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MRCP I > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Primary hypoparathyroidismGraves’ Disease features exclusive

A

eatures seen in Graves’ but not in other causes of thyrotoxicosis
* Eye signs: exophthalmos, ophthalmoplegia
* Pretibial myxedema
* Thyroid acropachy

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2
Q

Graves’ Disease antibodies

A

Autoantibodies
* Anti-TSH receptor stimulating
antibodies (90%)
* Anti-thyroid peroxidase
antibodies (50%)

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3
Q

Graves treatment

A

ATD titration
* Carbimazole is started at 40mg and ↓ gradually to maintain euthyroidism
* Typically continued for 12-18 months
* Patients following an ATD titration regime have been shown to suffer fewer side-effects than those
on a block-and-replace regime
Block-and-Replace
* Carbimazole is started at 40mg
* Thyroxine is added when the patient is euthyroid
* Treatment typically lasts for 6-9 months

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4
Q

The major complication of carbimazole

A

agranulocytosis (pancytopenia)

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5
Q

Radioiodine Treatment
* Contraindications

A

pregnancy (should be avoided for 4-6 months following treatment) and age < 16 years. Thyroid eye disease is a relative contraindication, as it may worsen the condition

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6
Q

Thyrotoxicosis causes

A

Causes
* Graves’ disease
* Toxic nodule goitres
* Subacute (de Quervain’s) thyroiditis
* Post-partum thyroiditis
* Acute phase of Hashimoto’s thyroiditis (later results in hypothyroidism)
* Toxic adenoma (Plummer’s disease)

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7
Q

Thyrotoxicosis labs

A
  • TSH down, T4 and T3 up
  • Thyroid autoantibodies
  • Other investigations are not routinely done but includes isotope scanning
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8
Q

Toxic Multinodular Goitre

A

describes a thyroid gland that contains a number of

autonomously functioning thyroid nodules that secrete excess thyroid hormones. Nuclear scintigraphy
reveals patchy uptake. The treatment of choice is radioiodine therapy

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9
Q

Thyroid Storm

A

rare but life-threatening complication of thyrotoxicosis. It is typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature. Iatrogenic thyroxine excess does not usually result in thyroid storm

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10
Q

Tyroid storm - Clinical features include:

A
  • Fever > 38.5oc
  • Tachycardia
  • Confusion and agitation
  • Nausea and vomiting
  • Hypertension
  • Heart failure
  • Abnormal liver function test
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11
Q

Tyroid storm Management

A

Symptomatic treatment e.g. Paracetamol
* Treatment of underlying precipitating event
* Anti-thyroid drugs: e.g. Methimazole or propylthiouracil
* Lugol’ s iodine
* Dexamethasone - e.g. 4mg IV QDS - blocks the conversion of T4 to T3
* Propranolol

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12
Q

Subacute Thyroiditis (De Quervain’s Thyroiditis)

A

thought to occur following viral infection and typically presents with hyperthyroidism
Features
* Hyperthyroidism
* Painful goiter
* Raised ESR
* Globally ↓ uptake on iodine-131 scan

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13
Q

Subacute Thyroiditis (De Quervain’s Thyroiditis)
Management

A

Management
* Usually self-limiting - most patients do not require treatment
* Thyroid pain may respond to aspirin or other NSAIDs
* In more severe cases steroids are used, particularly if hypothyroidism develops

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14
Q

Hashimoto’s Thyroiditis
Features

A

Features
* Features of hypothyroidism
* Goitre: firm, non-tender
* Positive microsomal antibodies, anti-thyroid peroxidase (Anti-TPO) and anti-Tg antibodies.

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15
Q

Subclinical Hyperthyroidism

A

Normal T3 – T4
* ↓ TSH (usually < 0.1 mu/l)

Causes
* Multinodular goitre, particularly in elderly ♀s
* Excessive thyroxine may give a similar biochemical picture

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16
Q

importance in recognising subclinical hyperthyroidism

A

effect on the cardiovascular system (atrial fibrillation) and bone metabolism (osteoporosis). It may also impact on quality of life and ↑ the likelihood of dementia

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17
Q

Subclinical Hyperthyroidism Management

A

Management
* TSH levels often revert back to normal - therefore levels must be persistently low to warrant
intervention
* A reasonable treatment option is a therapeutic trial of low-dose antithyroid agents for
approximately 6 months in an effort to induce a remission

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18
Q

Subclinical Hypothyroidism

A

Normal T3 – T4
* ↑TSH
* No obvious symptoms

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19
Q

Subclinical Hypothyroidism
Significance

A

Significance
* Risk of progressing to overt hypothyroidism is 2-5% per year (higher in men)
* Risk ↑ by presence of thyroid autoantibodies

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20
Q

Subclinical Hypothyroidism

A

Treat if
* TSH>10
* Thyroid autoantibodies positive
* Other autoimmune disorder
* Previous treatment of graves’ disease

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21
Q

Hypothyroidism
Causes:

A

Causes:
Hypothyroidism affects around 1-2% of women in the UK and is around 5-10 times more common in ♀s than ♂s.

