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FLASH FINALS > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Complications of Acromegaly (4)

A

Hypertension
Diabetes (>10%)
Cardiomyopathy
Colorectal cancer

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2
Q

First line test for Acromegaly and monitoring of disease:

A

Serum IGF-1 levels (no longer OGTT)

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3
Q

Test to confirm Acromegaly if IGF-1 raised:

A

OGTT

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4
Q

First line treatment Acromegaly:

A

Trans-sphenoidal surgery

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5
Q

Medical management of Acromegaly if surgery unsuitable:

A

Somatostatin analogue - inhibits release of GH (Octreotide)

Pegvisomant (GH receptor antagonist)

Dopamine antagonists (bromcriptine)

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6
Q

Addisons disease electrolyte imbalance:

A

HYPOnatraemia
HYPERkalaemia
HYPOglycaemia

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7
Q

Difference between primary Addisons and secondary Addisons (appearance)

A

Primary (adrenal cause) will cause HYPERPIGMENTATION, secondary (pituitary causes) will not.

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8
Q

Addisons investigation of choice:

A

ACTH (short synacthen test)

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9
Q

What is measured with ACTH stimulation test (synacthen test)

A

CORTISOL before and 30 minutes after administration of ACTH

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10
Q

Levels of 9 am cortisol in Addisons if ACTH test not available:

A

<100 = definitely abnormal
>500 Unlikely Addison’s
100-500 get SYNACTHEN test

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11
Q

Addison’s adrenal autoantibody:

A

Anti-21 hydroxylase

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12
Q

Addisons treatment:

A

Hydrocortisone and fludrocortisone

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13
Q

If concurrent illness in pre-established Addisons: what are you going to regarding steroids:

A

DOUBLE hydrocortisone

Keep fludrocortisone the same

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14
Q

Addisonian crisis management:

A

Hydrocortisone
1L saline with dextrose if hypoglycaemic
NO FLUDROCORTISONE IS REQUIRED as high cortisol exerts weak mineralocorticoid activity

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15
Q

Bartter’s syndrome condition which acts like taking which drug:

A

Large doses of LOOP diuretic (hypokalaemia, normotesnion)

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16
Q

Hypomaganesaemia may cause which other electrolyte disturbance:

A

Hypocalcaemia

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17
Q

Causes of congenital adrenal hyperplasia:

A

21–hydroxylase deficiency (90%)

11-B hydroxylase deficiency (5%)

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18
Q

Adrenal hyperplasia:
Androgens
Cortisol level:
ACTH level:

A

Low cortisol
High ACTH
High Androgens - Virilization of females, precocious puberty in males

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19
Q

Steroid FBC disturbance:

A

Neutrophilia (may seem paradoxical due to immuno-suppressive nature of drug)

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20
Q

When should steroids be withdrawn gradually:

A

If pt. has

  • received more than 40mg/day for more than 1 week
  • received more than 3 weeks of treatment
  • recently received repeated courses
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21
Q

Cushing’s syndrome electrolyte disturbance:

A

hypokalaemic metabolic alkalosis with impaired glucose tolerance.

Think of (for memory) : increased cortisol, increased aldosterone = increased Na retention and subsequent K loss -> K is positively charged, Pro-acidotic thus loss will = alkalosis.

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22
Q

First-line test for confirming Cushing’s syndrome:

A

Overnight dexamethasone suppression test

Cushing’s pts. will not have their cortisol morning spike suppressed.

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23
Q

Localisation test for Cushing’s:

A

High dose Dexamethasone suppression test

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24
Q

Localisation tests for Cushing’s:
Cortisol: NOT supressed
ACTH: suppressed
Interpretation:

A

Cushing’s syndrome (adrenal problem)

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25
Q

Localisation tests for cushings:
Cortisol: Suppressed
ACTH: Suppressed
Interpretation:

A

Cushing’s disease (ACTH pituitary adenoma)

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26
Q

Localisation tests for cushings:
Cortisol: NOT supressed
ACTH: NOT suppressed
Interpretation:

A

Ectopic ACTH syndrome

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27
Q

Test to differentiate between Cushings and pseudo-Cushing’s

A

Insulin stress test

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28
Q

Test to differentiate between Pituitary and Ectopic ACTH production

A

Petrosal sinus sampling

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29
Q

T1DM antibodies

A

anti-GAd (80%)

Islet cell antibodies (ICA) (70%)

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30
Q

T1DM diagnostic blood glucose levels

A 
Fasting (>7) 
Random glucose (11.1) or after 75g glucose tolerance test
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31
Q

If diagnostic doubt between T1DM and T2DM which test would you use?

A

C-peptide levels (low in T1) and specific autoantibodies

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32
Q

HBA1c should be checked:

A

Every 3-6 months till stable then 6 monthly

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33
Q

HBA1c targets:

A

Lifestyle - 48
Lifestyle + metformin - 48
includes drug which can cause hypoglycaemia (e.g sulphonylurea) - 53

Patient already on treatment: but has risen to 58 mmol - 53

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34
Q

Only add second drug at what HBA1c

A

58

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35
Q

GLP-1 mimetic example

A

Exenatide

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36
Q

GLP-1 mimetic (exenatide) criteria

only continued if:

A

if triple therapy not effective: consider Metformin, SU and GLP-1 if:
BMI > 35
BMI <35 but insulin would have adverse effect on ADLs or QoL
Only continued if wt.loss of 3% total in 6 months or reduction in HBA1c of 11

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37
Q

T2DM > 80 years old blood pressure target

A

150/90

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38
Q

Pre-diabtes
HBA1c:
Fasting glucose:

A

42-47

6.1-6.9

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39
Q

Meformin side effects:

Cannot be offered with GFR of less than:

A

Lactic acidosis GI upset

>30

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40
Q

Sulphonylurea electrolyte disturbance:

A

Hyponatraemia

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41
Q

Thiazolidinediones side effects:

A

Weight gain

Fluid retention

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42
Q

GLP-1 (Exenatide) side effects:

A

Nausea and vomiting

Pancreatitis

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43
Q

Which diabetic drugs may cause weight loss:

A

GLP-1 agoinst and SGLT2 inhibitors

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44
Q

Which insulin should be offered in T1DM -

A

Multiple daily basal bolus insulin regimen

twice daily insulin determir is the regime of choice.

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45
Q

How many times a day should you test blood glucose; T1DM

A

4

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46
Q

When should you conisder adding metformin in T1DM

A

if BMI > 25

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47
Q

Exception for stopping oral anti-diabetic medications on sick-day

A

If very dehydrated, metformin should be stopped due to effect on renal function.

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48
Q

What is DKA caused by:

A

LIPOLYIS = increased free fatty acids which are converted to ketones

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49
Q

Management of DKA:

A

Fluid replacement (isotonic saline)
Insulin (IV 0.1 unit/kg/hour)
once blood glucose <15, dextrose (5%) may be commenced
Correction of electrolyte disturbances (potassium may need replaced due to insulin-inudced hypokalemia)

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50
Q

DKA pt. regular insulin: what should be done?

A

Long-acting insulin continued, short-acting stopped

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51
Q

DKA resolution:

A

pH >7.3
blood ketones < 0.6
Bicarbonate > 15

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52
Q

Diabetic neuropathy first line treatment:

A

Amitryptiline, duloxetine, gabapentin or pregablin

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53
Q

Drug used as rescue therapy in neuropathic pain:

A

Tramadol

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54
Q

Causes of lower than expected HBA1c (due to reduced RBC lifespan)

A

Sickle cell anaemia
G6PD deficiency
Hereditary spherocytosis

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55
Q

Causes of higher than expected HBA1c (due to increased RBC lifespan)

A

VitB12/folate deficiency
Iron-deficiency anaemia
Splenectomy

56
Q

Graves disease thyroid scintigraphy:

A

Diffuse homogenous increased uptake of radioactive iodine

57
Q

Graves disease initial treatment to control symptoms

A

Propranolol

58
Q

ATD (antithyroid drug) therapy:

A

2 options

CARBIMAZOLE 40 mg then reduced till euthyroid

Block and replace (40mg carbimazole then thyroxine at euthyroid can be used for 6-9 months)

59
Q

IF ATD therapy is not working:

A

Radioiodine treatment - many require thyroxine supplementation after 5 years

60
Q

Hashimotos associations:

A

Other autoimmune conditions (coeliac, T1DM, vitiligo)

MALT lymphoma

61
Q

HHS result of increased serum osmolality (osmotic diuresis)

A

blood hyperviscosity - clot risk

62
Q

Key parameter to monitor in HHS fluid replacement therapy

A

Serum osmolality

63
Q

Goals of management in HHS:

A

1) Normalise the osmolality (gradually)
2) Replace fluid and electrolyte losses
3) Normalise blood glucose (gradually)

64
Q

Management of hypoglycaemia in
Community:
Hospital (alert vs. non-alert):

A

Initially oral glucose 10-20g in liquid gel or tablet.

If alert - short acting carbohydrate should be given
If unconscious or unable to swallow - SC or IM GLUCAGON may be given

Alternatively IV 20% glucose solution may be given through large vein

65
Q

Primary hypoparathyroidism treatment

A

Alfacalcidol

66
Q

Pseudohypoparathyroidism - due to target cells being insensitive to PTH - calcium, phosphate and PTH levels

Clinical features:

A

low calcium, high phosphate, HIGH PTH

Low IQ, short and shortened 4th and 5th metacarpals

67
Q

pseudopsuedohypoparathyroidism

A

same as psuedoPTH with normal biochemistry

68
Q

Hypothyroidism - when should lower starting dose of levothyroxine be used:

A

Elderly or pts. with ischaemic heart disease

standard dose is 50-100 mcg od)

69
Q

Therapeutic goal of thyroid therapy:

A

Normalisation of TSH (not thyroxine)

70
Q

Pregnant women should have their dose of thyroxine..

A

Increased by 25-50 mcg

71
Q

Side effects of thyroxine therapy:

A

Hyperthyroidism
Reduced bone mineral density
Worsening of angina (think about ischaemic heart disease in dosing)
Atrial fibrillation.

72
Q

Thyroxine interacts with

A

Iron and Calcium carbonate - give at least 4 hours apart

73
Q

pro-insulin is cleaved to form:

A

Insulin and C-peptide

74
Q

Insulin stress test: what should happen to cortisol and GH

A

They should both rise

75
Q

Which cardio drug reduces hypoglycaemic awareness

A

Beta-blockers

76
Q

Insulinoma: insulin/proinsulin findings

A

High insulin

Raised proinsulin:insulin ratio

77
Q

Insulinoma
Dx.
Mx.

A

Supervised long fast (72 hours)
CT pancreas

Diazoxide and somatostatin used if patient not for surgery

78
Q

Kallman’s syndrome
Give away:
Levels of sex hormone:

A

Lack of smell

Sex hormone levels usually low
LH/FSH typically low/normal

79
Q

Klinefelter’s syndrome

Karyotype:

Features:

Diagnosis by

A

47 XXY

Often taller than average
Small firm testes
Gynaecomastia
Elevated gonadotrophin but LOW testosterone

Chromosome analysis

80
Q

Liddle’s syndrome

electrolyte imbalance:

A

Hypokalaemic alkalosis (increased absorption of sodium)

Hypertension

81
Q

Meglitinides

MoA

Good for pts. with what kind of lifestyle?

Adverse effects:

A

Examples:
Repaglinide, nateglinide

work like SUs to INCREASE pancreatic insulin secretion

Erratic lifestyles

Weight gain and hypoglycaemia (but less than SUs)

82
Q

What is MODY

Inheritance

Treatment:

A

T2DM in a person of <25 years.

Autosomal dominant

Pts. V sensitive to SUs
Insulin not usually necessary

83
Q

MEN I conditions

Most common px.

Oncogene: MEN1

A

3 Ps

Parathyroid (hyperparathyroidism)
Pituitary adenoma
Pancreas (insulinoma, gastronoma -> recurrent peptic ulceration

HYPERCALCAEMIA

84
Q

MEN II:

Oncogene:

A

2Ps, 1M
Medullary Thyroid carcinoma
Parathyroid
Phaeochromocytoma

RET oncogene

85
Q

MEN IIb

A

Medullary thyroid cancer
Phaechromocytoma
Marfans
Neuromas

RET oncogene

86
Q

Myxoedema coma px:

A

Confusion and HYPOTHERMIA

87
Q

Myxoedema coma treatment:

A 
IV thyroid replacement 
IV fluid
IV corticosteroids
correct electrolytes 
occasionally, rewarming
88
Q

Neuroblastoma most commonly arises from =:

Ix.

A

Adrenal medulla

Raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA)
Calcification on x-ray
Biopsy

89
Q

Orlistat prescription requirements:

A

BMI > 28 w/ assoc. risk factors
BMI > 30
Continued wt. loss - 5% at 3 months

Orlistat usually used for <3 months

90
Q

1ry hyperparathyroidism indications for surgery :

A 
Elevated calcium (>1mg/dl) 
Hypercalciuria (>400mg/day) 
Creatinine clearance < 30% of normal 
Nephrolithiasis 
Age < 50 years 
Reduction in bone density
91
Q

Tertiary hyperparathyroidism:

A

Occurs as a result of ongoing hyperplasia of the PTH glands after correction of underlying renal disorder.

92
Q

Secondary hyperparathyroidism:

A

Renal failure

93
Q

Distinguishing primary hyperparathyroidism and FHH:

A

Urine calcium: creatinine clearance ratio <0.01 points towards FHH

94
Q

Phaeochromocytoma test:

A

24 hour urinary collection of METANEPHRINES (not catecholamines)

95
Q

Phaechromocytoma
Defnintive management:
Stabilisation management

A

Surgery

Alpha blocker GIVEN BEFORE
Beta blocker

96
Q

Pituitary blood profile:

A

GH, Prolactin, ACTH, FH, LSH, TFTs

97
Q

First-line medical management for Prolactinomas

surgery:

A

Dopamine agonist - Bromocriptine

If progression in size, transphenoidal surgery may be used

98
Q

Two types of impaired glucose regulation:

A

Impaired fasting glucose (IFG): Due to hepatic insulin resistance.

Impaired glucose tolerance (IGT): due to muscle insulin resistance.

IGT are more likely to develop T2DM and CV disease

99
Q

Is there an increase in thyroxine in pregnancy:

A

Technically yes as increase in TBG = increase in total thyroxine

But this does not affect the free thyroxine level.

100
Q

ATDs in pregnancy

A

1st trimester PTU

2nd/3rd trimester Carbimazole

101
Q

Can you breastfeed on thyroxine:

A

Yes

102
Q

Primary hyperaldosteronism

Electrolyte disturbance:

A

Hypertension,
Hypokalaemia - muscle weakness
Alkalosis

103
Q

Primary hyperaldosteronism

Ix:

A

1) Plasma Aldosterone/renin ratio is first line (high aldosterone, low renin)
2) High resolution CT and adrenal vein sampling is used to differentiate between unilateral and bilateral causes

If CT is normal, AVS used to distinguish between unilateral adenoma and bilateral hyperplasia

104
Q

Primary hyperaldosteronism.

tx.

A

Adrenal adenoma: surgery

Bilateral adrenocortical hyperplasia: Spironolactone

105
Q

Hyperparathyroidism sign on X-ray:

A

Pepperpot skull

106
Q

Hyperparathyroidism treatment:

A

Parathyroidectomy

conservative management may be offered if calcium < 0.25 above normal and pt. > 50 years and no evidence of end organ damage
Calcimimetic (circlet) may be used for those unsuitable for surgery

107
Q

Prolactin is under constant inhibition by:

A

Dopamine

108
Q

Drugs which can increase prolactin as a result of dopamine antagonism:

A

Metoclopramide and Anti-psychotics

109
Q

Sick euthyroid syndrome (non-thyroidal illness)

Levels:

A

Thyroxine, T3 low usually
TSH is normal range in majority of cases

No treatment needed.

