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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the definition of type 1 diabetes mellitus?

A

Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency

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2
Q

Describe the epidemiology of type 1 diabetes mellitus.

A

Usually at ages 5-15

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3
Q

What are the risk factors of type 1 diabetes mellitus?

A 
Northern European
Family History:
- HLA DR3-DQ2 or 
- HLA-DR4-DQ8
Other autoimmune diseases:
- Autoimmune thyroid
- Coeliac disease
- Addison’s disease
- Pernicious anaemia
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4
Q

Describe the pathophysiology of type 1 diabetes mellitus.

A
  1. Autoimmune destruction of beta cells in the Islets of Langerhans by autoantibodies
  2. Insulin deficiency and continued breakdown of liver glycogen
  3. Hyperglycaemia and Glycosuria
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5
Q

What does the absence of insulin in type 1 diabetes cause?

A

Increased hepatic gluconeogenesis and decreased peripheral glucose

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6
Q

What are the signs and symptoms of type 1 diabetes mellitus?

A

Polydipsia
Polyuria
Weight Loss
(Usually short history of severe symptoms)

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7
Q

How is type 1 diabetes mellitus diagnosed?

A

Symptoms/Signs mentioned above
Young
BMI < 25
Personal and/or FHx of autoimmune disease

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8
Q

What is the typical value of random plasma glucose in a patient with type 1 diabetes mellitus?

A

> 11mmol/l

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9
Q

How is type 1 diabetes mellitus treated?

A

INSULIN
Short acting
Short acting insulin analogues
Longer acting insulins

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10
Q

Give some examples of rapid insulins.

A

Lispro, aspart, glulisine

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11
Q

Give some examples of short acting insulins.

A

Regular

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12
Q

Give some examples of short acting insulin analogues (intermediate insulins).

A

NPH

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13
Q

Give some examples of longer acting insulins.

A

Detemir and glargine

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14
Q

What causes diabetic ketoacidosis?

A

Untreated T1DM
Undiagnosed DM
Infection/illness

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15
Q

Explain the pathophysiology of diabetic ketoacidosis.

A
  • Complete absence of insulin > unrestrained increased hepatic gluconeogenesis and decreased peripheral glucose uptake
  • Hyperglycaemia > osmotic diuresis > dehydration
  • Peripheral lipolysis increase FFA > oxidised to Acetyl CoA > ketones
    = ACIDOSIS
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16
Q

What are the symptoms of diabetic ketoacidosis?

A 
Diabetes Symptoms ++
 Nausea and vomiting
 Weight loss
 Drowsy/ Confused
Abdominal Pain
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17
Q

What are the signs of diabetic ketoacidosis?

A 
Reduced tissue turgor
Kussmaul’s breathing
Breath smell of ketones
Hypotension
Tachycardia
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18
Q

How is diabetic ketoacidosis investigated?

A

Hyperglycaemia: Random Plasma Glucose >11mmol/l
Ketonaemia: Plasma ketones > 3mmol/l
Acidosis: Blood pH < 7.35 or Bicarbonate <15mmol/l
Urine dipstick: glycosuria/ketonuria

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19
Q

What are the complications of diabetic ketoacidosis?

A 
Coma
Cerebral oedema
Thromboembolism
Aspiration Pneumonia
DEATH
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20
Q

How is diabetic ketoacidosis managed?

A

ABC
Replace fluid loss with 0.9% saline IV
IV insulin
Restore electrolytes e.g. K+

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21
Q

What is the definition of type 2 diabetes?

A

Combination of peripheral insulin resistance and less severe insulin deficiency

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22
Q

What is the clinical presentation of type 2 diabetes?

A 
Polydipsia
Polyuria
Glycosuria
Central obesity 
Slower onset
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23
Q

What are the risk factors of type 2 diabetes?

A 
Increase w/ age
M > F
Ethnicity: African-Carribean, Black African and South Asian
Obesity
Hypertension
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24
Q

What are the normal glucose levels in a non-diabetic patient?

A 
Random - <11.1
Fasting - <6.1
2h post prandial - <7.8
HbA1c (mmol/mol) - <42
HbA1c (%) <6.0
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25
Q

What are the normal glucose levels in a pre-diabetic patient?

A 
Random - N/A
Fasting - 6.1-6.9
2h post prandial - 7.8-11.0
HbA1c (mmol/mol) - 42-47
HbA1c (%) 6.0-6.4
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26
Q

What are the normal glucose levels in a diabetic patient?

A 
Random - 11.1
Fasting - 7.0
2h post prandial - 11.1
HbA1c (mmol/mol) - >47
HbA1c (%) >6.4
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27
Q

What does HbA1c measure?