In European countries primary atrophic hypothyroidism is the most cause causes of
hypothyroidism, whereas in North America Hashimoto’s thyroiditis appears to account for the
majority of cases. The reason for this discrepancy is unclear

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22
Q

Primary hypothyroidism

A

Primary atrophic hypothyroidism
2. Hashimoto’s thyroiditis
3. After thyroidectomy or radioiodine treatment
4. Drug therapy (e.g. lithium, amiodarone or anti-thyroid drugs such as carbimazole)
5. Dietary iodine deficiency

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23
Q

Primary atrophic hypothyroidism

A

Most common cause in Europe
* Autoimmune disease, associated with IDDM, Addison’s or pernicious anemia
* 5 times more common in women

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24
Q

Hashimoto’s thyroiditis

A

Autoimmune disease as above with goitre (Anti-TPO) * May cause transient thyrotoxicosis in the acute phase
* 10 times more common in women

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25
Q

Secondary hypothyroidism (rare)

A
  1. From pituitary failure
  2. Other associated conditions
    * Down’s syndrome
    * Turner’s syndrome
    * Coeliac disease
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26
Q

Hypothyroidism treatment

A
  • Initial starting dose of levothyroxine should be lower in elderly patients and those with ischemic heart disease (e.g. 25–50 mcg/day).
  • Following a change in thyroxine dose thyroid function tests should be checked after 6-8 weeks
  • The therapeutic goal is ‘normalisation’ of the thyroid stimulating hormone (TSH) level. As the majority unaffected people have a TSH value 0.5–2.5 mu/l it is now thought preferable to aim
    for a TSH in this range. Dosage changes should of course also take account of symptoms
  • There is no evidence to support combination therapy with levothyroxine and liothyronine
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27
Q

Side-effects of thyroxine therapy

A
  • Hyperthyroidism: due to over treatment
  • ↓ bone mineral density
  • Worsening of angina
  • Atrial fibrillation
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28
Q

thyroid function - Thyrotoxicosis (e.g. Graves

A

TSH low
T4 high
In T3 thyrotoxicosis, T4 will be normal

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29
Q

thyroid function -Primary (atrophic) hypothyroidism

A

TSH high
T3/4 low

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30
Q

thyroid function - Secondary hypothyroidism

A

TSH low
T3/4 low

Steroid therapy is required prior to thyroxine

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31
Q

thyroid function - Sick euthyroid syndrome*

A

TSH low
T3/4 low

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32
Q

thyroid function - Poor compliance with thyroxine

A

TSH high
T3/4 normal - high

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33
Q

thyroid function - Steroid therapy

A

TSH Low
T3/4 normal

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34
Q

Pendred’s Syndrome

A

Autosomal recessive disorder of defective iodine uptake

Features:
* Sensorineural deafness
* Goitre
* Euthyroid or mild hypothyroidism

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35
Q

Skin Manifestations of Thyroid Diseases:Hyperthyroidism

A

Pretibial myxedema: erythematous, edematous lesions above the lateral malleoli
* Thyroid acropachy: clubbing
* Scalp hair thinning
* ↑ sweating

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36
Q

Skin Manifestations of Thyroid Diseases:Hypothyoridism

A

Dry (anhydrosis), cold, yellowish skin
* Non-pitting edema (e.g. Hands, face)
* Dry, coarse scalp hair, loss of lateral
aspect of eyebrows
* Eczema
* Xanthomata

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37
Q

Propylthiouracil

A

antithyroid drug of choice in pregnancy. This
approach was supported by the 2007 Endocrine Society consensus guidelines. It also has the
advantage of being excreted to a lesser extent than carbimazole in breast milk.

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38
Q

Pregnancy: Thyroid Problems

A

pregnancy there is ↑ in the levels of thyroxine-binding globulin (TBG). This causes ↑ in the levels of total thyroxine but does not affect the free thyroxine level

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39
Q

Pregnancy: Thyrotoxicosis

A

ntreated thyrotoxicosis ↑ the risk of fetal loss, maternal heart failure and premature labour
* Graves’ disease is the most common cause of thyrotoxicosis in pregnancy. It is also recognised that activation of the TSH receptor by HCG may also occur - often termed transient
gestational hyperthyroidism. HCG levels will fall in second and third trimester

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40
Q

Pregnancy Hypothyroidism

A
  • Thyroxine is safe during pregnancy
  • Serum thyroid stimulating hormone measured in each trimester and 6-8 weeks post-partum
  • Some women require an ↑ dose of thyroxine during pregnancy
  • Breast feeding is safe whilst on thyroxine
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41
Q

Thyroid Cancer:

A

Papillary 70%
Follicular 20%
Medullary 5%
Anaplastic 1%
L ymphoma Rare

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42
Q

Thyroid Cancer:Papillary 70%

A

Often young ♀s - excellent prognosis (associated with FAP)

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43
Q

Thyroid Cancer:Follicular 20%

A

Spreads through blood vessels

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44
Q

Thyroid Cancer: medullary

A

Cancer of parafollicular cells, secrete calcitonin, part of MEN-2

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45
Q

Thyroid Cancer L ymphoma

A

Associated with Hashimoto’s and other autoimmune disorders

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46
Q

Management of papillary and follicular cancer

A
  • Total thyroidectomy
  • Followed by radioiodine (I-131) to kill residual cells
  • Yearly thyroglobulin levels to detect early recurrent disease (only after total thyroid ablation)
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47
Q

Primary Hyperparathyroidism

A

elderly ♀s with an unquenchable thirst and an inappropriately normal or raised parathyroid hormone level. It is most commonly due to a solitary adenoma

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48
Q

Causes of Primary Hyperparathyroidism

A

Causes of primary hyperparathyroidism
* 80%: solitary adenoma
* 15%: hyperplasia
* 4%: multiple adenoma
* 1%: carcinoma