110
Q

Stress response:
Hormones decreased:
Hormones which do not change:

A

Insulin
Testosterone
Oestrogen

TSH, LH, FSH

111
Q

Which hormones increase in stress response:

A

GH, Cortisol,

Renin, ACTH, Aldosterone, prolactin, ADH, Glucagon

112
Q

Subacute (De Quervains) thyroiditis:
presents with:

stages:

A

HYPERthyroidism

Phase 1: Hyperthyroid (3-6 weeks)
Phase 2: (1-3 weeks) euthyroid
Phase 3: Hypothyroid
Phase 4: thyroid function and structure back to normal

113
Q

Subacute (De Quervains) thyroiditis on scintigraphy:

A

Globally REDUCED uptake of iodine-131

114
Q

Subacute (De Quervains) thyroiditis tx.

A

Usually self-limiting - may respond to aspirin or NSAIDs

severe cases: steroids are used esp. if hypothyroid develops

115
Q

Subclinical hyperthyroidism

levels:

A

Normal thyroxine and T3

but LOW TSH.

116
Q

Subclinical hyperthyroidism

tx.

A

Most revert to normal TSH

reasonable to trial low dose antithyroid agents for 6 months to induce remission

117
Q

Subclinical HYPOthyroidism:

tx.

A

TSH high everything else normal

Start tx. even if asymptomatic with levothyroxine if <70 y/o

In older people (>80yrs) watch and wait.

118
Q

Can SUs be used in pregnancy and breast-feeding

A

No

119
Q

TZDs

adverse effects:

A

Wt. gain, liver impairment LFTs
Fluid retention - COMPLETE CONTRAINDICATION IN HEART FAILURE
Increased risk of FRACTURES
Bladder cancer (pioglitazone)

120
Q

Thyroid cancer:

Management of Papillary and follicular:

A

Total thyroidectomy
Followed by radio iodine (I-131) to kill residual cells
Yearly THYROGLOBULIN levels

121
Q

Thyroid cancer with
Lymphatic spread:
Haematogenous spread

A

Papillary

Follicular

122
Q

Calcitonin levels raised in which Thyroid cancer -

A

Medullary

123
Q

Anaplastic carcinoma:
Most common in:
Not responsive to:

A

Elderly

Not responsive to chemotherapy

124
Q

Most modifiable risk factor in development of thyroid eye disease:

A

Smoking

125
Q

Which thyroid treatment may worsen thyroid eye disease?

A

Radioiodine ablation

126
Q

Management of thyroid: eye disease

A

Topical lubricants
Steroids
Radiotherapy
Surgery

127
Q

What therapy is required before starting thyroxine

A

Steroid therapy

128
Q

What marker of thyroid function is used in TFTs

A

T4

129
Q

First line investigation for thyroid nodules:

A

Ultrasound and TFTs

130
Q

Thyroid storm management:

A

Symptomatic treatment: paracetamol

Treat underlying precipitating event

Beta-blocker: typically IV propranolol
ATDs - PTU or Methimazole
Lugol’s iodine
Dexamethasone (blocks conversion of T4 to T3)

131
Q

Dermatological features of thyrotoxicosis:

A 
Thyroid acropachy (clubbing fingers)
Pretibial myxoedema (erythema and oedema above the lateral malleoli) 
Increased sweating
132
Q

Toxic multi nodular goitre:
Thyroid disturbance:
Nuclear scintigraphy
Tx. of choice

A

Hyperthyroidism
Patchy uptake
Radioiodine therapy

133
Q

Psychogenic polydipsia

Starting plasma osmolality:

Final urine osmolality:

urine osmolality post DDAVP:

A

Low

> 400
400

134
Q

Cranial DI

Starting plasma osmolality:

Final urine osmolality:

urine osmolality post DDAVP:

A

High

<300
>600

135
Q

Nephrogenic DI

Starting plasma osmolality:

Final urine osmolality:

urine osmolality post DDAVP:

A

High

<300

<300

FLASH FINALS (34 decks)

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