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Y4 > Endocrinology > Flashcards

Endocrinology Flashcards

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
Q

side effects of SGLT2-I

A

urinary & genital infections
normoglycaemic ketoacidosis
increased risk of lower limb amputation

** patients often lose weight which can be beneficial in T2DM

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26
Q

how to monitor & adapt levothyroxine dose in pregnancy

A

increase dose by up to 50% as early as 4-6 weeks

serum TSH measured in each trimester and 6-8 weeks post partum

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27
Q

what is transient gestational hyperthyroidism

A

activation of the TSH receptor by HCG may also occur

HCG levels will fall in the second and third trimester

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28
Q

management of hyperthyroidism in pregnancy

A

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

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29
Q

features of subclinical hypothyroidism

A

TSH raised but T3, T4 normal
no obvious symptoms

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30
Q

management of subclinical hypothyroidism

A

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

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31
Q

should patients with T2DM be offered a statin?

A

only if QRISK >10%
then start atorvastatin 20mg

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32
Q

BP targets for those with T2DM

A

same as those without T2DM

<80 yrs
clinic: 140/90
home: 135/85

> 80 yrs
clinic: 150/90
home: 145/85

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33
Q

MOA of DPP-4 inhibitors

A

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

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34
Q

side effects of DPP-4 inhibitors

A

GI tract upset
Symptoms of upper respiratory tract infection
Pancreatitis

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35
Q

what is the range for impaired fasting glucose

A

6.1-6.9mmol/L

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36
Q

what is the range for impaired glucose tolerance

A

plasma glucose at 2 hours 7.8 – 11.1 mmol/l on an OGTT

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37
Q

MOA of TZD

A

agonists to the PPAR-gamma intracellular receptor
increase insulin sensitivity & decreases production of glucose from the liver

38
Q

side effects of TZD

A

weight gain
liver impairment: monitor LFTs
fluid retention: contraindicated in heart failure
increased risk of fractures
bladder cancer

39
Q

what is Grave’s disease

A

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
Q

management of Grave’s disease

A

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
Q

side effects of hyperthyroidism management

A

carbimazole - agranulocytosis

propylthiouracil - severe hepatic reactions

radioiodine - hypothyroidism

42
Q

contraindications for radioiodine

A

pregnancy (should be avoided for 4-6 months after)
<16 years
thyroid eye disease

43
Q

management of prediabetes

A

weight loss
exercise
change in diet

44
Q

how often should you monitor HbA1C for those with prediabetes

A

annually

45
Q

what are GLP-1 mimetics?

A

increase insulin secretion and inhibit glucagon secretion - mimic incretins
examples include exenatide & liraglutide

can cause weight loss

46
Q

key difference between exenatide & liraglutide

A

exenatide: subcut injection 60 mins before morning & evening meals

liraglutide: once daily subcut injection

47
Q

side effects of GLP-1 mimetics

A

nausea & vomiting
can cause pancreatitis

48
Q

when to consider giving GLP-1 mimetics?

A

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
Q

when & how often should patients with diabetes monitor their BM when driving?

A

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
Q

presentation of hypoglycaemia depending on blood sugar level

A

<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
Q

if a patient is asymptomatic, how many sets of tests need to be done to confirm diabetes

A

2 on separate occasions if asymptomatic

52
Q

what reduces hypoglycaemic awareness

A

frequent episodes of hypoglycaemia
beta-blockers

53
Q

complication of lipodystrophy

A

may cause erratic insulin absorption

54
Q

associated features of metabolic syndrome

A

PCOS
raised uric acid levels
non-alcoholic fatty liver disease

55
Q

symptoms of T2DM

A

polyuria & polydipsia
fatigue
opportunistic infections
slow healing
glucose in urine

56
Q

what is De Quervain’s thyroiditis

A

thought to occur following viral infection, presenting with fever, neck pain & tenderness, dysphagia, and features of hyperthyroidism

57
Q

phases of De Quervain’s thyroiditis

A

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
Q

management of De Quervain’s thyroiditis

A

self-limiting condition
NSAIDS/aspirin for the pain
beta blockers for symptomatic relief

59
Q

what is a thyroid storm/thyroid crisis?

