Endocrinology Conditions Flashcards
(113 cards)
1
Q
Diabetes Mellitus - Describe the clinical presentation (of young and old patients)
A
Young: 2-6 week history of thirst, polyuria and weight loss. Ketoacidosis if not picked up earlier (fruity breath). Older: Similar, but over longer period. Additionally lack of energy and eye problems (blurred vision). Neuropathy, eventually (glove and stockings). Exist on a spectrum.
2
Q
Diabetes Mellitus - Type 1 Pathophysiology
A
Caused by an autoimmune destruction of the pancreatic beta cells. Associated with HLA genetics (>90% with HLA-DR3/4 genes are affected) but triggered by environmental antigens. Will have the autoantibodies (bad ones) several years before onset.
3
Q
Diabetes Mellitus - Type 1 Pathophysiology of Polyuria
A
Renal glucose reabsorption cannot retrieve the amount of glucose that was filtered out of the blood and so it increases urea output (osmotic diuresis).
4
Q
Diabetes Mellitus - Type 1 Pathophysiology of Weight Loss
A
Fluid depletion and insulin deficiency leads to muscle and fat breakdown.
5
Q
Diabetes Mellitus - Type 2 Pathophysiology
A
Polygenic (not HLA related). Environmental factors trigger onset in the genetically susceptible.
Peripheral insulin resistance caused by the receptors that insulin acts on being overused so they don’t bind as well. After a while beta cell mass reduces, insulin secretion reduces and you can get pancreatic failure.
6
Q
Diabetes Mellitus - Type 2 causes (5)
A
Cushing’s disease, acromegaly, hyperthyroidism, pregnancy, pancreatitis
7
Q
Diabetes Mellitus - Type 1 Epidemiology
A
Onset usually <30 years. Usually fairly thin.
8
Q
Diabetes Mellitus - Type 2 Epidemiology
A
Onset usually >30 years. Usually overweight.
9
Q
Diabetes Mellitus - Investigations with results (4)
A
Test fasting glucose (not eaten for 8 hours), >7 mmol/L is positive.
Random glucose >11.1 mmol/L is positive.
HbA1c needs 6.5%/48mmol/mol
Low C peptide in type 1
Normal C peptide in type 2
10
Q
Diabetes Mellitus - Type 1 Treatment (3)
A
Glycaemic control through diet (low sugar, low fat, high starch) and insulin (twice daily and with meals)
Basal insulin - long acting insulin, lasts for 12-24 hours. Mixed with protamine or zinc
Bolus insulin - short acting soluble insulins work within 30-60 minutes
11
Q
Diabetes Mellitus - Type 2 Treatment (5)
A
Diet and exercise.
If that doesnt work use metformin, gliclazide, sitagliptin or insulin
12
Q
Diabetes Mellitus - Pharmacology (Drug class, example, mechanism of action, side effects 4)
A
- Biguanide, Metormin, Reduce gluconeogenesis in liver, increase glucose upatke in skeletal muscle, GI - abdo pain, anorxia, diarrhoea, neusea, Lactic acidosis
- Sulfonylurea, Gliclazide/Glipizide, Stimulate B cells to secrete insulin, Hypoglycaemia, weight gain
- DPP4 Inhibitors, Sitagliptin, Inhibits DPP4 which stimulates insulin secretion, no weight implications
- Glitazone, Pioglitazone, Enhance uptake of fatty acids and glucose, Fluid retention, wieght gain
13
Q
Diabetes Mellitus - List Complications (7)
A
- Hypoglycaemia
- Diabetic Ketoacidosis
- Hyperglycaemic hyperosmolar state
- Diabetic neuropathy
- Diabetic foot
- Diabetic retinopathies
- Diabetic nephropathy
14
Q
Diabetes Mellitus - Describe the normal insulin secretion process
A
- Hyperglycaemia leads to increase glucose uptake by cells
- Glucose metabolism leads to increased levels of ATP within cell
- Increased ATP causes K+ channels to close
- Causes depolarisation of cell membrane
- Ca2+ channels open and Ca2+ enters cells
- Increased Ca2+ causes exocytosis of insulin containing vesicles in pancreatic beta cells in the islets of langerhans and insulin in released.
