1
Q
What is addisons disease/hypoadrenalism and what happens?
A
Autoimmune destruction of adrenal glands
Reduced cortisol and aldosterone
2
Q
Features of addisons disease?
A
Lethargy, anorexia, weakness, nausea and vomiting, weight loss, salt cravings
Hyperpigmentation especially in palmar creases, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
3
Q
Electrolyte imbalances - addisons disease?
A
Hyponatraemia and hyperkalaemia and hypoglvyaemia
4
Q
Other causes of Primary adrenal insufficiency?
A
TB, metasteses, mengiococcal septicaemia, HIV, antiphospholipid syndrome
5
Q
What causes Secondary hypoadrenalism ?
A
Loss or damage to the pituitary gland
Due to congenital underdevelopment ( hypoplasia), surgery, infection, loss of blood flow or radiotherapy
6
Q
Hyperpigmentation in adrenal insufficiency- what does it suggest?
A
That theres a primary cause
7
Q
Investigations for addisons?
A
ACTH stimulation test (short synacthen test)
8
Q
What is the ACTH stimulation test?
A
Plasma cortisol before and 30 minutes and 60 minutes after giving synathen 250 IM
Synathen is a synthetic ACTH - cortisol level should at least double in response to synathen
If it doesn’t = indicates Addisons
9
Q
What is secondary adrenal insufficiency?
A
Inadequate ACTH stimulating teh adrenal glands, resulting in low levels of cortisol being released
10
Q
What is tertiary adrenal insufficiency?
A
Result of inadequate CRH release by the hypothalamus
11
Q
Describe path of cortisol/aldosterone
A
CRH from hypothalamus to anterior pituatary
ACTH from anterior pituatary to adrenal gland
Cortisol release from adrenal glands
12
Q
What causes tertiary adrenal insufficiency?
A
Usually result of long term oral steroids( more than 3 weeks) = suppression of the hypothalamus
13
Q
What happens when steroids are suddenly stopped- effect on hypothalamus?
A
Hypothalamus does not “wake up” fast enough and endogenous steroids are not adequately produced. Therefore, long term steroids should be tapered slowly to allow time for the adrenal axis to regain normal function.
14
Q
Features of adrenal insufficiency - babies
A
Lethargy, vomiting, poor feeding, hypoglycaemia, jaundice and failure to thrive
15
Q
investigations for adrenal insufficiency?
A
U&E’s, blood glucose
Check diagnosis with cortisol, ACTH, aldosterone and renin levels
Short synathen test for Addison
16
Q
What does cortisol, ACTH, aldosterone and renin look like in primary adrenal failure ?
A
Low cortisol
High ACTH - trying to increase levels
Low aldosterone - adrenal glands damaged
High renin - result of low aldosterone
17
Q
Management of Adrenal insufficiency?
A
Combination of hydrocortisone( glucocorticoid to replace cortisol) and fludrocortisone ( mineralocorticoid to replace aldosterone if its also in sufficient)
2-3 divided doses a day
18
Q
Patient education - steroids
A
Importance of not missing doses, medic alert bracelet and steroid card
Hydrocortisone injections for an adrenal crisis
19
Q
What is an addisonian crisis?
A
Acute presentation of severe Addisons
20
Q
Symptoms of addisons?
A
Hypotension
Hypoglycaemia, hyponatraemia and hyperkalaemia
Adrenal crisis can be the first presentation of Addison’s disease or triggered by infection, trauma or other acute illness in someone with established Addison’s.
21
Q
Management of addisonian crisis?
A
Hydrocortisone 100mg IM or IV
1 litre normal saline +/- dextrose if hypoglycaemic
Continue hydrocortisone until patient is stable
22
Q
What is hyperaldosteronism?
A
HIGH levels of aldosterone
HTN IS KEY FACTOR
23
Q
WHAT IS RENIN? Whats it produced by?
A
ENZYME produced by the juxtaglomerular cells in the afferent arterioles in the kidney
Sense the blood pressure in the vessels
Secrete more renin in response to low BP and less in response to high BP
24
Q
What does renin do? What is the knock on effect
A
Converts angiotensinogen into angiotensin I
Angiotensin I converts to angiotensin II in the lungs using ACE and Angiotensin II stimulates the release of aldosterone from the adrenal glands
25
What does aldosterone do?
Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts
26
What is primary hyperaldosteronism?
when the adrenal glands are directly responsible for producing too much aldosterone. Serum renin will be low as the high blood pressure suppresses it
27
Why would the adrenals produce too many aldosterone?- PRIMARY hyperaldosteronism
Bilateral adrenal hyperplasia (most common)
An adrenal adenoma secreting aldosterone (known as Conn’s syndrome)
Familial hyperaldosteronism (rare)
28
What is secondary hyperaldosteronism?
Caused by excessive renin stimulating the release of excessive aldosterone
29
What causes excessive renin release causing secondary hyperaldosteronism?
Excessive renin is released due to disproportionately lower blood pressure in the kidneys, usually due to:
Renal artery stenosis
Heart failure
Liver cirrhosis and ascites
30
Investigations for hyperaldosteronism?
aldosterone-to-renin ratio (ARR) is used as a screening test:
High aldosterone and low renin indicate primary hyperaldosteronism
High aldosterone and high renin indicate secondary hyperaldosteronism
Other investigations that relate to the effects of aldosterone include:
Raised blood pressure (hypertension)
Low potassium (hypokalaemia)
Blood gas analysis (alkalosis)
31
Investigations to work out underlying cause of hyperaldosteronism?
CT or MRI to look for an adrenal tumour or adrenal hyperplasia
Renal artery imaging for renal artery stenosis (Doppler, CT angiogram or MR angiography)
Adrenal vein sampling of blood from both adrenal veins to locate which gland is producing more aldosterone
32
Management of hyperaldosteronism?
Medical management is with aldosterone antagonists:
Eplerenone
Spironolactone
Treating the underlying cause involves:
Surgical removal of the adrenal adenoma
Percutaneous renal artery angioplasty via the femoral artery to treat renal artery stenosis
* adrenal adenoma: surgery (laparoscopic adrenalectomy)
* bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
33
Most common cause of secondary HTN?
Hyperaldosteronism
34
What is conns?
Adrenal adenoma = hyperdosteronism
35
What is acromegaly?