A

Glycosylated glucose

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28
Q

How can lifestyle be modified to treat type 2 diabetes?

A

Diet
Weight Control
Exercise

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29
Q

What is the first line therapy for type 2 diabetes?

A

Metformin (biguanide)

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30
Q

What is considered if HbA1c is still high after using metformin?

A 
If HbA1c still high consider dual therapy:
Metformin + DPP4 inhibitor
Metformin + Pioglitiazone
Metformin + sulfonylureas
Metformin + SGLT-2i
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31
Q

What is considered if HbA1c is still high after using dual therapy?

A

Triple therapy

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32
Q

What is considered if HbA1c is still high after using triple therapy?

A

Insulin

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33
Q

How does biguanide (e.g. metformin) work?

A

Decreased gluconeogenesis in liver and increase cell sensitivity to insulin

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34
Q

What are the side effects of biguanide?

A 
NOT hypoglycaemia
GI disturbances (anorexia, diarrhoea, nausea)
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35
Q

How does sulfonylureas e.g. gliclazide work?

A

Promote insulin secretion

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36
Q

What are the side effects of sulfonylureas?

A

Hypoglycaemia

Weight gain

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37
Q

Give an example of a biguanide.

A

Metformin

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38
Q

Give an example of a sulfonylureas.

A

Gliclazide

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39
Q

What is hyperosmolar hyperglycaemia characterised by?

A
  • Marked hyperglycaemia
  • Hyperosmolality
  • Mild/no ketosis
  • Uncontrolled T2DM
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40
Q

What is the clinical presentation of hyperosmolar hyperglycaemia?

A 
Decrease level of consciousness 
Severe dehydration
Hyperglycaemia
Hyperosmolality
No ketones in blood/urine
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41
Q

Describe the pathophysiology of hyperosmolar hyperglycaemia.

A

Decreased insulin levels insufficient to inhibit hepatic glucose production but sufficient to inhibit hepatic ketogenesis

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42
Q

How is hyperosmolar hyperglycaemia diagnosed?

A

Hyperglycaemia >11mmol/l
Urine dipstick: heavy glycosuria
Plasma osmolality: high

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43
Q

How is hyperosmolar hyperglycaemia treated?

A

Fluid replacement w/ 0.9% saline
LMWH e.g. SC enoxaparin to decrease risk of thromboembolism
Restore electrolyte loss (K+)

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44
Q

What causes Cushing’s syndrome?

A

Chronic excess of cortisol hormone released by the adrenal glands

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45
Q

What are the ACTH dependent causes of Cushing’s syndrome?

A

Cushing’s disease (most common)
Ectopic ACTH production
ACTH treatment

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46
Q

What causes Cushing’s disease?

A

Caused by an ACTH secreting pituitary adenoma

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47
Q

What does Cushing’s disease lead to?

A

Bilateral adrenal hyperplasia

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48
Q

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

A

Adrenal adenoma

Iatrogenic

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49
Q

What is the clinical presentation of Cushing’s syndrome?

A 
Central obesity
Plethoric complexion
Moon face
Mood change
Proximal muscle weakness
Purple abdominal striae
Gastric ulcers
Osteoporosis
Hirsutism
Emotional disturbance
Enlarged sella turcica
Cardiac hypertrophy (hypertension)
Buffalo hump
Adrenal tumour or hyperplasia
Thin, wrinkled face
Amenorrhea
Purpura
Skin ulcers (poor wound healing)
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50
Q

How is Cushing’s syndrome diagnosed?

A

Drug history – Cushing’s can be caused by oral steroids so first exclude this

Random plasma cortisol (screening). If high:

Overnight dexamethasone suppression test
+ Urinary free cortisol (24hr). If positive:

Test plasma ACTH

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51
Q

How is Cushing’s syndrome treated?

A

Dependent on cause
If cause is:
Pituitary adenoma - Transsphenoidal surgical resection
Adrenal adenoma - Adrenalectomy

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52
Q

What are the complications of Cushing’s syndrome?

A

Cardiovascular disease
Hypertension
Diabetes mellitus
Osteoporosis

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53
Q

What is primary adrenal insufficiency?

A

A disorder that affects the adrenal glands, causing decreased production of adrenocortical hormones

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54
Q

What is secondary adrenal insufficiency?

A

Occurs in patients with pituitary or hypothalamic involvement. This results in decreased ACTH secretion, which ultimately results in adrenal failure.

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55
Q

What is primary adrenal insufficiency also known as?

A

Addison’s disease

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56
Q

What causes adrenal insufficiency?

A

In developed countries autoimmune destruction (21-hydroxylase present in 60-90% of people)
TB is one of the commonest cause in developing countries.

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57
Q

Describe the pathophysiology of adrenal insufficiency.

A

Destruction of the adrenal cortex results in the decreased production of the hormones

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58
Q

What are the risk factors of adrenal insufficiency?

A

Female sex
Adrenocortical antibodies
Other autoimmune diseases

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59
Q

What is the cumulative risks for patients with positive tests for adrenocortical autoantibodies of developing Addison’s disease?

A

~50%

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60
Q

What are the symptoms of adrenal insufficiency?

A

Fatigue
Weakness
Weight loss

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61
Q

What are the signs of adrenal insufficiency?

A

Hyperpigmentation – Only in Addison’s
Postural hypotension
Hypoglycaemia
Other signs of autoimmunity may be present (vitiligo, hashimoto’s etc.)

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62
Q

How is adrenal insufficiency investigated?

A

Serum electrolytes: ↓ Sodium ↑ Potassium
FBC: Anaemia and eosinophilia
Morning serum cortisol: Reduced
Adrenal CT or MRI

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63
Q

How is adrenal insufficiency managed?

A

Glucocorticoid + Mineralocorticoid
Aim to mimic normal physiological state
Treat underlying cause

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64
Q

What is Conn’s syndrome?

A

Autonomous aldosterone production that exceeds the body’s requirements and is independent of the renin-angiotensin ll system

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65
Q

Explain the pathophysiology of Conn’s syndrome.

A
  1. Excess aldosterone
  2. Increased sodium reabsorption and potassium excretion in the kidneys
  3. Hypertension and potential hypokalaemia
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66
Q

What is the clinical presentation of Conn’s syndrome?

A 
Hypertension (mild to severe)
Nocturia and polyuria
Mood disturbance
Difficulty concentrating
Headache
Fatigue
Low potassium
Muscle cramps
Heart arrhythmia (atrial fibrillation is most common)
Anxiety, depression
Memory loss
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67
Q

How is Conn’s syndrome investigated?

A

Plasma potassium = Low

Aldosterone/renin ratio = High

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68
Q

What are the symptoms of Addison’s disease?

A 
Bronze pigmentation of skin
Changes in distribution of body hair
GI disturbances
Weakness
Hypoglycaemia
Postural hypotension
Weight loss
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69
Q

What are the symptoms of an adrenal crisis?

A 
Profound fatigue
Dehydration
Vascular collapse (very low BP)
Renal shut down
Low serum Na
High serum K
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70
Q

How is Conn’s syndrome treated?

A

If the cause is a single benign adrenal tumour - Unilateral adrenalectomy
If the cause is due to bilateral adrenal hyperplasia - Aldosterone antagonists (spironolactone)

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71
Q

What are the goals of Conn’s syndrome treatments?

A

Lower BP, decrease aldosterone levels and resolve any electrolyte imbalance

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72
Q

What is the definition of hypokalaemia?

A

<3.5mmol/L

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73
Q

What are the symptoms of hypokalaemia?

A 
Asymptomatic
Fatigue
Generalised weakness
Muscle cramps and pain
Palpitations
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74
Q

What are the signs of hypokalaemia?

A

Arrhythmias

Muscle paralysis and rhabdomyolysis

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75
Q

What causes hypokalaemia?

A

Increased excretion
Reduced intake
Shift to intracellular

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76
Q

What might cause increased excretion of potassium in hypokalaemia?

A

Drugs e.g. thiazide, loop
Renal disease - diuretics, other drugs, mineralocorticoid excess
GI loss - diarrhoea, vomiting, laxative abuse
Increased aldosterone

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77
Q

What might cause reduced intake of potassium in hypokalaemia?

A

Dietary deficiency

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78
Q

What might cause a shift to intracellular in hypokalaemia?

A

Drugs e.g. insulin, salbutamol

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79
Q

How is hypokalaemia diagnosed?

A

ECG: Flat T waves, ST depression, Prominent U waves, Prolonged PR
Urine osmolality, electrolytes
Bloods: FBC, U&E

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80
Q

How is hypokalaemia managed?

A

Potassium PO/IV
Other electrolyte replacements
Treat underlying cause

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81
Q

What is hyperkalaemia

A

> 5.5mmol/L

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82
Q

What are the symptoms of hyperkalaemia?

A

Fatigue
Generalised weakness
Chest pain
Palpitations

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83
Q

What are the signs of hyperkalaemia?

A

Arrhythmias
Reduced power
Reduced reflexes
Signs of underlying cause

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84
Q

What might cause impaired excretion of potassium in hyperkalaemia?

A

AKI and CKD
Drug effect
Renal tubular acidosis (T4)

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85
Q

What causes hyperkalaemia?

A

Impaired excretion
Increased intake
Shift to extracellular

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86
Q

What might cause increased intake of potassium in hyperkalaemia?

A

Intravenous therapy

Increased dietary intake

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87
Q

What might cause a shift to extracellular in hyperkalaemia?

A

Metabolic acidosis

Rhabdomyolysis

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88
Q

How is hyperkalaemia diagnosed?

A

ECG: ‘tall tented T waves’, prolonged PR interval (>200ms), widening of the QRS interval (>120ms), small/absent P waves
Urine osmolality, electrolytes
Bloods: FBC, U&E

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89
Q

How is hyperkalaemia managed?

A

ABC assessment
Consider cardiac monitoring
1. Protect myocardium: 10ml, 10% calcium gluconate
2. Drive K+ intracellularly: Insulin/Dextrose, Nebulised Salbutamol

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90
Q

What is a phaeochromocytoma?

A

Very rare adrenal medullary tumour that secretes catecholamines

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91
Q

What causes phaeochromocytomas?

A

Phaeochromocytomas occur in certain familial syndromes:
Multiple endocrine neoplasia (MEN) syndrome
Neurofibromatosis
Von-Hippel Lindau Disease

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92
Q

What are the symptoms of phaeochromocytomas?

A

Headache, Profuse Sweating, Palpitations, Tremor etc.

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93
Q

What are the signs of phaeochromocytomas?

A

Hypertension, Postural hypotension, tremor, hypertensive retinopathy, pallor

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94
Q

How are phaeochromocytomas investigated?

A

Plasma metanephrines and normetanephrines
24 hour urinary total catecholamines
CT – look for tumour

95
Q

How are phaeochromocytomas treated without HTN crisis?

A

1st Line: Alpha blockers: phenoxybenzamine

Most patients will eventually get the tumour removed and then managed medically.

96
Q

How are phaeochromocytomas treated with HTN crisis?

A

1st Line: Antihypertensive agents: phentolamine

97
Q

What is carcinoid syndrome?

A

Groups of symptoms due to release of serotonin and other vasoactive peptides into the systemic circulation from a carcinoid tumour

98
Q

What are the symptoms of carcinoid syndrome?

A

Diarrhoea

Flushing

99
Q

What are the signs of carcinoid syndrome?

A

Palpitations
Abdominal cramps
Signs of right heart failure
Bronchospasm

100
Q

What do carcinoid tumours tend to express?

A

Somatostatin receptors

101
Q

What organs do carcinoid tumours affect?

A

Affects lung, bowel, stomach, mets to liver

102
Q

Describe the pathophysiology of primary hyperthyroidism/Grave’s disease.

A

More made or more released

Antibodies binding to TSH receptor, causes more T3/T4 to be made

103
Q

What causes secondary hyperthyroidism?

A

Nodules, molar pregnancy, iodine overdose, amiodarone, IV contrast, pituitary tumour (secondary)

104
Q

What are the risk factors for hyperthyroidism?

A

Young/middle aged women, smokers, stress, HLA-DR3

105
Q

What are the symptoms of hyperthyroidism?

A

Hot and sweaty, diarrhoea, wt. loss, anxiety/restlessness, hyperphagia

106
Q

What are the signs of hyperthyroidism?

A

Periorbital swelling, goitre, tachycardia

107
Q

How is hyperthyroidism investigated?

A

Thyroid function tests- high t3/4, low TSH in primary, everything high in secondary cause

108
Q

How is hyperthyroidism managed?

A

Carbimazole/propylthiouracil - reduce synthesis and T4 conversion.
Surgery to remove nodules
Radioiodine

109
Q

What are the complications of hyperthyroidism?

A

Grave’s ophthalmopathy, hypothyroidism, thyroid storm - medical emergency

110
Q

What is primary hyperthyroidism?

A

Primary hyperthyroidism is the term used when the pathology is within the thyroid gland

111
Q

What is secondary hyperthyroidism?

A

Secondary hyperthyroidism is the term used when the thyroid gland is stimulated by excessive thyroid-stimulating hormone (TSH) in the circulation

112
Q

How can Hashimoto’s cause hypothyroidism?

A

Antibodies attack the thyroid causing inflammation and dysfunction, lowering T3/T4 levels

113
Q

What causes secondary hypothyroidism?

A

Damage, Hyperthyroidism treatments, Hypopituitarism

114
Q

What are the risk factors of hypothyroidism?

A

Other autoimmune diseases, postpartum

115
Q

What are the symptoms of hypothyroidism?