15
Q
Diabetes Mellitus - Hypoglycaemia (definition, symptoms 5, investigations, management)
A
- Insufficient glucose to the brain
- Aggression, sweating, tachycardia, hunger, pallor
- Blood glucose level test (<4mmol/L)
- Give glucose and glucagon
16
Q
Diabetes Mellitus - Diabetic Ketoacidosis pathology
A
- Without insulin there is increased hepatic gluconeogenesis
- High glucose leads to osmotic diuresis leading to dehydration
- Peripheral lipolysis increases circulating FFAs which are converted to acidic ketones in the liver
- Process is accelerated by stress hormones secreted because of dehydration
17
Q
Diabetes Mellitus - Diabetic Ketoacidosis Symptoms (5)
A
- Dehydration
- Vomiting and abdominal pain (electrolyte disturbances)
- Low BP
- Fruity breath (smells of ketones)
- Low body temperature
18
Q
Diabetes Mellitus - Diabetic Ketoacidosis Investigations (4)
A
- Blood tests for hyperglycaemia - blood glucose >11 mmol/L
- Ketonaemia - blood ketones
- Urine dipstick
- Serum U+E - urea and electrolytes. Urea raised, potassium low
19
Q
Diabetes Mellitus - Diabetic Ketoacidosis Treatment (3)
A
- Fluid replacement
- IV insulin
- Electrolytes
20
Q
Diabetes Mellitus - Hyperglycaemic Hyperosmolar State (description, symptoms 3, investigations, treatment)
A
- Characterised by hyperglycaemia, hyperosmolality and no ketosis
- Dehydration (osmotic diuresis), decreased consciousness (elevated plasma osmolality), polyuria
- Blood glucose level test (>40mmol/L)
- Fluid replacement, IV insulin, Electrolytes
21
Q
Diabetes Mellitus - Diabetic Neuropathy (description and symptoms 4)
A
Occlusion of the vasa nervorum and accumulation of fructose and sorbitol
- Glove and stocking sensation loss
- Hypersensitivity
- Muscle weakness
- Hyporeflexia
22
Q
Diabetes Mellitus - Diabetic foot (description, clinical presentation, treatment 3)
A
- Infection, ischaemia and neuropathy lead to tissue necrosis.
- Reduced sensation, signs of vascular disease in lower leg (thin skin, no hair, bluish)
- Swab for bacteria, local wound care, reconstructive vascular surgery
23
Q
Diabetes Mellitus - Diabetic Retinopathies (description, symptoms 6, investigation)
A
- Too much glucose in the blood causes glucose uptake into lens and blockages of the retinal blood vessels.
- Spots in vision, blurred vision, fluctuating vision, impaired colour vision, dark areas in vision, vision loss
- Fundoscopy (cotton wool spots and flare haemorrhages)
24
Q
Diabetes Melllitus - Diabetic Retinopathies Non-proliferative pathophysiology
A
- Retinal blood vessel walls weaken, microaneurysms leak into retina
- Large vessels dilate
- Retinal nerve fibres may swell
- Macular oedema may occur
25
Diabetes Melllitus - Diabetic Retinopathies proliferative pathophysiology
- Damaged blood vessels close off
- New abnormal blood vessels grow
- These can leak into the vitreous humour
- Scar tissue may cause retina to detach from back of eye
- Pressure may build up affecting optic nerve (glaucoma)
26
Diabetes Mellitus - Diabetic Nephropathy (causes 3, signs, treatment)
- Glomerular disease, ischaemic renal lesions, ascending UTIs
- Microalbuminuria progressing to intermittent albuminuria and persistent proteinuria
- BP control (ACE-1)
27
Diabetes Mellitus - Other forms (4)
- Mature Onset Diabetes of the Young - rare autosomal dominant form of T2DM affecting young people
- Latent Autoimmune Diabetes of Adults - form of T1DM with slower progression to insulin dependence later on in life
- Primary Neonatal Diabetes - Occurs in the first 6-12 months of life
- Gestational Diabetes - diabetes during pregnancy, usually third trimester
28
Hyperthyroidism - Epidemiology
- More females than males
- 2-5% of women
- Presents between 20-40
29
Hyperthyroidism - Causes (6)
- Graves’ disease - autoimmune induced excess production of thyroid hormone