Result of excessive GH
36
Where is GH produced from?
Anterior pituitary gland
37
Cause of acromegaly?
Usually due to a pituitary adenoma
Secondary to cancer - where tumor secretes ectopic growth hormone releasing hormone or growth hormone
38
Presentation of acromegaly?
* A space-occupying pituitary tumour can cause:
Headaches
Visual field defect (bitemporal hemianopia)
* Excess growth hormone causes tissue growth:
Prominent forehead and brow (frontal bossing)
Coarse, sweaty skin
Large nose
Large tongue (macroglossia)
Large hands and feet
Large protruding jaw (prognathism)
* Additional features include:
Hypertrophic heart
Hypertension
Type 2 diabetes
Carpal tunnel syndrome
Arthritis
Colorectal cancer
39
Bilateral carpal tunnel syndrome association
Acromegaly
40
Investigations for acromegaly?
Insulin like growth factor 1 - raised in acromegaly
Growth hormone suppression test 0 75g glucose drink wtih growth hormone tested at baseline and 2 hours following - should suppress the GH level if dont have acromegaly
MEN1 occasionally
MRI of pituitary
41
Treatment of acromegaly? - surgical
Trans-sphenoidal surgery to remove pituitary Tumor
Removal of cancer
42
Medical treatment of acromegaly?
Pegvisomant is a growth hormone receptor antagonist given daily by a subcutaneous injection
Somatostatin analogues (e.g., octreotide) block growth hormone release
Dopamine agonists (e.g., bromocriptine) block growth hormone release
43
Somatostatin function
Growth hormone inhibiting hormone
Normally secreted by the brain and GI tract and pancreas
Blocks GH release
44
What are carcinoid tumours?
Rare, slow growing malignant tumours that develop in the neuroendocrine system. The appendix and small intestine are common origins
5-10% release hormones especially serotonin
45
What is carcinoid syndrome?
sually occurs when metastases are present in the liver and release serotonin into the systemic circulation
* may also occur with lung carcinoid as mediators are not 'cleared' by the liver
46
Features of carcinoid tumours?
* flushing (often the earliest symptom)
* diarrhoea and abdo pain
* bronchospasm
* hypotension
* right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
* other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing's syndrome
* pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour
47
Investigations for carcinoid tumors?
* urinary 5-HIAA
* plasma chromogranin A y
48
Management for carcinoid tumours?
* somatostatin analogues e.g. octreotide
* diarrhoea: cyproheptadine may help
* surgical resection
49
What is Charcot athropathy?
Charcot arthropathy is a chronic destructive disease of the bone and joints in patients with neuropathy.
It is characterised by painful or painless bone and joint destruction in patients with limbs that have lost sensory innervation
Most common underlying aetiology is diabetes
50
Presentation of Charcot athopathy?
6 Ds
Destruction
Deformity
Degeneration
Dense bones
Debris
Classically, it affects the tarsometatarsal joints.
51
Management of Charcot athropathy?
Conservative:
Prolonged immobilisation (offloading)
Orthotics
Medications:
Bisphosphonates
Neuropathic pain agents
Topical aesthetics
Surgical:
Resection of bony prominences
Deformity correction
Amputation
52
What is cushings syndrome?
Prolonged elevation of cortisol
53
What is cushings disease?
Specific condition where a pituitary adenoma secretes excessive ACTH
54
Features of cushings syndrome?
Thick round middle, thin limbs, effects of stress
Round moon face, central obesity, buffalo hump, proximal limb muscle wasting
High stress levels: HTN, cardiac hypertrophy, hyperglycaemia (t2DM), depression and insomnia
Osteoporosis adn easy bruising
55
Causes of Cushings syndrome- ACTH dependent causes?
Cushings disease
Ectopic ACTH production e.g. small cell lung cancer
56
ACTH independent causes of cushings syndrome?
Exogenous steroids, adrenal adenoma, adrenal carcinoma, carney complex, micro nodular adrenal dysplasia
57
What is pseudo cushings?
MIMICS cushings
Due to alcohol excess or severe depression
Causes false positive dexamethasone suppression test or 24hr urinary free cortisol
Insulin stress used to differentiate
58
Investigations for cushings? - general findings
Hypokalaemia
metabolic alkalosis
Impaired glucose tolerance
Ectopic ACTH secretion associated with low potassium
59
2 tests for cushings
Dexamethasone suppression test and 24 hour urinary free cortisol test
60
What is the dexamethasone suppression test?
Low dose test
If low dose is normal- cushings excluded
If abnormal use high dose to differentiate underlying causes
Patient takes a dose of dexamethasone at. night and cortisol and ACTH is measured in the morning
Works out if dexamethasone surpasses their natural morning spike of cortisol
61
Low dose dexamethasone suppression test- explain findings and reasonings
1mg
A normal response = dexamethasone suppresses the release of cortisol by affecting the negative feedback on the hypothalamus and pituitary
Hypothalamus responds by reducing the CRH output. Pituitary responds by reducing ACTH output
If cortisol is not suppressed = cushings
62
High dose dexamethasone test - findings and reasonings
8mg
Cortisol supressed and ACTH surpassed = cushings disease ( pituitary adenoma
Cortisol not surpassed but ACTH supressed= cushings syndrome, adrenal adenoma
Neither cortisol or ACTH supressed - ectopic ACTH syndrome
63
CRH stimulation for cushings?
If pituitary source then cortisol rises
If ectopic/adrenal then no change
64
treatment of cushings?
Remove underlying cause
Surgical removal of tumor / removal both adrenal glands
Replacement steroid hormones for life!
65
What is diabetes insipidus?
Lack of ADH or lack of response to ADH
Prevents the kidneys from being able to concentrate urine
66
primary polydipsia?
When patient has a normally functioning ADH but just drinking too much h2o
67
What is nephrogenic DI?
Insensitivity of collecting ducts to ADH
68
What is Cranial DI?
When hypothalamus doesn't produce enough ADH
69
What are causes of nephrogenic DI?
Lithium, demeclocycine,
electrolytes: hypercalcaemia and hypokalaemia
Genetic = mutations in AVPR2 gene on X chromosome that codes for ADH receptor
Intrinsic kidney disease = obstruction, sickle cell, pyelonephritis
70
What causes cranial DI?
