Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 core conditions > endocrine > Flashcards

endocrine Flashcards

1
Q

who gets type 1 diabetes

A

10%
presents in children and young adults and persists into adult life

associated with HLA genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

cause of type 1 diabvetes

A

autoimmune destruction of beta cells in the islets of langerhans
initiated by poorly understood environmental factors acting on a genetically susceptible group of ppl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

risk factors for type 1 diabetes

A

genetics - 15% have first degree realtive with it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

presentation of type 1 diabetes

A

hyperglycaemia ( random >11)
polyuria, polydipsia, wieght loss, excessive tiredness, dehydration/thirst, starvation symptoms

ketoacidosis
atherosclerotic complications due to hyperlipidaemia
peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

normal blood glucose

A

3.5-5.5mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

diagnostic criteria for diabetes

  • fasting
  • 2hr plasma glucose
A

fasting >7

2hr >11.1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

investigations for type 1 diabetes

A

HbA1c - average Hb over 3 months
blood glucose - fasting, 2hr plasma
urine dipstick

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

treatment of type 1 diabetes

A

insulin therapy
blood glucose monitoring
diet, physical activity etc management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cause of type 2 diabetes

A

combinationof inuslin resistance/insensitivity and insulin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

risk factors for type 2 diabetes

A 
obesity and inactivity
family history
ethnicity
history of gestational diabtes
poor dietary habits
drug treatments - statins, corticosteroids, thizide+betablocker
metabolic syndrome
low birthweight for gestational age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

presentation of type 2 diabetes

A

persistnet hyperglycaemia
thirsty, polyuria, blurred bision, wieght loss, recurrent infections, tiredness
insulin resistance - acanthosis nigricans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

signs of type 2 diabetes on examination

A

diabetic neuropathy

diabetic retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

investigations for type 2 diabetes

A

HbA1c

plasma glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

treatment of type 2 diabtes

A

lifestyle advice and drugs
metformin - gradual increase of dose to minimise GI upset
monitor renal fucntion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

second line to metformin

A

metformin + gliptin

pioglitaxone or sulfonylurea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

who gets hypothyroidism

A

3% of pop

10x more in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

causes of hypothyroidism

A 
iodine deficiency
autoimmune thyroiditis (hashimotos or atrophic)
post ablative therapy or surgery
drugs
transient thyroiditis
thyroid infiltrative disorders
congenital
seocndfarycauses - pituitary or hypothalamic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

thyroid infiltrative disorders

A 
amyloidosis
sarcoidosis
haemochromatosis
tuberculosis
sclerodermas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

presentation of hypothyroidism

A

slow metabolism:
tiredness, weight gain, anorexia, cold intolerance, poor memoey, change in appearance, depression, low libido, goitre, puffy eyes, brittle hair, coarse skin, arthalgia, myalgia, muscle weakness/stiffness, constipation, menorrhagia, oligomenorrhagia, psychosis, coma, deafness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

signs of hypothyroidism on examination

A 
poverty of movement
peaches and cream complexion
loss of eyebrows
hypertension
eart fialure
bradycardia
pericardial effusion
carpal tunnel 
oedema
periorbital oedema
deep voice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

investigations for hypothyroidism

A

blood tests for TSH, serum T4 and thyrpid antibodies

T3/T4 low
TSH raised (if low, lesion of hypothalamus or pituitary is likely)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

treatment of hypothyroidism

A

lifelong tlevothyroxine

further assessment of thyroid function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

who gets hyperthyroidism

A

10x more in women
increases w age
higher in areas of iodine deficiency
0.75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

causes of hyperthyroidism

A

autoimmune - graves disease
TSH secreting pituitary adenoma
thyroiditis
exogenous intake of thyroid hormones - factitious thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

risk factors for hyperthyroidism

A

female
FHx
smoking
low iodine intake and autoimmune diseases (type 1 diabetes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

presentation of hyperthyroidism

A

weight loss, heat intolerance, sweating (stimualted metabolism)

tremor, nervousness, irritability, emotional disturbacne, tiredness, lethargy

cardiac features caused by beta adrenergic sympathetic activity, palpitations, tachycardia and arrhythmias

eye signs range in severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

thyroid storm

A

thyrotoxic crisis

  • precipitated by non-thyroid surgeyr, major trauma, infection, imaging studies withiodinated contrast medium in patients with unrecognised thyrotoxvicosis

