?

A
  • Bilateral adrenal hyperplasia

- Conn’s syndrome: adrenal adenoma secreting aldosterone

222
Q

What are the features of primary hyperaldosteronism?

A
  • Hypertension (aldosterone cuases Na+ reabsorption)
  • Hypernatraemia
  • Hypokalaemia (aldosterone promotes K+ excretion)
  • Alkalosis (aldosterone promotes H+ excretion)
223
Q

How is hyperaldosteronism investigated?

A

-Aldosterone/renin ratio
>aldosterone high, renin low
-U&E: ^K+, low Na+
-Imaging: HRCT abdo

224
Q

How is hyperadldosteronism managed?

A
  • Adrenal adenoma (Conn’s syndrome): surgical removal

- Bilateral adrenocortical hyperplasia: aldosterone antagonists eg spironolactone

225
Q

What is phaeochromacytoma?

A

-Catecolamine secreting tumour of the sympathetic nervous system (affects the adrenal medulla)

226
Q

What hormones are produced from a phaeochromacytoma?

A
  • Adrenaline
  • Noradrenaline
  • Dopamine
227
Q

What are some phaeochromacytomas associated with?

A

-Multiple endocrine neoplasia type 2

228
Q

What is the rule of 10s for phaeochromacytoma?

A

-10% bilateral
-10% malignant
-10% extra-adrenal
>most common site is the organ of Zuckerland (adjacent to the bifurcation of the aorta)

229
Q

What are the clinical features of phaeochromacytoma?

A

-Can be episodic
-Hypertension
>200 systolic
-Headaches
-Palpitations
-Sweating
-Anxiety
-Nausea
-Weight loss
-Tachycardia
-Pallor

230
Q

What are some differentials for phaeochromacytoma?

A
  • Hyperthyroidism

- Anxiety

231
Q

Investigations for phaeochromacytoma?

A
  • 24hr urinary collection of metanephrines
  • Raised plasma catecolamines
  • CT/MRI for location of tumour
232
Q

Management of phaeochromacytoma?

A
  • Surgery to excise tumour

- Medical management to stabilise pt: alpha blocker followed by beta blocker

233
Q

What are the features of MEN-1?

A

3Ps
>Pituitary adenoma
>Parathyroid hyperplasia
>Pancreatic tumour (insulinoma, gastrinoma)

234
Q

What’s the most common presentation of MEN-1?

A

-Symptoms of Hypercalcaemia

235
Q

What are the features of MEN-2A?

A

2Ps:
>Parathyroid hyperplasia
>Medullary thyroid cancer
>Phaeochromacytoma

236
Q

Which gene is MEN 2 associated with?

A

-RET oncogene

237
Q

What are the features of MEN-2B?

A
  • Mucosal neuromas
  • Marfanoid body habitus
  • Medullary thyroid cancer
  • Phaeochromacytoma
238
Q

Where is ADH produced and secreted?

A

-Synthesised in the hypothalamus and stored in the posterior pituitary

239
Q

When is ADH released?

A
  • When serum osmolality is high.
  • Released to retain more water and dilute plasma
  • When released in high concentrations > causes vasoconstriction
240
Q

What is diabetes insipidus?

A

-Condition characteriesed by either:
>deficiency of antidiuretic hormone
>An insensitivity to ADH

241
Q

What are the causes of cranial diabetes insipidus?

A
  • Idiopathic
  • Posthead injury
  • Pituitary surgery
  • Craniopharyngiomas
  • Histiocytosis X
  • Hypothalamic issues
242
Q

What are the causes of nephrogenic diabetes insipidus?

A
  • Genetic: vasopressin receptor and aquaporin channel gene mutations
  • Electrolytes: hypercalcaeima, hypokalaemia
  • Drugs: lithium
  • Renal disease: obstructions, sickle cell, pyelonephritis, renal tubular acidosis
243
Q

What are the features of diabetes insipidus?

