1
Q
Commonest cause of a diffuse Goitre
A
Grave’s Disease
2
Q
Plummer’s Disease
A
Single toxic nodule (adenoma) which is present on a background of a suppressed multinodular goitre
3
Q
De Querviains Thyroiditis Tx
A
- NSAIDS
- Corticosteroids
4
Q
Hashimoto’s antibodies
A
antibodies against thyroid peroxidase
Large firm swelling
5
Q
Drugs Causing Hypothyroidism
A
Lithium
Iodine
Amiodarone
6
Q
Most common Thyroid Cancer
A
Papillary Carcinoma (80%)
7
Q
Things to look for in Papillary Carcinomas
A
RF = radiation exposure, Young people Excellent prognosis Papillary pattern Calcified rings = Psamomma bodies Clear nuclei = ‘Orphan Annie Eye nuclei’
8
Q
Calcified rings = Psamomma bodies
Clear nuclei = ‘Orphan Annie Eye nuclei’
A
Papillary Carcinoma
9
Q
3 Facts about follicular thyroid carcinoma
A
Tend to metastasize to lung and bone
Presentation with Hurthle cells
Middle age
10
Q
Hurthle cells
A
Follicular Thyroid Carcinoma
11
Q
Medullary Thyroid Carcinoma
A
Familial pattern of inheritances
Associated with MEN 2A
Arises from parafollicular cells – C Cells
Increased secretion of calcitonin
12
Q
MEN2A
A
Parathyroid hyperplasia
Medullary Thyroid carcinoma
Pheochromocytoma
13
Q
MEN1
A
Pituitary adenoma
Parathyroid Hyperplasia
Pancreatic tumors
14
Q
MEN2B
A
Mucosal Neuromas
Marfanoid body habits
Medullary Thyroid Cancer
Phaeochromocytoma
15
Q
Oral Glucose Tolerance Test
A
2 Hours after an oral load of 75g glucose Diagnostic cut off is >11.1 mmol/L Impaired OGTT : Fasting plasma glucose is < 7.0 mmol/L With OGTT of 7.8 – 11.0 mmol/L
16
Q
HbA1c Cut off
A
Diagnostic is >48 mmol/mol (6.5%)
Remember two values
6% = 42 mmol/mol
7% = 53 mmol/mol
Addition of 11 mmol/mol
17
Q
DKA management rational
A
Progression to a point where there is an impairment of normal function
Hyperglycaemia
Acidotic
Hyperglycaemia leads to an osmotic diuresis
This can potentiate dehydration
Acidity may cause vomiting, diarrhoea which worsens dehydration
Treat dehydration and glucose level
Dehydration provides greatest risk so treat this with fluid management
18
Q
Sulphonylurea
A
Mechanism of action relates to increased secretion of insulin
Glibenclamide
Chlorpropamide
Tolbutamide
Often in those with uncontrolled Type 2 diabetes who are NOT obese
19
Q
Alpha Glucosidase Inhibitors
A
Acarbose
Act as competitive inhibitors to that digest carbohydrates
Prevent digestion of carbohydrates such as starch or sugar
Reduce amount of glucose entering blood
Particular use in:
Those not tolerating other medication
Those suffering with post-prandial hyperglycaemia
20
Q
Hypoglycaemia management
Group 1 – Adults who are conscious and orientated
A
- Give 15-20g of Quick Acting Carbohydrate such as Fruit Juice, Lucozade or sugar in water
- Repeat Capillary Blood Glucose and repeat until it reaches 4.0mmol/L or more
- If remains below 4mmol/L – Get Help! Consider 1mg Glucagon IM or IV 10% Glucose at 100ml/Hr
- Once above 4.0mmmol/L give a long acting Carbohydrate such as biscuits, slice of toast or 200-300mL milk
21
Q
Hypoglycaemia management
Group 2- Adults who are Conscious but confused, disorientated, unable to cooperate, aggressive but able to swallow
A
- If possible, follow Group 1
- If uncooperative but able to swallow give 1.5 – 2 tubes of glucogel squeezed onto the gums
- If unable to do this consider 1mg Glucogon IM
- If does not raise CBG to 4mmol/L consider IV 10% Glucose infusion at 100ml/hr and call for help
- Once above 4.0mmol/L give a long acting carbohydrate
22
Q
Hypoglycaemia management
Group 3 - Adults who are unconscious or experiencing seizures
A
- Must take an ABC approach first
- Stop any current insulin infusion
- Consider 1 of the following 3 based on local guidelines
1mg Glucagon IM
75-80mL 20% Glucose IV over 10-15mins
150-160 10% Glucose IV - Raise CBG to over 4.0mmol/L and regaining consciousness give a long acting carbohydrate meal
23
Q
What does calcitonin do?