= insomnia, anorexia, vomiting, diarrhoea, marked sweating, fever, tachycardia, immediate management is required

28
Q

investigations of hyperthyroidism

A

TFTs
decreased FSH
increased Y4 and T3 (except pituitary)
+ve serology for autoantibodies

radioactive iodine scan

29
Q

treatment of hyperthyroidism

A

medical - anithyroid drugs block hormone synthesis = carbimazole, beta blockers (tahcy and tremor), radioactive iodine,

surgical - total thyroidectomy (graves) or lobectomy (nodules or adenomas)
chpice for those not indcate d for I131 therapy and those with eye conditions

30
Q

differentials of hyperthyroidism

A

AF
panic attakcs
parkinsons

31
Q

who gets goitres/thyroid nodules

A

women >men

32
Q

causes of diffuse goitre

A 
physiological - puberty or pregnancy
autoimmune (graves or hashimotos)
acute viral thyroditis
iodine deficiency
dyshormonogenesis
goitrogens
33
Q

causes of nodular goitre

A

multinodular goitre
solitary nodule
fibrotic (reidells thyroiditis)
cysts

34
Q

types of tumour - goitre

A

adenoma
carcinoma
lymphoma

35
Q

causes of miscellaneous goitres

A

sarcoidosis

TB

36
Q

risk factors of goitr

A

family history
age - younger than 20 and older than 70
gender - male for cancer
radiation exposure

37
Q

presentation of goitre/nodules

A 
goite noticed
discomfort and pain in neck
occasional tracheal or oeseophageal compression - difficulty breathing and swallowing
bruit present and associated 
lymphadenopathy (malignant)

hoarseness of voice (hyperthyroidism)

38
Q

investigations of goitre

A

blood tests - thyroid function tests
imaging - thyroid USS, FNA under US, ches tand thoracic inlet xray - detect tahceal compression and large retrosternal extensions

thyroid scan using radioactive iodine

39
Q

treatment of goitre

A

usually not required apart from introducing euthyroidism
surgical intervention required for cosmetic effects of large goitre
pressure effects on trahcea or oesoep`hagus or confirmed/possible malignancy

40
Q

cushings disease

A

excess glucocorticoids reuslting from innapropriate ACTH secretion from the pituitary (usually microadenoma, less often cortophin hyperplasia)

41
Q

cushings syndrome

A

abnormalities reuslting from a chronic exces sof glucocorticoids whatever the cause

42
Q

cushings mortality if untreatewd

A

5 year mortality of 50% if untreated

43
Q

causes of cushings syndroem

A

exogenous = administration of synthetic steroids or ACTH for treatment of medical conditions

endogensou - adrenal tumour or excess ACTH - pituitary tumour = cushings disease or from ectopic site

spontaneous = rare- 2/3 from excess ACTH secretion from pituitary gland

pseudoushings - alcohol excess mimics cushings

44
Q

presetnation of cushings

A

obese - central, truncal obesity
plethoric complexion
moon face
easy brusing, purple striae on abdo, breast and thighs

45
Q

signs on examination of cushings

A 
mon face
plethora
depression/spychosis
ACNE
hirsutism
frontal balding
thin skin
bruising
poor wound healing
pigmentation 
skin infection 
hypertension
pathological fractures
osteoporosis
kyphosis
buffalo hump
central obesity
striae
oedema
proximal myopathy
proximal muscle wasting
glycosuria
46
Q

investigations of cushings

A

first confirm presenc eof cortisol excess then determine cause:

measure free cortisol - blood or saliva late at night

dexamethasone su[pression test (should suppress ACTH production and decrease cortisol, will not in cushings due to endogenous source of cortisol)

ACTH plasma levels - low = adrenal adenomas and carcinomas, high = cushings, ectopic ACTH production

imaging - MRI of pituitary (cushings), CT of adrenals, CT chest, abdo or pelvis (ectopic site suggesyed)

corticotrophin releasing hormone test

47
Q

treatment of cushings

A

exogenous medications gradually decreased (avoid sudden withdrawal)

pituitary adenoma - surgical excision

adrenal steroid inhibitors - ketoconazole +metyrapone +ectopic ACTH production

48
Q

who gets parathyroid adenomas?