- Toxic multinodular goitre - englarged thyroid gland produces too much thyroid hormone
- Toxic thyroid adenoma
- Pituitary adenoma - causes more TSH to be produced
- De Quervain’s thyroiditis - painful swelling of thyroid gland triggered by a viral infection
- Drug induced - iodine, amiodarone, lithium
30
Hyperthyroidism - Risk Factors
- Female
- Family history
- Stress
- Smoking
- Amiodarone (drug)
- HLA-DR3
31
Hyperthyroidism - Pathology of Graves Disease
Serum IgG antibodies called TSH receptor stimulating antibodies bind to TSH receptors on the ethyroid and simulate T3/4 production
This results in excess secretion, hyperplasia of the thyroid follicular cells, hyperthyroidism and goitre
32
Hyperthyroidism - Symptoms of Graves 4
Graves Ophthalmology - extraocular muscle swelling, eye discomfort, lacrimation, diplopia
Pretibial myxoedema - purple lesions on anterolateral shins
Thyroid Acropachy - clubbing, swelling of fingers and toes
Goitre - swollen thyroid
33
Hyperthyroidism - Thyroid tests (primary and secondary results, Graves)
- Primary - low TSH, high T3/4
- Secondary - high TSH, high T3/4
- TSH receptory antibodies (Graves)
34
Hyperthyroidism - Treatment 4
- Beta blockers decrease SNS activation
- Carbimazole - blocks thyroid hormone synthesis and is immunosuppressive so good for graves. Do it with thyroxine prevents hypo. Side effects - agranulocytosis
- Radioiodine therapy iodine taken up and local irradiation, the tissue damage causes return to normal function
- Thyroidectomy
35
Hyperthyroidism - Thyroid Crisis (description, treatment)
- Rare, life-threatening, can cause hyperpyrexia, tachycardia, restlessness, coma
- Carbimazole, propranolol, potassium iodine (blocks release of thyroid hormone), hydrocortisone (inhibits peripheral conversion of T4 to T3)
36
Hypothyroidism - Epidemiology
Affects females more than males
Affects 0.1-2% of the population
37
Hypothyroidism - Causes (4)
- Post-partum thyroiditis - following childbirth
- Autoimmune thyroiditis - anti-thyroid autoantibodies atrophies thyroid (Hashimotos)
- Drug induced - carbimazole, lithium, amiodarone
- Hashimoto’s - antibodies attach the thyroid causing inflammation and dysfunction, lowering TS/4 levels
38
Hypothyroidism - Symptoms (mneumonic)
**BRADYCARDIC**
**B**radycardia
**R**eflexes relax slowly
**A**taxia
**D**ry, thin hair
**Y**awning
**C**old hands
**A**scites
**R**ound puffy face
**D**efeated demeanour
**I**mmobile
**C**ongestive
39
Hypothyroidism - Investigations (3)
- Thyroid function test - primary (high TSH, low free T4), secondary (low TSH, low T3/4)
- Thyroid antibodies (TPO in Hashimotos)
- FBC test for anaemia
40
Hypothyroidism - Mangement
Lifelong oral Levothyroxine (T4), aim to get TSH >0.5
41
Hypothyroidism - Describe Secondary Hypothyroidism
Associated with pituitary gland or hypothalamus. Not enough TSH due to hypopituitarism
42
Cushing's Disease - Pathology
Excess ACTH stimulates excess cortisol or neoplasms in adrenals stimulate zona reticularis to produce more cortisol
43
Cushing's Disease - Differential diagnosis
Pseudo-cushing's syndrome caused by alcohol excess
44
Cushing's Disease - Causes
Mostly caused by real steroids
ACTH dependent - hypersecretion by pituitary adenoma, ectopic e.g. small cell lung cancer
45
Cushing's Disease - Symptoms (mneumonic)
**CUSHING**
**C**ataracts
**U**lcers
**S**triae
**H**ypertension and hyperglycaemia
**I**nfection
**N**ecrosis
**G**lucosuria
46
Cushing's Disease - Investigations (1st line and 2nd line)
Random cortisol (if high proceed to first line test)
*1st line:*
- Overnight dexamethasone suppression test 24hr (usually suppressed cortisol but if it doesn’t then likely cushings)
*2nd line:*
- If no suppression in 1st line do 48hr test
- If plasma ACTH is low do CT/MRI to detect adenoma or carcinoma.