A
Reduces Ca levels by opposing the effects of PTH
24
Q
Cushing’s Causes
A
- ACTH dependent (raised ACTH)
Cushing’s disease – pituitary adenoma secreting ACTH
Ectopic ACTH production – eg. small cell lung cancer - ACTH independent (suppressed ACTH)
Iatrogenic (most common) – pharmacological doses of steroids
Adrenal adenoma/cancer – secreting cortisol
25
BP and electrolyte changes in Cushing's
Hypertension (80%) and hypokalaemia
26
Cushing's Tx
Conservative
Iatrogenic: decrease steroid dose
Surgical
Cushing’s disease: remove tumour trans-sphenoidally
Ectopic ACTH production: removal of tumour or bilateral adrenalectomy if spread
Adrenal adenoma: unilateral adrenalectomy
Radiotherapy
If tumour can’t be removed eg. adrenal carcinoma
Pre-op to reduce size
Pharmacologically
Inhibit cortisol synthesis (ketoconazole)
27
Drug that decreases cortisol synthesis
ketoconazole
28
What is Conn's syndrome
Primary hyperaldosteronism is excess production of aldosterone, causing increased potassium excretion, increased sodium and water retention, and decreased renin release.
If caused by aldosterone-producing adenoma = Conn’s syndrome
29
Causes of primary hyperaldosteronism
1. Conn's syndrome
| 2. Bilateral adrenal hyperplasia
30
Conn's signs and symptoms
```
Symptoms: Asymptomatic?
Oedema
Signs of hypokalaemia
Weakness
Cramping
Paraesthesia
Polyuria/polydipsia
```
Signs
Hypertension
Hypokalaemia or alkalosis
Hypernatraemia (can be normal)
31
Conn's Tx
1. Medical
Spironolactone for 4 weeks pre-op to control BP and K
Androgen receptor antagonist and a K-sparing diuretic
Side effects: gynaecomastia, menstrual disturbances
2. Surgical
Laparascopic adrenalectomy
32
Phaeo symptom triad
Triad of PHEochromocytoma
Palpitations (episodic tachycardia)
Headache
Episodic sweating (diaphoresis)
33
Phaeo Tx
Management
Hypertensive crisis: α and β blockade (α first), such as short-acting IV α-blocker PHENTOLAMINE
Long-term
α -blockade eg. PHENOXYBENZAMINEP
β –blockade eg. Propanolol
Surgery
34
Hypoadrenal Diseases
1. Addison's
| 2. Congenital adrenal hyperplasia
35
Addisons definition and causes
Primary adrenocortical insufficiency: destruction of the adrenal cortex leading to glucocorticoid and mineralocorticoid deficiency.
Causes
Autoimmune (80% in UK)
TB (most common worldwide)
Iatrogenic (damage)
36
Addiosonian Crises Px
```
Vomiting
Abdominal pain
Weakness
Hypoglycaemia
Hypovolaemic shock
```
37
Addisons Tx
Management
Rehydration
Replace glucocorticoid: hydrocortisone (need more in infection/stress)
Replace mineralocorticoid: fludrocortisone
38
Causes of hyperprolactinaemia
physiological (pregnancy), drugs (eg. Metoclopramide) and due to disease (prolactinoma)
39
Cushing's Ix
1. 9am and 12 midnight cortisol levels
2. Low dose dexamethasone suppression test:
0.5mg dexamethasone every 6 hours for 48 hours
Cannot distinguish between different causes
3. High dose dexamethasone test:
2.0mg dexamethasone every 6 hours for 48 hours
Distinguishes between Cushing’s disease and other causes
4. 24 hour urine collection for urinary free cortisol (will be raised in disease)
5. In Cushing’s disease, cortisol will be SUPPRESSED
6. Imaging
Adrenal MRI/CT
Pituitary MRI/CT
40
Conn's Ix
1. Plasma aldosterone:renin ratio
In Conn’s syndrome, aldosterone will be raised and renin decreased
2. Adrenal MRI/CT
41
Phaeo Ix
24 hour urinary catecholamines
Plasma catecholamine levels
Imaging (CT/MRI)
42
Addisons Ix
1. Morning serum cortisol (between 8-9am)
2. Plasma ACTH level
3. Short synACTHen test:
Cortisol and ACTH levels measured at the start
IM injection 250 micrograms synthetic ACTH administered
Cortisol measured 30 and 60 minutes post-injection
In Addison’s disease, cortisol will NOT rise
43
Acromeglay Ix
1. Plasma GH hormone levels before and after oral glucose load (oral glucose tolerance test):
Normal – glucose causes GH levels to DROP
Acromegaly – GH levels remain HIGH
2. IGF-1 levels (will be HIGH in acromegaly)
3. Imaging: pituitary MRI
44
Hyperprolactinaemia Ix
Prolactin levels (>6000 confirms diagnosis)
Urinary HCG – rule out pregnancy!
