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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
What are the normal glucose levels in a pre-diabetic patient?
``` 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 ```
26
What are the normal glucose levels in a diabetic patient?
``` Random - 11.1 Fasting - 7.0 2h post prandial - 11.1 HbA1c (mmol/mol) - >47 HbA1c (%) >6.4 ```
27
What does HbA1c measure?
Glycosylated glucose
28
How can lifestyle be modified to treat type 2 diabetes?
Diet Weight Control Exercise
29
What is the first line therapy for type 2 diabetes?
Metformin (biguanide)
30
What is considered if HbA1c is still high after using metformin?
``` If HbA1c still high consider dual therapy: Metformin + DPP4 inhibitor Metformin + Pioglitiazone Metformin + sulfonylureas Metformin + SGLT-2i ```
31
What is considered if HbA1c is still high after using dual therapy?
Triple therapy
32
What is considered if HbA1c is still high after using triple therapy?
Insulin
33
How does biguanide (e.g. metformin) work?
Decreased gluconeogenesis in liver and increase cell sensitivity to insulin
34
What are the side effects of biguanide?
``` NOT hypoglycaemia GI disturbances (anorexia, diarrhoea, nausea) ```
35
How does sulfonylureas e.g. gliclazide work?
Promote insulin secretion
36
What are the side effects of sulfonylureas?
Hypoglycaemia | Weight gain
37
Give an example of a biguanide.
Metformin
38
Give an example of a sulfonylureas.
Gliclazide
39
What is hyperosmolar hyperglycaemia characterised by?
- Marked hyperglycaemia - Hyperosmolality - Mild/no ketosis - Uncontrolled T2DM
40
What is the clinical presentation of hyperosmolar hyperglycaemia?
``` Decrease level of consciousness Severe dehydration Hyperglycaemia Hyperosmolality No ketones in blood/urine ```
41
Describe the pathophysiology of hyperosmolar hyperglycaemia.
Decreased insulin levels insufficient to inhibit hepatic glucose production but sufficient to inhibit hepatic ketogenesis
42
How is hyperosmolar hyperglycaemia diagnosed?
Hyperglycaemia >11mmol/l Urine dipstick: heavy glycosuria Plasma osmolality: high
43
How is hyperosmolar hyperglycaemia treated?
Fluid replacement w/ 0.9% saline LMWH e.g. SC enoxaparin to decrease risk of thromboembolism Restore electrolyte loss (K+)
44
What causes Cushing's syndrome?
Chronic excess of cortisol hormone released by the adrenal glands
45
What are the ACTH dependent causes of Cushing's syndrome?
Cushing’s disease (most common) Ectopic ACTH production ACTH treatment
46
What causes Cushing's disease?
Caused by an ACTH secreting pituitary adenoma
47
What does Cushing's disease lead to?
Bilateral adrenal hyperplasia
48
What are the ACTH independent causes of Cushing's syndrome?
Adrenal adenoma | Iatrogenic
49
What is the clinical presentation of Cushing's syndrome?
``` 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) ```
50
How is Cushing's syndrome diagnosed?
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
51
How is Cushing's syndrome treated?
Dependent on cause If cause is: Pituitary adenoma - Transsphenoidal surgical resection Adrenal adenoma - Adrenalectomy
52
What are the complications of Cushing's syndrome?
Cardiovascular disease Hypertension Diabetes mellitus Osteoporosis
53
What is primary adrenal insufficiency?
A disorder that affects the adrenal glands, causing decreased production of adrenocortical hormones
54
What is secondary adrenal insufficiency?
Occurs in patients with pituitary or hypothalamic involvement. This results in decreased ACTH secretion, which ultimately results in adrenal failure.
55
What is primary adrenal insufficiency also known as?
Addison's disease
56
What causes adrenal insufficiency?
In developed countries autoimmune destruction (21-hydroxylase present in 60-90% of people) TB is one of the commonest cause in developing countries.
57
Describe the pathophysiology of adrenal insufficiency.
Destruction of the adrenal cortex results in the decreased production of the hormones
58
What are the risk factors of adrenal insufficiency?
