Endocrinology Flashcards
1
Q
Mechanism of action of metformin
A
Increases insulin sensitivity
Decreases glucose production by the liver
2
Q
SEs metformin
A
- GI symptoms, including pain, nausea, and diarrhoea
- Lactic acidosis
3
Q
SGLT-2 inhibitors naming
A
End in -gliflozin
4
Q
Mechanism of action of SGLT-2 inhibitors
A
Inhibit sodium-glucose co-transporter 2 protein found in proximal tubules of kidneys, causing glucose to be lost to urine
5
Q
Can SGLT-2 inhibitors cause hypoglycaemia?
A
Yes if combined with insulin or sulfonylureas
6
Q
Use of SGLT-2 inhibitors in heart failure
A
Reduce risk of cardiovascular disease, empagliflozin and dapagliflozin licensed for heart failure
7
Q
Use of SGLT-2 inhibtors in CKD
A
Dapagliflozin licensed in CKD
8
Q
SEs SGLT2 inhibitors
A
- Glycosuria
- Increased UO and frequency
- Genital and urinary tract infections
- Weight loss
- DKA (with only moderately raised glucose)
- Lower-limb amputation (with canagliflozin)
- Fournier’s gangrene
9
Q
Thiazolidinedione e.g.
A
Pioglitazone
10
Q
Mechanism of action of pioglitazone
A
- Increases insulin sensitivity
- Decreases liver production of glucose
11
Q
SEs pioglitazone
A
- Weight gain
- Heart failure
- Increased risk of bone fractures
- Small increase risk of bladder cancer
12
Q
Sulfonylurea e.g.
A
Gliclazide
13
Q
Mechanism of action of sulfonylureas
A
Stimulate insulin release from pancreas
14
Q
SEs sulfonylureas
A
Weight gain
Hypoglycaemia
15
Q
DPP-4 inhibitors e.g.
A
Sitagliptin
Alogliptin
16
Q
SEs DPP-4 inhibitors
A
Headaches
Acute pancreatitis
17
Q
GLP-1 mimetics e.g.
A
Exenatide
Litaglutide
18
Q
Route of administration GLP-1 mimetics
A
SC injection
19
Q
Other use of litaglutide
A
Weight loss in non-diabetic obese patients
20
Q
SEs GLP-1 mimetics
A
Reduced appetite
Weight loss
GI symptoms, including discomfort, nausea, and diarrhoea
21
Q
Rapid acting insulin e.g.
A
NovoRapid
22
Q
Cause acromegaly
A
Excess GH secreted by pituitary adenoma in 95% cases
Minority cases caused by ectopic GNRH or GH production by tumours, e.g. pancreatic
23
Q
Features acromegaly
A
Coarse facial appearance, spade-like hands, increase in shoe size
Large tongue, prognathism, interdental spaces
Excessive sweating and oily skin
24
Q
Features of pituitary tumour
A
Hypopituitarism
Headaches
Bitemporal hemianopia
25
Complications acromegaly
Hypertension
Diabetes
Cardiomyopathy
Colorectal cancer
26
Prolactin in acromegaly
1/3 of patients have raised prolactin → galactorrohoea
27
First line investigation acromegaly
Serum IGF-1 levels
28
What to do if serum IGF-1 raised
OGTT
29
Interpretation of OGTT in acromegaly
In normal patients, GH suppressed to <2mu/L with hyperglycaemia
In acromegaly no suppression of GH
30
Further investigations acromegaly
Pituitary MRI may demonstrate pituitary tumour
31
What is Addison's disease
Autoimmune destruction of adrenal glands, leading to reduced cortisol and aldosterone - accounts for 80% of cases of primary hypoadrenalism
32
Features Addison's disease
Lethargy
Weakness
Anorexia, nausea and vomiting, weight loss
Salt craving
Hyperpigmentation, esp palmar creases
Vitiligo
Loss of pubic hair in women
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia
33
Features Addisonian crisis
Collapse
Shock
Pyrexia
34
Other cause of primary hypoadrenalism
TB
Metastases, e.g. bronchial carcinoma
Meningococcal septicaemia
HIV
Antiphospholipid syndrome
35
Secondary causes hypoadrenalism
Pituitary disorders - tumours, irradiation, infiltration
36
First line investigation Addison's disease
ACTH stimulation test (short Synacthen test)
37
How is short synacthen test carried out
Plasma cortisol measured before and 30 mins after 250ug IM synacthen
38
Investigations of Addison's when SST not available
9am serum cortisol
39
Interpretation 9am serum cortisol in Addisons
>500nmol/L makes Addison's very unlikely
<100nmol/L definately abnormal
100-500nmol needs ACTH stimulation
40
Electrolyte abnormalities in Addison's
Hyperkalaemia
Hyponatraemia
Hypoglycaemia
Metabolic acidosis
41
Management Addison's disease
Hydrocortisone - 2 to 3 divided doses, typically need 20-30mg/day