A

more severe presentation of hyperthyroidism with pyrexia, tachycardia, and delirium

60
Q

management of a thyroid storm

A

admission for monitoring

fluid resuscitation
anti-arrhythmic medication
beta blockers

61
Q

features of hyperthyroidism

A

sweating
anxiety/irritability
diarrhoea
fatigue
weight loss
tachycardia

62
Q

causes of hyperthyroidism

A

Grave’s disease
toxic multi-nodular goitre (2nd most common cause)
Solitary toxic thyroid nodule (benign adenoma)
thyroiditis e.g. de Quervain’s

63
Q

role of parathyroid gland & PTH

A

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
Q

main cause of primary hyperparathyroidism

A

solitary adenoma
**treated with surgical excision

65
Q

symptoms of hyperparathyroidism

A

**bones, stones, abdominal groans, and psychic moans

polyuria, polydipsia
abdominal groans - nausea and vomiting, constipation
bone pain
renal stones
depression, fatigue, psychosis

66
Q

characteristic xray finding of hyperparathyroidism

A

pepperpot skull

67
Q

symptoms of hypocalcaemia

A

paraesthesia in fingertips, toes, and lips
facial twitching
depression, fatigue
muscle pains or cramps

68
Q

cause of secondary hyperparathyroidism

A

insufficient vitamin D or chronic renal failure
low calcium leads to raised PTH, results in hyperplasia of the glands

69
Q

tertiary hyperparathyroidism

A

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
Q

autoantibodies associated with hashimoto’s thyroiditis

A

anti-thyroid peroxidase
anti-thyroglobulin

71
Q

Hashimoto’s thyroiditis is associated with an increased risk of what?

A

MALT lymphoma

other autoimmune conditions

72
Q

when to consider stopping/stopping metformin?

A

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
Q

what is the importance in recognising subclinical hyperthyroidism

A

effects on the cardiovascular system - supraventricular arrhythmias, AF

bone metabolism - osteoporosis

74
Q

cause & management of subclinical hyperthyroidism

A

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
Q

role of dexamethasone in cerebral metastases

A

reduce cerebral oedema
reduce the risk of seizures

76
Q

side effects of thyroxine therapy

A

hyperthyroidism
worsening of angina
AF
osteoporosis - reduced bone mineral density

77
Q

different criteria for starting levothyroxine therapy

A

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
Q

causes of hypothyroidism

A

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
Q

symptoms of hypothyroidism

A

weight gain
fatigue
cold intolerance
depression
constipation
dry skin, coarse hair
fluid retention
heavy/irregular periods

80
Q

use of radioactive isotope when diagnosing thyroid conditions e.g. diffuse, focal, and cold areas

A

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
Q

pathophysiology of DKA

A

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
Q

common causes of DKA

A

infection, MI, missed insulin doses

83
Q

features of DKA

A

hyperglycaemia
dehydration
ketosis
metabolic acidosis
potassium imbalance

polyuria, polydipsia
dehydration & subsequent hypotension
abdominal pain
nausea & vomiting
acetone smell to breath

84
Q

diagnosing DKA

A

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
Q

diagnosing DKA

A

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
Q

management of DKA

A

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
Q

what is important in the prevention of thyroid eye disease

A

stopping smoking
radioiodine therapy is a contraindication

88
Q

features of thyroid eye disease

A

*** 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
Q

features of thyroid eye disease

A

*** 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
Q

why are GLP-1 mimetics sometimes used in combination with insulin

A

minimise insulin related weight gain

90
Q

management of Addison’s disease in concurrent illness

A

double hydrocortisone dose
*** during illness the body usually increases cortisol levels as a stress response

keep fludrocortisone dose the same

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