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49
Q

Feature of Primary Hyperparathyroidism

A

Features:
‘Bones, stones, abdominal groans and psychic moans’
* Polydipsia, polyuria
* Peptic ulceration/constipation/pancreatitis
* Bone pain/fracture
* Renal stones
* Depression
* Hypertension

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50
Q

Association of Primary Hyperparathyroidism

A

Associations
* Hypertension
* Multiple endocrine neoplasia: MEN I and II

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51
Q

Investigations Primary Hyperparathyroidism

A

nvestigations
* Raised calcium, low phosphate
* PTH may be raised or normal
* Technetium-MIBI subtraction scan

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52
Q

Treatment Primary Hyperparathyroidism

A

IV Fluids
* Total parathyroidectomy
* Bisphosphonates

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53
Q

Primary hypoparathyroidism

A

↓ PTH secretion
* E.g. Secondary to thyroid surgery
* Low calcium, high phosphate
* Treat with alfacalcidol

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54
Q

Pseudohypoparathyroidism

A

Target cells being insensitive to PTH
* In type I pseudohypoparathyroidism there is a complete receptor defect whereas in type II the
cell receptor is intact.
* Due to abnormality in a G protein
* Autosomal dominant fashion*
* Associated with low IQ, short stature, shortened 4th and 5th metacarpals
* Low calcium, high phosphate, high PTH
* Diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of
PTH. In hypoparathyroidism this will cause ↑ in both cAMP and phosphate levels. In pseudohypoparathyroidism type I neither cAMP nor phosphate levels are ↑ whilst in pseudohypoparathyroidism type II only cAMP rises.

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55
Q

Pseudopseudohypoparathyroidism

A

Similar phenotype to pseudohypoparathyroidism but normal biochemistr

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56
Q

Diabetes Insipidus - Cranial DI causes

A
  • Idiopathic
  • Post head injury
  • Pituitary surgery
  • Craniopharyngiomas
  • Histiocytosis X
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57
Q

DIDMOAD

A

association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)

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58
Q

Causes of nephrogenic DI

A
  • Genetic (primary)
  • Electrolytes: hypercalcemia, Hypokalemia
  • Drugs: demeclocycline, lithium
  • Tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
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59
Q

Diabetes Insipidus investigations

A

High plasma osmolarity, low urine osmolarity
* Water deprivation test

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60
Q

Water Deprivation Test Normal

A

starting os Normal (275-299)
Final urine os > 600 HIGH
Urine os post DDVAVP - > 600 HIGH

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61
Q

Psychogenic polydipsia water dep results

A

starting os LOW
Final urine os > 400
Urine post DDAVP >400

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62
Q

Cranial DI Water Deprivation Test

A

starting os HIGH
Final urine os <300 LOW
Urine post DDAVP <600 HIGH

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63
Q

Water Deprivation Test Nephrogenic DI

A

starting os HIGH
Final urine os <300 LOW
Urine post DDAVP <300 LOW

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64
Q

Diabetes Mellitus

A

f the patient is symptomatic:
* Fasting glucose ≥7.0 mmol/l
* Random glucose ≥11.1 mmol/l (or after 75g oral glucose tolerance test)
If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.

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65
Q

Impaired fasting glucose (IFG):

A

fasting glucose 6.1 - 7.0 mmol/l implies impaired fasting glucose

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66
Q

Impaired glucose tolerance (IGT)

A

fasting plasma glucose < 7.0 and OGTT 2-hour 7.8 - 11.1

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67
Q

Sulfonylureas

A

increasing pancreatic insulin secretion (B cells must be present)

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68
Q

Sulfonylureas Common adverse effects

A

Hypoglycaemic episodes (more common with long acting preparations such as chlorpropamide)
* ↑ appetite and weight gain
Sulfonylureas should be avoided in breast feeding and pregnancy

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69
Q

Metformin CI

A

Chronic kidney disease: NICE recommend reviewing metformin if the creatinine is > 130
μmol/l and stopping metformin if > 150 μmol/l
* Do not use during suspected episodes of tissue hypoxia (e.g. Recent MI, sepsis)
* Alcohol abuse is a relative contraindication
* Stop 2 days before general anaesthetic, restart when renal function normal
* Stop prior to IV contrast e.g. Angiography, restart when renal function norm

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70
Q

Metformin Adverse effects

A

Adverse effects
* Gastrointestinal upsets are common (nausea, anorexia, diarrhea), intolerable in 20%
* ↓ vitamin B12 absorption - rarely a clinical problem
* Lactic acidosis* with severe liver disease or renal failure
* High dose (>2gm) interferes with enterohepatic circulation of bile salt → diarrhea.

71
Q

Metformin

A

Mechanism of action
* ↑ Insulin sensitivity
* ↓ hepatic gluconeogenesis
* May also ↓ gastrointestinal absorption of carbohydrates

72
Q

Thiazolidinediones

A

They are agonists to the PPAR-gamma receptor and ↓ peripheral insulin resistance

Peroxisome Proliferator-Activated Receptor Gamma (PPAR-gamma receptor) is an intracellular nuclear receptor. Its natural ligands are free fatty acids and it is thought to control adipocyte differentiation and function

73
Q

Thiazolidinediones adverse effects

A

Adverse effects
* Weight gain
* Liver impairment: monitor LFTs
* Fluid retention - therefore contraindicated in heart failure. The risk of fluid retention is ↑
if the patient also takes insulin
* Recent studies have indicated an ↑ risk of fractures
* Rosiglitazone is not recommended for use in patients with ischemic heart disease or peripheral
arterial disease. The risk of complications may be ↑ if rosiglitazone is combined with insulin

74
Q

NICE guidance on thiazolidinediones

A

Only continue if there is a reduction of > 0.5 percentage points in HbA1c in 6 months

75
Q

glucagon-like peptide-1 (GLP- 1),

A

hormone released by the small intestine in response to an oral glucose load

In normal physiology an oral glucose load results in a greater release of insulin than if the same load is given intravenously - this known as the incretin effect. This effect is largely mediated by GLP-1 and is known to be ↓ in T2DM.