A

Wt. gain, depression, constipation, cold intolerance, “brain fog”

Hair loss
Apathy
Lethargy
Dry skin (coarse and scaly)
Muscle aches and weakness
Receding hairline
Facial and eyelid oedema
Extreme fatigue
Thick tongue - slow speech
Anorexia
Brittle hair and nails
Menstrual disturbances
116
Q

What are the signs of hypothyroidism?

A

Bradycardia, delayed reflexes

117
Q

How is hypothyroidism investigated?

A

Thyroid function tests- low T3/4 high TSH (1st), everything low (2nd)

118
Q

How is hypothyroidism managed?

A

Levothyroxine (T4)

119
Q

What are the complications of hypothyroidism?

A

Heart disease, pregnancy problems, myxoedema coma - medical emergency

120
Q

What is acromegaly?

A

Too much growth hormone, usually from a pituitary tumour

121
Q

Explain the pathophysiology of acromegaly.

A

Growth hormone stimulates bone and muscle growth, increased protein synthesis, fat/glycogen breakdown. ILGF-1 drives growth too

122
Q

What are the symptoms of acromegaly?

A

Large hands, box jaw, thick skin, arthritis, sight problems

123
Q

What are the signs of acromegaly?

A

Hypertension, insulin resistance, bitemporal hemiopia

124
Q

How is acromegaly investigated?

A

Insulin like growth factor-1 blood test, ask about changes in ring or shoe size over time

125
Q

How is acromegaly managed?

A

Tumour surgery
Dopamine agonist (cabergoline)
Somatostatin analogue (octreotide)
GH receptor antagonist (pegvisomant)

126
Q

What are the complications of acromegaly?

A

Diabetes, sleep apnoea, heart disease

127
Q

Explain the pathophysiology of prolactinoma.

A

Tumour secretes prolactin which initiates lactation, breast development, controls osmolality, and carbs/fat metabolism

128
Q

What are the symptoms of prolactinoma?

A

Amenorrhea, galactorrhoea, gynaecomastia, low libido, possible cerebral symptoms

129
Q

What are the signs of prolactinoma?

A

Low testosterone, infertility

130
Q

How is prolactinoma investigated?

A

Prolactin levels, CT head

131
Q

How is prolactinoma managed?

A

Surgery

bromocritipine/cabergoline - dopamine agonists

132
Q

What are the complications of prolactinoma?

A

Infertility, sight loss, raised intracranial pressure

133
Q

What causes SIADH?

A

Brain injury, infection, hypothyroidism, cancers, lung diseases

134
Q

Explain the pathophysiology of SIADH.

A

ADH inappropriately released causing water to be reabsorbed in the collecting duct

135
Q

What are the symptoms of SIADH?

A

N+V, headache, lethargy, cramps, weakness, confusion

136
Q

What are the signs of SIADH?

A

Raised JVP, oedema, ascites

137
Q

How is SIADH investigated?

A

ADH levels

U and Es (low sodium normal potassium), fluid status

138
Q

How is SIADH managed?

A

Fluid restriction
Increase osmolarity
Treat underlying cause

139
Q

What are the complications of SIADH?

A

Cerebral oedema, Seizure and coma, death - a medical emergency

140
Q

What causes nephrogenic diabetes insipidus?

A

Poor kidney response to vasopressin, lithium

141
Q

What causes neurogenic diabetes insipidus?

A

Hypothalamus/pituitary injury)

142
Q

Explain the pathophysiology of diabetes insipidus.

A

Reduced ADH causes excessive water loss

143
Q

What are the symptoms of diabetes insipidus?

A

Polyuria, polydipsia

144
Q

What are the signs of diabetes insipidus?

A

Dry mucosa, sunken eyes, changes to skin turgidity

145
Q

How is diabetes insipidus investigated?

A

Water deprivation test
ADH suppression test- shows neurogenic
Urine dip, glucose, U and E, fluid status

146
Q

How is diabetes insipidus managed?

A

Rehydration
Desmopressin
Thiazide diuretics - bendroflumethiazide

147
Q

What are the complications of diabetes insipidus?

A

Dehydration, electrolyte imbalance

148
Q

What causes hypocalcaemia?

A

Hypoparathyroidism, vit D deficiency, hyperventilation, drugs, malignancy, toxic shock

149
Q

What is calcium used in?

A

Neurotransmission and muscle contraction

150
Q

What are the symptoms of hypocalcaemia?

A

CATs go numb- Convulsions, arrhythmias, tetany and numbness

151
Q

What are the signs of hypocalcaemia?

A

Chevostek’s - tapping facial nerve induces spasm, Trousseau’s - BP cuff causes wrist to flex and fingers to draw together

152
Q

How is hypocalcaemia investigated?

A

Corrected Calcium levels, ECG (prolonged QT)

Parathyroid function

153
Q

How is hypocalcaemia managed?