Idiopathic
Haemochromatosis
Wolframs syndrome
Head tumors, injury
Surgery of the brain
Brain infections
Infilitrative e.g. sarcoidosis
71
Presentation of diabetes insipidus?
Polyuria, dehydration, postural hypotension, hypernatreamia
72
Presentation of diabetes insipidus?
Polyuria, dehydration, postural hypotension, hypernatreamia
73
Presentation of diabetes insipidus?
Polyuria, dehydration, postural hypotension, hypernatreamia
74
Presentation of diabetes insipidus?
Polyuria, dehydration, postural hypotension, hypernatreamia, polydipsia
75
Investigations for diabetes inspidus?
Water deprivation test
High plasma osmolality, low urine osmolality
76
Method for the water deprivation test?
Fluid deprivation for 8 hours
Urine osmolality measured and synthetic ADH is administered
8 hours later - measure the urine osmolality
77
After deprivation and after ADH - results for cranial DI, nephrogenic DI and primary polydipsia: urine osmolality
Cranial DI - low after deprivation, high after ADH
Neprhogenc DI - low after deprivation, low after ADH
Primary polydipsia - high after deprivation, high after ADH
78
Management of diabetes insipidus?
Nephrogenic: thiazides, low salt/protein diet
Cranial: desmopressin
79
Type 1 diabetes- overview?
Autoimmune where insulin producing beta cells of islets of langerhans are destroyed by the pancreas
Results in absolute deficiency of insulin = increase in glucose levels
Typically presents in childhood/early adult
80
Type 2 diabetes - overview
Most common cause of diabetes in developed world
Caused by relative deficiency of insulin due to excess of adipose tissue
Not enough insulin to go around all the excess fatty tissue
81
Maturity onset diabetes of the young
Group of inherited genetic disorders affecting production of insulin
Results in younger patients developing symptoms similar to T2DM e.g. asymptomatic hyperglycaemia with progression to more severe complications e.g. DKA
82
Latent autoimmune diabetes of adults
Develop problems later in life
83
What is Diabetes Mellitus type 1 ?
When pancreas stops being able to produce insulin
Body cant take glucose and use it for fuel= HYPERGLYCAEMIA
84
What can trigger diabetes type 1??
Coxsackie virus B
Enterovirus
85
What does insulin do?
Decreases blood sugar levels
Produced by pancreas, reduces blood sugar levels
Produced by beta cells in the islets of lagerhans in the pancreas
Anabolic
Reduces blood sugar in 2 ways - causes cells to absorb glucose and use for fuel and causes liver and muscle cells to absorb glucose and use for glycogen
86
What does glucagon do?
Increases blood sugar levels
Produced by alpha cells in the Islets of Langerhans
Catabolic
Tells the liver to break down stores glycogen into glucose and tells hte liver to convert fats and proteins into glucose
Produced when theres LOW blood sugar and when you're stressed
87
what is ketogenesis?
Occurs when theres an insufficient supply of glucose and glycogens stores are exhausted
Liver takes fatty acids and coverts them itno ketones
Ketoacidosis = acertone smell to breath
88
What is glycogenesis
Liver to break down stored glycogen into glucose
89
What is gluconeogenesis
Liver converts fats and proteins itno glucose
90
Presentation of DM1
Hyperglycaemia - polyuria, polydipsia and weight loss
OR
DKA - abdo pain, vomiting and reduced consciousness
OR
Less typical e.g. Secondary enuresis - bed wetting ( in previously dry child) and recurrent infections
91
Features of DKA?
Abdo pain, polyuria, dehydration, kussamul respiration, acetone breath
92
Investigations for DKA?
Finger prick bedside glucose
FBC, renal, glucose
HbA1c
Thyroid function
TTG
Glucose tolerance test
Urine dipstick
C peptide = low
DM specific antibodies
93
What is Hba1c
Amount of glycated haemoglobin nd represented average blood glucose over 2-3 months
94
What is Hba1c
Amount of glycated haemoglobin nd represented average blood glucose over 2-3 months
95
DM specific antibodies?
Anti GAD- T1
ICA- T1
IAA- T1
96
Diagnostic criteria for T1DM
If symptomatic
- Fasting glucose greater than 7
Random glucose greater than 11.1
if asymptomatic - above criteria on 2 separate occasions
97
Typical t1dm clinical ideas -
Ketosis, rapid weight loss, age <50, bmi below 25, personal or family history of autoimmune conditions
98
When would you consider further investigations in adults with suspected t1dm? What does further investigations mean?
Measurement of C peptide and/or diabetes specific autoantibody titres
Age 50+, Bmi of >25, slow evolution
^ atypical factors
99
Management of T1DM?
Insulin
Monitor glucose levels and risk factors e.g. CVD
100
How is insulin given for T1DM?
Long acting background once a day
Short acting 30 minutes before eating carbohydrates
^
basal bolus regime
OR
insulin pump
101
What is a basal bolus regime?
Basal: long acting insulin e.g. Lantus
Bolus: short acting insulin e.g. act rapid
102
2 types of insulin pump?
1. Tethered : have replaceable infusion sets and insulin
2. Patch: sit directly on skin without any visible tubes
103
Short term complications of insulin?
Hypoglycaemia - too much insulin, not enough carbs Hyperglycaemia
104
Symptoms of hypoglycaemia?
Hunger, tremor, sweating, dizziness, irritability, pallor ----> reduced consciousness, coma
105
Treatment of hypoglycaemia?
Rapid acting glucose e.g. Lucozade and slower acting e.g. biscuits
Severe: IV dextrose and IM glucagon
106
Causes of hypoglycaemia?
hypothyroidism, glycogen storage disorder, growth hormone deficiency, liver cirrhosis, MCADD
107
What is nocturnal hypoglycaemia?
Common complication in t1DM
Sweaty
108
Long term complications of diabetes?
Chronic exposure to hyperglycaemia = damage to endothelial cells of blood vessels, leaky malfunctioning vessels unable to regerate, suppression of the immune system and optimal environment for infectious organisms to thrive
109
Macrovascular complications of diabetes?
CAD, peripheral isschaemia, stroke, HTN
110
Microvascular complications of diabetes?
Peripheral neuropathy, retinopathy, kidney disease e.g. gomerulosclerosis
111
Infection related complications of diabetes?