- If it is high but supressed = pituitary adenoma
- High but no suppression = ectopic
47
Cushing's Disease - Treatment (3)
- Stop steroids
- Remove pituitary adenoma
- Radiotherapy on adrenal adenoma
48
Acromegaly - Physiology of growth hormones (including inhibition )
Hypothalamus → Growth Hormone Releasing Factor → Pituitary gland → Growth hormone → Liver → Insulin-like Growth Factor 1 → Protein synthesis and Cell Division
Inhibited by somatostatin and high glucose
GH acts on tissues e.g. liver/muscles/bone/fat to change metabolism
IFG-1 increases lipolysis and calcium retention, decreases blood glucose, stimulates hypertrophy and hyperplasia of bone and skeletal muscle
49
Acromegaly - Epidemiology
3 per million, mean diagnosis age 40, equally male and female
50
Acromegaly - Causes
Benign GH-reducing adenoma
Ectopic GH-releasing hormone forms. Carcinoid tumour (rare)
51
Acromegaly - Risk Factors
Multiple endocrine neoplasia-1 (MEN-1)
52
Acromegaly - Pathology
Increased GH travels to tissues e.g. liver binding to receptors increasing IF-1
Skeletal and soft tissue growth
53
Acromegaly - Symptoms
Local tumour expansion in pituitary causes compression of surrounding structures resulting in headaches and visual field loss
Metabolic effects cause sweating, decreased libido, amenorrhoea/oligomenorrhea
Signs - big hands/feet/jaw, widely spaced teeth, puffy lips/eyelids/skin, deep voice
54
Acromegaly - Investigations (4)
Oral glucose tolerance test - should suppress GH if not then his is diagnostic
Serum IF-1 levels (almost always raised and fluctuate less than GH)
MRI for pituitary adenoma
Visual field tests
55
Acromegaly - Treatment
1st line - transphenoidal surgery to remove adenoma (can cause infection, hypopituitary, diabetes insipidus)
2nd line - somatostatin analogues/dopamine agonists inhibit GH secretion, GH antagonist, external radiotherapy
56
Conn's Syndrome - Causes
Solitary aldosterone producing adrenal adenoma 2/3
Bilateral adrenocortical hyperplasia 1/3
57
Conn's Syndrome - Pathology
Excess aldosterone independent of RAAS causes increased K+ loss, Na+ and water retention → raised BP, decreased renin release, hypokalaemia
58
Conn's Syndrome - Symptoms
Usually asymptomatic
Hypertension, increased risk of cardiac arrhythmias
Symptoms of hypokalaemia: constipation, muscle weakness, cramps,polyuria
59
Conn's Syndrome - Differential Diagnosis
Secondary hyperaldosteronism (excess renin which stimulates aldosterone release)
60
Conn's Syndrome - Investigations
U&Es - decreased renin, increased aldosterone
ECG - flat T, ST depression, long QT, long PR
61
Conn's Syndrome - Treatment
Laparoscopic adrenalectomy
Oral spironolactone (aldosterone antagonist)
62
Addison's Disease - Epidemiology
Very rare, more common in females
63
Addison's Disease - Pathology
Reduced cortisol level leads to increased CRH and ACTH (hyperpigmentation) production
64
Addison's Disease - Causes of adrenal insufficiency (primary and secondary)
Primary
- Adrenal TB
- Surgical removal of adrenal glands
- Adrenal haemorrhage
- Addison's
Secondary
- Steroids
- Congenital
- Trauma
- CRH deficiency
- Radiotherapy
Most common worldwide is TB, most common in the UK is Addison’s
65
Addison's Syndrome - Symptoms
Non specific symptoms (nausea ,abdominal pain, weight loss, anorexia, depression)