A

10ml calcium gluconate/chloride 10% slow IV, oral calcium and Vit D

154
Q

What are the complications of hypocalcaemia?

A

Seizure, cardiac arrest (decreases heart rate and contractility) - a medical emergency

155
Q

What causes hypercalcaemia?

A

Hyperparathyroidism, malignancy, sarcoidosis, thyrotoxicosis, drugs

156
Q

What are the symptoms of hypercalcaemia?

A

Soft weak bones, Abdo pain, N+V, constipation, depression/cognitive impairment

157
Q

What are the signs of hypercalcaemia?

A

Kidney stones, short QT

158
Q

How is hypercalcaemia investigated?

A

Corrected calcium levels, ECG

look for cause

159
Q

How is hypercalcaemia managed?

A

Treat underlying cause
increase circulation volume, increase excretion.
Bisphosphonates, glucocorticoids, gallium, dialysis

160
Q

What are the complications of hypercalcaemia?

A

Pancreatitis, confusion, coma, death - a medical emergency

161
Q

What causes primary hyperparathyroidism?

A

Adenomas, hyperplasia

162
Q

What causes secondary hyperparathyroidism?

A

Low vit D/CKD

163
Q

What does parathyroid hormone do?

A

PTH increases calcium through bone resorption, gut absorption, renal reabsorption and activating Vit D

164
Q

What are the risk factors for hyperparathyroidism?

A

Women, 50-60yo

165
Q

What are the symptoms of hyperparathyroidism?

A

Bones, stones, groans and psychic moans

166
Q

What are the signs of hyperparathyroidism?

A

Hypercalcaemia

167
Q

How is hyperparathyroidism investigated?

A

PTH/bone profile- high PTH, high calcium low phosphates

DEXA, X ray (salt and pepper degradation of bone), ultrasound for stones

168
Q

How is hyperparathyroidism investigated?

A

Watchful waiting

Surgery to remove the dodgy gland

169
Q

What are the complications of hyperparathyroidism?

A

Hungry bone - rapid decrease in calcium/phosphate

pancreatitis, kidney stones causing damage, fractures

170
Q

What causes hypoparathyroidism?

A

Autoimmune, congenital, acquired damage leads to low calcium

Other autoimmune diseases

171
Q

What are the symptoms of hypoparathyroidism?

A

CATs go numb- convulsions, arrhythmias, tetany and numbness

172
Q

What are the signs of hypoparathyroidism?

A

Hypocalcaemia, Chevostek’s and Trousseau’s

173
Q

How is hypoparathyroidism investigated?

A

Bone profile - low calcium normal/high phosphate, low PTH

174
Q

How is hypoparathyroidism managed?

A

IV calcium

adcald3

175
Q

What are the complications of hypoparathyroidism?

A

Cardiac arrest - a medical emergency

176
Q

What is a positive Chevostek sign?

A

Contraction of facial muscle when light tapping of facial nerve in front of the ear

177
Q

What is hypoglycaemia defined as?

A

Defined as plasma glucose < 3mmol/L

178
Q

What is the cause of hypoglycaemia in diabetics?

A

Due to insulin or sulphonylurea treatment - commonest cause:

- E.g. with increased activity, missed meal, accidental or non- accidental overdose

179
Q

What causes hypoglycaemia in non-diabetics?

A

Ex -Exogenous drugs - insulin, oral hypoglycaemic, alcohol binge with no food
P - Pituitary insufficiency
L - Liver failure
A - Addison’s disease
I - Islets cell tumour (insulinoma) & immune hypoglycaemia
N - Non-pancreatic neoplasm e.g. fibrosarcomas and haemangiopericytomas

EXPLAIN

180
Q

How does hypoglycaemia present?

A
  • Autonomic:
    • Sweating, anxiety, hunger, tremor, palpitations, dizziness -
  • Neuroglycopenic:
    • Confusion, drowsiness, visual trouble, seizures, coma
    • Rarely there are focal symptoms such as transient hemiplegia, mutism,
    personality change, restlessness and incoherence
181
Q

How is hypoglycaemia diagnosed?

A
  • Fingerpick blood during attack (on filter-paper at home) - and then can be sent for analysis
  • Take drug history and exclude liver failure
  • Bloods - glucose, insuline, C-peptide, plasma ketones
182
Q

What causes hypoglycaemic hyperinsulinaemia?

A

Due to insulinoma, sulfonylurea or insulin injection (no C-peptide in serum) or congenital

183
Q

What causes low insulin but no excess ketones?

A

Due to non-pancreatic neoplasms or anti-insulin receptor antibodies

184
Q

What causes low insulin and increased ketones?