Fludrocortisone
42
Management Addison's during intercurrent illness
Glucocorticoid dose should be doubled, fludrocortisone dose stays the same
43
Use of carbimazole
Used in thyrotoxicosis - typically given in high doses for 6 weeks until patient becomes euthyroid before being reduced
44
Adverse effects carbimazole
Agranulocytosis
Crosses placenta (can be used in low doses during pregnancy)
45
Glucocorticoid vs mineralocorticoid activity fludrocortisone
MInimal gluco
Very high mineralo
46
Glucocorticoid vs mineralocorticoid activity hydrocortisone
Some gluco
High mineralo
47
Glucocorticoid vs mineralocorticoid activity prednisolone
Predominant glucoco
Low mineralo
48
Glucocorticoid vs mineralocorticoid activity dexamethasone/betmethasone
Very high gluco
Minimal mineralo
49
Endocrine SEs glucocorticoids
Impaired glucose regulation
Increased appetite/weight gain
Hirsuitism
Hyperlipidaemia
Cushing's
50
MSK SEs glucocorticoids
Osteoporosis
Proximal myopathy
Avascular necrosis of femoral head
51
Immunosuppressive SEs glucocorticoids
Increased susceptibility severe infection
Reactivation of TB
52
Psychiatric SEs glucocorticoids
Insomnia
Mania
Depression
Psychosis
53
GI SEs glucocorticoids
Peptic ulceration
Acute pancreatitis
54
Opthalmic SEs glucocorticoids
Glaucoma
Cataracts
55
Other SEs glucocorticoids
Suppression of growth in children
Intracranial HTN
Neutrophilia
56
SEs mineralocorticoids
Fluid retention
Hypertension
57
When is gradual withdrawal of steroids required
More than 40mg pred daily for more than 1 week
More than 3 weeks of treatment
Recently received repeated courses
58
ACTH dependant causes Cushing's syndrome
Cushing's disease
Ectopic ACTH production, e.g. SCLC
59
What is Cushing's disease
Pituitary tumour secreting ACTH → adrenal hyperplasia
60
ACTH independent causes Cushin's syndrome
Iatrogenic - steroids
Adrenal adenoma
Adrenal carcinoma
Carney complex (syndrome including cardiac myxoma)
Micronodular adrenal dysplasia
61
Causes pseudo-Cushing's
Alcohol excess
Severe depression
62
How to differentiate Cushings syndrome and pseudocushings
Insulin stress test
63
Features Cushing's
Round face
Central obesity
Abdominal striae
Buffalo hump
Proximal limb muscle wasting
Hirsuitism
Easy bruising, poor skin healing
64
Findings on gas Cushings
Hypokalaemic metabolic alkalosis
65
First line test Cushing's syndrome
Overnight dexamethasone suppression test
66
Other tests to confirm Cushing's syndrome
24 hr urinary free cortisol
Bedtime salivary cortisol
Both need 2 measurements
67
Finding on overnight dexamethasone supression test in Cushing's
Patients with Cushing's do not have their morning cortisol spike suppressed
68
First line localisation tests Cushing's syndrome
9am and midnight plasma ACTH and cortisol
69
Interpretation 9am and midnight ACTH in Cushing's
If ACTH suppressed, non-ACTH dependent cause likely
70
Other localisation tests Cushing's syndrome
High-dose dexamethasone suppression test
CTH stimulation
Petrosal sinus sampling of ACTH
Insulin stress test
71
Interpretation high-dose dexamethasone suppression test
If cortisol suppressed and ACTH suppressed, Cushing's disease (pituitary adenoma → ACTH secretion
If cortisol not suppressed but ACTH is, Cushing's syndrome due to other causes
If neither cortisol or ACTH suppressed, ectopic ACTH syndrome
72
Interpretation CRH stimulation in Cushings
If pituitary source, cortisol rises
If ectopic/adrenal, no change in cortisol
73
Use of petrosal sampling in Cushing's
Differentiate between pituitary and ectopic ACTH secretion
74
Use of insulin stress test in Cushing's
Differentiate between Cushing's and pseudo-Cushings
75
C-peptide in T1DM
Typically low
76
Use of antibodies in diagnosis of diabetes mellitus
Useful to distinguish between T1DM and T2DM
77
Antibodies in T1DM
Anti-GAD
Islet cell antibodies
Insulin autoantibodies
Insulinoma associated 2 autoantibodies (IA-2A)
78
Diagnostic criteria T1DM
If symptomatic:
- Fasting glucose greater than or equal to 7.0mmol/L
- Random glucose greater than or equal to 11.1mmol/L
If asymptomatic, above criteria on 2 seperate occasions