A
  • Polyuria (dilaute urine, >3L/24hrs)
  • Nocturia
  • Compensatory polydipsia
244
Q

What are differentials of diabetes insipidus?

A
  • Hyperglycaemia from diabetes mellitus

- Primary psychogenic polydipsia

245
Q

How is diabetes insipidus investigated?

A

-Urine volume >3L/day
-High plasma osmolality
-Low urine osmolality
(<700)
-Hypernatraemia
-Water deprivation test: continue to pass dilute urine even though dehydrated
-MRI hypothalamus if cranial cause suspected

246
Q

How is diabetes insipidus treated?

A
  • Tumour/TB/Sarcoid - treat
  • Idiopathic and cranial in origin: DESMOPRESSIN
  • Nephrogenic in origin: THIAZIDE DIURETICS
247
Q

How do thiazide diuretics work when treating nephrogenic diabetes insipidus?

A

-Causes increased Sodium excretion whichc breaks polydipsia polyuria cycle

248
Q

What is SIADH?

A
  • Syndrome of inappropriate ADH secretion > too much ADH

- Hyponatraemia secondary to dilutional effecs of excessive water retention

249
Q

Causes of SIADH?

A
  • Cancer: SCLC, pancreas, prostate
  • Neuro: stroke, SAH, subdural haemorrage, meningitis/encephalitis
  • Infectious: TB, pneumonia
  • Drugs: sulofnylureas, SSRIs, TCA, carbamazepine
250
Q

What are the clinical features of SIADH?

A
  • Nausea
  • Irritability
  • Headache
  • Fits and coma (in severe hyponatraemia)
251
Q

Investigations for SIADH?

A
  • Low serum sodium
  • Low plasma osmolality
  • Inappropriately high urine osmolality
  • Continued urinary sodium excretion
252
Q

How is SIADH managed?

A
  • Fluid restriction
  • Demeclocycline
  • Hypertonic saline and furosemid
253
Q

How does demeclocylcine work for a pt with SIADH?

A

-Reduces the responsiveness of collecting tubules to ADH

254
Q

Why must hyponatraemia and SIADH be corrected slowly?

A

-To prevent central pontine myelinolysis

255
Q

What are the main causes of hypocalcaemia?

A
  • Vit D deficiency
  • CKD
  • Hypoparathyroidism
256
Q

Symptoms of hypocalcaemia?

A
  • Increased excitability of muscles and nerves
  • Numbness around mouth and in extremities
  • Cramps and tetany
  • Convulsions and death if left untreated
257
Q

Specific signs of hypocalcaemia?

A
  • Chvostek’s sign
  • Troussau’s sign
  • Papilloedema
  • Long QT on ECG
258
Q

What is Chvostek’s sign?

A

-Tapping of the facial nerve in the parotid region causes the face to twinge in the presence of hypocalcaemia

259
Q

What is Trousseau’s sign?

A

-Carpopedal spasm when a BP cuff is pumped up higher than the systolic BP in the presence of hypocalcaemia

260
Q

How is acute hypocalcaemia treated?

A
  • IV calcium gluconate

- ECG monitoring

261
Q

How is perisistent hypocalcaemia treated?

A
  • Vitamin D deficiency: vit D2/D3

- Hypoparathyroidism: alfacalcidol

262
Q

What are the causes of hypokalaemia with alkalosis?

A
  • Vomiting
  • DIuretics (loop and thiazide)
  • Cushing’s syndrome
  • Pyloric stenosis
  • Conn’s syndrome (hyperaldosteronism)
263
Q

What are the causes of hypokalaemia with acidosis?

A
  • Diarrhoea
  • Renal tubular acidosis
  • Acetazolamide
  • Partially treated DKA
264
Q

Clinical features of hyokalaemia?

A
  • Muscle weakness
  • Hypotonia
  • Hyporeflexia
  • Cramps
  • Tetany
  • Constipation
  • Cardiac arrhythmias
265
Q

Which cardiac medication is dangerous in an episode of hypokleamaia?