TFTs
Pituitary MRI
45
Bone disorders:
| Cause of Hypercalcaemia
Primary hyperparathyroidism
Malignancy
Causes
PTH suppressed: malignancy, rarer causes e.g. sarcoidosis, vitamin D excess
PTH raised or inappropriately normal: primary hyperparathyroidism
46
Bone disorders:
| Cause of Hypocalcaemia
Osteomalacia
Renal disease
Non-PTH driven: vitamin D deficiency, chronic kidney disease, PTH resistance (pseudohypoparathyroidism)
Due to low PTH: iatrogenic (post-thyroidectomy), autoimmune hypoparathyroidism, congenital absence of parathyroid glands (DiGeorge syndrome)
47
Bone disorders:
| Cause of normal calcium and other abnormality
Neutral
Osteoporosis
Paget’s disease
48
Hypercalcaemia symptoms
```
Symptoms
STONES: renal stones
BONES: bone pain
GROANS: abdominal pain, nausea and vomiting
THRONES: constipation, polyuria
MOANS: confusion, psychosis, depression
Fatigue
```
49
High Ca, low phosphate, high/normal PTH, normal Vit D, normal/raised ALP
Primary Hyperparathyroidism
50
Primary Hyperparathyroidism causes
Parathyroid adenoma (85-90%)
Chief cell hyperplasia
Parathyroid carcinoma
51
Hypercalcaemia of malignancy Tx
Treatment
IV fluids to combat volume depletion
Bisphosphonates eg pamidronate, or calcitonin
Treat underlying disease
52
Hypocalcaemia symptoms
Muscle twitching/spasms
Tingling
Numbness
Hyper-reflexia
Chvostek’s sign (tapping on the cheek causes facial twitching)
Trousseau’s sign (applying a blood pressure cuff causes carpal spasm)
53
Low/N Ca, low /N phosphate, high PTH, low Vit D, raised ALP
Osteomalacia/Ricketts
54
Low Ca, high phosphate, high PTH (negative feedback), normal Vit D and Raised/normal ALP
CKD
55
CKD
Decreased calcium reabsorption and decreased phosphate excretion
Hypocalcaemia and hyperphosphataemia
Results in secondary hyperparathyroidism
Due to lack of negative feedback, there is increase of PTH
Can progress to tertiary hyperparathyroidism (autonomous parathyroid glands resulting in hypercalcaemia)
56
Osteoporosis Tx
Treatment
Conservative: smoking cessation, reduce alcohol intake, weight-bearing exercise
Medical: calcium/vitamin D supplements, bisphosphonates, teriparatide (recombinant PTH), HRT
57
Osteoporosis RF
1. Reduced oestrogen exposure: Late menarche, Early menopause, Amenorrhoea e.g. anorexia nervosa
2. Nutritional: Low BMI e.g. anorexia nervosa, Malabsorption e.g. coeliac disease, IBD, gastric surgery
3. Endocrine: Cushing’s syndrome, Hyperthyroidism, Hyperparathyroidism, Diabetes mellitus
4. Musculoskeletal: Immobility, Rhematoid arthritis
5. Iatrogenic: STEROIDS, Heparin, Anti-epileptics, PPIs
58
Normal Ca, phosphate, PTH and Vit D. Raised ALP
Paget's Disease
59
Tx of Acromeglay
1. Transphenoidal surgery
| 2. Somatostatin analogue: octreotide
60
Carcinoid Syndrome
Constellation of symptoms caused by systemic release of humoral factors (amines, prostaglandins, polypeptides) from carcinoid tumors (neural crest origin).
Release of serotonin, histamine, and other vasoactive peptides causing systemic circulation
61
Mainly gut tutors, high mets risk
carcinoid syndromes
62
Carcinoid Syndrome
Syndromes: flushing, diarrhoea, wheeze, bronchoconstriction, sweating, palpitations
Sings: facial flushing, telangiectasia, RHS murmurs, signs of RHF
63
High dose dexamethasone suppression test suppresses what in Cushings
suppreses cortisol when the cause is pituitary tumour.
64
Diabetes Insipidus Tests
1. serum and urine osmolarity
2. water deprivation test
3. AVP stimulation test
65
Management of Diabetes Insipidus
- Cranial: vasopressin
| - Nephrogenic: Thiazide diuretics to stimulate RAS , Na/K restrict
66
Retinopathy All stages
Background: microanurysems, blot haemorrhages, hard exudates
Pre-Proliferative: retinal haemorrhages, cotton wool spots
Proliferative: revascularization, fibrosis
Maculopathy: hard exudates involving macula
67
Background Retinopathy
Background: microanurysems, blot haemorrhages, hard exudates
68
Pre-proliferative Retinopathy
Pre-Proliferative: retinal haemorrhages, cotton wool spots
69
Proliferative Retinopathy
Proliferative: revascularization, fibrosis
70
Maculopathy
hard exudates involving macula
71
DKA Management
Problem: inceased glucose and ketones, decreased pH
1. Fluids IV infusion pump (NaCl soln 0.9%)
2. IV insulin infusion
3. Asses basic jobs of pt
4. Aim to maintain K in normal range
72
Complications of DKA
- hyper/hypokalaemia
- cerebral odema
- hypoglycaemia
- pulmonary odema
73
Management of Type II DM
1. Monotherapy (metformin unless contraindicated lactic acidosis or CKD )
2. Dual therapy
3. Triple therapy or start insulin
74
SIADH is characterised by what?
- hypotonic hyponatermia
- concentrated urine
- euvolemic shock
headaches, nausea and vomiting, muscle crams, irratibility, confusion, coma
75
Tx of SIADH
| Acute and Chronic
Acute:
1. IV hypertonic saline and fluid restrict
+/- treat underlying cause, vasopressin antagonist, frusemide
Chronic:
1st: fluid restrict, treat underlying cause
2nd: tolvaptan
3rd: sodium chloride and fruosemide
76
Delayed sexual development and small testes and gynecomastia
Klienfelter's (XXY)
77
isloated GnRH deficiency, with anosmia and colourbliness
Kallman's
78
Loss of critical region on ch15, causing obesity, short stature, almond shaped eyes, learning difficulty and postnatal hypotonia
Prader-Willi
79
Obesity, polydactyly, retinitis, pigmentosa, learning difficulty
Laurence-moon-biedi syndrome
80
Short stature, high arched palate, widely spaced nipples, lowe posterior hairline,
Turners sundrome
81
Pituitary apoplexy
haemorrhage/infarction of pituitary tutor
| lofe threatening: headache, visual loss, CN palsies
82
Sheen's Syndrome
pituitary infarction, haemorrhage, necrosis following post part haemorrhage
83
Myxodema Coma
```
hypothermia
hypoventilation
hyponatemia
HF
confusion
coma
SLOWLY RELAXING REFLEXES
```
84
Myxodema Coma Tx
```
oxygen
rewarming therapy
rehydrated
IV T3
IV hydrocortisone
```
85
Obesity definition
BMI > 30
86
Hypokalaemia signs
muscle weakness, cramps, parasthesia, tetany
87
PCOS diagnostic criteria
Rotterdam (2003) pt must have 2 of the following:
- hyperandrogemism +/or hyperandrogenaemia
- oligo or anovulation
- polycystic ovaries on US
88
Thiazolidinediones work by
activating peroxisome proliferator-activated
receptor-γ, which regulates the expression of several genes involving metabolism, and work by enhancing the actions of endogenous insulin.
They are used as a third-line therapy in combination with metformin and
sulphonylurea, however they cause sodium and fluid retention and should
not be used in patients with cardiac failure, such as in this case.
89
Thiazolidinediones are used as..
third-line therapy in combination with metformin and
sulphonylurea, however they cause sodium and fluid retention and should
not be used in patients with cardiac failure, such as in this case.
90
Thiazolidinediones are contraindicated in
cardiac failure pts
91
The most common cause of hypocalcaemia is .
hypoalbuminaemia with a normal ionised calcium concentration (hence why it is important to
correct calcium concentrations according to serum albumin). Other causes include alkalosis, vitamin D deficiency, chronic renal failure,
pseudohypoparathyroidism, acute pancreatitis and hypomagnesaemia.
92
Pseudohypoparathyroidism is an autosomal dominant condition
| characterised by end-organ resistance to parathyroid hormone. Features include
.... mental retardation, short stature and short fourth and fifth metacarpals, accompanied by a low PTH, low calcium and high phosphate levels.
Pseudopseudohypoparathyroidism describes the condition where
you get all the phenotypic features of pseudohypoparathyroidism but in
conjunction with a normal biochemistry
93
phaeocytochroma Ix
24-hour urinary vanillylmandelic acid
| An abdominal CT will help localize the tumour.
Resp
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