A

Alcohol, pituitary insufficiency, Addison’s disease

185
Q

How is hypoglycaemia treated?

A
  • If cannot swallow then give 50% GLUCOSE IV
  • Or IM GLUCAGON if no IV access
  • If episodes are often then advise many small high-starch meals - In diabetics re-educate on insulin use and safety!!
186
Q

What is Graves’ disease?

A

Autoimmune induced excess production of thyroid hormone

187
Q

What is the most common cause of hyperthyroidism?

A

Graves’ disease

188
Q

Describe the epidemiology of Graves’ disease.

A
  • More common in FEMALES than males
  • Typically presents at 40-60yrs (appear earlier if maternal family
    history)
189
Q

What are the risk factors of Graves’ disease?

A
  • FEMALE - biggest risk factor (onset is common postpartum)
  • Genetic - association with HLA-B8, DR3 & DR2
  • E.coli and other gram-NEGATIVE organisms
  • Smoking
  • Stress
  • High iodine intake
  • Autoimmune disease:
    • Vitiligo (pale white patches on skin)
    • Addison’s disease
    • Pernicious anaemia
    • Myasthenia gravis
    • Type 1 DM
190
Q

Explain the pathophysiology of Graves’ disease.

A
  • Serum IgG antibodies, specific for Graves’ disease, known as TSH receptor stimulating antibodies (TSHR-Ab) bind to TSH receptors in the thyroid
  • Thereby stimulating thyroid hormone production (T3 & T4) - essentially they behave like TSH
  • Resulting in excess secretion of thyroid hormones and hyperplasia of thyroid follicular cells resulting in hyperthyroidism and diffuse goitre
  • Persistent high levels predict a relapse when drug treatment is stopped
  • Similar auto antigen can also result in retro-orbital inflammation - graves opthalmopathy
191
Q

How does Graves’ disease present?

A

Graves’ opthalmopathy - Eye discomfort, grittiness, increased tear production, photophobia, diplopia, reduced acuity

Exophthalmos - appearance of protruding eye and proptosis - eye protrudes beyond orbit

Pretibial myxoedema - raised, purple-red symmetrical skin lesions over the anterolateral aspects of the shin

Thyroid acropachy - clubbing, swollen fingers and periosteal bone formation

192
Q

How is Graves’ disease investigated?

A

Eyes are examined via CT/MRI of orbit

193
Q

How is Graves’ disease treated?

A

Conservative treatment includes smoking cessation and sunglasses
Treated with IV METHYLPREDNISOLONE and surgical decompression or eyelid surgery

194
Q

What is Hashimoto’s thyroiditis?

A

Form of autoimmune hypothyroidism

195
Q

Who is Hashimoto’s thyroiditis commonly seen in?

A

More common in FEMALES then males

Most common in middle age and commoner in women aged 60-70yrs

196
Q

Explain the pathophysiology of Hashimoto’s thyroiditis.

A

Produces atrophic changes with regeneration that results in GOITRE FORMATION due to lymphocytic and plasma cell infiltration
Gland is usually firm and rubbery but may range from soft to hard Thyroid peroxidase is an enzyme essential for the production and storage of thyroid hormone
Thyroid peroxidase antibodies (TPO-Ab) are present in HIGH TITRES Patients may be hypothyroid or euthyroid (normal thyroid function)

197
Q

How is Hashimoto’s thyroiditis treated?

A

LEVOTHYROXINE THERAPY may shrink the goitre, even when the patient is not hypothyroid

198
Q

What is De Quervain’s thyroiditis?

A

Transient hyperthyroidism sometimes results from acute inflammation of the thyroid gland, probably due to viral infection

199
Q

How is De Quervain’s thyroiditis diagnosed?

A

Typical for there to be globally reduced uptake on technetium thyroid
scan

200
Q

What are the symptoms of De Quervain’s thyroiditis?

A

Usually accompanied by fever, malaise and pain in the neck

201
Q

How is De Quervain’s thyroiditis treated?

A

Treat with aspirin and only give prednisolone for severely symptomatic cases

202
Q

Describe the epidemiology of thyroid carcinoma.

A
  • Not common, but are responsible for 400 deaths annually in the UK
  • More common in FEMALES than males
203
Q

What are the risk factors of thyroid carcinoma?

A

Radiation

204
Q

What are the different types of thyroid carcinoma?

A 
Papillary
Follicular
Anaplastic
Lymphoma
Medullary cell
205
Q

What percentage of thyroid carcinomas are papillary?

A

70%

206
Q

Where do papillary thyroid carcinomas arise from?

A

Thyroid epithelium

207
Q

How do papillary thyroid carcinomas behave?

