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Endocrinology Flashcards

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1
Q

what is the step wise management of obesity

A

conservative: diet & exercise
medical
surgical

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2
Q

what is orlistat & its side effects

A

pancreatic lipase inhibitor used in the medical treatment of obesity

loose stool/diarrhoea
flatulence
faecal urgency/incontinence

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3
Q

what is the criteria for orlistat to be prescribed

A

BMI of 28 kg/m^2 or more with associated risk factors, or
BMI of 30 kg/m^2 or more
continued weight loss e.g. 5% at 3 months

orlistat is normally used for < 1 year

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4
Q

contraindications for orlistat

A

critical medications e.g. COCP, anti-epileptics

increased transit time through the gut caused by orlistat could reduce absorption & efficacy of vital medications

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5
Q

what should patients on long term steroids do to their dose when have a concurrent illness?

A

double hydrocortisone dose

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6
Q

side effects of glucocorticoids

A

endocrine: impaired glucose regulation, increased appetite/weight gain, hirsutism

cushing’s syndrome

MSK: osteoporosis, proximal myopathy, avascular necrosis of femoral head

immunosuppression: TB reactivation

psychiatric: insomnia, mania, depression, psychosis

GI: peptic ulceration, pancreatitis

ophthalmic: glaucoma, cataracts

suppression of growth in children
intracranial hypertension
neutrophilia

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7
Q

side effects of mineralocorticoids

A

hypertension
fluid retention

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8
Q

what is an Addisonian crisis/adrenal crisis

A

an acute presentation of severe Addison’s, where the absence of steroids leads to a life threatening presentation

can be first presentation of Addison’s
triggered by trauma, infection, or other acute illness
can happen if someone stops steroids abruptly

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9
Q

presentation of adrenal crisis

A

hypotension
hyponatremia, hyperkalaemia
hypoglycaemia
reduced consciousness
patients can be very unwell

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10
Q

management of adrenal crisis

A

Intensive monitoring if unwell
Parenteral steroids (i.e. IV hydrocortisone 100mg stat then 100mg every 6 hours)
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance

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11
Q

unique features of Grave’s disease

A

exophthalmos
ophthalmoplegia

pretibial myxoedema

thyroid acropachy:
clubbing
soft tissue swelling of hands and feet
periosteal new bone formation

** all due to TSH receptor antibodies

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12
Q

what is pretibial myxoedema

A

dermatological condition
deposits of mucin under the skin of the anterior aspect of the leg

gives a discoloured, waxy, oedematous appearance to the skin over the area

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13
Q

pathophysiology of hyperaldosteronism

A

in the afferent arterioles of the kidneys there are juxtaglomerular cells which detect BP in the vessels

if low, they secrete renin
Liver in turn release a protein called angiotensinogen, which renin converts to angiotensin I
Angiotensin I –> 2 in the lungs by ACE
Angiotensin II stimulates release of aldosterone from the adrenal glands

results in:
Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts

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14
Q

what type of steroid is aldosterone

A

mineralocorticoid

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15
Q

features of primary hyperaldosteronism

A

hypertension
hypokalemia
***muscle weakness
alkalosis

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16
Q

causes of primary hyperaldosteronism

A

adrenal glands producing too much aldosterone, resulting in low renin

bilateral adrenal hyperplasia**
adrenal adenoma
Familial hyperaldosteronism type 1 and type 2

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17
Q

causes of secondary hyperaldosteronism

A

excessive renin being produced which simultaneously produces more aldosterone
occurs when BP in the kidneys is proportionately lower to the BP in the rest of the body

renal artery stenosis
renal artery obstruction
HF

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18
Q

investigations for hyperaldosteronism

A

aldosterone/renin ratio

BP, U&Es, blood gas

Then:
high resolution CT abdomen** / MRI to look for an adrenal tumour
Renal doppler ultrasound, CT angiogram or MRA for renal artery stenosis or obstruction

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19
Q

management of hyperaldosteronism

A

adenoma:surgery

hyperplasia: aldosterone antagonists e.g. spironolactone, Eplerenone

percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis

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20
Q

drug causes of gynaecomastia

A

spironolactone***
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids

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21
Q

pathophysiology of androgen insensitivity syndrome

A

x linked recessive condition
cells unable to respond to androgens due to a lack of receptor

Patients are genetically male with XY sex chromosome
However, due to no response to testosterone & excess androgens being converted to estrogen = female phenotype externally

testes in the abdomen or inguinal canal, and absence of a uterus, upper vagina, cervix, fallopian tubes and ovaries. The female internal organs do not develop because the testes produce anti-Müllerian hormone, which prevents males from developing an upper vagina, uterus, cervix and fallopian tubes

insensitivity to androgens also results in a lack of pubic hair, facial hair and male type muscle development. Patients tend to be slightly taller than the female average.