76
Q

Glucagon-Like Peptide-1 (GLP-1) Mimetics (e.g. exenatide)

A

↑ insulin secretion and inhibit glucagon secretion
* Licensed for use in T2DM
* Must be given by subcutaneous injection within 60 minutes before the morning and evening
meals. It should not be given after a meal
* May be combined with metformin, a sulfonylurea or a thiazolidinedion

77
Q

Glucagon-Like Peptide-1 adverse effect

A

Typically results in weight loss
* Major adverse effect is nausea and vomiting
* The Medicines and Healthcare products Regulatory Agency has issued specific warnings on the
use of exenatide:
o increased risk of severe pancreatitis o increased risk of renal impairment

78
Q

NICE guidelines on the use of Exenatide

A

Should be used only when insulin would otherwise be started, obesity is a problem (BMI > 35
kg/m2) and the need for high dose insulin is likely
* Continue only if beneficial response occurs and is maintained (> 1.0 percentage point HbA1c
reduction and weight loss > 3% in 6 months)

79
Q

Dipeptidyl Peptidase-4 (DPP-4) Inhibitors (e.g. Vildagliptin, sitagliptin) NICE guideline

A
  • Continue DPP-4 inhibitor only if there is ↓ of > 0.5 percentage points in HbA1c in 6 months
  • NICE suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight
    gain would cause significant problems, a thiazolidinedione is contraindicated or the person has had a poor response to a thiazolidinedione
80
Q

T2DM - Dietary advice

A

Encourage high fibre, low glycaemic index sources of carbohydrates
* Include low-fat dairy products and oily fish
* Control the intake of foods containing saturated fats and trans fatty acids
* Limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care
should be taken to avoid excess energy intake
* Discourage use of foods marketed specifically at people with diabetes
* Initial target weight loss in an overweight person is 5-10%

81
Q

HbA1c targets

A
  • The general target for patients is 6.5%. HbA1c levels below 6.5% should not be pursued
  • However, individual targets should be agreed with patients to encourage motivation
  • HbA1c should be checked every 2-6 months until stable, then 6 monthly
82
Q

Blood pressure T@DM

A

Target is < 140/80 mmHg (or < 130/80 mmHg if end-organ damage is present)
* ACE inhibitors are first-line

83
Q

treatment if patient is at risk from hypoglycemia (

A

) then a DPP-4 inhibitor or
thiazolidinedione should be considered rather than a sulfonylurea

84
Q

consider Meglitinides

A

hould be considered for patients with an erratic lifestyle

85
Q

If HbA1c > 7.5%

A

consider human insulin

Metformin treatment should be continued after starting insulin

86
Q

Starting insulin

A

Usually commenced if HbA1c > 7.5%
* NICE recommend starting with human NPH insulin (isophane, intermediate acting) taken at
bed-time or twice daily according to need

87
Q

T2DM Other risk factor modification

A
  • Aspirin to all patients > 50 years and to younger patients with other significant risk factors
  • The management of blood lipids in T2DM has changed slightly. Previously all patients with
    T2DM > 40-years-old were prescribed statins. Now patients > 40-years-old who have no obvious cardiovascular risk (e.g. Non-smoker, not obese, normotensive etc) and have a cardiovascular risk < 20%/10 years do not need to be given a statin.
  • If serum cholesterol target is not reached consider increasing simvastatin to 80mg HS.
  • If target still not reached consider using a more effective statin (e.g. Atorvastatin) or adding
    ezetimibe
  • Target total cholesterol is < 4.0 mmol/l
  • If serum triglyceride levels are > 4.5 mmol/l prescribe fenofibrate
88
Q

Diabetic Neuropathy treatment

A

First-line: oral duloxetine. Oral amitriptyline if duloxetine is contraindicated.
* Second-line treatment: if first-line treatment was with duloxetine, switch to amitriptyline or
pregabalin, or combine with pregabalin. If first-line treatment was with amitriptyline, switch to
or combine with pregabalin
* Other options: pain management clinic, tramadol (not other strong opioids), topical lidocaine
for localised pain if patients unable to take oral medication
* Consider capsaicin ointment (red pepper extract) local application

89
Q

Hypoglycemia: causes

A

Causes
* Insulinoma - ↑ ratio of proinsulin to insulin
* Self-administration of insulin/sulphonylureas
* Liver failure
* Addison’s disease
* Alcohol
Other possible causes in children
* Nesidioblastosis - β cell hyperplasia

90
Q

The level of HbA1c therefore is dependent on

A

Red blood cell lifespan
* Average blood glucose concentration

As HbA1c is produced by the glycosylation of hemoglobin at a rate proportional to the glucose concentration.