UTIs, pneumonia, skin and soft tissue e.g. in feet, fungal infections
112
Monitoring for diabetes ?
hBa1c - every 3-6 months, shows the glucose level every 3 months as thats the lifespan of RBC
Cap blood glucose
Flash glucose monitoring - sensor in skin - 5 min lag, interstitial fluid
113
Risk factors for t2dm?
Older age, ethnicity, family history, obesity, sedentary lifestyle, high carbohydrate diet
114
Presentation of t2dm?
Fatigue, polydipsia and polyuria, unintentional weight loss, slow healing, glucose in urine
115
What Is the oral glucose tolerance test? ( diabetes checking)
Do it in the morning before breakfast
Baseline plasma glucose, 75g glucose drink, plasma glucose 2 hours later
Tests ability for body to cope with carbohydrate meal
116
Pre diabetes ?
Indication you're heading towards diabetes
Impaired fasting glucose - body struggles to keep glucose in normal ranges
Impaired tolerance - body struggles to cope pressing carbohydrate meals
117
Pre diabetes diagnosis - values?
HbA1c- >48
random glucose >11
Fasting glucose >7
OGTT>11
118
diabetes t2 diagnosis - values?
HbA1c- >48
random glucose >11
Fasting glucose >7
OGTT>11
Note if symptomatic
if asymptomatic - must be on 2 occasions
119
Pre diabetes values - diagnosis?
HBA1c- 42-47
Impaired fasting glucose - 6.1-6.9
Impaired glucose tolerance - plasma glucose at 2 hours 7.8-11
120
Management for T2DM?
Dietary advice
medications
121
Targets for HBA1c for t2dm
48 - new t2dm
53- if moved beyond metformin alone
122
Medications used for t2dm?
Metformin
+ SGLT2 if hf/cvd etc etc
no cvd---> dpp4/pioglitazone/ sulphonyurea
If metformin doesnt work use a different one
123
What does metformin do? - name, side effects?
Biguanide
Increases insulin sensitivity and decreases liver production of glucose
Weight neutral
Side effects: diarrhoea and Abdo pain, lactic acidosis,
124
Thiazolidinedione - what does it Do, example, side effects?
Increases insulin sensitivity and decreases liver production of glucose
Side effects = weight gain, fluid retention, anaemia, HF
Extended use = bladder cancer use increased
125
Sulfonylurea - what does it do? Example? Side effects?
Stimulates insulin release from the pancreas
Gliclazide
Side effects= weight gain, hypoglycaemia, increased risk of CVD and MI when used as monotherapy
126
Incretins - what does it do?
Hormones produced by GI tract, secreted in response to large meals
Increase insulin secretions, inhibit glucagon production, slow absorption by GI tract
127
DPP4 inhibitor
- Reduces the peripheral breakdown of incretins
Inhibits Dpp4 enzyme and increases GLP1 activity
e.g. sitagliptin
Side effects = GI tract upset, URTI symptoms, pancreatitis
128
SGLT2 inhibitors
end with suffix gliflozin
SGLT2 is responsible for reabsorbing glucose from urine into theblood
Block the acting of this protein
Side effects- glucouria, increased rate of UTIs, weight loss
129
First line management of t2dm ?
Assess cardiovascular risk
No = metformin
Yes = metformin and once established + SGLT2 inhibitor
A second drug should be added in type 2 diabetes mellitus if the HbA1c is > 58 mmol/mol
130
If metformin is not tolerated?
e.g. Due to GI side effects
Switch to modified release
130
If metformin is contraindicated?
- If they have risk of CVD/CVD/chronic hf----> SGLT2 monotherapy
- If they don’t have a risk of CVD etc ---> DPP-4 inhibitor OR pioglitazone OR sulfonylurea.
131
Risk factor modification for t2dm?
HTN - ARB or ACE inhibitors
Atorvastatin 20mg , 80mg if known CVdisease
132
What is a DKA?
Not enough insulin to use glucose
133
Ketoacidosis in DKA?
Ketogenesis begins as body has no fuel
= increased glucose and ketones ( liver takes fatty acids and converts them into ketones)
Initially kidney produces bicarbonate to counteract ketone acids and maintain normal pH but overtime = blood is acidic
134
Dehydration in DKA?
Hyperglycaemia overwhelms kidneys
Glucose draws h2o out = osmotic diuresis
Polyuria and polydipsia
135
Potassium imbalance in DKA?
Insulin usually drives K into cells - no insulin so total body K is low as none in cells but serum K is low or high as kidney balances
When treatment with insulin starts patients can get severe hypokalaemia( low in blood) = fatal arrthymia
136
Presentation of DKA?
Hyperglycaemia
Dehydration
Ketosis
Metabolic acidosis
Potassium imbalance
Abdo pain
Polyuria and polydipsia
Kassmasul respiration = deep hyperventilation
Acetone breath
Altered consciousness
137
Diagnosis for DKA?
Hyperglycaemia ( glucose >11)
Ketosis >3
Acidosis
Bicarb >15
138
Complications of DKA?
Gastric stasis, thromboembolism, arrthymias ( hyperkalaemia), acute resp distress, aki,
Iatrogenic - incorrect fluid - cerebral oedema
139
Treatment of DKA?
FIGPICK
F- fluids
Insulin - IV started at 0.1unit/kg/house
Glucose monitoring - ready to give dextrose if needed
Potassium
Infection
Chart
Ketones
140
Specifics for DKA in children for treatment?- key complication?
Cerebral oedema - children at high risk
dehydration and hyperglycaemia causes h2o to move from intracellular space to extracellular space
Causes brain cells to shrink
Rapid corrections can cause rapid shift = brain swells and becomes oedematous
Slow IV fluids, IV mannitol and IV hypertonic saline
141
KA management in children - key things to note
Correct dehydration evenly over 48 hours
Give fixed rate insulin infusion
Avoid fluid bolus
treat underlying triggers
Prevent hypoglycaemia with IV dextrose once glucose falls below 14
Add potassium to IV fluids and monitor
Monitor for oedema
Monitor glucose, ketones and pH
142
What is diabetic neuropathy?
Diabetes leading to sensory loss
Glove and stocking
143
Management of diabetic neuropathy?
First line - amitryptilline, duloxetine, gabapentin or pregablin
Tramadol - exacerbations
Topical capsin - localised pain
Pain management clinics
144
Gastrointestinal autonomic neuropathy?