Female sex Adrenocortical antibodies Other autoimmune diseases
59
What is the cumulative risks for patients with positive tests for adrenocortical autoantibodies of developing Addison's disease?
~50%
60
What are the symptoms of adrenal insufficiency?
Fatigue Weakness Weight loss
61
What are the signs of adrenal insufficiency?
Hyperpigmentation – Only in Addison’s Postural hypotension Hypoglycaemia Other signs of autoimmunity may be present (vitiligo, hashimoto’s etc.)
62
How is adrenal insufficiency investigated?
Serum electrolytes: ↓ Sodium ↑ Potassium FBC: Anaemia and eosinophilia Morning serum cortisol: Reduced Adrenal CT or MRI
63
How is adrenal insufficiency managed?
Glucocorticoid + Mineralocorticoid Aim to mimic normal physiological state Treat underlying cause
64
What is Conn's syndrome?
Autonomous aldosterone production that exceeds the body’s requirements and is independent of the renin-angiotensin ll system
65
Explain the pathophysiology of Conn's syndrome.
1. Excess aldosterone 2. Increased sodium reabsorption and potassium excretion in the kidneys 3. Hypertension and potential hypokalaemia
66
What is the clinical presentation of Conn's syndrome?
``` 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 ```
67
How is Conn's syndrome investigated?
Plasma potassium = Low | Aldosterone/renin ratio = High
68
What are the symptoms of Addison's disease?
``` Bronze pigmentation of skin Changes in distribution of body hair GI disturbances Weakness Hypoglycaemia Postural hypotension Weight loss ```
69
What are the symptoms of an adrenal crisis?
``` Profound fatigue Dehydration Vascular collapse (very low BP) Renal shut down Low serum Na High serum K ```
70
How is Conn's syndrome treated?
If the cause is a single benign adrenal tumour - Unilateral adrenalectomy If the cause is due to bilateral adrenal hyperplasia - Aldosterone antagonists (spironolactone)
71
What are the goals of Conn's syndrome treatments?
Lower BP, decrease aldosterone levels and resolve any electrolyte imbalance
72
What is the definition of hypokalaemia?
<3.5mmol/L
73
What are the symptoms of hypokalaemia?
``` Asymptomatic Fatigue Generalised weakness Muscle cramps and pain Palpitations ```
74
What are the signs of hypokalaemia?
Arrhythmias | Muscle paralysis and rhabdomyolysis
75
What causes hypokalaemia?
Increased excretion Reduced intake Shift to intracellular
76
What might cause increased excretion of potassium in hypokalaemia?
Drugs e.g. thiazide, loop Renal disease - diuretics, other drugs, mineralocorticoid excess GI loss - diarrhoea, vomiting, laxative abuse Increased aldosterone
77
What might cause reduced intake of potassium in hypokalaemia?
Dietary deficiency
78
What might cause a shift to intracellular in hypokalaemia?
Drugs e.g. insulin, salbutamol
79
How is hypokalaemia diagnosed?
ECG: Flat T waves, ST depression, Prominent U waves, Prolonged PR Urine osmolality, electrolytes Bloods: FBC, U&E
80
How is hypokalaemia managed?
Potassium PO/IV Other electrolyte replacements Treat underlying cause
81
What is hyperkalaemia
>5.5mmol/L
82
What are the symptoms of hyperkalaemia?
Fatigue Generalised weakness Chest pain Palpitations
83
What are the signs of hyperkalaemia?
Arrhythmias Reduced power Reduced reflexes Signs of underlying cause
84
What might cause impaired excretion of potassium in hyperkalaemia?
AKI and CKD Drug effect Renal tubular acidosis (T4)
85
What causes hyperkalaemia?
Impaired excretion Increased intake Shift to extracellular
86
What might cause increased intake of potassium in hyperkalaemia?
Intravenous therapy | Increased dietary intake
87
What might cause a shift to extracellular in hyperkalaemia?
Metabolic acidosis | Rhabdomyolysis
88
How is hyperkalaemia diagnosed?
