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phase 2a > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What investigation results do you need to have to diagnose diabetes?

A

2 of: or 1 + symptoms:

random blood glucose over 11
fasting blood glucose over 7
more than 11 after glucose tolerance test

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2
Q

what is C peptide?

A

used to test for diabetes especially if atypical
Produced in the breakdown of insulin
So if T1DM there will be no C peptide

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3
Q

when should you take bolus insulin?

A

30 mins before a meal

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4
Q

what is the criteria for borderline diabetes?

A

oral glucose tolerance test above 7.8
fasting glucose above 6.1
hba1c above 42

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5
Q

what indications are there that metformin is not sufficient?

A

HbA1c is above 58

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6
Q

gliclazide is what type of drug, what does this do?

A

gliclazide = sulphonylurea
stimulate insulin release
= hypoglycaemia

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7
Q

what kind of drug is dapaglifozin?

A

SGLT2 inhibitor

glucose excretion into urine (fozin like urine)

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8
Q

exanatide is what kind of drug?

A

GLP-1 analogue

increase insulin and satiety

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9
Q

sitagliptin is what kind of drug?

A

DPP-4 inhibitor (prevents breakdown of GLP-1)

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10
Q

pioglitazone is what kind of drug?

A

thiazolidinedione
increased insuline sensitivity and decrease liver gluconeogenesis
CV side effects

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11
Q

in type II diabetes what type of insulin do you start with?

A

basal

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12
Q

what amount of glucose is level 2 hypoglycaemia?

A

3-3.9

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13
Q

diagnostic triad for hypoglycaemia?

A

symptomatic
biochemical
resolves with glucose

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14
Q

what is the pathophysiology of diabetic ketoacidosis?

A

lack of insulin = metabolise amino acids and triglycerides for energy
lipolysis = high serum levels of free fatty acids and alanine
glucagon stimulates ketogenesis (fatty acids – ketones)
= metabolic acidosis

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15
Q

what 3 things must there be in DKA?

A

hyperglycaemia
urinary ketones
metabolic acidosis

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16
Q

treatment of DKA?

A

slow rehydration
insulin
replace electrolytes
treat underlying cause

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17
Q

what can hyperosmolar hyperglycaemic state cause?

A

AKI
hypotension
coma
stroke etc (as hyperviscosity of blood because not enough water)

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18
Q

management of hyperosmolar hyperglycaemic state?

A

fluid (saline)! To dilute

insulin after that if still needed

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19
Q

3 macrovascular complications of diabetes?

A

stroke
IHD
heart failure
peripheral vascular disease

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20
Q

3 microvascular complications of diabetes?

A

neuropathy (inc autonomic = GI disturbance)
renal dysfunction
retinopathy

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21
Q

two stages of retinopathy and what briefly happens in them?

A

non proliferative: fluid leaks into macula = blurred vision

proliferative: new blood vessels try to grow but are not very strong

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22
Q

how does MODY1 present?

A

neonatal macrosomia and hyperglycaemia

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23
Q

what is MODY2?

A

GCK glucose sensor mutation

produces a mild diabetes

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24
Q

what is MODY-3?

A

most common

responds to sulphonylurea eg gliclazide

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25
Q

what is HNF MODY diabetes caused by?

A

decreased beta cell proliferation

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26
Q

how does adrenal disease impact glucose/diabetes?

A

acromegaly, cushings, increased adrenal activity = decreased insulin sensitivity – diabetes like picture

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27
Q

what is the simple function of thyroid hormone?

A

increases BMR, increases use of the body’s resources

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28
Q

what is the basic function of growth hormone?

A

breakdown of fat and carbs for growth

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29
Q

what is the basic function of cortisol?

A

mobilises glucose for fight or flight

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30
Q

what is the basic function of aldosterone?

A

increase BP, sodium and fluid retention

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31
Q

what is the effect of ADH on sodium?

A

high ADH = low sodium

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32
Q

what is Graves?

A

hyperthryoidism

because of antibodies to TSH receptors

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33
Q

what is toxic multinodular goitre?

A

high thyroid

in response to low iodine

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34
Q

what is Hashimoto’s?

A

hypothyroid

because of autoimmune attack of the thyroid gland

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35
Q

what is Conn’s syndrome?

A

high aldosterone

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36
Q

what is Addisons disease?

A

low aldosterone, cortisol and androgens

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37
Q

what is diabetes insipidus?

A

low ADH

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38
Q

what is the most common type of thyroid cancer?

A

papillary

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39
Q

what class of antibodies (MADGE) are in Graves disease?

A

IgG

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40
Q

are the affects of PTH mediated by osteoclasts or osteoblasts?

A

osteoblasts

osteoclasts haven’t got a PTH receptor

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41
Q

what kind of thyroid disturbance does tyhroiditis cause?

A

transient hyperthyroidism

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42
Q

amiodarone and lithium cause what endocrine disturbance?

A

hyperthyroidism

amiodarone can also cause hypothyroidism

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43
Q

a choriocarcinoma can cause what endocrine disturbance?

A

hyperthyroidism
choriocarcinomas secrete hCG
hCG increases thyroid hormone in preparation for pregnancy

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44
Q

5 symptoms of hyperthyroidism?

A 
tremour 
increased heart rate 
yawning
restlessness 
oligomenorrhoea 
irritability
diarrhoea 
intolerance to heat 
sweating
muscle wasting
eyelid lad/stare
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45
Q

some symptoms of hyperthyroidism that indicate Grave’s is the cause?

A 
other autoimmune eg diabetes etc 
bulging eyes 
acropathy 
pretibial myxedema 
Goitre
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46
Q

What do the individual levels of T3/T4 mean?

A

high T3 and T4 = hyperthyroidism
high T3 = hyperthyroidism
normal T3 high T4 - not significant

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47
Q

what antibodies are there in Graves?

A

anti TSHR IgG

may see:
anti TPO (thyroid peroxidase)
anti thyroglobulin

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48
Q

how can you look at the thyroid gland to see the type of goitre?

A

radioactive iodine uptake scan

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49
Q

what drug is used for hyperthyroidism?

A

carbimazole

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50
Q

what is gestational thyrotoxicosis?

A

nausea and vomitting
wernickes encephalopathy
no goitre or autoimmunity, low TSH high T4

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51
Q

what can happen in pregnancy if too much thyroid hormone?

A 
poor foetal growth
low birth weight 
pre eclampsia 
miscarriage 
still birth
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52
Q

what is atropic thyroiditis?

A

an extreme form of hashimotos, = hypothyroidism

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53
Q

symptoms of hypothyroidism?

A 
weight gain
cold intolerance
oedema
slow cerebration
delayed reflexes
fatigue
dry cold skin
loss of lateral aspect of eyebrows
goitre
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54
Q

what antibodies are there in Hashimoto’s?

A

anti-TPO

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55
Q

what is subclinical hypothyroidism?

A

high TSH but (inappropriately) normal T4

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56
Q

what is the drug for hypothyroidism?

A

levothyroxine

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57
Q

what can happen if not enough thyroid hormone in pregnancy?

A 
hypertension
placental abruption
post partum haemorrhage
low birth weight (this can also happen if hyperthyroid)
preterm 
neonatal goitre
neonatal resp distress
If you take levothyroxine you need to increase the dose in pregnancy
58
Q

3 signs/symptoms of thyroid cancer?

A 
trachial deviation
dysphagia
hoarse voice
palpable nodule in thyroid 
raised or decreased thyroid hormone or symptoms  of that
59
Q

what 2 types of thyroid cancer secrete thyroglobulin?

A

papillary and follicular

thyroglobulin is used to make T3 and T4

60
Q

what cells is medullary thyroid cancer from?

A

the C cells that make calcitonin

61
Q

what are the 3 effects of grehlin?

A

increases hunger
increases fat deposition
stimulates growth hormone

62
Q

What inhibits growth hormone release? - 3

A

somatostatin (from hypothalamus)
glucose
dopamine
high IGF-1 or GH, by negative feedback

63
Q

what organ produces IGF-1?

A

liver

64
Q

3 effects of IGF-1?

A

Cartilege formation
bone growth
protein synthesis
cell proliferation

65
Q

apart from acral enlargement, give 5 other features of acromegaly?

A 
sweating
large hands/feet
carpal tunnel
arthralgia
headache
bitemporal hemianopia
hypogonadal dysfunction
diabetes like - polyuria polydipsia
hyperprolactinaemia
66
Q

3 tests for acromegaly?

A

GH - pulsatile so high GH means little but very low GH suggests is not a tumour
GnRH - if high suggests a problem in hypothalamus

glucose tolerance test.

    • glucose inhibits GH release
    • glucose = fall in IGF-1 normally, if not could be acromegaly

pituitary MRI after you have pos results, to find the tumour

67
Q

what treatment is first line for acromegaly caused by pituitary tumour?

A

transsphenoidal pituitary surgery

68
Q

give 3 drugs you could give for acromegaly?

A

somatostatin analogue eg octroetide

dopamine agonist eg bromocriptine

pegvisomant: GH antagonist

69
Q

Cushings disease vs syndrome?

A

cushings disease = pituitary tumour

cushings syndrome = glucocorticoid excess from any other cause

70
Q

two primary causes of cushings?

A

adrenal adenoma
adrenal hyperplasia
micronodular adrenal dysplasia
carney complex syndrome

71
Q

what is a carney complex syndrome?

A

multiple benign tumours
myxomas (in conn tissue esp heart)
tumours in endocrine glands (– Cushings etc)
spotty skin

72
Q

5 signs / symptoms of Cushings disease?

A 
moon face
bufallo hump
purple striae 
muscle wasting
central obesity
achne 
bloating
weiight gain
tiredness 
menstrual irregularity
73
Q

how does cortisol affect the BMR?

A

cortisol decreases metabolism, this is why cushings = weight gain

74
Q

what is dexamethasone an analogue of?

A

cortisol

75
Q

how does the dexamethasone test work, what do you use it for?

A

use it to investigate high cortisol

dexamethasone = cortisol analogue
so AcTH should decrease in response to it (neg feedback)
if AcTH does not decrease is pathological

Cushings disease – only responds to high dose dexamethasone
ectopic AcTH secreting tumour (eg small cell lung cancer) – still no response to v high dexamethasone

76
Q

in Cushings when is the best time to measure cortisol?

A

Midnight, when it should be lowest

If cortisol is still high at this time you know there is a problem

77
Q

In Cushings when should you measure AcTH, what will the results tell you?

A

measure at 9am
as cortisol is highest at 9am, ACTH should be lowest
If it is low the problem could be with the adrenals
If it is high the ACTH is being produced when it shouldnt be so the problem is secondayr

78
Q

3 causes of pseudocushings?

A

alcohol
depression
obesity
pregnancy

79
Q

what is secondary hyperaldosteronism caused by?

A

high renin, eg

    • renal artery stenosis
    • heart failure (resulting in poor renal perfusion)
80
Q

how does renin cause aldosterone release?

A

renin = angiotensinogen – AT1

AT 2 = aldosterone release from the adrenals

81
Q

what does aldosterone do in the kidney?

A

increases Na+K+ channels on the luminal membrane of principle cells in the DCT
increases ENaC on the apical membrane of principle cells in the DCT
= increased sodium reabsorption and increased potassium excretion

Increases H+K+ excretion pump = potassium excretion & alkalosis

82
Q

some symptoms of Conns syndrome?

A

Conns = too much aldosterone

resistant hypertension
alkalosis
hypokalaemia – cramps
lethargy

83
Q

how would you find renal artery stenosis?

A

CT angiography
doppler
magnetic resonance angiography (MRA)

84
Q

first line investigation for hyperaldosteronism?

A

renin:aldosterone ratio

85
Q

is Conns primary or secondary?

A

Conns is primary hyperaldosteronism, caused by an adrenal tumour/hyperplasia etc

86
Q

treatment for hyperaldosteronism?

A

aldosterone antagonist - spironolactone, eplerenone
percutanous renal artery angioplasty/stent - if renal artery stenosis
adrenalectomy - if problem is a unilateral tumour
low dose glucocorticoids for familial hyperaldosteronism

87
Q

in this country what is the most common cause of adrenal insufficiency?

A

Autoimmune adrenalitis

antibodies against glands or enzymes especially 21 a hydroxylase

88
Q

3 causes of Addisons disease?

A 
autoimmune adrenalitis 
TB 
congenital
metastatic tumour 
haemorrhage 
amyloidosis
89
Q

what is the most common cause of tertiary adrenal insufficiency?

A

steroids

90
Q

what stimulates AcTH release from the anterior pituitary?

A

CRH release from the hypothalamus

91
Q

give 4 physiological functions of cortisol?

A 
increases HR 
increases BP
bronchodilation
glycogenolysis 
decreases digestion
decreases urine output 
decreases BMR
92
Q

symptoms of Addisons disease?

A 
hyperpigmented patches of skin
weight loss
muscle wasting 
fatigue
poor recovery from inf 
hypotension
hyponatraemia 
hyperkalaemia 
vitiligo
hair loss 
dehydration
93
Q

symptoms of addisonian crisis?

A 
metabolic acidosis
hyperkalaemia 
hyponatraemia 
hypovolaemic shock
confusion
94
Q

when do you measure cortisol if you suspect adrenal insufficiency and what result indicates adrenal insufficiency?

A

measure at 9am when it should be highest, if low is bad!
100 = hospitalise
more than 500 = fine

95
Q

what is synacthen and how can you use it as a test?

A

AcTH analogue
should stimulate AcTH receptors = cortisol release
if cortisol is not released in response there is a problem with the adrenals (primary adrenal insufficiency / Addisons disease)

96
Q

why should you measure aldosterone if there is low cortisol?

A

aldosterone is also released from the adrenals but not under pituitary control

so if aldosterone is normal, problem is with AcTH - pituitary, hypothalamus, steroids

if aldosterone is low the problem is primary, a problem with the adrenals

97
Q

3 causes of hyperkalaemia?

A 
adrenal insufficiency 
renal dysfunction
tumour lysis syndrome
rhabdomyolysis/ trauma / burns 
metabolic acidosis 
diabetic ketoacidosis
potassium sparing diuretics eg spironolactone 
ACEi because they decrease aldosterone
diet 
NSAIDs because they impair renal function
98
Q

normally is potassium intracellular or extracellular?

A

potassium lives in the cell

99
Q

what ECG signs do you see in hyperkalaemia?

A

tall tented T waves
flat P
wide QRS

100
Q

symptoms of hyperkalaemia?

A 
arrythmia
weakness
paresthesia 
lightheadedness
tachycardia
diarrhoea
hyper reflexia
101
Q

a traumatic blood taking can alter the level of what electrolyte?

A

potassium

because it is released from lysed cellls

102
Q

what drug for mild (below 6) hyperkalaemia?

A

calcium resonium

103
Q

what drugs for bad hyperkalaemia?

A

insulin/dextrose
calcium gluconate

nebulised salbutamol
IV fluid
sodium bicarb

104
Q

5 causes of hypokalaemia?

A

conns
cushings
nephrotic syndrome = low kidney BP = RAAS
inadequate diet / malabsorption / laxative
potassium wasting diuretics
renal failure
genetic - barrters / liddles / gietelmans
alkalosis
alcohol

105
Q

5 symptoms of hypokalaemia?

A 
arrythmia / palpitations / ectopic beats 
muscle weakness / hypotonia 
rhabdomyolysis 
paralytic ileus 
hypotension
respiratory depression
tetany
106
Q

ECG changes in hypokalaemia?

A

flat inverse T wave
U wave
ST depression
prolonged QU

107
Q

what is the oral potassium replacement called?

A

sandok

108
Q

3 causes of nephrogenic diabetes insipidus?

A 
lithium
CKD
post obstructive uropathy 
hypokalaemia 
hypercalcaemia 
inherited V2 receptor defect 
diabetes mellitus
109
Q

3 causes of cranial diabetes insipidus?

A 
brain tumour
head injury
hypophysitis 
meningitis 
sarcoidosis 
pregnancy
110
Q

is ADH released when serum osmolarity is high or low?

A

released when it is high
this means the blood is concentrated and we dont want to be losing anymore water so we will secrete ADH to keep the water

111
Q

presentation of diabetes insipidus?

A 
polyuria 
polydipsia
dehydration
postural hypotension
hypernatraemia 
concentrated blood, diluted urine
112
Q

what is desmopressin an agonist of and how is desmopressin used as a test?

A

desmopressin = V2 agonist

test for diabetes insipidus

113
Q

what can you use as a marker of DI instead of desmopressin?

A

copeptin
released in the production of ADH
water deprivation should induce copeptin release

114
Q

treatment for DI? Is this for cranial or nephrogenic?

A

desmopressin
works well in cranial
no good treatment for nephrogenic but can try desmopressin

115
Q

symptoms of hyponatraemia?

A 
nausea
anorexia
lethargy
headache
weakness
myalgia
ataxia
confusion
seizures
LOC
myoclonus
respiratory arrest
116
Q

3 causes of SIADH?

A 
head injury
brain abscess 
guillian barre
pneumonia
asthma
drugs eg carbamazepine
small cell lug cancer
117
Q

what is the difference in presentation of Addisons and SIADH?

A

both have low serum sodium and high urine sodium
in addisons there is usually hypovolaemia but in SIADH the body compensates for this
In addisons there are dark patches on the skin
in addisons ACTH is high
in addisons you also lack cortisol

118
Q

what happens if the person is hyponatraemic and you give them sodium too quickly?

A

osmotic demyelination

119
Q

treatment for SIADH?

A

replace sodium with hypertonic saline
tolvaptan
fluid restrict
furosemide

120
Q

If you suspect acromegaly, what are the 1st, 2nd and 3rd line tests?

A

1st line: IGF-1
2nd : oral glucose tolerance test
3rd: pituitary function tests inc prolactin
4th: MRI pituitary

121
Q

what is the gold standard test for phaeochromocytoma?

A

elevated free plasma metanephrine

122
Q

3 cancers that cause SIADH?

A

small cell lung
prostate
pancreatic

thymus
lymphoma

123
Q

complications of acromegaly?

A 
obstructive sleep apnoea 
carpal tunnel
diabetes 
cardiomyopathy 
HTN 
stroke
124
Q

what is the most common cause of primary hyperparathyroidism?

A

solitary adenoma

125
Q

in hyperaldosteronism what is the most obvious electrolyte distubance?

A

hyperkalaemia

126
Q

how does carbimazole work?

A

prevents thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin

127
Q

what cells is a phaeochromocytoma made of?

A

chromaffin cells

128
Q

4 causes of hypocalcaemia?

A
  • low vit D
  • low PTH (surgery/ digeorge / magnesium deficiency)
  • pseudohypoparathyroidism (mutation in PTH receptor)
  • kidney disease (so cant reabsorb it)
  • osteomalacia

pancreatitis
resp alkalosis
rhabdomyolysis

129
Q

how does calcium affect QT?

A 
lOng = hypOcalcaemia 
short = hypercalcemia
130
Q

two signs of hypocalcaemia?

A

Trousseau: hand spasm with BP cuff

Chovstek: face twitch

131
Q

parasthesia, spasm, long QT, seizures and basal ganglia calcification suggest high or low calcium?

A

low

low calcium = everything more excitable, the QT interval is opposite to what you’d think

132
Q

thirst, hyporeflexia, short QT, pyrexia, hypertension suggest high or low calcium?

A

high

133
Q

primary vs secondary hyperparathyroidism?

A

primary: high PTH = high Ca

secondary = low Ca = high PTH

134
Q

how does high calcium affect the neurones?

A

high calcium = hyperpolarisation = slow and sluggish neurones

135
Q

symptoms of high calcium?

A

bones (pain)
stones (kidney)
moans (depression)
thrones (constipation)

hyporeflexia 
hypertension
vomitting 
confusion - coma 
pyrexia
136
Q

what happens in hypercalcaemia of malignancy?

A

tumour produces ectopic PTHrP

137
Q

what happens in carcinoid syndrome?

A 
tumour produces serotonin, bradykinin and histamine 
= vasodilation
itching
SOB
diarrhoea
138
Q

plasma chromogranin A and urinary 5-HIAA are tests for what?

A

carcinoid syndrome

139
Q

a drug for carcinoid syndrome?

A

octreotide

140
Q

3 causes of decreased pituitary function?

A 
adenoma 
metastates 
developmental cyst - rathkes or mucocoele
syphilis
sarcoidosis 
granulomatosis with polyangiitis
anneurysm 
autoimmune 
perisellar meningeoma
141
Q

what cells is prolactinoma a tumour of?

what are some symptoms of prolactinoma?

A

lactotroph

inhibits FSH and LH = infertility, amenorrhoea
galactorrhoea
low libido

phase 2a (10 decks)

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