A

-Digoxin

266
Q

ECG features of hypokalaemia?

A
  • U waves
  • ST depression
  • Prolonged PR interval
  • Small or absent T waves
267
Q

Treatment for hypokalaemia?

A
  • Mild: oral supplement
  • Severe: IV K+ cautiously
  • Change to K+ sparing diuretic if on thiazide
268
Q

What is the role of parathyroid hormone?

A 
-Raises serum calcium levels to
>increase absorption from the gut
>increase vit D conversion by the kidney
-Incrased resorption from bone
-Increased reabsorption by kidneys
269
Q

What’s the definition of primary hyperparathyroidism?

A
  • Parathyroid gland in origin

- Usually a solitary adenoma

270
Q

What’s the definition of secondary hyperparathyroidism?

A

-Parathyroid gland hyperplasia as a result of chronically low calcium

271
Q

What’s the definition of tertiary hyperparathyroidism?

A

-Hyperplasia of 4 pararthyroid glands, no underlying renlal disorder

272
Q

Describe the typical pt for primary hyperparathyroidism?

A
  • Elderly female
  • Unquenchable thirst
  • Raised PTH levels
273
Q

What would be seen on the hormone profile of someone with primary hyperparathyroidism?

A
  • Raised PTH
  • Raised Calcium
  • Low phosphate
  • Urine calcium: creatinine clearance ration >0.01
274
Q

What imaging findings would you see for someone who has primary hyperparathyroidism>

A

-Pepperpot skull on xray

275
Q

Causes of primary hyperparathyroidism?

A
  • Solitary adenoma (80%)
  • Multifocal disease
  • Parathyroid cancer (<1%)
276
Q

Clinical features of primary hyperparathyroidism?

A

-Symptoms of hypercalcaemia: bones, stones, abdominal groans, psychic moans
-Depression,
hypertension

277
Q

What are some associations with hyperparathyroidism?

A
  • Hypertension

- MEN 1 + 2

278
Q

How is pirmary hyperparathyroidism treated?

A

-Total parathyroidectomy

279
Q

What would the hormone profile be for secondary hyperparathyroidism?

A
  • Raised PTH
  • Low or normal Calcium
  • Raised phosphate
  • Low vitamin D
280
Q

What causes secondary hyperparathyroidism?

A

-Parathyroid gland Hyperplasia due to chronically low calcium

281
Q

Clinical features of hyperparathyroidism?

A
  • Bone disease
  • Ostetitis fibrosa cystical
  • Soft tissue calcifications
282
Q

Hormone profile for tertiary hyperparathyroidism?

A
  • Raised alk phos.
  • Raised PTH
  • Calcium Normal/high
283
Q

Clinical features of tertiary hyperparathyroidism?

A
  • Metastatic calcification
  • Bone pain and/or fractures
  • Nephrolithiasis
  • Pancreatitis
284
Q

How does CKD lead to bone problems?

A
  • Low vit D (due to loss of 1-alpha hydroxylation enzyme function)
  • Phosphate retnetion
  • Low calcium (lack of vit D and high phosphate)
  • Secondary hyperparathyroidism (low calcium, high pho, low vit D - bone breakdown)
285
Q

How is renal bone disease managed?

A

-Phopshate binders (calcium acetate) and vitamin D

286
Q

What are the causes of raised alkaline phosphatase?

A
  • Liver: Cholestasis, hepatitis, fatty liver, neoplasia
  • Pagets
  • Osteomalacia
  • Bone mets
  • Hyperparathyroidism
  • Renal failure
  • Physiological ie pregnancy
287
Q

What causes raised ALP and raised calcium?

A
  • Bone mets

- Hyperparathyroidism

288
Q

What causes raised ALP and low calcium?

A
  • Osteomalacia

- Renal failure

Phase 3B (14 decks)

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