Signs - hypotension, hyperpigmentation, vitiligo, hypoglycaemia
TANED TIRED TONED TEARFUL
66
Addison's Syndrome - Investigations (3)
- **Short ACTH stimulation test** - take baseline cortisol levels, give ACTH then measure cortisol, will remain low in Addison’s
- **Plasma ACTH levels** - high ACTH with low or normal cortisol = primary hypoadrenalism. Low ACTH and cortisol = secondary or tertiary hypoadrenalism
- **U&E** - shows high plasma renin due to low aldosterone and raised urea
67
Addison's Syndrome - Treatment
- **Glucocorticoids** - oral hydrocortisone/prednisolone to replace cortisol
- **Mineralocorticoids** - fludrocortisone to replace aldosterone
68
Thyroid Cancer - Symptoms
Thyroid nodules
Dysphagia (difficulty swallowing)
Hoarse voice
Enlarged lymph nodes
69
Thyroid Cancer - Investigations
Biopsy - to distinguish benign and malignant
Ultrasound
70
Thyroid Cancer - Treatment
Follicular and papillary:
- Total thyroidectomy
- Ablative radioiodine
Anaplastic and lymphoma:
- Radiotherapy
- Largely palliative treatment
71
SIADH - Pathology
- Excess ADH → insertion of aquaporin 2 channels → water retention → dilution of blood plasma → hyponaetraemia
- Water retention also decreases RAAS aldoseterone secreting Na+ so body is removing sodium from blood that already has low concentration
72
SIADHS - Causes (5 with examples)
**Malignancy**
- Small cell lung carcinoma
- Prostate
- Thymus
- Pancreas
**Drugs**
- Opiates
- Chlorpropamide
- Carbamazepine
- Vincristine
**Brain issues**
- Meningitis
- Cerebral abcess
- Head injury
- Tumour
**Lung**
- Pneumonia
- TB
- Abscesses
- Asthma
- CF
**Metabolic**
- Porphyria
- Alcohol withdrawal
73
SIADHS - Symtoms (7)
- Confusion
- Irritability
- Headaches
- Anorexia
- Nausea
- Concentrated urine
- Mild dilutional hyponatraemia
74
SIADHS- Investigation
1-2L of 0.9% saline - sodium depletion will respond, SIADH will not
75
SIADHS - Diagnostic Criteria (5)
- Low serum sodium
- Low plasma osmolality with inappropriate urine osmolarity
- Continued urinary sodium excretion
- Absence of hypokalaemia, hypotension and hypovolaemia (body losing fluid)
- Normal renal, adrenal and thyroid function
76
SIADHS - Treatment (4)
- **Restrict fluid** - to increase Na+ concentration
- **Demeclocycline** - inhibits action of vasopressin on kidney
- **Tolvaptan** - vasopressin receptor antagonist, treats the hyponatraemia
- **Oral furosemide** - salt and loop diuretics to prevent circulatory overload
77
Diabetes Insipidus - Pathology (types)
- **Cranial** - too little ADH from posterior pituitary gland
- **Nephrogenic** - kidney not responding to ADH
78
Diabetes Insipidus - Causes
Cranial:
- Neurosurgery
- Head trauma
- Pituitary tumour
- Congenital defect in ADH gene
Nephrogenic:
- Drugs
- Hypokalaemia
- Hpercalcaemia
- Sickle cell disease
79
Diabetes Insipidus - Symptoms (3)
- Polyuria (excess urination)
- Polydipsia (excessive thirst)
- Dehydration
80
Diabetes Insipidus - Investigations (3)
- **Water deprivation test** - determines whether kidneys continue to produce dilute urine despite dehydration. Restrict fluid then measure urine osmolarity. If it stays he same = Nephrogenic. Osmolarity increases = cranial
- **Plasma biochemistry**
- **MRI of hypothalamus**
81
Diabetes Insipidus - Treatment