Gastroparesis
Symptoms include cranial blood glucose control, bloating and vomiting
Management = metoclopramide
Chronic diarrhoea often at night
GORD - decreased lower oesphgeal sphincter pressure
145
What is metaclopramide?
Anti sickness
146
What is diabetic nephropathy?
Most common cause of glomerular pathology adn CKD in UK
Chronic high level of glucose passing through - scarring = glomerulosclerosis
Proteinuria = key sign = damage to glomerulus allows proteins to leak
147
Screening for diabetic nephropathy?
Annual screening using urinary albumin and creatinine ratio
Should be an early morning specimen
ACR >2.5 - microalbuminuria
148
Management for diabetic nephropathy?
Dietary protein control
Glycaemic contro
BP control
ACE inhibitor or any II antagonist, if 3 mol or more ( not dual therapy)
Control dyslipidaemia e.g. statins
149
BP control aim for diabetic nephropathy?
<130/80
150
What is gestational diabetes?
Triggered by pregnancy
Caused by reduced insulin sensitivity
151
Complication of gestational diabetes?
Large for dates baby
Macrosomea ( big baby)
Implications for birth - risk of shoulder dystocia
152
Risk factors for gestational diabetes ?
BMI >30 kg/m2
Previous gestational diabetes
Previous macrosucie baby
First degree relative with diabetes
Ethnic origin ( black carribean, south Asian and middle eastern)
153
Screening for gestational diabetes?
oral glucose tolerance test
24-28 WEEKS: Used in patients with risk factors or features that suggest gestational diabetes: large for dates, polyhydraminos( high amniotic fluid), glucose on urine dipstick
If had gestational previously: Perform ASAP and at 24-28 weeks If its normal
Performed in the morning after a fast - measure glucose
75g glucose drink and measure after 2 hours
154
What result indicates gestational diabetes?
5678
>5.6 fasting
>7.8 at 2 hours
155
Management of gestational diabetes?
Joint diabetes and antenatal clinics ASAP
Dietician and exercise
Self monitoring of blood glucose
4 weekly USS to monitor fatal growth and amniotic fluid volume from 28-36 weeks gestation
156
Specifics - when to give medication for gestational diabetes?
<7 - exercise and diet for 1-2 weeks, followed by metformin and then insulin
>7- insulin +/- metfmronin
6-6.9 + evidence of complications = insulin +/- metformin
157
Pre existing diabetes- pregnant patients
Weight loss for BMI >27
5mg folic acid from preconception till 12 weeks gestation
Stop oral hypoglycaemic medications -apart from metformin and insulin
Retinopathy screening
Planned delivery between 27 and 38 weeks
Tight glycemic control
Annually scan at 20 weeks including heart
158
Causes of galactorrhea?
Idiopathic, prolactinoma, drugs e.g. antipsychotics, SSRIs, cimetidine, beta blockers
Metabolic contiions e.g. hypothyroidism, liver disease, chronic renal impairment
159
Smooth goitre causes?
◦ Graves
◦ Hasmiotos
◦ Drugs e.g. lithium and amiodarone
◦ Iodine deficiency/ excress
◦ De Quervains thyroiditis ( painful)
◦ Infiltration ( e..g sarcoid and haemochormatosis)
160
Nodular goitre causes?
◦ Toxic solitary adenoma
◦ non functional thyroid adenoma
◦ Multinodular
◦ Thyroid cyst
◦ Cancer
161
Primary hyperlipidaemia?
Often due to genetic factors interacting with environmental factors
Familial hypercholesteraemia is caused by mutation in the LOLR gene - autosomal dominant
162
What is secondary hyperlipidaemia? What are the types?
Described based on the type of lipid elevated in the blood
Secondary cholesterolaemia and secondary hypertriglyceridaemia
163
Causes of secondary hypercholesterolaemia?
Hyperthyroidism, pregnancy, nephrotic syndrome, anorexia, drugs e.g. glucocorticoids and androgens
164
Causes of secondary ypertriglyceridaemia?
T2DM, CKD, obesity, excess alcohol, hepatocellular disease and drugs e.g. B blockers and glucocorticoids
165
Clinical features of hyperlipidaemia?
Often asymptomatic
Can present with features of acute pancreatitis
History commonly includes CVD history, FH of CVD< alcohol, smoking, obesity
Xanthomata, xanthelasmata, corneal arcus
166
What are tendon xanthomata?
Hard painless nodules over bones
FH
167
What are xantholesma?
Lipid laden nodules on eyelids
168
What is premature corneal arcus?
Bluish rims around irises
169
Investigations for hyperlipidaemia?
Lipid profile
TC/hdl ratio
Excess alcohol - lfts - GGT
ckd - renal function - high urea and creatinine
Nephrotic disease - low albumin, dipstick for proteinuria
Thyroid function
170
Simon Broome criteria
For familial hypercholesteraemia
171
HHS- what is it
Hyperglycaemia results in osmotic diuresis with associated sodium and potassium loss
Severe volume depletion results in raised serum osmolarity and hyperviscocity of the blood
SEVERE electrolyte loss but patient may not look as dehydrated as they are
T2DM
172
Presentation of HHS?
Fatigue, lethargy, nausea and vomiting
Altered consciousness, headaches, papilloedema, weakness
Haematological: hyperciscosity = MI, stroke, peripheral arterial thrombosis
Cardio - dehydration, HTN and bradycardia
173
Diagnosis of HHS?
Hypovolaemia
Marked hyperglycaemia WITHOUT KETONAEMIA OR ACIDOSIS
Significantly raised serum osmolarity
174
Management of HHS?
Normalise osmolality = serum osmolality, if not available can be estimated by 2(NA+glucose+urea)
Replace fluids and electrolytes
Normalise blood glucose
Fluid replacement ( IV sodium chloride ) THEN insulin then potassium
175
What is hyperparathyroidism?
High PTH = high calcium
176
How does PTH increase blood calcium?
Increasing osteoclast activity in bones.
Increasing calcium absorption from the gut
Increasing calcium absorption from the kidneys
Increasing vitamin D activity - vitamin D increases calcium absorption from the intestines
177
Symptoms of hyperparathyroidism?
Symptoms of hypercalcaemia
Renal stones, painful bones, abdo groans - constipation, nausea and vomiting, psychic moans - fatigue, depression and psychosis
peptic ulceration, pancreatitis, HTN, polyuria, polydipsia, anorexia
178
Primary hyperparathyroidism
Uncontrollable PTH produced directly by a tumor of parathyroid glands
Leads to hypercalcaemia
Sterotypically seen in elderly females with unquenchable thirst and inappropriately normal or raised PTH
179
Commonest tumor - primary hyperparathyroidism?
Solidativity adenoma
Hyperplasia
Multiple adenoma
180
Associations of primary hyperparathyroidism?
HTN, multiple endocrine neoplasia = MEN I and II
181
Investigations for primary hyperparathyroidism?
Raised Ca, low phosphate , high PTH
PTH may be raised
Pepperpot skull - XRAY
182
Treatment for primary hyperparathyroidism?
Total parathyroidectomy
and Cinacalcet - calimimetic... mimics the action of calcium on tissues by allosteric activation the calcium sensing receptor- reduces production of PTH
183
Secondary hyperparathyroidism?
Insufficient vitamin D or chronic renal failure leads to low absorption of calcium from intestines, kidneys and bones
Hypocalcaemia - tingling in mouth/feet and fingers, seizures, stiffening
Parathyroid glands react by excreting more PTH-overtime cells in glands increase - hyperplasia, glands become bulkier
HIGH PTH, LOW CALCIUM, phosphate high, vitamin D low
184
How to treat secondary hyperparathyroidism?
Correct vitamin D deficiency/ renal transplant
185
Tertiary hyperparathyroidism?
Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder
or
high level of PTH without previous pathology = high levels of absorption of calcium = hypercalcaemia
HIGH CALCIUM AND HIGH PTH, phoshate decreased or normal
ALP high
186
Presentation of tertiary hyperparathyroidism?
Metastatic calcification
Bone pain and / or fracture
Nephrolithiasis
Pancreatitis
187
What is hashimotos?
Autoimmune disorder of the thyroid gland associated with hypothyroidism
May be transient thyrotoxicosis in the acute phase
More common in women
188
Features of hashmitos? What type of antibodies?
features of hypothyroidism
goitre: firm, non-tender
anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies
189
Associations of hashimotos?
other autoimmune conditions e.g. coeliac disease, type 1 diabetes mellitus, vitiligo
Hashimoto's thyroiditis is associated with the development of MALT lymphoma
190
Symptoms of hypotesosteronism?
lethargy, weakness, weight gain, libido loss, ED, gynaecomastia, depression
191
Primary hypoparathyroidism?
Decrease in PTH secretion due to e.g. thyroid surgery
LOW calcium, HIGH phosphate
192
What is the treatment for primary hypoparathyroidism?
Alfacalcidol
193
Symptoms of hypoparathyroidism?
Tetany - muscle twitching, cramping, spasm
Perioral paraesthesia
Trousseaus sign: carpal spasm if brachial artery occluded by blood pressure cuff inflation
Chvotecks sign: tapping over parotid causes facial muscles to twitch
ECG: QT interval prolonged
Chronic - depression and cataracts
194
What is pseudohypoparathyroidism?
Target cells insensitive to PTH
Due to abnormality in a G protein
Associated with low IQ, short stature, shortened 4th and 5th metacarpals
Low calcium, high phosphate and high PTH
195
Diagnosis of psuedohypoparathyroidism?
Urinary cAMP and phosphate levels following pTH infusion
Type 1 - neither of them rises
type 2- cAMP rises
196
What is pseudopsuedohypoparathyroidism?
Similar phenotype to pseudo but normal biochem
197
Hypothyroidism?
More common in females
Inadequate output of thyroid gland
Can be congenital or acquired and primary of secondary
198
Congenital hypothyroidism?
Child born with under-active thyroid gland
Either underdevelopment of the gland or not enough hormone
Screened at birth with newborn blood spot screening test
199
Symptoms of congenital hypothyroidism?
Prolonged neonatal jaundice, poor feeding, constipation, increased sleeping, reduced activity, slow growth ad development
200
Types of acquired hypothyroidism?
Hashimotos, dietary iodine deficiency, subacute, riedel thyroidits, secondary to hyperthyroidism treatment, medications
201
Hashmiotos associations?
T1DM, coeliac, pernicious anaemia
May cause transient thyrotoxicosis
Associated with anti TPO and antithryoglobulin antibodies
202
Medications that can cause acquired hypothyroidism?
Lithium ( inhibits thyroid hormone production = goitre and hypothyroidism)
Amiodarone - interfere with thyroid hormone production = CAN CAUSE BOTH HYPER AND HYPO
203
What is secondary hypothyroidism?
Pituitary gland fails to produce enough TSH, associated with lack of other hormones e.g. ACTH
204
Causes of secondary hypothyroidism?
Tumors, infection, vascular, radiation
205
Associated conditions for secondary hypothyroidism?
Coeliac, turners, downs
206
Presentation and features of hypothyroidism?
Weight gain, fatigue, dry skin, coarse skin and hair loss, heavy/irregular periods, constipation, fluid reunion, hoarse voice, non pitting oedema, loss of lateral aspect of the eyebrows, decreased deep tendon reflexes, carpal tunnel
207
What do thyroid function tests show for primary hypothyroidism?
Thyroid gland
High TSH
Low t3 and t4
208
What do thyroid function tests show for secondary hypothyroidism?
Pituitary gland
Low TSH
Low T3 and t4
209
Management of hypothyroidism?
Levothyroxine
210
Side effects of levothyroxine?
Hyperthyroidism, reduced bone mineral density, angina worsening, AF
211
Interactions - levothyroxine?
Iron, calcium carbonate tablets can reduce absorption
212
Causes of hypercalcaemia?
Primary hyperparathyroidism
malignancy
drugs e.g. thiazides, dehydration, granulomas, vitamin D toxication, Addisons, throtoxicosis, acromegaly, pages disease of hte bone
213
Causes of hypercalcaemia?
Primary hyperparathyroidism
malignancy
drugs e.g. thiazides, dehydration, granulomas, vitamin D toxication, Addisons, throtoxicosis, acromegaly, pages disease of the bone
214
Features of hypercalcaemia?
