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Year 6 > Endo > Flashcards

Endo Flashcards

1
Q

in a pregnant lady under 25 with type 1 diabetes, what are the chances ( x in x) of her baby getting T1DM?

A

1 in 25

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1
Q

what can trigger Waterhouse Friderichsen Syndrome

A

Neisseria meningitides or strep pneumo infection

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2
Q

what pathological process that Waterhouse Friderichsen Syndrome lead to?

A

DIC

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3
Q

sulfonylurea MoA

A

increase insulin secretions

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4
Q

examples of sulfonylureas

A

glimepiride, gliclazide

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5
Q

name a drug that reduces the absorption of levothyroxine

A

calcium carbonate
iron

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6
Q

blood ketones in DKA

A

> 3 mmol/L

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7
Q

bicarb in DKA

A

< 15

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8
Q

Side effects of thyroxine over replacement [4]

A

hyperthyroidism
worsening angina
AF
osteoporosis

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9
Q

3 keys features of primary hyperaldosteronism

A

hypokalaemia
hypertension
metabolic alkalosis

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10
Q

if CT is normal, how can unilateral and bilateral causes of hyperaldosteronism be differentiated

A

adrenal venous sampling

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11
Q

treatment of bilateral adrenal hyperplasia

A

spirinolactone

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12
Q

what is the principle of management of Addisons disease?

A

steroid replacement with hydrocortisone and fludrocortisone

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13
Q

what patient education must be provided for those with Addisons? [4]

A
  • emphasise the importance of not missing glucocorticoid doses
  • consider MedicAlert bracelets and steroid cards
  • patients should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis
  • discuss how to adjust the glucocorticoid dose during an intercurrent illness
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14
Q

how should hydrocortisone and fludrocortisone dose change with intercurrent illness in Addisons?

A

double the hydrocortisone
keep fludrocortisone the same

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15
Q

how is hydrocortisone replacement given in Addison’s disease?

number of doses in the day and time of day

A

2-3 doses a day, usually within the first half of the day

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16
Q

which conditions can cause a lower than usual HbA1c reading [3]

A

G6PD deficiency
hereditary spherocytosis
haemodialysis

i.e. anything that reduced RBC survival

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17
Q

which conditions can cause a higher than usual HbA1c reading [3]

A

splenectomy
IDA
vitamin B12/folate def

anything that make more RBCs, bigger RBCs or survive longer

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18
Q

how can you differentiate HHS from DKA

A
  • happens over a longer time frame
  • no significant ketosis <3
  • very high glucose >30
  • no significant acidosis bicarb >15, pH >7.3
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19
Q

key diagnostic features of HHS [4]

A

hypovolaemia
hyperglycaemia
raised serum osmolarity
no significant ketosis/acidosis

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20
Q

treatment of HHS [3]

A

IV fluids
insulin
VTE prophylaxis

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21
Q

complication of HHS

A

hyperviscosity leading to MI and stroke

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22
Q

causes of hypernatraemia: increase in salt [3]

A
  • high intake
  • Conn’s/BAH
  • Renal artery stenosis

both cause high aldosterone

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23
Q

causes of hypernatraemia: loss of water [3]

A
  • osmotic diuresis
  • diabetes insipidus
  • GI loss and sweat
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24
Q

4 causes of nephrogenic DI

A

hypercalcaemia
hypokalaemia
lithium
sickle cell anaemia

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25
Q

complication of rapid hypernatraemia correction

A

cerebral oedema

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26
Q

complication of rapid hyponatraemia correction

A

central pontine myelinolysis

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27
Q

hypervolaemic hyponatraemia: 3 causes and the mechanism causing hyponatraemia

A

cardiac failure
cirrhosis
renal failure

first two lead to excess water being held because of increased ADH due to low pressure states

renal failure is unable to get rid of water

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28
Q

euvolaemic hyponatraemia [4]

A
  • psychogenic polydipsia
  • hypothyroidism (low BP, ADH released)
  • adrenal insufficiency (no Aldo)
  • SIADH (water retention, suppress RAAS, less Aldo)
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29
Q

drugs that can cause SIADH [5]

A

SSRI
TCA
PPI
carbamazepine
sulphonylureas

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30
Q

2 drug treatments for SIADH

A

demeclocycline
tolvaptan

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31
Q

symptoms of central pontine myelinolysis [4]

A

quadriplegia,
dysarthria
seizure
coma and death

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32
Q

6 causes of hyperkalaemia

A

1.low GFR
2. high Renin (Type 4 RTA and NSAIDs)
3. ACE inhibitors
4. ARBs (Angiotensin 2 Receptor Blockers)
5. Addison’s disease
6. Aldosterone antagonists (i.e. spironolactone)

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33
Q

4 categories of causes of hyperkalaemia

A
  • renal impairment
  • drugs
  • release from cells
  • low aldosterone
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34
Q

features of hyperkalaemia on ECG [4]

A
  • tall tented T waves
  • PR prolongation
  • broad QRS
  • flat P wave
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35
Q

late ECG sign in hyperkalaemic indicating peri-arrest

A

sine wave

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36
Q

causes of hypokalaemia [5, non drug]

A
  • GI losses
  • Cushing’s
  • Conn’s
  • RTA (1 and 2)
  • hypomagnesaemia
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37
Q

drugs that causes hypokalaemia

A

loop and thiazide diuretics
insulin
beta agonists

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38
Q

ECG features of hypokalaemia [3]

A

ST depression
flat T waves
U waves

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39
Q

when measuring aldosterone: renin ratio, what does a high aldosterone indicate?

what does a high renin indicate?

A

high aldosterone –> Conn’s

high renin –> RAS

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40
Q

treatment of mild/mod hypokalameia

A

oral KCl e.g. SandoK

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41
Q

treatment of severe hypokalaemia [2]

A

IV KCl (3x 1L bag of saline with 40mmol KCl)

cardiac monitoring

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42
Q

ECG finding in hypocalcaemia

A

long QT

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43
Q

main electrolyte abnormality in refeeding syndrome

A

hypophosphataemia

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44
Q

signs of refeeding syndrome [4]

A

rhabdo
low resp rate
arrhythmia
shock and seizures

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45
Q

management of refeeding syndrome

A

phosphate supplementation

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46
Q

ECG sign in hypercalcaemia

A

short QT

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47
Q

1st line bloods in investigating polyuria

A

U&Es, glucose, paired serum & urine osmolarity, serum calcium

2nd line: water deprivation test

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48
Q

which arteries does fibromuscular dysplasia (FMD) affect predominantly

A

renal and cervical arteries

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49
Q

signs of renal artery FMD [3]

A

resistant hypertension
unilateral small kidneys
bruits

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50
Q

signs of cervical artery FMD [2]

A

chronic migraines
pulsatile tinnitus

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51
Q

gold standard investigation for FMD

A

CTA, catheter angiography

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52
Q

management of FMD [4]

A

1) stop smoking
2) clopidrogrel
3) ACEi or ARB
4) stenting of arteries

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53
Q

tongue sign of B12 def

A

glossitis

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54
Q

highly sensitive AB in Vitamin B12 def

A

anti parietal

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55
Q

highly specific AB in vitamin B12 def

A

anti Intrinsic factor

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56
Q

1st and 2nd line AB to check in vitamin B12 def

A

1st: anti IF
2nd: anti parietal cell (not used)

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57
Q

management of vit b12 def: what are the two preparations of B12 replacement

A

cyanocobalamin PO

hydroxycobalamin IM

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58
Q

2 metabolic disorders that cause hypomagnesaemia

A

Gitelman’s and Barter’s

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59
Q

two electrolyte abnormalities causing low Mg

A

hypokalaemia
hypocalcaemia

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60
Q

what drug toxicity can hypomagnesaemia exacerbate

A

digoxin

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61
Q

treatment of hypomagnesaemia

A

PO or IV MgSO4 depending on severity (<> 0.4 mmol/L)

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62
Q

when should an SGLT-2 inhibitor be added to meds for a diabetic

A

used in addition to metformin as initial therapy for T2DM if CVD, high-risk of CVD or chronic heart failure

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63
Q

how should Muslim diabetics take metformin during Ramadan?

A

dose should be split one-third before sunrise (Suhoor) and two-thirds after sunset (Iftar)

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64
Q

The standard HbA1c target in type 2 diabetes mellitus

A

48 mmol/mol

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65
Q

LH and testosterone levels in Klinefelter’s?

A

High LH
Low testosterone

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66
Q

Radioiodine uptake in Grave’s disease

A

diffuse homogenous uptake

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67
Q

Key investigation for Addison’s

A

short synacthen test

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68
Q

Key investigation for Cushing’s

A

overnight dexamethsone

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69
Q

high aldosterone:renin ration mean

A

Indicates aldosterone is being produced independently of renin, so the cause is primary (originating in the adrenals).

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70
Q

low aldosterone: renin ratio means

A

indicates aldosterone is raised due to renin being raised, so the cause is pathology of the renin-angiotensin-aldosterone axis e.g. renal artery stenosis

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71
Q

useful serology to diagnose T1DM

A

low C-peptide

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72
Q

how do you distinguish between type 1 and type 2 diabetes in the bloods

A

diabetes-specific autoantibodies:
- Antibodies to glutamic acid decarboxylase (anti-GAD)
- Islet cell antibodies

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73
Q

in what % of patients are eye signs seen in graves

A

30% therefore absence does not rule it out

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74
Q

Characteristic histology in papillary thyroid cancer

A

Orphan Annie eyes

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75
Q

tumour marker for papillary and follicular thyroid cancer

A

thyroglobulin

76
Q

drug treatment for prolactinoma [2]

A

cabergoline, bromocriptine

77
Q

triad seen in phaeochromocytoma

A

sweating
headaches
palpitations

in association with severe headache

78
Q

management of phaechromocytoma before definitive surgery

A

alpha blockade e.g. phenoxybenzamine followed by beta blockade e.g. propranolol

79
Q

what must be done with an incidentaloma found in the pituitary sella

which scan is best

A

all patients with a pituitary incidentaloma, including those without symptoms, undergo clinical and laboratory evaluations for hormone hypersecretion and hypopituitarism.

MRI

80
Q

Most common pituitary adenoma

A

prolactinoma

After prolactinomas, non-secreting adenomas are the next most common, then GH-secreting and then ACTH-secreting adenomas.

81
Q

How do non-functional pituitary adenomas present

A

depletion of a hormone(s) (due to compression of the normal functioning pituitary gland) therefore, present with generalised hypopituitarism

82
Q

treatment of GH-secreting adenomas

A

somatostatin analogues (e.g., octreotide, lanreotide) and GH receptor antagonists (e.g., pegvisomant)

83
Q

First line treatment for most patients with a pituitary tumour causing acromegaly

A

trans-sphenoidal surgery

84
Q

two common side effects of sulfonylureas

A

weight gain
hypos

85
Q

what hypoaldosteronism condition is caused by meningococcal septicaemia

A

Waterhouse-Friedrichsen syndrome

86
Q

drugs that can raise prolactin [4]

A

metoclopramide, domperidone
phenothiazines
haloperidol

very rare: SSRIs, opioids

87
Q

TFTs in sick euthyroid syndrome

A

low T3/T4 and normal TSH with acute illness

88
Q

when is insulin started in HHS

A

if the glucose stops falling while giving IV fluids

89
Q

what key thing must also be given in HHS treatment alongside fluids and insulin

A

thromboprophylaxis due to hyperviscosity

90
Q

cardiac complication of acromegaly

A

cardiomyopathy

91
Q

6% of acromegaly patients have _____

A

MEN-1

92
Q

causes of hypogonadotrophic hypogonadism

A

haemochromatosis
Kallman’s

93
Q

management of gastroparesis in diabetes

A

pro kinetics e.g. metoclopramide, domiperidone

94
Q

treatment of neuropathic pain in diabetes

A

amitriptyline, duloxetine

95
Q

waking target in T1DM

A

5-7 mmol/L

96
Q

how often should BM monitoring be done during illness

A

every 4 hours

97
Q

what is the alternative to basal-bolus regimen

A

pre-mixed regimen given at the start of breakfast and dinner

98
Q

pre-diabetes HbA1c threshold

how is this managed

A

42-48

diabetes prevention programme

99
Q

what drugs are given to address cardiovascular risk factors in DM

A

aspirin
ACEI/ARB
statin

100
Q

MoA of metformin

A

increase insulin sensitive and decrease hepatic gluconeogenesis

101
Q

contraindications of metformin [4]

A

eGFR <30
tissue hypoxia e..g MI, surgery
iodine contrast
alcohol abuse

102
Q

when does diabetic therapy become dual therapy

A

when HbA1c rises to >58 /7.5%

103
Q

when starting dual therapy for DM, what does the HbA1c target become

A

< 53 mmol/L or 7%

104
Q

which cancer is a contraindication to pioglitazone

A

bladder cancer

105
Q

treatment of MODY

A

sulfonylurea

106
Q

treatment of late onset DM (LADA)

A

hypoglycaemics followed by insulin

107
Q

investigation for MODY and LADA

A

MODY: C peptides
LADA: GAD antibodies and low C-peptide

108
Q

rate of insulin infusion on DKA

A

0.1U/kg/hr

109
Q

Treatment algo for DKA [5]

A

fluids
insulin with 10% detrose
potassium replacement
VTE prophylaxis

110
Q

insulin infusion rate in HHS

when is it started?

A

0.05U/kg/hr sliding scale once BM stop dropping or ketones start rising

111
Q

TSH and T4 in thyrotoxicosis

A

TSH LOW
T4 HIGH

112
Q

TSH and T4 in primary hypothyroid

A

TSH HIGH
T4 LOW

113
Q

TSH and T4 in secondary hypothyroid

A

TSH LOW
T4 LOW

114
Q

TSH and T4 in sick euthyroid syndrome

A

TSH LOW/NORMAL
T4 LOW
T3 very low

115
Q

TSH and T4 in subclinical hypothyroid

A

TSH HIGH
T4 NORMAL

116
Q

TSH and T4 in poor thyroxine compliance

A

TSH HIGH
T4 NORMAL

117
Q

TSH and T4 in steroid therapy

A

TSH LOW
T4 NORMAL

118
Q

when should USS and FNA of a thyroid lump be done

A

> 1cm

119
Q

management of thyroid cancer

A

Hemi thyroidectomy + iodine 131 too kill remaining cells

follow up: measure TG or calcitonin, I-123 body scans

120
Q

Causes of hyperthyroid that cause low uptake [2]

A

Sub acute thyroiditis/Viral thyroiditis/de Quervains

post partum thyroiditis

121
Q

features of thyroid acropachy [3]

A

digital clubbing
soft tissue swelling
periostea new bone formation

122
Q

best preventative measure of Grave’s

A

stop smoking

123
Q

treatment of Graves in primary care

A

propanolol

124
Q

1st line anti thyroid

A

carbimazole

125
Q

2nd line antithyroid

A

PTU

126
Q

what is used to treat Graves if antithyroid medication don’t work

what are the side effects

A

radioiodine

SE: hypothyroid, thyroid storm

127
Q

treatment of thyroid storm

A

Propanolol IV
PTU
Prednisolone/Hydrocortisone
POtassium iodide

128
Q

investigation of Hashimoto’s thyroiditis

A

anti TPO abs

129
Q

most common cause of hypothyroidism in the UK and the developing world

A

UK: hashimotos

developing world: iodine deficiency

130
Q

when should sub-clinical hypothyroidism be treate; with what?

A

when TSH >10 with levothyroxine

otherwise just observe

131
Q

treatment of myxoedema coma [3]

A

thyroxine IV
hydrocortisone IV
fluids IV

132
Q

1st line investigation in Addison’s

A

(9 am) plasma cortisol

if <500 –> short synacthen then measure cortisol after 30 minutes, cortisol will still be <500

133
Q

signs and symptoms of pituitary adenoma [4]

A
  • excess hormones (acromegaly, Cushing’s, amenorrhoea)
  • hormone depletion
  • bitemporal hemianopia
  • headaches
134
Q

investigations for prolactinoma [3]

A

bloods for pituitary hormones
visual field testing
MRI brain with contrast

135
Q

investigation for acromegaly [2]

A

1st Serum IGF-1
if raised –> OGTT with serial GH measurements to confirm diagnosis

MRI brain with contrast

136
Q

2nd line treatment of acromegaly

A

somatostatin analogue e.g. octreotide

137
Q

Causes of Cushing’s syndrome can be split into exogenous and endogenous. Endogenous causes are further split into ACTH dependent and ACTH independent

what are the dependent causes [2]

A

Cushing’s disease (adenoma)
Ectopic ACTH production

138
Q

Causes of Cushing’s syndrome can be split into exogenous and endogenous. Endogenous causes are further split into ACTH dependent and ACTH independent

what are the INdependent causes [4]

A

iatrogenic steroids
adrenal adenoma
adrenal carcinoma
Carney complex

139
Q

what are the causes of pseudo Cushings [2]

how can you differentiate it from true Cushing’s

A

alcohol XS or severe depression

causes a false positive dexamethasone suppression test

differentiate with insulin stress test

140
Q

1st line investigation of Cushings [2]

A

salivary cortisol
low dose dex suppression test [fails to suppress]

141
Q

how is a low dose dex suppression test carried out

A

dose taken before bed at 11pm (1mg) and cortisol is measured at 9 am the next day

in Cushing’s, the cortisol will still be high

142
Q

how do you distinguish pituitary dependent Cushing’s to ectopic ACTH Cushing’s

A

Inferior Petrosal Sinus Sampling

catheter fed into the jugular vein

143
Q

management of Cushing’s
- pituitary adenoma
- adrenal adenoma [2]
- ectopic [3]

A
  • pituitary adenoma –> surgery
  • adrenal mass –> adrenalectomy + steroid replacement
  • ectopic –> ketoconazole, metryapone, mifepristone
144
Q

3 investigations in Conn’s

A

plasma aldosterone:renin ratio
HR-CT
adrenal venous sampling (uni vs bi)

145
Q

cause of high aldosterone: renin ratio and normal ratio

A

high in Conn’s and normal in renal artery stenosis

both end with high aldosterone.
in RAS the high renin leads to aldosterone production

146
Q

management of Conns

A

solitary adenoma–> spironolactone/epleronone + surgery

bilateral or elderly –> spironolactone/epleronone

147
Q

how does hypocalcaemia present [2]

A

pareasthesia in fingers toes and periorally
muscle cramps and spasms

148
Q

calcium level in secondary hyperparathyroidism

A

LOW

149
Q

definitive treatment of hyperparathyroidism

A

total parathyroidectomy

cinacalcet if non surgical candidate

150
Q

which forms of multiple myeloma have no CRAB features or Signs & Symptoms

A

MGUS and smouldering myeloma

151
Q

difference between MGUS and smouldering myeloma [3]

A

monoclonal serum protein; BM plasma cell levels and risk of progression

< 30g/L serum protein and <10% plasma cells in MGUS
low risk of progression to MM

> 30g/L serum protein and >10% plasma cells in SM
10% risk of progression to MM

152
Q

which Ig protein in found in Walderstroms

A

IgM

153
Q

investigation to do in subclinical hypothyroidism

A

check for thyroid peroxidase antibodies

154
Q

what should be done for those with TSH is between 5.5 - 10mU/L and the free thyroxine level is within the normal range and asymptomatci

A

observe and do TFT in 6 months

155
Q

what should be done for those with TSH is between 5.5 - 10mU/L and the free thyroxine level is within the normal range and are < 65 years consider

A

offering a 6-month trial of levothyroxine if:
the TSH level is 5.5 - 10mU/L on 2 separate occasions 3 months apart,and
there are symptoms of hypothyroidism

156
Q

If a triple combination of drugs has failed to reduce HbA1c, what is done

A

switching one of the drugs for a GLP-1 mimetic is recommended, particularly if the BMI > 35

157
Q

complications of thyroid eye disease

A

Exposure keratopathy
this is the most common complication of thyroid eye disease
due to eyelid retraction and proptosis (exophthalmos) → cornea becomes excessively exposed, disrupting the normal tear film → dryness, irritation, and corneal ulceration
symptoms include foreign body sensation, pain, and photophobia
in severe cases, it can lead to corneal scarring and vision impairment.

Optic neuropathy
one of the most serious complications of thyroid eye disease
occurs when enlarged extraocular muscles compress the optic nerve at the apex of the orbit → a reduction in visual acuity, colour vision deficits, and visual field defect
it requires urgent medical intervention to prevent permanent vision loss.

Strabismus and diplopia
fibrosis and enlargement of the extraocular muscles can result in restrictive strabismus → misalignment of the eyes → double vision (diplopia)
this not only affects visual function but can also significantly impair the quality of life.

158
Q

adverse effects of gliflozins [3]

A

urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored

159
Q

how often should you monitor BMs

A

at least 5 times a day for children and young people
at leas 4 a day for adults

before meals and before bed

160
Q

1st line insulin regime in newly diagnosed type 1 diabetics

A

basal–bolus using twice‑daily insulin detemir

161
Q

when should metformin be added to the management of type 1 diabetes

A

when BMI >= 25

162
Q

beneficial side effect of SGLT-2 inhibitors

A

weight loss

163
Q

how does pioglitazone cause weight gain

A

fat and fluid retention

164
Q

features of Kallmans [6]

A

‘delayed puberty’
hypogonadism, cryptorchidism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above-average height

165
Q

LH and FSH levels in Kallmans

A

low to normal

166
Q

treatment of Kallmans [2]

A

testosterone supplementation
gonadotrophin supplementation may result in sperm production if fertility is desired later in life

167
Q

thyroxine requirements in pregnancy

A

women require an increased dose of thyroxine during pregnancy
by up to 50% as early as 4-6 weeks of pregnancy

168
Q

‘unrecordable’ blood glucose always means

A

BMs are very high

169
Q

criteria for DKA resolution [3]

A

pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L

170
Q

what should be done if ketonaemia and acidosis have NOT resolved within 24 hours

A

call senior

171
Q

when can IV insulin be changed to SC insulin in DKA management [2]

A

ketonaemia and acidosis have resolved according to criteria
and
pt is eating and drinking

patient should be reviewed by the diabetes specialist nurse prior to discharge

172
Q

complication associated with DKA management

A

cerebral oedema

173
Q

DVLA count a ‘severe’ episode as one in which…. (hypos)

A

help is required

174
Q

what effect does magnesium have on calcium

A

Magnesium is required for both PTH secretion and its action on target tissues. Hypomagnesaemia may both cause hypocalcaemia and render patients unresponsive to treatment with calcium and vitamin D supplementation.

175
Q

genotypically male children (46XY) to have a female phenotype. Rudimentary vagina and testes present but no uterus.

A

androgen insensitivity syndrome [x-linked]

elevated testo, LH and oestrogen

176
Q

inability of males to convert testosterone to dihydrotestosterone (DHT). Individuals have ambiguous genitalia in the newborn period.

A

5-α reductase deficiency[AR]

Hypospadias is common. Virilization at puberty.

177
Q

investigation of neuroblastoma

A

raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels
calcification may be seen on abdominal x-ray
biopsy

178
Q

where do neuroblastoma arise from

A

neural crest tissue of the adrenal medulla (the most common site) and sympathetic nervous system.

179
Q

Consider further investigation in adults that involves measurement of C‑peptide and/or diabetes‑specific autoantibody titres if:

A

type 1 diabetes is suspected but the clinical presentation includes some atypical features (for example, age 50 years or above, BMI of 25 kg/m² or above, slow evolution of hyperglycaemia or long prodrome)

180
Q

Minimal glucocorticoid activity, very high mineralocorticoid activity,

A

Fludrocortisone

181
Q

Glucocorticoid activity, high mineralocorticoid activity,

A

Hydrocortisone

182
Q

Predominant glucocorticoid activity, low mineralocorticoid activity

A

Prednisolone

183
Q

Very high glucocorticoid activity, minimal mineralocorticoid activity

A

Dexamethasone
Betmethasone

184
Q

alcoholic ketoacidosis vs diabetic ketoacidosis

A

alcoholic ketoacidosis has normal glucose levels unlike DKA

185
Q

which drug needs to be stopped before CT with contrast

A

metformin

can worsen contrast induced nephropathy

186
Q

management of diabetic neuropathic pain if GFR <30

A

amitriptyline

duloxetine can’t be used if GFR <30

187
Q

what would bony mets do to PTH

A

suppress it

in primary hyperPTH, PTH can be normal

Year 6 (19 decks)

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