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22
Q

presentation of androgen insensitivity syndrome

A

often presents in infancy with inguinal hernias containing testes
or at puberty with primary amennorhoea

Raised LH
Normal or raised FSH
Normal or raised testosterone levels (for a male)
Raised oestrogen levels (for a male)

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23
Q

what is there an increased risk of in androgen insensitivity syndrome

A

testicular cancer
requires a bilateral orchidectomy

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24
Q

management of androgen insensitivity syndrome

A

Bilateral orchidectomy (removal of the testes) to avoid testicular tumours

Oestrogen therapy

Vaginal dilators or vaginal surgery can be used to create an adequate vaginal length

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25
side effects of SGLT2-I
urinary & genital infections normoglycaemic ketoacidosis increased risk of lower limb amputation ** patients often lose weight which can be beneficial in T2DM
26
how to monitor & adapt levothyroxine dose in pregnancy
increase dose by up to 50% as early as 4-6 weeks serum TSH measured in each trimester and 6-8 weeks post partum
27
what is transient gestational hyperthyroidism
activation of the TSH receptor by HCG may also occur HCG levels will fall in the second and third trimester
28
management of hyperthyroidism in pregnancy
propylthiouracil in the 1st trimester (carbimazole associated with congenital abnormalities) at the start of the 2nd trimester, should be transferred back to carbimazole maternal free thyroxine levels should be kept in the upper third of the normal reference range to avoid fetal hypothyroidism thyrotrophin receptor stimulating antibodies should be checked at 30-36 weeks gestation - helps to determine the risk of neonatal thyroid problems
29
features of subclinical hypothyroidism
TSH raised but T3, T4 normal no obvious symptoms
30
management of subclinical hypothyroidism
if TSH 4-10 if <65yrs and have symptoms, trial levothyroxine >80 yrs, watch and wait if no symptoms, repeat TFTs in 6 months TSH >10 <70yrs start treatment even if asymptomatic in older people follow a watch & wait approach
31
should patients with T2DM be offered a statin?
only if QRISK >10% then start atorvastatin 20mg
32
BP targets for those with T2DM
same as those without T2DM <80 yrs clinic: 140/90 home: 135/85 >80 yrs clinic: 150/90 home: 145/85
33
MOA of DPP-4 inhibitors
prevent the breakdown of incretins **hormones produced by the GI tract in response to large meals, reducing the blood sugar levels Increase insulin secretions Inhibit glucagon production Slow absorption by the GI tract
34
side effects of DPP-4 inhibitors
GI tract upset Symptoms of upper respiratory tract infection Pancreatitis
35
what is the range for impaired fasting glucose
6.1-6.9mmol/L
36
what is the range for impaired glucose tolerance
plasma glucose at 2 hours 7.8 – 11.1 mmol/l on an OGTT
37
MOA of TZD
agonists to the PPAR-gamma intracellular receptor increase insulin sensitivity & decreases production of glucose from the liver
38
side effects of TZD
weight gain liver impairment: monitor LFTs fluid retention: contraindicated in heart failure increased risk of fractures bladder cancer
39
what is Grave's disease
an autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism These are abnormal antibodies produced by the immune system Most common cause of hyperthyroidism
40
management of Grave's disease
propranolol = controls symptoms NICE recommend referring these patients to secondary care for ongoing treatment 1) carbimazole leaving them with normal thyroid function after 4-8 weeks - the dose is carefully titrated to maintain normal levels (known as “titration-block”) - or the dose is sufficient to block all production and the patient takes levothyroxine titrated to effect (known as “block and replace”) 2) propylthiouracil 3) radioiodine treatment
41
side effects of hyperthyroidism management
carbimazole - agranulocytosis propylthiouracil - severe hepatic reactions radioiodine - hypothyroidism
42
contraindications for radioiodine
pregnancy (should be avoided for 4-6 months after) <16 years thyroid eye disease
43
management of prediabetes
