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J3 > Endo > Flashcards

Endo Flashcards

1
Q

What is the most common cell type in the anterior pituitary and what does it produce?

A

somatotrophs (50%) - growth hormone

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2
Q

What are the various cell types in the anterior pituitary and what do they produce?

A

somatotrophs growth hormone

thyrotrophs - TSH

lactotrophs - prolactin

corticotrophs - ACTH

gonadotrophs -LH/FSH

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3
Q

Name the 3 conditions associated with growth hormone defects

A

Gigantism = growth hormone excess in childhood/puberty

Dwarfism = growth hormone deficiency in childhood

Acromegaly = growth hormone excess after puberty; will not cause people to grow taller, grow wider instead

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4
Q

Disorders of the posterior pituitary

A

Diabetes insipidus (lack of ADH)

Syndrome of inappropriate anti-diuretic hormone (SIADH) -> causes hyponatremia

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5
Q

Which hormone should be replaced first with panhypopituitarism?

A

cortisol

This is because giving thyroxine first will speed up the metabolic rate, increasing the body’s steroid requirement

Lack of cortisol is life threatening

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6
Q

causes of hypopituitarism

A
  • Tumours
  • Radiotherapy
  • Infarction / haemorrhage (apoplexy)
  • Trauma
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7
Q

types of Pituitary tumours (size)

A

< 1cm microadenoma

> 1cm macroadenoma -> more likely to compress the optic chiasm

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8
Q

types of Pituitary tumours (function)

A

Non-functioning (majority) -> visual field defect

Functioning
•	Prolactin (prolactinoma) 
•	GH (acromegaly)
•	ACTH (Cushing’s disease) 
•	TSH (TSHoma)
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9
Q

Causes of high prolactin

A

Prolactinomas

Lactation / pregnancy

Drugs (block dopamine) - Tricyclics / antiemetics / antipsychotics

“stalk” effect - Tumour that blocks connection between hypothalamus and posterior pituitary -> blocks dopamine inhibition of prolactin

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10
Q

Prolactinoma clinical features

A
  • Galactorrhoea – milky discharge from breasts
  • Headaches
  • Mass effect
  • Visual field defect
  • Amenorrhoea / erectile dysfunction

Clinical features result from suppression of gonadotrophic hormones -> hypogonadrotrophic hypogonadism (negative feedback on gonadotropins)

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11
Q

Prolactinoma treatment

A

Dopamine agonists (cabergoline / bromocriptine)

Surgery if there is a failure of medical therapy or with a large tumour with visual field effects

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12
Q

Acromegaly

A

Pituitary tumour (macroadenoma) secreting Growth Hormone

Excessive production of GH (and IGF-1) in adults

Growth plates have fused, and therefore cannot cause increase in height

Cartilage, muscles and tendons can still grow

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13
Q

Acromegaly clinical features

A
  • Sweats and headaches
  • Alteration of facial features
  • Increased hand and feet size
  • Visual impairment
  • Cardiomyopathy
  • Increased inter-dental space
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14
Q

Acromegaly complications

A
  • Hypertension
  • diabetes or impaired glucose tolerance
  • Increased risk of bowel cancer
  • heart failure
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15
Q

Acromegaly diagnosis

A

Glucose tolerance test
• Glucose load fails to suppress GH

IGF-1 level

Pituitary MRI

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16
Q

Acromegaly treatment

A

surgery to debulk tumour

pituitary radiotherapy

pharmacological management

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17
Q

Cushing’s disease

A
  • Pituitary tumour releasing ACTH
  • One of the causes of Cushing’s syndrome

• Surgery is first line treatment

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18
Q

TSHoma

A
  • Pituitary tumour releasing TSH

* Causes high TSH and high fT4

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19
Q

Diabetes insipidus (DI)

A
  • ADH deficiency – central or cranial
  • lack of ADH and inability to reabsorb water

chronic excessive thirst accompanied by excessive fluid intake – polyuria

• Low urine osmolality and high plasma osmolality

Cranial DI = deficiency
Nephrogenic DI = resistance

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20
Q

Hypoglycaemia

A

in DM: plasma glucos <4mmol/L

in non-DM: plasma glucose <3 mmol/L

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21
Q

hypoglycaemic symptoms

A

autonomic:

  • sweating
  • tremors
  • palpitations
  • nausea

neuroglycopaenic:

  • impaired concentration
  • drowsiness
  • slurred speech
  • headache
  • seizures
  • coma

autonomic symptoms occur before neuroglycopenic symptoms

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22
Q

Whipple’s triad

A

– Symptoms consistent with hypoglycaemia
– Low plasma glucose concentration (venous sample)
– Relief of those symptoms after the plasma glucose level is raised

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23
Q

Arterial Calcium Stimulation

A

IV administered calcium stimulates insulin release from insulinoma, but not from normal beta cells.