91
Q

Hyperosmolar Hyperglycaemic State

A
  1. Glucose > 33.3 mmol/l
  2. pH > 7.30
  3. Serum bicarbonate > 15 mmol/l
  4. Serum osmolality > 320 mosmol/kg
  5. Traces of ketones may be present in urines
92
Q

Diabetic Ketoacidosis path-his

A

The low-insulin condition in DKA stimulate → lipolysis →
production of ketone bodies, β-
hydroxybutyrate and acetoacetate
, which can be used as metabolic fuel

93
Q

DKA - American Diabetes Association diagnostic criteria are as fol

A

Blood glucose >13.8 mmol/l
* pH < 7.30
* Serum bicarbonate <18 mmol/l
* Anion gap > 10
* Ketonemia

94
Q

DKA management

A

Fluid replacement: most patients are depleted ≈ 5-8 litres. 0.9% saline is used initially
* Insulin: an intravenous infusion should be started at 6U/hour. Once blood glucose is < 15
mmol/l an infusion of 5% dextrose should be started
* Correction of Hypokalemia
* LMWH to prevent DVT

95
Q

Complications of DKA and its treatment

A
  • Gastric stasis
  • Cerebral edema
  • Thromboembolism
  • Acute respiratory distress syndrome
  • Acute renal failure
96
Q

Risk factors for gestational diabetes

A
  • BMI of > 30 kg/m2
  • Previous macrosomic baby weighing 4.5 kg or above.
  • Previous gestational diabetes
  • First-degree relative with diabetes
  • Family origin with a high prevalence of diabetes (South Asian, black Caribbean and Middle
    Eastern)
97
Q
A
98
Q

Screening for gestational diabetes

A

If a women has had gestational diabetes previously an oral glucose tolerance test (OGTT)
should be performed at 16-18 weeks and at 28 weeks if the first test is normal
* Women with any of the other risk factors should be offered an OGTT at 24–28 weeks

99
Q

Gestational diabetes
Management

A

Weight loss for women with BMI of > 27 kg/m2
* Stop oral hypoglycaemic agents, apart from metformin*, and commence insulin
* Folic acid 5 mg/day from pre-conception to 12 weeks gestation
* Detailed anomaly scan at 18-20 weeks including 4-chamber view of the heart and outflow tracts
* Tight glycaemic control ↓ complication rates
* Treat retinopathy as can worsen during pregnancy

100
Q

Adhesive capsulitis (frozen shoulder) is strongly associated

A

Adhesive capsulitis (frozen shoulder) is strongly associated diabetes type-I with as many as
40% of patients developing this problem at some stage

101
Q

Type 1 Diabetes Mellitus is caused by

A

destruction of the β-cells of the pancreas. Identical twins show a genetic concordance of 40%. It is associated with HLA-DR3 and DR4. It is inherited in a polygenic fashion

102
Q

Type 2 diabetes mellitus is thought to be caused by

A

relative deficiency of insulin and the phenomenon of insulin resistance. Age, obesity and ethnicity are important aetiological factors. There is almost 100% concordance in identical twins and no HLA associations.

103
Q

Type 1 DM Pathophysiology:

A
  • Autoimmune disease
  • Antibodies against β cells of pancreas
  • HLA DR4 > HLA DR3
  • Various antibodies such as islet-associated antigen (IAA) antibody and glutamic acid
    decarboxylase (GAD) antibody are detected in patients who later go on to develop type 1 DM - their prognostic significance is not yet clear
104
Q

Maturity-Onset Diabetes Of The Young (MODY) is characterized by

A

the development of type 2 diabetes mellitus in patients < 25 years old. It is typically inherited as an autosomal dominant condition. Over six different genetic mutations have so far been identified as leading to MODY. Ketosis is not a feature at presentation. Usually there is a strong family history

105
Q

MODY 3

A

60% of cases
* Due to a defect in the HNF-1 α gene (Hepatocyte Nuclear Factor).

106
Q

MODY 2

A
  • 20% of cases
  • Due to a defect in the glucokinase gene
107
Q

MODY 1

A

<10%
* Due to defect in HNF-4 α gene.

108
Q

Insulinoma

A

Basics
* Most common pancreatic endocrine tumour
* 10% malignant, 10% multiple
* Of patients with multiple tumours, 50% have MEN-1
Features
* Of hypoglycemia: typically early in morning or just before meal, e.g. Diplopia, weakness etc
* Rapid weight gain may be seen
* High insulin, raised proinsulin:insulin ratio
* High C-peptide
Diagnosis
* Supervised, prolonged fasting (up to 72 hours)
* CT pancrea

109
Q

Insulin Stress Test

A

Basics
* Used in investigation of hypopituitarism
* IV insulin given, GH and cortisol levels measured
* With normal pituitary function GH and cortisol should rise
Contraindications
* Epilepsy
* Ischemic heart disease
* Adrenal insufficiency

110
Q

Cushing’s Syndrome
causes :

A

CTH dependent causes
* Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
* Ectopic ACTH production (5-10%): e.g. Small cell lung cancer

CTH independent causes
* Iatrogenic: steroids
* Adrenal adenoma (5-10%)
* Adrenal carcinoma (rare)
* Carney complex: syndrome including cardiac myxoma
* Micronodular adrenal dysplasia (very rare)

111
Q

cushings investigations

A
  1. hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance.

Tests to confirm Cushing’s syndrome:

  • Overnight dexamethasone suppression test (most sensitive)
  • 24 hr urinary free Cortisol

Localisation tests: the first-line localisation is 9am and midnight plasma ACTH (and cortisol) levels.

112
Q

High-dose dexamethasone suppression test

A

If pituitary source then cortisol suppressed
* If ectopic/adrenal then no change in cortisol

113
Q

CRH (corticotrophin-releasing hormone) stimulation

A

ff pituitary source then cortisol rises
* If ectopic/adrenal then no change in cortisol

114
Q

Liddle’s Syndrome

A

Hypokalemia + Hypertension

iddle’s Syndrome is an autosomal dominant disorder that mimics hyperaldosteronism, resulting in Hypokalemia associated with hypertension. It is thought to be caused by disordered sodium channels in the distal tubules leading to increased reabsorption of sodium, leading to hypokalemia and alkalosis.

115
Q

Gitelman’s Syndrome:

A

defect in the thiazide-sensitive Na+ Cl- transporter in the distal convoluted tubule

Features
* Hypokalemia
* Hypomagnesemia
* Hypocalciuria
* Metabolic alkalosis
* Normotension

116
Q

Bartter’s Syndrome

A

inherited cause (usually autosomal recessive) of severe Hypokalemia due to defective chloride absorption at the Na+ K+ 2Cl- cotransporter in the ascending loop of Henle

eatures:
* Usually presents in childhood, e.g. Failure to thrive
* Polyuria, polydipsia
* Renal stones, nephrocalcinosis is commom
* W eakness

Nomotension
MG normal

117
Q

Primary Hyperaldosteronism:
features

A

Features
* Hypertension
* Hypokalemia (e.g. Muscle weakness)
* Alkalosis
* Hypernatremia
* Not related to posture

118
Q

Primary Hyperaldosteronism
Investigations: the best is

A

enin:Aldosterone Ratio
* High serum aldosterone
* Low serum renin
* High-resolution CT abdomen

119
Q

Primary HyperaldosteronismManagement

A

Primary Hyperaldosteronism
Management
* Na+ restriction
* Adrenal adenoma: surgery
* Bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. Spironolactone

120
Q

Addison’s Disease
features

A

autoimmune destruction of the adrenal glands is the commonest cause of hypoadrenalism in the UK, accounting for 80% of cases
Features
* Lethargy, weakness, anorexia, nausea & vomiting, weight loss
* Hyperpigmentation, vitiligo, loss of pubic hair in women
* Crisis: collapse, shock, pyrexia

121
Q

Dehydroepiandrosterone

A

most abundant circulating adrenal steroid. Adrenal glands are the
main source of DHEA in ♀s - loss of functioning adrenal tissue as in Addison’s disease may result
in symptoms secondary to androgen deficiency, such as loss of libido. Research is ongoing as to
whether routine replacement of DHEA is beneficial

122
Q

Hyponatremia and high potassium

A

in a patient with lethargy is highly suggestive of Addison’s

123
Q

addisions Investigations:

A

with suspected Addison’s disease the definite investigation is a short ACTH test. Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM. Adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated

124
Q

Addisons Associated electrolyte abnormalities

A

Hyperkalemia
* Hyper-Renin
* Hypo-Aldosterone
* Hyponatremia
* Hypoglycemia
* Metabolic acidosis (Hypo pH)

125
Q

SIADH Criteria

A

Normal Renal, Normal Adrenal and Normal Thyorid
* Hyponatremia <135 mEq/L
* Hypotonic plasma - POsm <270 mOsm/kg.
* Inappropriately ↑ urine osmolality
* Urine sodium >20 mEq/L (inappropriate natriuresis)

126
Q

SIADH causes

A

Causes:
1. Malignancy
* Especially small cell lung cancer
* Also: pancreas, prostate
2. Neurological
* Stroke
* Subarachnoid hemorrhage
* Subdural hemorrhage
* Meningitis/encephalitis/abscess
3. Infections * TB
* Pneumonia
4. Drugs
* Sulfonylureas
* SSRIs, tricyclics

  • Carbamazepine
  • Vincristine
  • Cyclophosphamide
    5. Other causes
  • Positive end-expiratory pressure (PEEP) * Porphyrias
127
Q

Pheochromocytoma:

A

are catecholamine secreting neuroendocrine tumor of the medulla of the adrenal glands (originating in the chromaffin cells), or extra-adrenal chromaffin tissue. It secretes excessive amounts of catecholamines, usually adrenaline if in the adrenal gland (not extra-adrenal) and noradrenaline. Extra-adrenal paragangliomas (extra-adrenal pheochromocytomas) are closely related, though less common. About 10% are familial and may be associated with MEN type II, neurofibromatosis and Von Hippel-Lindau syndrome.

128
Q

Pheochromocytoma: investigations

A

24hr urinary collection of catecholamines is preferred to one of vanillylmandelic acid as it has a higher sensitivity. Three 24 hour collections are needed as some patients have intermittently raised levels
Surgery is the definitive management.

129
Q

PHEochromocytoma immediate treatment

A

give PHEnoxybenzamine before beta-blockers

130
Q

GFR = ACD

A

Zona Glomerulosa (on outside): mineralocorticoids, mainly Aldosterone
* Zona Fasciculata (middle): glucocorticoids, mainly Cortisol
* Zona Reticularis (on inside): androgens, mainly Dehydroepiandrosterone

131
Q

Dynamic Pituitary Function Test

A

A normal dynamic pituitary function test has the following characteristics:
* GH level rises > 20mu/l
* Cortisol level rises > 550 mmol/l
* TSH level rises by > 2 mu/l from baseline level
* LH and FSH should double

132
Q

Growth hormone (GH)

A

anabolic hormone secreted by the somatotroph cells of the anterior lobe of the pituitary gland.