A

Well differentiated

Local spread and good prognosis

208
Q

Who are papillary thyroid carcinomas commonly seen in?

A

Young people

209
Q

What percentage of thyroid carcinomas are follicular?

A

20%

210
Q

Who are follicular thyroid carcinomas commonly seen in?

A

Middle age

211
Q

Where do follicular thyroid carcinomas arise from?

A

Thyroid epithelium

212
Q

How do follicular thyroid carcinomas behave?

A

Spread to lung/bone, usually good prognosis

Well differentiated

213
Q

What percentage of thyroid carcinomas are anaplastic?

A

<5%

214
Q

Where do anaplastic thyroid carcinomas arise from?

A

Thyroid epithelium

215
Q

How do anaplastic thyroid carcinomas behave?

A

Very undifferentiated Aggressive, local spread but poor prognosis

216
Q

What percentage of thyroid carcinomas are lymphomas?

A

2%

217
Q

What percentage of thyroid carcinomas are medullary cell?

A

5%

218
Q

Where do medullary cell thyroid carcinomas arise from?

A

Calcitonin C cells of thyroid gland

219
Q

Explain the pathophysiology of thyroid carcinomas.

A
  • Minimally active hormonally

- Over 90% secrete thyroglobulin which can be used as a tumour marker after thyroid ablation

220
Q

How do thyroid carcinomas present?

A
  • In 90% they present as thyroid nodules
  • Occasionally (5%) they present with cervical lymphadenopathy or with lung,
    cerebral, hepatic or bone metastases
  • If thyroid gland increases in size, becomes hard and is irregular in shape -
    think carcinoma
  • Patients may complain of dysphagia or hoarseness of voice due to tumour compression on surrounding structures i.e. oesophagus and laryngeal nerve
221
Q

What is the differential diagnosis of thyroid carcinoma?

A

Goitre

222
Q

How are thyroid carcinomas diagnosed?

A
  • Fine needle aspiration cytology biopsy:
    • To distinguish between benign or malignant nodules - Blood test - to check TFTs (TSH, T4 & T3):
    • To check if hyperthyroid or hypothyroid - needs to be treated before carcinoma surgery
  • Ultrasound of thyroid:
    • Can differentiate between benign or malignant
223
Q

How is thyroid carcinoma treated?

A

Thyroid LOVES iodine so will readily take up radioactive iodine which in turn will locally irradiate and destroy cancer - providing very little radiation damage to other surrounding structures
Administer lots of LEVOTHYROXINE (T4) to keep TSH reduced as this is a growth factor for the cancer!
Chemotherapy helps to reduce risk of spread and treats micro-metastases that have been undetected

224
Q

How are papillary and follicular thyroid carcinomas treated?

A
  • Total thyroidectomy

* Ablative radioactive iodine

225
Q

How are anaplastic thyroid carcinomas and lymphomas treated?

A
  • DO NOT respond to radioactive iodine

* External radiotherapy provides brief respite - mainly palliative

226
Q

How are medullary thyroid carcinomas treated?

A

Thyroidectomy and lymph node removal

227
Q

What is a thyroid crisis/storm?

A
  • MEDICAL EMERGENCY!

- Rare, life threatening condition in which there is a rapid deterioration of thyrotoxicosis (RAPID T4 INCREASE)

228
Q

What are the features of a thyroid crisis?

A

Hyperpyrexia, tachycardia, extreme restlessness

and eventually delirium, coma and death

229
Q

What causes a thyroid crisis?

A

Usually precipitated by stress, infection, surgery or radioactive iodine therapy in an unprepared patient

230
Q

How is a thyroid crisis treated?

A

Treated with LARGE DOSES of:

  • ORAL CARBIMAZOLE
  • ORAL PROPRANOLOL
  • ORAL POTASSIUM IODIDE (to block acutely the release of thyroid hormone from gland)
  • IV HYDROCORTISONE (to inhibits peripheral conversion of T4 to T3)
231
Q

What is tertiary hyperparathyroidism?

A

Occurs after many years of secondary hyperparathyroidism that occurs from chronic kidney disease or vitamin D deficiency

232
Q

Explain the pathophysiology of tertiary hyperparathyroidism.

A

Causes glands to act autonomously having undergone hyper plastic or adenomatous change resulting in excess PTH secretion that is unlimited by feedback control

233
Q

When is tertiary hyperparathyroidism commonly seen?

A

Most often seen in CHRONIC RENAL FAILURE

234
Q

What test results indicate tertiary hyperparathyroidism?

A
  • PTH - High
  • Ca2+ - High
  • Phosphate - High
  • Alkaline phosphatase - High

Phase 2a (25 decks)

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