Cranial:
- Desmopressin
Nephrogenic:
- Bendroflumethiazide - causes more Na+ secretion in DCT → increased water loss causes GFR reduction
- NSAIDs - reduce GFR by inhibiting prostaglandin synthase
82
Hyperkalaemia - Pathology
Blood potassium rises → reduces difference in electrical potential between cardiac myocytes and outside → action potential threshold decreases → arrhythmias → cardiac arrest
83
Hyperkalaemia - Causes (4)
- Excess fluids
- Adrenal insufficiency (aldosterone not stimulating secretion of K+ in kidneys)
- Drugs - ACE inhibitors (block aldosterone), Spironolactone (potassium-sparing diuretic), NSAIDs
- Acute kidney injury (decreased filtration rate)
84
Hyperkalaemia - Symptoms (6)
- Muscle weakness
- Impaired neuromuscular transmission
- Flaccid paralysis
- Chest pain
- Metabolic acidosis
- Tachycardia
85
Hyperkalaemia - Investigations
- U&Es - over 5.5mmol/L = hyperkalaemic, over 6.5 = emergency
- ECG - tall tented T waves, small P waves, wide QRS
86
Hyperkalaemia - Treatment
Mild to moderate
- Treat underlying cause
- Dietary potassium restriction
- Furosemide
Severe
- Calcium gluconate - reduces excitability of cardiac myocytes
- Insulin and dextrose - drives K+ into cells
- Polystyrene sulphonate resin - binds K+ in gut decreasing uptake
87
Hypokalaemia - Pathology
- Low K+ in serum causes water concentration gradient out of cell
- Hyperpolarisation of the myocyte membrane decreases myocyte excitability
88
Hypokalaemia - Causes (4)
- Anorexia
- High aldosterone (Cushings/Conns)
- Increased renal excretion
- GI losses (vomiting, laxatives)
89
Hypokalaemia - Symptoms (5)
- Muscle weakness
- Cramps
- Tetany
- Palpitations
- Constipation
90
Hypokalaemia - Investigations
- **U&E** - <3.5mmol/L = hypokalaemia, <2.5 = emergency
- **ECG** - Small/inverted T waves, depressed ST segments, long PR, long QT, prominent U waves
91
Hypokalaemia - Treatment
Mild
- Oral K+
Severe
- IV K+
92
Hypoparathyroidism - Causes (5)
- Autoimmune destruction of parathyroid glands
- Vit D deficiency
- Magnesium deficiency
- Congenital
- Parathyroidectomy
93
Hypoparathyroidism - Symptoms (mneumonic)
**SPASMODIC**
**S**pasms
**P**erioral paraesthesia (burning feeling around the mouth)
**A**nxious, irritable, irrational
**S**eizures
**M**uscle tone increases
**O**rientation impaired
**D**ermatitis
**I**mpetigo herpetiformis
**C**hvostek’s sign (tapping over parotid gland causes twitching of ipsilateral facial muscles)
94
Hypoparathyroidism - Treatment (3)
- Calcium supplement
- Calcitriol (active vit D)
- Synthetic PTH
95
Hyperparathyroidism - Causes (primary, secondary, tertiary)
Primary
- Single parathyroid adenoma
Secondary
- Compensatory hypertrophy of glands in response to hypocalcaemia
Tertiary
- Parathyroid hyperplasia after secondary
- Plasma calcium and PTH raised
- Treated by parathyroidectomy
96
Hyperparathyroidism - Symptoms (7)
- Painful bones
- Renal stones
- Psychiatric moans
- Abdominal groans
- Thirst
- Polyuria
- Fractures
97
Hyperparathyroidism - Investigations (3)
- **Bloods** - primary ( inc PTH, inc Ca, dec phosphate), secondary (inc PTH, dec Ca, inc phosphate) tertiary (inc everything)
- **Abdominal X-ray** - renal calculi or nephrocalcinosis
- **Radioisotope scanning** - adenomas
98