79
Features favouring T1DM over T2DM
Ketosis
Rapid weight loss
Age of onset below 50
BMI below 25
Personal and/or family history autoimmune disease
80
When to consider further tests to distinguish T1DM from T2DM
If T1DM suspected, but clinical presentation involves some atypical features, e.g. over 50, BMI over 25, slow evolution of hyperglycaemia
81
Features favouring T2DM over T1DM
Over 40
Respond well to oral hypoglycaemic
82
Criteria for diagnosis of T2DM
If symptomatic:
- Fasting glucose greater than or equal to 7.0mmol/L
- Random glucose greater than or equal to 11.1mmol/L
- HbA1c ≤48mmol/mol (6.5%)
If asymptomatic, above criteria on 2 seperate occasions
83
When can't HbA1c be used to diagnose diabetes
Haemoglobinopathies
Haemolytic anaemia
Untreated iron deficiency anaemia
Suspected gestational diabetes
Children
HIV
CKD
Taking medications that may cause hyperglycaemia, e.g. corticosteroids
84
Criteria impaired fasting glucose
Fasting glucose ≥6.1 but <7.0
85
Criteria impaired glucose tolerance
Fasting plasma glucose less than 7.0, OGTT value ≥7.8mmolL but less than 11.1
86
Diabetic drug adjustments for Ramadan
For patients taking metformin, dose split 1/3 before sunrise and 2/3 after sunset
For patients on OD sulfonylureas, change to after sunset. For BD, larger proportion of dose taken after sunset
87
Screening for diabetic foot disease
At least annually
Ischaemia - palpating for dorsalis pedis and posterior tibial pulse
Neuropathy - 10g monofilament various parts of sole of foot
88
Low risk diabetic foot disease criteria
No risk factors except callus alone
89
Moderate risk diabetic foot disease criteria
Deformity
Neuropathy
Non-critical limb ischaemia
90
High risk diabetic foot disease criteria
Previous ulceration
Previous amputation
Renal replacement therapy
Neuropathy and non-critical limb ischaemia
Neuropathy with callus and/or deformity
Non-critical limb ischaemia with callus and/or deformity
91
Diagnostic criteria DKA
Glucose >11 or known diabetes
pH >7.3
Bicarb <15
Ketones >3mmol/L or urine ketones ++
92
Management DKA
- Fluid replacement
- Insulin
- Correcting electrolyte disturbance
93
Insulin regime in DKA
IV insulin infusion started at 0.1unit/kg/hour
Once glucose <14, infusion of 10% dextrose should be started at 125ml/hour in addition to 0.9% NaCl regime
94
Management of potassium in DKA
Serum potassium often high on admission, but quickly falls with insulin treatment, resulting in hypokalaemia, so potassium added to replacement fluids
If rate of K infusion greater than 20mmol/hour, cardiac monitoring
95
Management of regular insulin in DKA
Long acting insulin continued, short acting insulin stopped
96
How much potassium to add to replacement fluids in DKA
If K over 5.5, none
If K 3.5-5.5, 40mmol/L
If K below 3.5, senior review
97
DKA resolution defined as
pH >7.3
Blood ketones <0.6mmol/L
Bicarb >15
98
When should DKA resolution be achieved by
Within 24 hours - if not, senior review from endocrinologist
99
When can patient switch to SC insulin in DKA
Once resolution criteria met and patient eating and drinking
100
Complications DKA
- Gastric stasis
- Thromboembolism
- Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
- ARDS
- AKI
Iatrogenic due to incorrect fluids - cerebral oedema, hypokalaemia, hypoglycaemia
101
Who is at most risk from cerebral oedema in DKA treatment
Children/young adults
102
Presentation cerebral oedema in DKA treatment
Headache
Irritability
Visual disturbance
Focal neurology
103
When does cerebral oedema occur in DKA treatment
4-12 hours after commencing treatment
104
Investigation suspected cerebral oedema in DKA treatment
CT head
105
Presentation diabetic peripheral neuropathy
Typically sensory loss not motor - glove and stocking distribution
106
First line treatment pain from diabetic peripheral neuropathy
Amitriptyline, duloxetine, gabapentin, or pregabalin
107
'Rescue therapy' for exacerbation of pain diabetic peripheral neuropathy
Tramadol
108
Treatment localised neuropathic pain in diabetes
Topical capsaicin
109
GI autonomic neuropathy in diabetes causes...