Mechanism of action
* Acts on a transmembrane receptor for growth
* Binding of GH to the receptor leads to receptor dimerization
* Acts directly on tissues and also indirectly via insulin-like growth factor 1 (IGF-1), primarily
secreted by the liver

133
Q

Acromegaly

A

there is excess growth hormone secondary to a pituitary adenoma in over 95% of cases. A minority of cases are caused by ectopic GHRH or GH production by tumours e.g. pancreatic.

134
Q

Acromegaly Features

A
  • Coarse, oily skin , large tongue, prognathism, interdental spaces
  • Spade-like hands, ↑ in shoe size
  • Sweating due to sweat gland hypertrophy
  • Features of pituitary tumour: hypopituitarism, headaches,
    bitemporal hemianopia
  • Raised prolactin in 1/3 of cases → galactorrhoea
  • 6% of patients have MEN-1
135
Q
A
135
Q

Acromegaly Investigations:

A

Growth hormone (GH) levels vary during the day and are therefore not diagnostic. The definitive test is the oral glucose tolerance (OGTT) with serial GH measurements. Serum IGF-1 may also be used as a screening test and is sometimes used to monitor disease

136
Q

Disorder + investigation
Cushing

A

Overnight Dexamethasone Test

137
Q

Disorder + investigation Cushing- vs. Pseudo-cushing

A

Insulin Stress Test

138
Q

Disorder + investigation Addison

A

Short Synacthen Test

139
Q

Disorder + investigation Pheochromocytoma

A

24H Urinary Catecholamines

140
Q

Disorder + investigation acromegaly

A

Oral Glucose Tolerance Test

141
Q

Dopamine agonists

A

For example bromocriptine.
* The first effective medical treatment for acromegaly, however now superseded by somatostatin
analogues
* Effective only in a minority of patient

142
Q

Somatostatin analogue

A
  • For example octreotide
  • Effective in 50-70% of patients
  • May be used as an adjunct as it helps to control cardiometabolic risk factors prior to surgery.
143
Q

Prolactin

A

secreted by the anterior pituitary gland with release being controlled by a wide variety of physiological factors. Dopamine acts as the primary prolactin releasing inhibitor and hence dopamine agonists such as bromocriptine may be used to control galactorrhoea. It is important to differentiate the causes of galactorrhoea (due to the actions of prolactin on breast tissue) from those of gynaecomastia

144
Q

Features of excess prolactin

A
  • Men: impotence, loss of libido, galactorrhoea
  • Women: amenorrhoea, galactorrhoea
145
Q

Causes of raised prolactin

A

Prolactinoma
* Pregnancy
* Estrogens
* Physiological: stress, exercise, sleep
* Acromegaly: 1/3 of patients
* Polycystic ovarian syndrome
PRIMARY HYPOTHYROIDISM (due to thyrotrophin releasing hormone (TRH) stimulating prolactin release)

146
Q

Drug causes of raised prolactin

A

Metoclopramide, domperidone
* Phenothiazines
* Haloperidol
* Very rare: SSRIs, opioids

147
Q

Gynaecomastia
Causes

A
  • Physiological: normal in puberty
  • Syndromes with androgen deficiency: kallman’s, klinefelter’s
  • Testicular failure: e.g. Mumps
  • Testicular cancer e.g. Seminoma secreting HCG
  • Liver disease
  • Ectopic tumour secretion
  • HYPERTHYROIDISM NOT HYPOTHYROIDISM
  • Hemodialysi
148
Q

Drug causes of gynaecomastia

A

Spironolactone (most common drug cause)
* Cimetidine
* Digoxin
* Cannabis
* Finasteride
* Estrogens, anabolic steroids

149
Q

For a diagnosis of metabolic syndrome at least 3 of the following should be identified:

A
  • Elevated waist circumference: men > 102 cm, women > 88 cm
  • Elevated triglycerides: > 1.7 mmol/l
  • ↓ HDL: < 1.03 mmol/l in ♂s and < 1.29 mmol/l in ♀s
  • Raised blood pressure: > 130/85 mmHg, or active treatment of hypertension
  • Raised fasting plasma glucose > 5.6 mmol/l, or previously diagnosed type 2 diabetes
150
Q

Obesety: Therapeutic options:

A

The management of obesity consists of a step-wise approach:
* Conservative: diet, exercise
* Medical
* Surgical

151
Q

Orlistat

A

pancreatic lipase inhibitor used in the management of obesity. Adverse effects include faecal urgency/incontinence and flatulence. A lower dose version is now available without prescription (‘Alli’).

152
Q

orlistat indication

A
  • BMI of 28 kg/m2 or more with associated risk factors, or
  • BMI of 30 kg/ m2 or more
  • Continued weight loss e.g. 5% at 3 months
  • Orlistat is normally used for < 1 year
153
Q

NICE guidelines on bariatric surgery for adults

A
  • They have a BMI of 40 kg/m2 or more, or between 35 kg/ m2 and 40 kg/ m2 and other significant disease (e.g T2DM, hypertension) that could be improved if lost weight.
  • All appropriate non-surgical measures have failed to achieve or maintain adequate clinically beneficial weight loss for at least 6 months
  • They are receiving or will receive intensive specialist management
  • They are generally fit for anaesthesia and surgery
  • They commit to the need for long-term follow-up
  • Consider surgery as a first-line option for adults with a BMI of more than 50 kg/ m2 in whom
    surgical intervention is considered appropriate.
  • Consider orlistat before surgery if the waiting time is long
154
Q