Hyperparathyroidism - Treatments (primary, secondary, tertiary)
Primary
- Parathyroid adenoma - surgical removal
- Parathyroid hyperplasia - all 4 glands removed
- Calcimimetic - increases sensitivity to Ca2+ → less PTH secretions
Secondary and tertiary
- Treat cause
Emergency
- Rehydrate
- Bisphosphonates (inhibits osteoclasts → prevents bone resorption)
99
Pseudohypoparathyroidism - Description, Investigation, Treatment
Resistance to PTH due to genetic mutation
Bloods show low calcium and high PTH
Treat as normal hypoparathyroidism
100
Hypocalcaemia - Causes (7)
- **Vit D deficiency** - low phosphate, low calcium uptake in GI and decreased absorption in kidneys leads to osteomalacia
- **Hypoparathyroidism** - high phosphate
- **Acute pancreatitis** - high phosphate
- **Osteomalacia** - low phosphate, soft bones due to low calcium and vit D deficiency
- **Chronic Kidney Disease** - high phosphate, poor uptake of calcium in kidneys caused by low production of vit D
- **Pseudohypoparathyroidism** - resistance to PTH
- **Drugs** - *calcitonin* (decreases calcium and phosphate), *bisphosphonates* (reduce osteoclast activity)
101
Hypocalcaemia - Symptoms (mnemonic)
**SPASMODIC**
**S**pasms
**P**erioral paraesthesia (burning feeling around the mouth)
**A**nxious, irritable, irrational
**S**eizures
**M**uscle tone increases
**O**rientation impaired
**D**ermatitis
**I**mpetigo herpetiformis
**C**hvostek’s sign (tapping over parotid gland causes twitching of ipsilateral facial muscles)
102
Hypocalcaemia - Investigations
ECG - long QT interval
103
Hypocalcaemia - Treatments
Mild - adcal supplement (calcium corbonate)
Severe - Calcium gluconate
104
Hypercalcaemia - Epidemiology
Mostly affects older women
105
Hypercalcaemia - Causes
Most common is hyperparathyroidism or cancer
**CHIMPANZEES**
**C**alcium supplementation
**H**yperparathyroidism
**I**atrogenic drugs
**M**ilk alkali syndrome
**P**aget’s disease of bone
**A**cromegaly and Addison’s
**Z**olinger-Ellison Syndrome
**E**xcess vit D
**E**xcess vit A
**S**arcoidosis
106
Hypercalcaemia - Symptoms (5)
- **Painful bones** - osteitis fibrosa cystica
- **Renal stones** - calcium deposition in renal tubules causes polyuria and nocturia
- **Psychiatric moans** - lethargy, fatigue, memory loos, psychosis, depression
- **Abdominal groans** - nausea, vomiting, constipation, indigestion
- **Cardiac arrest**
107
Hypercalcaemia - Investigations
- **ECG** - tented T, short QT interval
- **Bloods** - undetectable PTH excludes primary hyperparathyroidism (check for tumour)
108
Hypercalcaemia - Treatments
- Treat underlying cause
- **IV saline** - dilutes calcium
- **Bisphosphonates** - encourage osteoclasts to undergo apoptosis so less breakdown
109
Hyperprolactinaemia - Epidemiology
Common in young women
110
Hyperprolactinaemia - Causes
Prolactin secreting pituitary adenoma (prolactinoma)
Any tumour inhibiting dopamine (as this inhibits prolactin)
111
Hyperprolactinaemia - Symptoms (4)
- Increased prolactin → increased milk production
- Reduced fertility (prolactin inhibits GnRH)
- Decreased libido, erectile dysfunction
- Amenorrhoea
112
Hyperprolactinaemia - Investigations (3)
- Serum prolactin level
- Thyroid function tests
- MRI of pituitary
113
Hyperprolactinaemia - Treatment
Dopamine agonist - Cabergoline or Bromocriptine