Gastroparesis
Chronic diarrhoea
GORD
110
Symptoms gastroparesis diabetes
Erratic glucose control
Bloating
Vomiting
111
Management gastroparesis diabetes
Metoclopramide
Domperidone
Erythromycin
112
Features chronic diarrhoea caused by diabetic neuropathy
Often occurs at night
113
Causes of falsely low HbA1c
Sickle cell anaemia
G6PD deficiency
Hereditary spherocytosis
Haemodialysis
114
Causes of falsely high HbA1c
Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy
115
What is Graves disease
Autoimmune thyroid disease in which body produces IgG antibodies to TSH receptor, stimulating it
116
Features specific to Graves disease
Eye signs - exopthalmos, opthalmoplegia
Pretibial myxoedema
Thyroid acropachy - digital clubbing, soft tissue swelling of hands and feet, periosteal new bone formation
117
Autoantibodies seen in Graves
TSH receptor stimulating antibodies (90%)
Anti-thyroid peroxidase antibodies (75%)
118
Thyroid scintigraphy in Graves
Diffuse, homogenous, increased uptake of radioactive iodine
119
Initial treatment to control symptoms in Grave's diseasea
Propanolol
120
First line definitive treatment Grave's disease
Anti-thyroid drugs
121
Anti-thyroid drug therapy in Graves
Carbimazole - started at 40mg and reduced gradually to maintain euthyroidism
122
How long is carbimazole continued for in Grave's
Typically 12-18 months
123
Major complication of carbimazole therapy
Agranulocytosis
124
Second line definitive treatment Grave's disease
Radioiodine treatment
125
Indications radioiodine treatment in Graves
Relapse following or resistance to anti-thyroid drug treatment
126
Contraindications radioiodine treatment for Graves
Pregnancy (should be avoided for 4-6 months after)
Age <16
Thyroid eye disease relative contraindication - may worsen condition
127
Aftermath of radioiodine treatment
Majority of patients need thyroxine supps after 5 years
128
Pathophysiology gynaecomastia
Due to increased oestrogen:androgen ratio
129
Causes of gynaecomastia
Physiological - normal in puberty
Syndromes with androgen deficiency - Kallmans, Klinefilters
Testicular failure, e.g. mumps
Liver disease
Testicular cancer
Ectopic tumour secretion of oestrogen
Hyperthyroidism
Haemodialysis
Drugs
130
Drugs causing gynaecomastia
Spironolactone
Cimetidine
Digoxin
Cannabis
Finasteride
GnRH agonists, e.g. goserelin, buserelin
Oestrogens, anabolic steroids
131
What is Hashimoto's thyroiditis
Autoimmune disorder of thyroid gland, typically associated with hypothyroidism but may be transient thyrotoxicosis in acute phase
132
Features Hashimoto's thyroiditis
Features of hypothyroidism
Firm, non-tender goitre
133
Antibodies in Hashimoto's thyroiditis
Anti-thyroid peroxidase (TPO)
Anti-thyroglobulin (Tg) antibodies
134
Conditions associated with Hashimoto's thyroiditis
Other autoimmune conditions, e.g. coeliac, T1DM, vitiligo
MALT lymphoma
135
Most common causes hypercalcaemia (90% of cases)
Primary hyperparathyroidism
Malignancy
136
Causes of hypercalcaemia in malignancy
PTHrP from tumour, e.g. squamous cell lung cancer
Bone mets
Myeloma
137
Other causes hypercalcaemia
Sarcoidosis
Vitamin D intoxication
Acromegaly
Thyrotoxicosis
Milk-alkali syndrome
Thiazides, calcium containing antacids
Dehydration
Addison's disease
Paget's disease of bone
138
HHS precipitating factors
Intercurrent illness
Dementia
Sedative drugs
139
Presentation HHS
Comes on over many days, so dehydration and metabolic distubances may be worse than DKA
Dehydration, polyuria, polydipsia
Lethargy, N&V
Altered consciousness, focal neurological deficits
Hyperviscosity - MI, stroke, thrombosis
140
HHS not diagnostic criteria but what you see
Hypovolaemia
Marked hyperglycaemia (>30mmol/L)
Significantly raised serum osmolarity (>320mosmol/kg)
No significant hyperketonaemia
No significant acidosis
141
Management HHS
Fluid replacement
VTE prophylaxis
142
Fluid losses in HHS estimation
100-220ml/kg
143
Fluid used for replacement HHS
0.9% NaCl
144
Role of insulin in HHS
Should not be given unless blood glucose stops falling while giving IV fluids
145
Causes hypoglycaemia
Insulinoma
Insulin/sulphonylureas
Liver failure
Addison's disease
Alcohol
146
Effects of glucose <3.3
Causes autonomic symptoms due to release of glucagon and adrenaline, causing:
- Sweating
- Shaking
- Hunger
- Anxiety
- Nausea
147
Effects of glucose <2.8
Cause neuroglycopenic symptoms due to inadequate glucose supply to brain:
- Weakness
- Vision changes
- Confusion
- Dizziness
148
Investigation hypoglycaemia
If cause of hypoglycaemia unclear, measure insulin and c-peptide
149
High insulin and high c-peptide interpretation
Endogenous insulin production - insulinoma, sulphonylurea use/abuse
150
High insulin, low c-peptide interpretation
Exogenous insulin administration - exogenous insulin overdose, factitious disorder
151
Low insulin, low c-peptide interpretation
Non-insulin related cause, e.g. alcohol-induced hypoglycaemia, critical illness, adrenal insufficiency, GH deficiency, fasting/starvation
152
Community management hypoglycaemia
Oral glucose 10-20g in liquid, gel, or tablet form
153
Hospital management hypoglycaemia
If patient alert, quick acting carbohydrate
If patient unconscious or unable to swallow, SC or IM injection glucagon, or IV 20% glucose solution
154
Bloods in primary hypoparathyroidism
Low calcium, high phosphate
155
Treatment primary hypoparathyroidism
Alfacalcidol
156
Symptoms of hypoparathyroidism
Secondary to hypocalcaemia:
- Tentany - muscle twitching, cramping, spasm
- Perioral paresthesia
- Trousseau's sign
- Chvostek's sign
- Depression
- Cataracts
157
What is Trousseau's sign
Carpal spasm if brachial artery occluded by BP cuff and pressure maintained above systolic
158
What is Chvostek's sign
Tapping parotids causes facial muscles to twitch
159
ECG findings hypoparathyroidism
Prolonged QT interval
160
Cause pseudohypoparathyroidism
Target cells insensitive to PTH
161
Other features associated with pseudohypoparathyroidism
Low IQ
Short stature
Shortened 4th and 5th metacarpals
162
Bloods pseudohypoparathyroidism
Low calcium
High phosphate
High PTH
163
Diagnosis pseudohypoparathyroidism
Measuring urinary cAMP and phosphate levels following infusion of PTH - in hypoparathyroidism, this will cause increase in cAMP and phosphate. In pseudohypoparathyroidism type I, neither rise. In type II, only cAMP rise
164
Most common cause hypothyroidism
Hashimoto's thyroiditis
165
Other causes hypothyroidism
Subacute (de Quervain's) thyroiditis
Riedel thyroiditis
After thyroidectomy or radioiodine treatment
Drug therapy
Dietary iodine deficiency
166
Drug therapy causing hypothyroidism
Lithium
Amiodarone
Anti-thyroid drugs, e.g. carbimazole
167
Starting dose levothyroxine
50-100mcg OD
25mcg if cardiac disease, 50+, or severe hypothyroidism
168
When to check thyroid after dose change thyroxine
8-12 weeks
169
Therapeutic goal of thyroxine therapy
Normalisation of TSH (0.5-2.5)
170
Adjustment to levothyroxine in pregnancy
Dose increase by at least 25-50mch, TSH monitored carefully aiming for low-normal value
171
SEs thyroxine
Hyperthyroidism