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
89
How is hyperkalaemia managed?
ABC assessment Consider cardiac monitoring 1. Protect myocardium: 10ml, 10% calcium gluconate 2. Drive K+ intracellularly: Insulin/Dextrose, Nebulised Salbutamol
90
What is a phaeochromocytoma?
Very rare adrenal medullary tumour that secretes catecholamines
91
What causes phaeochromocytomas?
Phaeochromocytomas occur in certain familial syndromes: Multiple endocrine neoplasia (MEN) syndrome Neurofibromatosis Von-Hippel Lindau Disease
92
What are the symptoms of phaeochromocytomas?
Headache, Profuse Sweating, Palpitations, Tremor etc.
93
What are the signs of phaeochromocytomas?
Hypertension, Postural hypotension, tremor, hypertensive retinopathy, pallor
94
How are phaeochromocytomas investigated?
Plasma metanephrines and normetanephrines 24 hour urinary total catecholamines CT – look for tumour
95
How are phaeochromocytomas treated without HTN crisis?
1st Line: Alpha blockers: phenoxybenzamine | Most patients will eventually get the tumour removed and then managed medically.
96
How are phaeochromocytomas treated with HTN crisis?
1st Line: Antihypertensive agents: phentolamine
97
What is carcinoid syndrome?
Groups of symptoms due to release of serotonin and other vasoactive peptides into the systemic circulation from a carcinoid tumour
98
What are the symptoms of carcinoid syndrome?
Diarrhoea | Flushing
99
What are the signs of carcinoid syndrome?
Palpitations Abdominal cramps Signs of right heart failure Bronchospasm
100
What do carcinoid tumours tend to express?
Somatostatin receptors
101
What organs do carcinoid tumours affect?
Affects lung, bowel, stomach, mets to liver
102
Describe the pathophysiology of primary hyperthyroidism/Grave's disease.
More made or more released | Antibodies binding to TSH receptor, causes more T3/T4 to be made
103
What causes secondary hyperthyroidism?
Nodules, molar pregnancy, iodine overdose, amiodarone, IV contrast, pituitary tumour (secondary)
104
What are the risk factors for hyperthyroidism?
Young/middle aged women, smokers, stress, HLA-DR3
105
What are the symptoms of hyperthyroidism?
Hot and sweaty, diarrhoea, wt. loss, anxiety/restlessness, hyperphagia
106
What are the signs of hyperthyroidism?
Periorbital swelling, goitre, tachycardia
107
How is hyperthyroidism investigated?
Thyroid function tests- high t3/4, low TSH in primary, everything high in secondary cause
108
How is hyperthyroidism managed?
Carbimazole/propylthiouracil - reduce synthesis and T4 conversion. Surgery to remove nodules Radioiodine
109
What are the complications of hyperthyroidism?
Grave’s ophthalmopathy, hypothyroidism, thyroid storm - medical emergency
110
What is primary hyperthyroidism?
Primary hyperthyroidism is the term used when the pathology is within the thyroid gland
111
What is secondary hyperthyroidism?
Secondary hyperthyroidism is the term used when the thyroid gland is stimulated by excessive thyroid-stimulating hormone (TSH) in the circulation
112
How can Hashimoto's cause hypothyroidism?
Antibodies attack the thyroid causing inflammation and dysfunction, lowering T3/T4 levels
113
What causes secondary hypothyroidism?
Damage, Hyperthyroidism treatments, Hypopituitarism
114
What are the risk factors of hypothyroidism?
Other autoimmune diseases, postpartum
115
What are the symptoms of hypothyroidism?
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
What are the signs of hypothyroidism?
Bradycardia, delayed reflexes
117
How is hypothyroidism investigated?
Thyroid function tests- low T3/4 high TSH (1st), everything low (2nd)
118
How is hypothyroidism managed?
Levothyroxine (T4)
119
What are the complications of hypothyroidism?
Heart disease, pregnancy problems, myxoedema coma - medical emergency
120
What is acromegaly?
Too much growth hormone, usually from a pituitary tumour
121
Explain the pathophysiology of acromegaly.
Growth hormone stimulates bone and muscle growth, increased protein synthesis, fat/glycogen breakdown. ILGF-1 drives growth too
122
What are the symptoms of acromegaly?
Large hands, box jaw, thick skin, arthritis, sight problems
123
What are the signs of acromegaly?
Hypertension, insulin resistance, bitemporal hemiopia
124
How is acromegaly investigated?
Insulin like growth factor-1 blood test, ask about changes in ring or shoe size over time
125
How is acromegaly managed?
Tumour surgery Dopamine agonist (cabergoline) Somatostatin analogue (octreotide) GH receptor antagonist (pegvisomant)
126
What are the complications of acromegaly?
Diabetes, sleep apnoea, heart disease
127
Explain the pathophysiology of prolactinoma.
Tumour secretes prolactin which initiates lactation, breast development, controls osmolality, and carbs/fat metabolism
128
What are the symptoms of prolactinoma?
Amenorrhea, galactorrhoea, gynaecomastia, low libido, possible cerebral symptoms
129
What are the signs of prolactinoma?
Low testosterone, infertility
130
How is prolactinoma investigated?
Prolactin levels, CT head
131
How is prolactinoma managed?
Surgery | bromocritipine/cabergoline - dopamine agonists
132
What are the complications of prolactinoma?
Infertility, sight loss, raised intracranial pressure
133
What causes SIADH?
Brain injury, infection, hypothyroidism, cancers, lung diseases
134
Explain the pathophysiology of SIADH.
ADH inappropriately released causing water to be reabsorbed in the collecting duct
135
What are the symptoms of SIADH?
N+V, headache, lethargy, cramps, weakness, confusion
136
What are the signs of SIADH?
Raised JVP, oedema, ascites
137
How is SIADH investigated?
ADH levels | U and Es (low sodium normal potassium), fluid status
138
How is SIADH managed?
Fluid restriction Increase osmolarity Treat underlying cause
139
What are the complications of SIADH?
Cerebral oedema, Seizure and coma, death - a medical emergency
140
What causes nephrogenic diabetes insipidus?
Poor kidney response to vasopressin, lithium
141
What causes neurogenic diabetes insipidus?
Hypothalamus/pituitary injury)
142
Explain the pathophysiology of diabetes insipidus.
Reduced ADH causes excessive water loss
143
What are the symptoms of diabetes insipidus?
Polyuria, polydipsia
144
What are the signs of diabetes insipidus?
Dry mucosa, sunken eyes, changes to skin turgidity
145
How is diabetes insipidus investigated?
Water deprivation test ADH suppression test- shows neurogenic Urine dip, glucose, U and E, fluid status
146
How is diabetes insipidus managed?
Rehydration Desmopressin Thiazide diuretics - bendroflumethiazide
147
What are the complications of diabetes insipidus?
Dehydration, electrolyte imbalance
148
What causes hypocalcaemia?
Hypoparathyroidism, vit D deficiency, hyperventilation, drugs, malignancy, toxic shock
149
What is calcium used in?
Neurotransmission and muscle contraction
150
What are the symptoms of hypocalcaemia?
CATs go numb- Convulsions, arrhythmias, tetany and numbness
151
What are the signs of hypocalcaemia?
Chevostek’s - tapping facial nerve induces spasm, Trousseau’s - BP cuff causes wrist to flex and fingers to draw together
152
How is hypocalcaemia investigated?
Corrected Calcium levels, ECG (prolonged QT) | Parathyroid function
153
How is hypocalcaemia managed?
10ml calcium gluconate/chloride 10% slow IV, oral calcium and Vit D
154
What are the complications of hypocalcaemia?
Seizure, cardiac arrest (decreases heart rate and contractility) - a medical emergency
155
What causes hypercalcaemia?
Hyperparathyroidism, malignancy, sarcoidosis, thyrotoxicosis, drugs
156
What are the symptoms of hypercalcaemia?
Soft weak bones, Abdo pain, N+V, constipation, depression/cognitive impairment
157
What are the signs of hypercalcaemia?
Kidney stones, short QT
158
How is hypercalcaemia investigated?
Corrected calcium levels, ECG | look for cause
159
How is hypercalcaemia managed?
Treat underlying cause increase circulation volume, increase excretion. Bisphosphonates, glucocorticoids, gallium, dialysis
160
What are the complications of hypercalcaemia?
Pancreatitis, confusion, coma, death - a medical emergency
161
What causes primary hyperparathyroidism?
Adenomas, hyperplasia
162
What causes secondary hyperparathyroidism?
Low vit D/CKD
163
What does parathyroid hormone do?
PTH increases calcium through bone resorption, gut absorption, renal reabsorption and activating Vit D
164
What are the risk factors for hyperparathyroidism?
Women, 50-60yo
165
What are the symptoms of hyperparathyroidism?
Bones, stones, groans and psychic moans
166
What are the signs of hyperparathyroidism?
Hypercalcaemia
167
How is hyperparathyroidism investigated?
PTH/bone profile- high PTH, high calcium low phosphates | DEXA, X ray (salt and pepper degradation of bone), ultrasound for stones
168
How is hyperparathyroidism investigated?
Watchful waiting | Surgery to remove the dodgy gland
169
What are the complications of hyperparathyroidism?
Hungry bone - rapid decrease in calcium/phosphate | pancreatitis, kidney stones causing damage, fractures
170
What causes hypoparathyroidism?
Autoimmune, congenital, acquired damage leads to low calcium Other autoimmune diseases
171
What are the symptoms of hypoparathyroidism?
CATs go numb- convulsions, arrhythmias, tetany and numbness
172
What are the signs of hypoparathyroidism?
Hypocalcaemia, Chevostek's and Trousseau's
173
How is hypoparathyroidism investigated?
Bone profile - low calcium normal/high phosphate, low PTH
174
How is hypoparathyroidism managed?
IV calcium | adcald3
175
What are the complications of hypoparathyroidism?
Cardiac arrest - a medical emergency
176
What is a positive Chevostek sign?
Contraction of facial muscle when light tapping of facial nerve in front of the ear
177
What is hypoglycaemia defined as?
Defined as plasma glucose < 3mmol/L
178
What is the cause of hypoglycaemia in diabetics?
Due to insulin or sulphonylurea treatment - commonest cause: | - E.g. with increased activity, missed meal, accidental or non- accidental overdose
179
What causes hypoglycaemia in non-diabetics?
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
How does hypoglycaemia present?
- 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
How is hypoglycaemia diagnosed?
- 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
What causes hypoglycaemic hyperinsulinaemia?
Due to insulinoma, sulfonylurea or insulin injection (no C-peptide in serum) or congenital
183
What causes low insulin but no excess ketones?
Due to non-pancreatic neoplasms or anti-insulin receptor antibodies
184
What causes low insulin and increased ketones?
Alcohol, pituitary insufficiency, Addison’s disease
185
How is hypoglycaemia treated?
- 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
What is Graves' disease?
Autoimmune induced excess production of thyroid hormone
187
What is the most common cause of hyperthyroidism?
Graves' disease
188
Describe the epidemiology of Graves' disease.
- More common in FEMALES than males - Typically presents at 40-60yrs (appear earlier if maternal family history)
189
What are the risk factors of Graves' disease?
- 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
Explain the pathophysiology of Graves' disease.
- 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
How does Graves' disease present?
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
How is Graves' disease investigated?
Eyes are examined via CT/MRI of orbit
193
How is Graves' disease treated?
Conservative treatment includes smoking cessation and sunglasses Treated with IV METHYLPREDNISOLONE and surgical decompression or eyelid surgery
194
What is Hashimoto's thyroiditis?
Form of autoimmune hypothyroidism
195
Who is Hashimoto's thyroiditis commonly seen in?
More common in FEMALES then males | Most common in middle age and commoner in women aged 60-70yrs
196
Explain the pathophysiology of Hashimoto's thyroiditis.
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
How is Hashimoto's thyroiditis treated?