Types of bariatric surgery:

A

Primarily restrictive: laparoscopic-adjustable gastric banding (LAGB) or sleeve gastrectomy
* Primarily malabsorptive: classic biliopancreatic diversion (BPD) has now largely been replaced
by biliopancreatic diversion with duodenal switch
* Mixed: Roux-en-Y gastric bypass surgery

155
Q

Obesity: physiology:

A

Leptin ↓ appetite
* Ghrelin ↑ appetit

156
Q

Leptin

A

hought to play a key role in the regulation of body weight. It is produced by adipose tissue and acts on satiety centres in the hypothalamus to ↓ appetite. More adipose tissue (e.g. in obesity) results in high leptin levels. Leptin stimulates the release of melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH). Low levels of leptin stimulates the release of neuropeptide Y (NPY)

157
Q

Ghrelin

A

Where as leptin induces satiety, ghrelin stimulates hunger. It is produced mainly by the fundus of the stomach and the pancreas. Ghrelin levels ↑ before meals and ↓ after meals

158
Q

Remnant hyperlipidemia

A

Rare cause of mixed hyperlipidemia (raised cholesterol and triglyceride levels)
* Also known as Fredrickson type III hyperlipidemia, broad-β disease and
dysbetalipoproteinemia
* Associated with APO-E2 homozygosity
* High incidence of ischemic heart disease and peripheral vascular disease
* Thought to be caused by impaired removal of intermediate density lipoprotein from the
circulation by the liver

159
Q

Familial hypercholesterolemia (FH)

A

Familial hypercholesterolemia (FH) is an autosomal dominant condition that is thought to affect around 1 in 500 people. It results in high levels of LDL-cholesterol which, if untreated, may cause early cardiovascular disease (CVD). FH is caused by mutations in the hepatic proteins involved in clearance of LDL-cholesterol from the circulation

160
Q

Primary prevention: statin

A

10-year risk of 20% is cut-off

First-degree relative with a history of premature coronary heart disease (defined as < 55 years in ♂s and < 65 years in ♀s) - ↑ risk by 1.5 times if one relative affected or up to 2.0 times if more than one relative affected
* South asian ethnicity - ↑ risk by 1.4 times

161
Q

Along with lifestyle changes drug treatment should be considered for patients with a 10-year CVD risk of 20% or greater

A

Simvastatin 40mg on is the first line treatment
* There is no target level for total or LDL cholesterol for primary prevention
* Liver function tests should be check at baseline, within 3 months and at 12 months but not again
unless clinically indicated

162
Q

In prolonged cholestasis features include:

A

↑ serum cholesterol, moderate ↑ in triglyceride, serum
is not lipaemic, ↓ HDL levels. Clinical features include: palmar xanthomas; tuberous xanthomas
(particularly on extensor surfaces); tendinous xanthomas are rare. Xanthomas usually only occur
if cholestasis has persisted for more than 3 months sometimes fat deposits may involve bone and
peripheral nerves.

163
Q

Palmar xanthoma

A

Remnant hyperlipidemia
* May less commonly be seen in familial hypercholesterolemia

164
Q

Causes of eruptive xanthoma

A

Eruptive xanthoma are due to high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees)

  • Familial hypertriglyceridemia
  • Lipoprotein lipase deficiency
165
Q

Flushing, diarrhea, bronchospasm, tricuspid stenosis, pellagra

A

carcinoid with liver mets
diagnosis: urinary 5-HIAA

166
Q

Carcinoid syndrome:

A
  • Usually occurs when metastases are present in the liver and release serotonin into the systemic circulation
  • May also occur with lung carcinoid as mediators are not ‘cleared’ by the liver

Hypo- not hypertension is seen in carcinoid syndrome secondary to serotonin release

167
Q

Primary HYPOparathyroidism is usually the first endocrine manifestation of

A

ype 1 autoimmune
POLYendocrinopathy syndrome. While (MEN) → hyperparathyroidism is a common finding

168
Q

Autoimmune Polyendocrinopathy Syndrome

A

Addison’s disease (autoimmune hypoadrenalism) is associated with other endocrine deficiencies in approximately 10% of patients. There are two distinct types of autoimmune polyendocrinopathy syndrome (APS), with type 2 (sometimes referred to as Schmidt’s syndrome) being much more common.

polygenic inheritance and is linked to HLA DR3/DR4. Patients have Addison’s disease plus either:
* Type 1 diabetes mellitus
* Autoimmune thyroid disease (Hypothyroid)

169
Q

Features of APS type 1 (2 out of 3 needed)

A

Chronic mucocutaneous candidiasis (typically first feature as young child)
* Addison’s disease
* Primary hypoparathyroidism

170
Q

MEN I

A

Mnemonic ‘three P’s’:
* Parathyroid (95%):
hyperparathyroidism due to
parathyroid hyperplasia
* Pituitary (70%)
* Pancreas (50%, e.g
gastrinoma)
* Also: adrenal and thyroid

171
Q

MEN IIA
ret

A
  • Pheochromocytoma 95%
  • Medullary thyroid CA 70% * Parathyroid (60%)
172
Q

MEN IIB
ret

A

Medullary thyroid cancer
* PHEOCHROMOCYTOMA
* Marfanoid body habitus
* Neuromas
* Intestinal polyps
histologically ganglioneromas usually asymptomatic)

MRCP I (12 decks)

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