Reduced bone mineral density
Worsening of angina
AF
172
Drug interactions levothyroxine
Iron, calcium carbonate - reduce absorption, so should give at least 4 hrs apart
173
Inheritance Kallman's syndrome
X linked recessive
174
Features Kallmans syndrome
Delayed puberty
Hypogonadism, cryptorchidism
Anosmia
Cleft lip/palate and visual/hearing defects in some patients
175
Blood tests Kallman's syndrome
Sex hormones low
LH/FSH levels low or inappropriately normal
176
Management Kallman's syndrome
Testosterone supplementation
Gonadotrophic supplementation for sperm production if fertility desired
177
Karyotype Klinefilters
47 XXY
178
Features Klinefelter's
Taller than average
Lack of secondary sexual characteristics
Small, firm testes
Infertile
Gynaecomastia
179
Bloods Klinefelter's
Elevated gonadotrophins, low testosterone
180
Examples meglitinides
Repaglinide
Nateglinide
181
Mechanism of action meglitanides
Increase pancreatic insulin secretion
182
What kind of patients are meglitanides often used for
Those with erratic lifestyle
183
Tumours associated with MEN I
Parathyroid
Pituitary
Pancreas, e.g. insulinoma, gastrinoma
Adrenal
Thyroid
184
Tumours associated with MEN IIa
Medullary thyroid cancer
Parathyroid
Phaeochromocytoma
185
Tumours associated with MEN IIb
Medullary thyroid cancer
Pheochromocytoma
Marfanoid body habitus
Neuromas
186
Presentation myxoedema coma
Confusion
Hypothermia
187
Causes myxodema coma
Severe hypothyroidism
188
Treatment myxoedema coma
IV thyroid replacement
IV fluid
IV corticosteroids (until possibility of co-existing adrenal insufficiency excluded)
Electrolyte imbalance correction
Sometimes rewarming
189
BMI underweight
<18.49
190
Normal BMI
18.5 - 25
191
Overweight BMI
25-30
192
Obese class 1 BMI
30-35
193
Obese class 2 BMI
35-40
194
Obese class 3 BMI
>40
195
Medical management obesity
Orlistat
Liraglutide
196
Adverse effects orlistat
Faecal urgency/incontinence
Flatulence
197
Criteria prescription orlistat
Part of overall plan for managing obesity in patients wtih:
BMI 28+ with associated risk factors
BMI 30+
Continued weight loss, e.g. 5% at 3 months
198
Duration of use orlistat
<1 year
199
Criteria prescription liraglutide for obesity
BMI 35+
Prediabetic hyperglycaemia 42-47
200
Associations phaeochromocytoma
MEN II
Neurofibromatosis
Von Hippel-Lindau syndrome
201
Symptoms phaeochromocytoma
Usually episodic
- Hypertension
- Headaches
- Palpitations
- Sweating
- Anxiety
202
Investigations phaeochromocytoma
24 hour urinary collection of metanephrines
203
Treatment phaeochromocytoma
Definitive treatment with surgery, first stabilise with:
Alpha-blocker, e.g. phenoxybenzamine, given before
Beta blocker, e.g. propanolol
204
Diagnostic criteria prediabetes
Fasting plasma glucose 6.1-6.9mmol/L
HbA1c 42-47 (6-6.4%)
205
Management prediabetes
Lifestyle modification - weight loss, increased exercise, change in diet
At least yearly f/u with blood tests
Metformin if blood tests progressive despite participation in intensive lifestyle-change programme
206
Cause impaired fasting glucose
Hepatic insulin resistance
207
Cause impaired glucose tolerance
Muscle insulin resistance
208
Whats worse, impaired fasting glucose or impaired glucose tolerance
Impaired glucose tolerance more likely to develop T2DM and cardiovascular disease
209
Impaired fasting glucose diagnostic criteria
Fasting glucose ≥6.1 but <7
210
Impaired glucose tolerance diagnostic criteria
Fasting plasma glucose <7, but OGTT ≥7.8 but <11.1
211
Causes primary hyperaldosteronism
Bilateral idiopathic adrenal hyperplasia (most common)