LEVOTHYROXINE THERAPY may shrink the goitre, even when the patient is not hypothyroid
198
What is De Quervain's thyroiditis?
Transient hyperthyroidism sometimes results from acute inflammation of the thyroid gland, probably due to viral infection
199
How is De Quervain's thyroiditis diagnosed?
Typical for there to be globally reduced uptake on technetium thyroid scan
200
What are the symptoms of De Quervain's thyroiditis?
Usually accompanied by fever, malaise and pain in the neck
201
How is De Quervain's thyroiditis treated?
Treat with aspirin and only give prednisolone for severely symptomatic cases
202
Describe the epidemiology of thyroid carcinoma.
- Not common, but are responsible for 400 deaths annually in the UK - More common in FEMALES than males
203
What are the risk factors of thyroid carcinoma?
Radiation
204
What are the different types of thyroid carcinoma?
``` Papillary Follicular Anaplastic Lymphoma Medullary cell ```
205
What percentage of thyroid carcinomas are papillary?
70%
206
Where do papillary thyroid carcinomas arise from?
Thyroid epithelium
207
How do papillary thyroid carcinomas behave?
Well differentiated | Local spread and good prognosis
208
Who are papillary thyroid carcinomas commonly seen in?
Young people
209
What percentage of thyroid carcinomas are follicular?
20%
210
Who are follicular thyroid carcinomas commonly seen in?
Middle age
211
Where do follicular thyroid carcinomas arise from?
Thyroid epithelium
212
How do follicular thyroid carcinomas behave?
Spread to lung/bone, usually good prognosis | Well differentiated
213
What percentage of thyroid carcinomas are anaplastic?
<5%
214
Where do anaplastic thyroid carcinomas arise from?
Thyroid epithelium
215
How do anaplastic thyroid carcinomas behave?
Very undifferentiated Aggressive, local spread but poor prognosis
216
What percentage of thyroid carcinomas are lymphomas?
2%
217
What percentage of thyroid carcinomas are medullary cell?
5%
218
Where do medullary cell thyroid carcinomas arise from?
Calcitonin C cells of thyroid gland
219
Explain the pathophysiology of thyroid carcinomas.
- Minimally active hormonally | - Over 90% secrete thyroglobulin which can be used as a tumour marker after thyroid ablation
220
How do thyroid carcinomas present?
- 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
What is the differential diagnosis of thyroid carcinoma?
Goitre
222
How are thyroid carcinomas diagnosed?
- 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
How is thyroid carcinoma treated?
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
How are papillary and follicular thyroid carcinomas treated?
* Total thyroidectomy | * Ablative radioactive iodine
225
How are anaplastic thyroid carcinomas and lymphomas treated?
* DO NOT respond to radioactive iodine | * External radiotherapy provides brief respite - mainly palliative
226
How are medullary thyroid carcinomas treated?
Thyroidectomy and lymph node removal
227
What is a thyroid crisis/storm?
- MEDICAL EMERGENCY! | - Rare, life threatening condition in which there is a rapid deterioration of thyrotoxicosis (RAPID T4 INCREASE)
228
What are the features of a thyroid crisis?
Hyperpyrexia, tachycardia, extreme restlessness | and eventually delirium, coma and death
229
What causes a thyroid crisis?
Usually precipitated by stress, infection, surgery or radioactive iodine therapy in an unprepared patient
230
How is a thyroid crisis treated?
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
What is tertiary hyperparathyroidism?
Occurs after many years of secondary hyperparathyroidism that occurs from chronic kidney disease or vitamin D deficiency
232
Explain the pathophysiology of tertiary hyperparathyroidism.
Causes glands to act autonomously having undergone hyper plastic or adenomatous change resulting in excess PTH secretion that is unlimited by feedback control
233
When is tertiary hyperparathyroidism commonly seen?
Most often seen in CHRONIC RENAL FAILURE
234
What test results indicate tertiary hyperparathyroidism?
* PTH - High * Ca2+ - High * Phosphate - High * Alkaline phosphatase - High

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