A

post menopausal women mostly

49
Q

what gene is parathyroid adenoma associated with?

A

MEN1

50
Q

how does parathyroid adenoma present?

A

bones - aches/pains localised in larger joints

stones - calcium based renal stones

Moans - psychological/psychiatric symptoms (lethargy, depressed mood)

Groans - non specific GI symptoms (abdo pain, constipation)

51
Q

signs on examination of parathyroid adenoma

A

polyuria, polydipsia and nocturia

hypercalcaemic crisis in those exposed to severe dehydration (diarrhoea, vomiting)

52
Q

investigations for parathyroid adenoma

A

raised corrected serum calcium if unexplained = very suggestive

increased serum parathyroid hormone concentration in presence of hypercalcaemia is diagnostic

high resolution US may identify tumours

53
Q

treatment of parathyroid adenoma

A

without localisation scans, bilateral neck expolration and removal of large tumours is standard

if location is known, minimally invasive parathyroidectomy

54
Q

who gets primary hyperparathyroidism

A

mostly post menopausal women

55
Q

causes of primary hyperparathyroidism

A

most have single parathyroid adenoma

some have multiglandular hyperplasia - sporadic disease or in association with familial disease

parathyroid cancer is rare

56
Q

risk factor for parathyroid adenoma

A

MEN syndromes

57
Q

presentation of primary hyperparathyroidism

A

BONES, STONES, MOANS and GROANs

  • Bones: Aches/pains localised in larger joints
  • Stones: Calcium based renal stones
  • Moans: Psychological/psychiatric symptoms (lethargy, depressed mood)
  • Groans: Non-specific GI symptoms (abdominal pain, constipation)
58
Q

signs on examination of primary hyperparathyroidism

A

polyuria, polydipsia, nocturia common symptoms

many non specific symptosm put down to getting older

hypercalcaemic crisis if exposed to severe dehydration

59
Q

investigations of primary hyperparathyroidism

A

increased PTH in presence of hypercalcaemia is diagnostic

high res US to identify tumours
sestamibi scanning used to localised adenomas

60
Q

treatment of primary hyperparathyroidism

A

minimally invasive parathyroidectomy

61
Q

causes of addisons disease

A

Autoimmune response that attacks the cortex of the adrenal gland where cortisol and aldosterone is made

most of the time by organ specific autoantibodies. assoicated with autoimmune conditions such as thyroid disease, ovarian fialure, pernicious anaemia, DM T1

Rarer causes - adrenal gland tuberculosis, surgical removal, haemorrhage, malignant infiltration

62
Q

secondary hypoadrenalism

A

pituitary disease

63
Q

tertiary hypoadrenalism

A

hypothalamic disease

64
Q

signs on exmaination of Addison’s disease

A

lethargy, depression, anorexia, weight loss

postural hypotension - salt and water loss is an early sign

hyperpigmentation

vitiligo and loss of body hair in women

crisis presentation: vomiting, abod pain, profound weakness, hypoglycaemia and hypovolaemic shock

65
Q

investigations of Addison’s disease

A

3 fold to demonstrate low cortisol secretion and determine if independent or dependent on ACTH secretion

  • single cortisol measurement
  • short ACTH stimulation test (diagnostic but does not diff between secondary and primary)
  • plasma ACTH level (high ACTH + low cortisol = primary, both low = secondary or tertiary)
  • adrenal antibodies are detected in most cases
66
Q

treatment of addisons disease

A

lifelong steroid replacement

  • hydrocortisone 20mg waking and 10mg in eve to mimic diurnal rhythm
  • fludrocortisone - 50-300mg daily

Year 3 core conditions (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions