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Finals Studying - Condensed > Endocrine > Flashcards

Endocrine Flashcards

1
Q

thyroid hormones

  • highest
  • lowest
A

highest - night

lowest - morning

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2
Q

neck lump that moves up on swallowing

A

thyroid goitre

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3
Q

neck lump that moves up on swallowing and sticking out tongue

A

thyroglossal cyst

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4
Q

branchial cyst presentation

A

large neck swelling on side

teenage years

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5
Q

cystic hygroma presentation

A

congenital

large neck swelling

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6
Q

orphan annie nuclei

A

papillary thyroid cancer

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7
Q

psomomma bodies

A

papillary thyroid cancer

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8
Q

spread of papillary thyroid cancer

A

lymphatic

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9
Q

spread of papillary follicular cancer

A

haematogenous

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10
Q

medullary thyroid ca association

A

MEN IIa or IIb

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11
Q

what is medullary thyroid ca

A

ca of parafollicular cells

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12
Q

Mx of thyroid ca

A

total thyroidectomy + radio-iodine

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13
Q

antibody in graves disease

A

tsh receptor antibody

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14
Q

Mx graves for rapid symptom relief

A

propanolol

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15
Q

Mx graves

A

carbimazole alone

or

carbimazole + thyroxine (block and replace) for 12-18m then withraw

  1. radio-iodine
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16
Q

drug causing thyrotoxicosis

A

amiodarone

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17
Q

antibody in hashimotos thyroiditis

A

anti-TPO antibody

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18
Q

subacute de-quervains thyroiditis

A

post-viral with painful goitre

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19
Q

progression of subacute de-quervains thyroiditis

A

starts with hyperthyroid – euthyroid – hypothyroid

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20
Q

drugs causing hypothyroidism

A

lithium

amiodarone

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21
Q

Monitoring primary hypothyroidism

A

TSH

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22
Q

Monitoring secondary hypothyroidism

A

T4

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23
Q

hormones releases by the anterior pituitary

A 
ACTH
TSH
GH
LH
FSH
Prolactin
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24
Q

hormones released by the posterior pituitary

A

Oxytocin

ADH

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25
Q

cranial diabetes insipidus

A

failure of the posterior pituitary to release ADH

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26
Q

causes of cranial diabetes insipidus

A

idiopathic
neoplasm
post-surgery
trauma

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27
Q

wolfram’s syndrome

A

‘DIDMOAD’

Diabetes Insipidus
Diabetes Mellitus
Optic Atrophy
Deafness

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28
Q

nephrogenic diabetes insipidus

A

failure of the kidneys to respond to ADH

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29
Q

causes of nephrogenic diabetes insipidus

A

genetic
electrolyte abnormalities -
hypercalcaemia, hypokalaemia
drugs - lithium

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30
Q

drug that causes nephrogenic diabetes insipidus

A

lithium

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31
Q

presentation diabetes insipidus

A

polyuria (large volumes of dilute urine)

polydipsia

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32
Q

Ix diabetes insipidus

A

plasma osmolality - high

urine osmolality - low

water deprivation test - will continue to pee ++ volumes

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33
Q

Mx cranial diabetes insipidus

A

Desmopressin (synthetic analogue of ADH)

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34
Q

what is a ‘non-functioning’ pituitary adenoma

A

doesn’t secrete active hormones

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35
Q

classification of non-functioning pituitary adenoma

A

micro-adenoma = <1cm

macro-adenoma = >1cm

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36
Q

presentation of a non-functioning pituitary adenoma

A 
headache
worsening visual acuity 
double vision
panhypopituitarism
CN palsies - III, IV, VI compression 
bitemporal hemianopia
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37
Q

Ix pituitary adenoma

A
  1. pituitary blood profile

2. MRI brain with contrast

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38
Q

Mx pituitary adenoma

A

observation

surgical removal - transsphenoidal approach, post op XRT

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39
Q

what are the 2 most common hormones to be secreted by a pituitary adenoma

A

prolactin (prolactinoma)

GH (acromegaly)

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40
Q

presentation of a prolactinoma

A

Females:

  • amenorrhoea
  • infertility
  • galactorrhoea
  • reduced libido
  • wt gain

Males:

  • erectile dysfunction
  • reduced facial hair
  • osteoporosis
  • galactorrhoea
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41
Q

Mx prolactinoma

A

Dopamine Agonists:

  • bromocriptine
  • cabergoline
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42
Q

presentation of acromegaly

A 
coarse facial hair
large hands
increase in shoe size
excessive sweating 
macroglossia 
acanthosis nigricans
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43
Q

what genetic condition is associated with acromegaly

A

MEN I

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44
Q

Ix acromegaly

A
  1. IGF-1 levels
    - if raised,
  2. Oral Glucose Tolerance Test (OGTT)
    - give 75g oral glucose, take level a 0, 30, 0, 90, 120, 150mins
    - GH normally inhibited by hyperglycaemia
    - if raised,
  3. MRI brain with contrast
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45
Q

Mx acromegaly

A
  1. surgical removal (trans-sphenoidal approach)
  2. somatostatin analogues (inhibit GH) - octreotide
  3. GH antagonists - pegvisomat
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46
Q

HbA1c level

  • normal
  • diabetes diagnosis
A

normal = <41 mmol/L

diabetes = >48 mmol/L

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47
Q

Fasting glucose level

  • normal
  • diabetes diagnosis
A

normal = <6 mmol/L

diabetes = >7 mmol/L

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48
Q

2hr OGTT level

  • normal
  • diabetes diagnosis
A

normal = < 7.7 mmol/L

diabetes = > 11.1 mmol/L

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49
Q

Random glucose level

  • normal
  • diabetes diagnosis
A

normal = < 7.7. mmol/L

diabetes = > 11.1 mmol/L

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50
Q

Ix T1DM

A
  1. random blood glucose
  2. fasting blood glucose
  3. HbA1c
  4. 2h OGTT
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51
Q

rapid acting insulins

A

novorapid

Humalog

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52
Q

short-acting insulins

A

actrapid
Humulin S
insuman rapid

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53
Q

intermediate acting insulins

A

Humulin I
Insulatard
Insuman Basal

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54
Q

long acting insulins

A

Lantus

Levemir

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55
Q

how much insulin in total should someone be taking a day

A

0.2 - 0.4 units/kg/day

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56
Q

what is a basal bolus regime

A

basal = 1/2 of the total daily dose of insulin is taken before bed

bolus = 1/2 of the total daily dose of insulin is split over meal times

57
Q

what is Latent Autoimmune Diabetes of Adulthood

A

autoimmune diabetes that develops in an older person and is often misdiagnosed as having T2DM

58
Q

presentation of LADA

A

young adult 25-40
non-obese
auto ab +ve
non-insulin requiring at diagnosis

59
Q

Ix T2DM

A
  1. random blood glucose
  2. fasting blood glucose
  3. HbA1c
  4. 2h OGTT
60
Q

metformin - class of drug

A

biguanide

61
Q

biguanides - mode of action

A

improve sensitivity to insulin

62
Q

benefits of biguanides

A

no hypo risk
CVS benefits
weight reduction
safe in preg

63
Q

s/e of biguanides

A

GI upset

lactic acidosis

64
Q

glicazide - class of drug

A

sulphonylurea

65
Q

sulphonylureas - mode of action

A

promote insulin release from islet cells

66
Q

benefits of sulphonylureas

A

quick reduction in hyperglycaemia

67
Q

s/e of sulphonylureas

A

hypo risk
weight gain
no CVS benefits

68
Q

dapagliflozin - class of drug

A

SGLT2 inhibitors

69
Q

SGLT2 inhibitors - mode of action

A

enhance glucose excretion by the kidney

70
Q

benefits of SGLT2 inhibitors

A

no hypo risk
wt loss
CVs benefits

71
Q

s/e of SGLT2 inhibitors

A

increased thrush and urine infections

72
Q

pioglitazone - class of drug

A

TZDs (PPARy agonists)

73
Q

TZDs - mode of action

A

promote glucose uptake

74
Q

s/e of TZDs

A

weight gain
fluid retention
increased risk of hip # in elderly

75
Q

sitagliptin - class of drug

A

DPP-IV inhibitors (gliptans)

76
Q

DPP-IV inhibitors - mode of action

A

act on the incretin pathway

77
Q

s/e of DPP-IV inhibitors

A

no CVS benefits
low/mod efficacy
weight neutral

78
Q

exenatide - class of drug

A

GLP -1 agonist

79
Q

GLP-1 agonists - mode of action

A

acts on the incretin pathway

80
Q

benefits of GLP -1 agonists

A

SC injection
wt loss
low hypo risk

81
Q

s/e of GLP -1 agonist

A

nausea

pancreatitis

82
Q

Mx of T2DM

A
  1. Lifestyle
  2. Metformin
    • sulphonylurea OR SGLT-2 inhibitor OR DPP inhibitor OR TZD
    • one of the above or injectable
83
Q

what is maturity onset diabetes of the young (MODY)

A

familial form of early onset T2DM

84
Q

types of MODY

A

glucokinase (GCK)

transcription factor

85
Q

presentation of MODY

A

strong FHx
renal cysts
GAD -ve
c-peptide +ve

86
Q

Mx MODY

A

GCK MODY - no Tx

Transcription Factor MODY - sulphonylurea

87
Q

what is the hallmark of diabetic nephropathy

A

proteinuria

88
Q

Ix of diabetic nephropathy

A

urinary albumin : creatinine ratio

89
Q

normal urinary albumin : creatinine ratio

A

Males < 2.5

Females < 3.5

90
Q

Mx diabetic nephropathy

A

ACEi

91
Q

Mx DKA

A
  1. fluid replacement (most are depleted 5-8 litres)
  2. Insulin infusion (0.1 unit/kg/hr)
  3. start 5% dextrose infusion when BG <15mmol/L
  4. correct hypokalaemia (caused by the insulin)
92
Q

What do you do with a T1DM insulin when they are being treated for DKA

A

continue their basal insulin, omit bolus insulin

93
Q

pathogenesis of hyperosmolar hyperglycaemic state (HHS)

A 
hyperglycaemia - 
osmotic diuresis - 
loss of Na + K - 
increase serum osmolality -
increase hyperviscosity of blood
94
Q

Mx HHS

A
  1. Fluid Replacement - 0.9% saline IVI over 48h

if ketotic - give insulin

95
Q

mild hypoglycaemia

  • presentation
  • Mx
A

pt conscious, orientated, able to swallow

Mx = 15-20g of quick acting carbohydrate

96
Q

moderate hypoglycaemia

  • presentation
  • Mx
A

pt conscious, able to swallow, disorientated/confused

Mx = 1.5-2 tubes of glucose gel squeezed into mouth between teeth and gums

97
Q

severe hypoglycaemia

  • presentation
  • Mx
A

pt unconscious, fitting, very aggressive or NBM

Mx = IV glucose 150ml 10% or 75ml 20%

98
Q

causes of primary hyperparathyroidism

A

solitary adenoma (80%)
hyperplasia of glands
parathyroid Ca
genetic (MEN)

99
Q

biochem primary hyperparathyroidism

A

PTH - raised
Ca - raised
Phosphate - low
Alk phos - high

100
Q

Mx primary hyperparathyroidism

A

surgical candidate:
parathyroidectomy

non-surgical candidate:
monitoring + bisphosphonates

101
Q

causes of secondary hyperparathyroidism

A

this is a physiological response to a low Ca

  • chronic renal failure
  • vitamin D deficiency
102
Q

biochem secondary hyperparathyroidism

A

PTH - raised (appropriately)

Ca - low

103
Q

cause of tertiary hyperparathyroidism

A

hyperplastic change to the parathyroid glands -

the parathyroid becomes autonomous after many years of secondary hyperparathyroidism

104
Q

biochem tertiary hyperparathyroidism

A

PTH - raised ++ (inappropriately)

Ca - raised

105
Q

what is familial benign hypocalciuric hypercalcaemia

A

autosomal dominant defect in Ca sensing

106
Q

presentation of hypoparathyroidism

A

related to low Ca
‘SPASMODIC’

Spasms
Paraesthesiae
Anxious
Seizures
Muscle tone increase
Orientation confused
Impetigo Herpetiformis
Chvostek's sign
107
Q

Mx primary hypoparathyroidism

A

oral Ca supplements + calcitriol

108
Q

pseudohypoparathyroidism

A

genetic condition

  • failure of target cells to respond to PTH
  • high PTH, low Ca
109
Q

pseudopseudohypoparathyroidism biochem

A

normal biochem!

110
Q

secretions of the renal cortex

A

Glomerulosa - Mineralocorticoids
Fasiculata - Glucocorticoids
Reticularis - Sex Steroids

111
Q

what stimulates glucorticoid release from the adrenal cortex

A

ACTH

112
Q

what stimulates mineralocorticoid release from the adrenal cortex

A

RAAS system

113
Q

what stimulates sex steroid release from the adrenal cortex

A

ACTH

114
Q

secretions of the renal medulla

A

catecholamines (adrenaline)

115
Q

what is addisons disease

A

primary hypoadrenalism - low cortisol and aldosterone

116
Q

presentation of addisons disease

A 
ski pigmentation + buccal mucosa ("bronze diabetes") 
abdo pain
fatigue
vomiting 
diarrhoea 
low BP
117
Q

Ix for Addisons

A

short syacthen test

  • give 250mcg IM synthetic ACTH
  • measure cortisol before and 30mins after
  • if cortisol stays low = Addison’s
118
Q

Mx Addisons

A

replace the cortisol = hydrocortisone, dexamethasone or prednisolone
replace the aldosterone = fludrocortisone

119
Q

what is cushings syndrome

A

the clinical state caused by excess cortisol

120
Q

causes of cushings syndrome

A

ACTH dependent causes:

  • cushings diease (ACTH secreting pituitary adenoma)
  • ectopic ACTH (small cell lung cancer)

ACTH independent causes:

  • adrenal tumours
  • steroids
121
Q

screening tests for cushings syndrome

A
  1. Overnight dexamethasone suppression test
    - give dexa 1mg at night, measure cortisol at 8am
  2. 24h urinary free cortisol
122
Q

diagnostic test for cushings syndrome

A

48h dexamethasone suppression

123
Q

conn’s syndrome

A

aldosterone producing adenoma - the most common cause of hyperaldosteronism

124
Q

presentation hyperaldosteronism

A
  • HTN
  • hypokalaemia
    (main ones to be aware of)
  • nocturia
  • polyuria
  • lethargy
  • mood disturbance
125
Q

screening tests for hyperaldosteronism

A 
plasma K (low)
aldosterone/renin ratio (raised)
126
Q

Ix for Conn’s syndrome

A
  1. fludrocortisone suppression test

2. high res CT abdo

127
Q

Mx conn’s syndrome

A

unilateral tumour - laparoscopic adrenalectomy

bilateral tumour - aldosterone antagonists (spironolactone)

128
Q

presentation of phaechromocytoma

A

episodic headache
sweating
tachycardia
+/- high BP

129
Q

Ix phaeochromocytoma

A
  1. bloods - plasma metanephrine levels

2. CT & MRI

130
Q

Mx phaechromocytoma

A 
1. alpha blockade (doxazosin, prazosin)
 THEN 
beta blockade (atenolol, propranolol)
  1. surgical excision
131
Q

Mx gynaecomastia

A

address underlying cause
surgery (cosmetic)
anti-oestrogens (tamoxifen)

132
Q

causes of hypoglycaemia in a non-diabetic patient

A

‘EXPLAIN’

EX = Exogenous drugs - alcohol, quinine sulfate, ACEi, aspirin poisoining 
P = pituitary insuffiency
L = liver failure 
A = Addison's disease
I = islet cell tumours e.g. insulinoma 
N = non=pancreatic neoplasms
133
Q

most important modifiable risk factor in the development of thyroid eye disease

A

smoking

134
Q

T2DM BP target with no end organ damage

A

< 140/80 mmHg

135
Q

T2DM BP target with end organ damage

A

< 130/80 mmHg

136
Q

Mx of intercurrent illness in a person with Addison’s

A

double their hydrocortisone dose

137
Q

triad of renal cell carcinoma

A

haematuria
abdominal mass
loin pain

138
Q

Mx renal cell carcinoma

A

radical nephrectomy

Finals Studying - Condensed (22 decks)

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