Distinguishes focal (Insulinoma) from diffuse disease

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24
Q

causes of non-diabetic fasting hypoglycaemia

A

Remember: causes of non-diabetic fasting hypoglycaemia = ExPLAIN

  • Ex = exogenous drugs
  • P = pituitary insufficiency
  • L = Liver failure
  • A = Addison’s disease/Autoimmune
  • I = Islet cell tumours (insulinoma)
  • N = non-pancreatic neoplasms
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25
Q

Impaired glucose tolerance

A

a period of increased insulin resistance

Usually develops due to combination of lifestyle and genetic factors

Insulin signalling impaired at cellular level

Pancreas is overworking to try and keep the blood glucose within a normal range

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26
Q

Pathogenesis of type 2 diabetes

A

1) Insulin resistance + beta cell compensation
2) Beta cell failure - decreased insulin production
3) increased blood glucose

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27
Q

Which drugs act as insulin sensitisers?

A

metformin

pioglitazone

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28
Q

Mechanism of action: metformin

A

Inhibits mitochondrial glycerophosphate dehydrogenase in the liver, activates AMPK

acts as an insulin sensitising agent and reduces hepatic gluconeogenesis

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29
Q

Which diabetes therapies cause weight gain?

A

insulin
sulphonylureas
thiazolidinediones

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30
Q

Which diabetes therapies may cause hypoglycaemia?

A

insulin

sulphonylureas

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31
Q

incretin effect

A

the difference in insulin response between orally delivered and intravenously delivered glucose.

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32
Q

Which diabetes therapies cause weight loss?

A

GLP-1 receptor agonists

SGLT-2 inhibitors

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33
Q

Which GLP-1 receptor agonist has proven cardiovascular benefits?

A

liraglutide

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34
Q

Which SGLT-2 inhibitors have proven cardiovascular benefits?

A

empagliflozin

canagliflozin

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35
Q

Diabetes mellitus

A

A metabolic disorder characterized by chronic hyperglycaemia with disturbed carbohydrate, protein and fat metabolism resulting from defects in insulin secretion and/or insulin action

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36
Q

Symptoms of Hyperglycaemia

A

Glycosuria - Depletion of Energy Stores
o Tired, weak, weight loss, difficulty concentrating, irritability

Glycosuria - Osmotic Diuresis
o Polyuria, polydipsia, thirst, dry mucous membranes, reduced skin turgor, postural hypotension

Glucose Shifts - Swollen Ocular Lenses
o Blurred vision

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37
Q

DKA symptoms

A 
nausea
vomiting
abdominal pain
heavy/rapid breathing
acetone breath
drowsiness
coma
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38
Q

Diagnostic Criteria for DM

A

Fasting blood glucose
o > 7: diabetes

OGTT (oral glucose tolerance test) 2 hr glucose
o > 11.1: diabetes

Need 2 abnormal tests, or 1 + symptoms

Symptoms
	Polydipsia
	Fatigue
	Polyuria
	Blurred vision
	Thrush (oral/genital)

HbA1c >48 (6.5%)

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39
Q

Pathogenesis of type 1 diabetes

A

Type 1 diabetes results from autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans.

Occurs in genetically susceptible individuals and is probably triggered by one or more environmental agents.

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40
Q

MODY

A

any of several hereditary forms of diabetes mellitus caused by mutations in an autosomal dominant gene disrupting insulin production

“monogenic diabetes”

most common is a mutation of hepatic nuclear factor 1-alpha -> results in deficiency of one of the islet transcription factors

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41
Q

Gestational diabetes mellitus

A

Carbohydrate intolerance with onset, or diagnosis during pregnancy

  • Fasting venous plasma glucose ≥ 5.1 mmol/l, or
  • One hour value ≥ 10 mmol/l, or
  • Two hours after OGTT ≥ 8.5 mmol/l

Women become very resistant to their own insulin, mainly in the third trimester of pregnancy

If the threshold for insulin is already very high, this pushes the woman over to hyperglycaemia

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42
Q

Risk factors for Gestational diabetes mellitus

A 
o	high BMI >30
o	previous macrosomic baby 
o	previous gestational diabetes 
o	family history of diabetes
o	ethnic prevalence of diabetes

all women with risk factors should have an OGTT at 24 to 28 weeks

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43
Q

What are some causes of Secondary Diabetes?