Bones, groans, stones and psychic mones
Corneal calcification
Shortened QT
HTN
215
Malignancy causing hypercalcaemia?
PTH from a tumor
bony metastes
Myeloma - increased bone resorption caused by coal cytokines released by myeloma cells
216
Management of hypercalcaemia?
Rehydration with normal saline - 3-4 litres a day
Bisphosphates- take 2-3days to work, most effect seen at 7 days
Calcitonin
Steroids in sarcoidosis
217
Causes of hypocalcaemia?
Vit D deficiency, CKD, hypoparathyroidism, psuedohypoparathyroidsm, rhabdo, magnesium deficiency, blood transfusion, acute pancreatitis
218
management of hypocalcaemia?
IV calcium gluconate 10ml of 10% solution over 10 minutes
IV CaCl2 - local irritation
ECG monitoring
219
Prolonged QT< seizures, carpopedal spasm?
Hypocalcaemia
220
MEN type I presentation?
Tumors in parathyroid, pituitary, pancreas
MENI gene
HYPERCALCAEMIA
221
MEN TYPE II presentation?
Medullary thyroid cancer
Parathyroid tumor
Phaeochromocytoma
RET oncogene
222
MENII type b
Medullary thyroid cancer
Phaeochromocytoma
Neuromas
RET oncogene
223
Management of obesity?
Conservative e.g. diet and exercise
Medical
Surgical
224
Medical management of obesity and indications for treatment?
Orlistat
Pancreatic lipase inhibitor
Can give faecal urgency
ONLY prescribed if: BMI of 28 + risk factors or BMI of 30 or continued weight loss or if normally used for < 1 year .
225
What is bariatric surgery for obesity
primary restrictive - gastric banding. sleeve gastrectomy
Primary malabsorptive options- biliopancreatic diversion with duodenal switch
Mixed operations- gastric bypass surgery
226
What is a pheochromocytoma?
A phaeochromocytoma is a tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline)
Tumour of the chromatin cells
INTERMITTENT symptoms - bursts of adrenaline
227
Which genetic disorders are phaeochromocytomas more common in?
MEN 2
NF1
Von hip Lindau disease
228
Presentation of phaeochromocytomas?
Anxiety
Sweating
Headache
Tremor
Palpitations
Hypertension
Tachycardia
- EXCESSIVE adrenaline
- intermittent
229
Diagnosis of phaeochromocytoma?
Plasma free meanephrines - breakdown product of adrenaline
24 hour urinary catecholamines - adrenaline over 24 hours
CT or MRI to look for the tumour
Genetic testing to look for genetic cause
230
management of pheochromocytoma?
Alpha blockers (e.g., phenoxybenzamine or doxazosin)
Beta blockers, only when established on alpha blockers
Surgical removal of the tumour
231
Causes of infertility?
male factor 30%
unexplained 20%
ovulation failure 20%
tubal damage 15%
other causes 15%
232
Basic investigations for infertility?
Serum analysis
Serum progesterone 7 days prior to expected next period
233
Genetic causes of infertility?
Turner's syndrome (XO), Kleinfelter's syndrome (XXY).
234
Ovulation/endocrine disorders - causes of infertility?
Polycystic ovary syndrome
Pituitary tumours
Sheehan's syndrome (pituitary infarction due to haemorrhagic shock during labour)
Hyperprolactinaemia
Cushing's syndrome
Premature ovarian failure
235
tubal abnormalities causing infertility?
Congenital anatomical abnormalities, Adhesions following pelvic inflammatory disease - secondary to chlamydia or gonorrhoea
236
Uterine abnormalities causing infertility?
Bicornate uterus, Fibroids Asherman's syndrome (adhesions of the uterus)Endometriosis
237
Testiular disorders that can cause infertility?
Cryptorchidism, Varicocele. Testicular cancer
238
What is a pituitary adenoma?
Benign tumour of the pituitary gland
Prolactin's are the most common
239
Classification of pituitary adenomas?
Size and Hormonal
240
Size and hormone classification of pituitary adenomas?
Size = micro adenoma <1cm, macro adenoma >1cm
Hormonal - secretory vs non secretory
241
How do pituitary adenoma cause symptoms?
Excess hormone e.g. excess GH
Depletion of hormone due to compression of normal functioning pituitary gland
Stretching of drug within the pituitary fossa = headaches
Compression of the optic chasm = bitemporal hemianopia
OR if incidental = pituitary icidentaloma
242
Investigations for pituitary adenomas
Pituitary blood profile ie GH, prolactin, ACTH
Formal visual field testing
MRI brain WITH contrast
243
Differentials for pituitary adenoma?
Pituitary hyperplasia, craniopharyngylgioma, meningioma, brain metastases, lymhoma, vascular malformations
244
Treatment for pituitary adenoma?
Hormone therapy
Surgery
Radiotherapy
245
What are prolactinomas?
Type of pituitary adenoma
Most common type
Produce an excess of prolactin
246
Presentation of prolactinomas?
excess prolactin in women
amenorrhoea
infertility
galactorrhoea
osteoporosis
excess prolactin in men
impotence
loss of libido
galactorrhoea
other symptoms may be seen with macroadenomas
headache.
visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia)
symptoms and signs of hypopituitarism
247
Diagnosis of prolactinoma?
MRI
248
Management of prolactinomas?
symptomatic patients are treated medically with dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland
surgery is performed for patients who cannot tolerate or fail to respond to medical therapy. A trans-sphenoidal approach is generally preferred unless there is a significant extra-pituitary extension
249
What is subclinical hyperthyroidism?
* Mildly reduced TSH and normal t3 and t4
* no obvious symtpoms
250
Causes of subclinical hyperthyroidism?
* Multinodular goitre, especially in elderly females
251
Management of subclinical hyperthyroidism?
Excluding other causes of a raised TSH such as inter-current illness.
Rechecking thyroid function in 3-6 months.
Most patients require no treatment.
Thyroxine replacement is an option although there is little evidence to show benefit.
252
What is subclinical hypothyroidism?
Mildly increased TSH and normal t3 and t4
253
What medication can suppress TSH?
Steroids, lithium, antiparkinson medication
254
What causes benign thyroid nodules?
Multinodular goitre, thyroid adenoma. hashmitos, cysts
255
What causes malignant thyroid nodules?