Adrenal adenoma (Conn's syndrome)
Unilateral hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma
212
Features primary hyperaldosteronism
Hypertension
Hypokalaemia
Metabolic alkalosis
213
Who needs screening for primary hyperaldosteronism
Hypertension with hypokalaemia
Treatment resistant hypertension
214
First line investigation suspected primary hyperaldosteronism
Aldosterone/renin ratio
215
Findings plasma aldosterone/renin ratio in primary hyperaldosteronism
High aldosterone levels with low renin levels (negative feedback due to sodium retention from aldosterone)
216
Further investigation if aldosterone/renin ratio suggests primary hyperaldosteronism
High resolution CT
Adrenal vein sampling
Tests to differentiate between unilateral adenoma and bilateral hyperplasisa
217
Management adrenal adenoma
Laparoscopic adrenalectomy
218
Management bilateral adrenocortical hyperplasia
Aldosterone antagonist, e.g. spironolactone
219
Causes primary hyperparathyroidism
Solitary adenoma (85%)
Hyperplasia
Multiple adenoma
Carcinoma
220
Symptoms primary hyperparathyroidism
Those of hypercalcaemia
Polydipsia, polyuria
Depression
Anorexia, nausea, constipation
Peptic ulceration
Pancreatitis
Bone pain/fracture
Renal stones
Hypertension
221
Associations primary hyperparathyroidism
Hypertension
MEN 1 and 2
222
Blood findings primary hyperparathyroidism
Raised calcium, low phosphate
PTH may be raised or inappropriately normal
223
X ray findings primary hyperparathyroidism
Pepperpot skul
Osteitis fibrosa cystica
224
Definitive management primary hyperparathyroidism
Total parathyroidectomy
225
Conservative management primary hyperparathyroidism
Cinacalcet
226
Criteria for conservative management primary hyperparathyroidism
Calcium level less than 0.25 above upper limit of normal
Patient >50
No evidence of end organ damage
227
Features of high prolactin in men
Impotence
Loss of libido
Galactorrhoea
228
Features of high prolactin women
Amenorrhoea
Galactorrhoea
Osteoporosis
Infertility
229
Causes of raised prolactin
Prolactinoma
Pregnancy
Oestrogens
Physiological - stress, exercise, sleep
Acromegaly
PCOS
Primary hypothyroidism
230
Drugs causing raised prolactin
Metoclopramide, domperidone
Phenothiazines
Haloperidol
SSRIs
Opioids
231
Symptoms seen with pituitary macroadenoma
Headache
Visual disturbance, classically bitemporal hemianopia or upper temporal quadrantanopia
Signs and symptoms of hypopituitarism
232
Diagnosis prolactinoma
MRI
233
Management prolactinoma
Majority of symptomatic patients managed with dopamine agonists, e.g. cabergoline, bromocriptine
Surgery if can't tolerate/fail to respond - trans-sphenoid approach unless significant extra-pituitary extension
234
What is Riedels thyroiditis
Rare cause of hypothyroidism characterised by dense fibrous tissue replacing normal thyroid parenchyma
235
Examination findings Riedels thyroiditis
Hard, fixed, painless goitre
236
Associations Riedels thyroiditis
Retroperitoneal fibrosis
237
Examples SGLT inhibitors
Canagliflozin
Dapagliflozin
Empagliflozin
238
Adverse effects SGLT2 inhibiotrs
Urinary and genital infection
Fourniers gangrene
Normoglycaemia ketoacidosis
Increased risk of lower limb amputation
239
Blood tests sick euthyroid syndrome
TSH, thyroxine, and T3 low
TSH may be inappropriately normal
240
Treatment sick euthyroid syndrome
No treatment needed - recovers when better from acute illness
241
Cause subacute (De Quervain's) thyroiditis
Occurs following viral infection
242
Phase 1 subacute (De Quervain's) thyroiditis
Lasts 3-6 weeks - hyperthyroidism, painful goitre, raised ESR
243
Phase 2 subacute (De Quervain's) thyroiditis
Lasts 1-3 weeks - euthyroid
244
Phase 3 subacute (De Quervain's) thyroiditis
Lasts weeks - months - hypothyroidism
245
Phase 4 subacute (De Quervain's) thyroiditis
Thyroid structure and function returns to normal
246
Thyroid scintigraphy subacute (De Quervain's) thyroiditis
Globally reduced uptake iodine-131
247
Management subacute (De Quervain's) thyroiditis
Usually self limiting, most patients don't need treatment
Thyroid pain may respond to aspirin or other NSAIDs
In more severe cases, steroids used
248
Criteria subclinical hypothyroidism
TSH raised, T3/4 normal
No obvious symptoms
249
Significance subclinical hypothyroidism
Risk of processing towards overt hypothyroidism
250
When should levothyroxine therapy be considered in subclinical hypothyroidism
If TSH >10 on 2 occasions 3 months apart
If TSH 5.5-10, <65 and symptoms of hypothyroidism
251
Management asymptomatic subclinical hypothyroidism with TSH 5.5-10
Observe and repeat thyroid function in 6 months
252
Adverse effects sulfonylureas
Hypoglycaemic episodes
Weight gain
Less commonly:
Hyponatraemia secondary to SIADH
Bone marrow suppression
Hepatotoxicity
Peripheral neuropathy
253
Sulfonylureas in breastfeeding and pregnancy
Avoid
254
Example thiazolidinediones
Pioglitazone
Rosiglitazone withdrawn due to concerns about CVS side effects
255
SEs pioglitazone
- Weight gain
- Liver impairment
- Fluid retention
- Increased risk of cancer
- Bladder cancer
256
CIs pioglitazone
Heart failure
257
Monitoring pioglitazone
LFTs
258
Features hypothyroidism
- Weight gain
- Lethargy
- Cold intolerance
- Dry, cold, yellowish skin
- Non-pitting oedema
- Dry, coase scalp hair, loss of lateral aspect of eyebrows
- Constipation
- Menorrhagia
- Decreased deep tendon reflexes
- Carpal tunnel syndrome
259
Features hyperthyroidism
- Weight loss
- Manic, restlessness
- Heat intolerance
- Palpitations
- Increased sweating
- Pretibial myxoedema
- Thyroid acropachy
- Diarrhoea
- Oligomenorrhoea
- Anxiety
- Tremor
260
What is pretibial myxoedema
Erythematous, oedematous lesions above lateral malleoli
261
TSH/T4 in thyrotoxicosis
TSH low, T4 high
262
TSH/T4 in primary hypothyroidism
TSH low, T4 low
263
TSH/T4 in secondary hypothyroidism
TSH low, T4 low
264
TSH/T4 in sick euthyroid syndrome
TSH low, T4 low
265
TSH/T4 in subclinical hypothyroidism
TSH low, T4 normal
266
TSH/T4 in poor compliance with thyroxine
TSH high, T4 low
267
Most common condition TSH receptor antibodies seen in
Grave's
268
Most common condition anti-TPO antibodies seen in
Hashimoto's thyroiditis
269
What is thyroid storm
Rare but life-threatening complication of thyrotoxicosis
270
Thyroid storm precipitating events
Thyroid or non-thyroidal surgery
Trauma
Infection
Acute iodine load, e.g. CT contrast media
271
Clinical features thyroid storm
Fever >38.5
Tachycardia
Confusion and agitation
N&V
Hypertension
Heart failure
Abnormal liver function test
272
Management thyroid storm
Symptomatic treatment, e.g. paracetamol
Treatment of underlying precipitating event
Beta blockers, usually IV propanolol
Anti thyroid drugs
Lugol's iodine
Dexamethasone
273
Anti thyroid drugs used in thyroid storm
Methimazole or propylthyiouracil
274
Causes thyrotoxicosis
Graves disease
Toxic nodular goitre
Acute phase of hypothyroid conditions
Amiodarone
Contrast
275
Conditions causing thyrotoxicosis in the acute phase
Subacute thyroiditis
Post-partum thyroiditis
Hasmimoto's thyroiditis