weight loss exercise change in diet
44
how often should you monitor HbA1C for those with prediabetes
annually
45
what are GLP-1 mimetics?
increase insulin secretion and inhibit glucagon secretion - mimic incretins examples include exenatide & liraglutide can cause weight loss
46
key difference between exenatide & liraglutide
exenatide: subcut injection 60 mins before morning & evening meals liraglutide: once daily subcut injection
47
side effects of GLP-1 mimetics
nausea & vomiting can cause pancreatitis
48
when to consider giving GLP-1 mimetics?
If triple therapy is not effective or tolerated BMI ≥ 35 kg/m² and specific psychological or other medical problems associated with obesity or BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months
49
when & how often should patients with diabetes monitor their BM when driving?
Patients on medication for diabetes with potential to cause hypoglycaemia eg. insulin, sulphonylureas, are required to check their BM prior to driving and every 2 hours of the journey
50
presentation of hypoglycaemia depending on blood sugar level
<3.3mmol/L: autonomic symptoms due to release of glucagon & adrenaline: sweating shaking anxiety nausea hunger <2.8 neuroglycopenic symptoms due to inadequate glucose supply to the brain weakness vision changes confusion dizziness severe: convulsion coma
51
if a patient is asymptomatic, how many sets of tests need to be done to confirm diabetes
2 on separate occasions if asymptomatic
52
what reduces hypoglycaemic awareness
frequent episodes of hypoglycaemia beta-blockers
53
complication of lipodystrophy
may cause erratic insulin absorption
54
associated features of metabolic syndrome
PCOS raised uric acid levels non-alcoholic fatty liver disease
55
symptoms of T2DM
polyuria & polydipsia fatigue opportunistic infections slow healing glucose in urine
56
what is De Quervain's thyroiditis
thought to occur following viral infection, presenting with fever, neck pain & tenderness, dysphagia, and features of hyperthyroidism
57
phases of De Quervain's thyroiditis
phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR phase 2 (1-3 weeks): euthyroid phase 3 (weeks - months): hypothyroidism phase 4: thyroid structure and function goes back to normal
58
management of De Quervain's thyroiditis
self-limiting condition NSAIDS/aspirin for the pain beta blockers for symptomatic relief
59
what is a thyroid storm/thyroid crisis?
more severe presentation of hyperthyroidism with pyrexia, tachycardia, and delirium
60
management of a thyroid storm
admission for monitoring fluid resuscitation anti-arrhythmic medication beta blockers
61
features of hyperthyroidism
sweating anxiety/irritability diarrhoea fatigue weight loss tachycardia
62
causes of hyperthyroidism
Grave's disease toxic multi-nodular goitre (2nd most common cause) Solitary toxic thyroid nodule (benign adenoma) thyroiditis e.g. de Quervain's
63
role of parathyroid gland & PTH
4 parathyroid glands of the thyroid, where the chief cells release PTH in response to hypocalcemia PTH increases calcium levels in the blood by: - increasing osteoclast activity - increasing vitamin D activity - increasing calcium absorption from the gut & kidneys
64
main cause of primary hyperparathyroidism
solitary adenoma **treated with surgical excision
65
symptoms of hyperparathyroidism
**bones, stones, abdominal groans, and psychic moans polyuria, polydipsia abdominal groans - nausea and vomiting, constipation bone pain renal stones depression, fatigue, psychosis
66
characteristic xray finding of hyperparathyroidism
pepperpot skull
67
symptoms of hypocalcaemia
paraesthesia in fingertips, toes, and lips facial twitching depression, fatigue muscle pains or cramps
68
cause of secondary hyperparathyroidism
insufficient vitamin D or chronic renal failure low calcium leads to raised PTH, results in hyperplasia of the glands
69
tertiary hyperparathyroidism
happens when the cause of secondary hyperparathyroidism is treated, but PTH remains high due to the hyperplasia of the glands ***treated by surgically removing part of the parathyroid gland to return to normal functioning
70
autoantibodies associated with hashimoto's thyroiditis
anti-thyroid peroxidase anti-thyroglobulin
71
Hashimoto's thyroiditis is associated with an increased risk of what?
MALT lymphoma other autoimmune conditions
72
when to consider stopping/stopping metformin?
metformin dose should be reviewed if the creatinine is > 130 µmol/l (or eGFR < 45 ml/min) AND stopped if the creatinine is > 150 µmol/l (or eGFR < 30 ml/min)
73
what is the importance in recognising subclinical hyperthyroidism
effects on the cardiovascular system - supraventricular arrhythmias, AF bone metabolism - osteoporosis
74
cause & management of subclinical hyperthyroidism
cause - multinodular goitre, especially in elderly women management - TSH levels usually revert to normal, so need a persistently low TSH can try a low dose of anti-thyroid medication for approx 6 months to induce remission
75
role of dexamethasone in cerebral metastases
reduce cerebral oedema reduce the risk of seizures
76
side effects of thyroxine therapy
hyperthyroidism worsening of angina AF osteoporosis - reduced bone mineral density
77
different criteria for starting levothyroxine therapy
those suffering from cardiac disease, severe hypothyroidism, >50 yrs - started on 25mcg with dose slowly titrated others should start on 50-100mcg following a change in dose, TFTs should be checked after 8-12 weeks
78
causes of hypothyroidism
hashimoto's thyroiditis (autoimmune) iodine deficiency hyperthyroidism medication e.g. carbimazole, propylthiouracil, radioactive iodine, surgery drugs - lithium, amiodarone secondary cause: dysfunction of the pituitary gland due to tumour, infection, vascular cause (Sheehan syndrome)
79
symptoms of hypothyroidism
weight gain fatigue cold intolerance depression constipation dry skin, coarse hair fluid retention heavy/irregular periods
80
use of radioactive isotope when diagnosing thyroid conditions e.g. diffuse, focal, and cold areas
Diffuse high uptake is found in Grave’s Disease Focal high uptake is found in toxic multinodular goitre and adenomas “Cold” areas (i.e. abnormally low uptake) can indicate thyroid cancer
81
pathophysiology of DKA
as cells have no fuel and think they are starving, lipolysis starts and ketogenesis occurs initially the body produces enough bicarbonate to counteract the ketone acids, but eventually it is used up --> ketoacidosis due to hyperglycaemia, more glucose is excreted in the urine, water follows due to osmotic diuresis leading to polyuria and dehydration insulin normally drives potassium into cells, serum potassium is high or normal, total body potassium is low as none is being stored in the cells
82
common causes of DKA
infection, MI, missed insulin doses
83
features of DKA
hyperglycaemia dehydration ketosis metabolic acidosis potassium imbalance polyuria, polydipsia dehydration & subsequent hypotension abdominal pain nausea & vomiting acetone smell to breath
84
diagnosing DKA
Hyperglycaemia (i.e. blood glucose > 11 mmol/l) Ketosis (i.e. blood ketones > 3 mmol/l or urine ketones ++ on dipstick) Acidosis (i.e. pH < 7.3)
85
diagnosing DKA
Hyperglycaemia (i.e. blood glucose > 11 mmol/l) Ketosis (i.e. blood ketones > 3 mmol/l or urine ketones ++ on dipstick) Acidosis (i.e. pH < 7.3)
86
management of DKA
IV fluids insulin (add dextrose infusion if blood sugars go below a certain level) potassium supplementation ** if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required
87
what is important in the prevention of thyroid eye disease
stopping smoking radioiodine therapy is a contraindication
88
features of thyroid eye disease
*** patient may be hypo-, eu-, or hyperthyroid at point of presentation exophthalmos conjunctival oedema optic disc swelling ophthalmoplegia inability to close lids may lead to sore, dry eyes ---> exposure keratopathy
88
features of thyroid eye disease
*** patient may be hypo-, eu-, or hyperthyroid at point of presentation exophthalmos conjunctival oedema optic disc swelling ophthalmoplegia inability to close lids may lead to sore, dry eyes ---> exposure keratopathy
89
why are GLP-1 mimetics sometimes used in combination with insulin
minimise insulin related weight gain
90
management of Addison's disease in concurrent illness
double hydrocortisone dose *** during illness the body usually increases cortisol levels as a stress response keep fludrocortisone dose the same

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