Papillary, folicular,medullary, anaplastic carcinomas and lymphoma
256
Investigations for thyroid nodules?
thyroid function
Ultrasonography
257
Causes of thyroxotoxicosis?
Graves, multi nodular goitre, acute phase of subacute thyroiditis, acute phase of hashimotos, amiodarone therapy
258
Investigations for thyrotoxicosis?
TSH down, t4 and t3 up
Thyroid autoantibodies
Thyroid scintigraphy - diffuse, homogenous increased uptake of radioactive iodine
259
Features of thyrotoxicosis?
General = weight loss, manic, restlessness, heat intolerance
High output cardiac failure, palpitations, tachy
Sweating, pretibial myxoedema- redness, oedematous lesions above lateral malleoli, clubbing
Diarrhoea, oligomenorrhoea, anxiety, tremor
260
treatment of thyrotoxicosis?
Thionamide drugs = antithyroid drugs, methimazole pTU, carbimazole
Radioactive iodine
beta blockers
261
What is hyperthyroidism?
Overproduction of thyroid hormone by thyroid gland
262
Primary hyperthyroidism?
Thyroid itself is behaving abnormally and producing excess thyroid hormone
263
Secondary hyperthyroidism?
Due to excessive TSH - pituitary pathology
264
What is graves?
Autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism
Mimic TSH
265
What is toxic multi nodular goitre?
Plummers disease
Nodules develop on thyroid gland
Act independently of normal feedback system and continuously produce excessive thyroid hormone
266
What is exophthalmos?
Buldging of the eyeball out oft the socket caused by graves
Due to inflammation, swelling and hypertrophy of the tissue behind eyeball - forces eyeball forward
267
What is exophthalmos?
Buldging of the eyeball out oft the socket caused by graves
Due to inflammation, swelling and hypertrophy of the tissue behind eyeball - forces eyeball forward
268
What is pretibial myxoedema?
Derm condition
Deposits of mucin under the skin on the anterior aspect of the lung
Discoloured, waxy, oedematous skin appearance
Reaction to TSH receptor antibodies- specfici to Graves
269
De quervains thyroiditis?
Viral infection with neck pain, fever, hyperthyroidism symptoms
Hyperthryodi phase followed by hypothyroid phase
Self limiting conditions - NSAIDs and beta blockers
270
What is a thyroid storm?
Rare presentation of hyperthyroidism
Severe presentation with pyrexia, tachycardia, delirium
Admission - anti arrthymic, beta blockers, fluid rescuitations
271
Treatment for hyperthyroidism?
Carbimazole first line
Propylthiouracil second line
Radioactive iodine
Beta blockers
Surgery
272
Radioactive iodine - hyperthyroidism
Drinking a dose
Taken up by thyroid gland + radiation destroys some cells = decrease in thyroxine production =remission from hyperthyroidism
Remission can take 6 months
MUST NOT BE PREGNANT
273
BETA BLOCKERS - hyperthyroidism ?
Block adrenaline related symptoms
Propranol - on selective instead of others that only work on the heart
Great for thyroid storm
274
What is Waterhouse fiderichsens syndrome?
caused by a severe bacterial infection which results in disseminated intravascular coagulation and subsequent adrenal haemorrhage and failure.
The adrenal haemorrhage is usually bilateral but can be unilateral.
275
Causes of Waterhouse fiderichsens syndrome?
The most common cause is Neisseria meningitidis but other bacterial infections may also be responsible e.g. streptococcus pneumoniae.
276
Clinical features - Waterhouse fiderichsens syndrome
non-specific infection which progresses into a macular, petechial and subsequently purpuric rash along with septic shock
277
Surgery for hyperthyroidism - what must you consider after
They will be hypothyroid =LEVOTHYROXINE
278
2nd line for T2DM management - if targets are not met
- Dual therapy: add one of the following:
○ Metformin + DPP4 inhibitor
○ Metformin + pioglitazone
○ Metformin + sulfonylurea
○ Metformin + SGLT2 inhibitor
279
Sick day rules - T2DM
- Temporarily stop some oral hypoglycaemics during an acute illness
- Medication may be restarted once person feeling better and eating and drinking for 24-48 hours
○ Metformin stopped if risk of dehydration to reduce lactic acidosis risk
○ Sulphonyureas may increase hypo risk
- Monitor blood glucose more frequently
280
Sick day rules - T1DM
If on insulin- MUST NOT STOP IT! - risk of DKA.
Check blood glucose more frequently.
Maintain normal meal pattern- or carbohydrate containing drinks like milkshakes, fruit juices and aim to drink 3L of fluid a day to prevent dehydration
281
Investigating hypoglycaemia? What do markers show?
Serum insulin and c-peptide levels can be measured
High insulin, High C peptide = endogenous insulin production - insulinoma or sulfonylurea abuse
High insulin , low C peptide = exogenous insulin administration
282
What is sick euthyroid syndrome/
TSH, thyroxine etc low
NO TREATMENT NEEDED.
changes are reversible on recovery from systemic illness
283
What can reduce teh absorption of levothyroxine?
Ferrous sulphate/ calcium carbonate tablets
284
Thyroid eye Disease
Effects people with graves
Smoking most important risk factors
Exposure keratopathy
285
AAAMedicine
flashcards
Decks in class (42)
# Cards
-
Respiratory Conditions237
-
Renal327
-
Gastro conditions396
-
Neurology conditions326
-
Cardiology Conditions281
-
Endocrine286
-
Breast104
-
murmurs and arrythmias21
-
Psych192
-
Neonates69
-
Paediatrics495
-
Drugs2
-
Rheumatology199
-
Opthalmology conditions141
-
Ortho206
-
Anaesthetics127
-
ENT Conditions104
-
Dermatology conditions225
-
Vascular conditions113
-
Haematology196
-
Infectious diseases31
-
quick Acute + Pharma68
-
Pharma2
-
Resp quick80
-
Renal quick7
-
Cardio quick49
-
Neuro quick66
-
Older person - dementia, palliative29
-
Dermy quick39
-
Renal quick54
-
Endo quick38
-
Oppy quick34
-
GI quick56
-
MSK quick61
-
Paeds quick72
-
ENT quick26
-
O+G and sex health quick3
-
Other quick60
-
Psychy quick41
-
Gynaecology171
-
OBS263
-
Sexual Health & Contraception116