A

Pancreatitis
Pancreatic Carcinoma
CF
Haemochromatosis

Any excess of counter-regulatory hormones (e.g. GH/cortisol)

Drug induced

  • Anti Psychotics – Clozapine/Olanzapine
  • Glucocorticoids/Tacrolimus/Ciclosporin
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44
Q

Most common Auto-antibodies in Type 1 DM

A
  • ICA (islet cell antibody)
  • I-A2 (insulinoma-associated antigen-2)
  • GAD65 (glutamic acid decarboxylase 65)
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45
Q

Basal insulin

A

Basal = maintains some constant insulin in circulation

• Usually administered once daily = long acting

Different versions
– glargine
– detemir (twice daily)
– Tresiba

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46
Q

Bolus insulin

A

Dose of insulin changes depending on the amount of carbohydrates ingested
-e.g. humulin S (short-acting)

If you have no carbs, you shouldn’t necessarily need bolus insulin

Patients are encouraged to use carb counting

1 unit of short acting insulin for 10g of carbohydrate

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47
Q

Advantages of Insulin pens

A

More convenient and easier to transport

more accurate dosages

Easier to use for those with impairments in visual and fine motor skills

Less injection pain

Can be used without being noticed

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48
Q

Continuous Subcutaneous Insulin infusion (CSII)

A

continuous infusion of a short-acting insulin driven by mechanical force and delivered via a needle or soft cannula under the skin

can improve glycaemic control and quality of life

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49
Q

Hypoglycaemia and driving

A

CBG (capillary blood glucose) > 5mmol/l before driving, carry CHO, identifiers

Remember: at least five to drive!

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50
Q

precipitants of ketoacidosis

A
  • new onset diabetes
  • MI
  • Infection
  • Steroids
  • CSII Pump failure
  • Substance abuse
  • Deliberate omission of Insulin dose
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51
Q

Treatment of DKA

A

Hypovolaemia - Intravenous fluid
• restoration of circulatory volume: crystalloid
• clearance of ketones: 10% dextrose – Give dextrose to stop FFA catabolism

Insulin deficiency - Intravenous insulin. Will cause fall in glucose and potassium

Hypokalaemia - Intravenous potassium

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52
Q

Hyperglycaemic Hyperosmolar State (HHS)

A

Complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis

RELATIVE insulin deficiency

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53
Q

Hyperglycaemic Hyperosmolar State precipatants

A
  • Infection (majority)
  • Poor compliance
  • Drugs
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54
Q

HHS treatment

A

Strategies are broadly the same as DKA, but all need to be administered with much more caution due to comorbidities and the potential for over-rapid replacement

Fluid

Insulin (if glucose doesnt fall with fluid alone)

K+ - NB: Chronic renal impairment may make the patient less able to excrete potassium

LMWH - Hypercoagulable due to severe dehydration

Foot protection – ulceration is common

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55
Q

How does thyroid hormone circulate in the blood?

A

Free (0.5%) / bound (99.5%)

Bound to thyroid binding globulin, transthyretin and albumin

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56
Q

Primary hypothyroidism

A

High TSH and low T4

Disease is in the thyroid gland

Treat with thyroxine

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57
Q

Secondary hypothyroidism

A

Low TSH and low T4

Pituitary cause of disease
May also have other pituitary axis hormone deficits

NB: Make sure their cortisol is okay before commencing thyroxine treatment

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58
Q

Primary hyperthyroidism

A

Low TSH and high T4

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59
Q

Sick euthyroidism

A

low TSH and low T4

Effect on thyroid hormones with other illness (e.g. malignancy), but not fundamental thyroid disease

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60
Q

Investigation of thyroid function

A 
Measure: 
o	TSH
o	free T4
o	total T3 
o	TSH receptor antibodies 
o	TPO - thyroid peroxisomal antibody
  • Primary hypothyroidism – High TSH and low T4
  • Secondary hypothyroidism – Low TSH and low T4
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61
Q

radioiodine uptake scan

A

Used for investigation of hyperthyroidism

different conditions will cause different uptake patterns

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62
Q

Causes of hyperthyroidism

A

Auto-immune (Graves’ disease)

Toxic adenoma – solitary nodule over secreting thyroid hormones

Multinodular goitre - can be either:
o toxic multinodular goitre (causes hyperthyroidism)
o non-toxic (does not make too much thyroid hormone)

Thyroiditis (acute early phase) - generally caused by an attack on the thyroid, resulting in inflammation and damage to the thyroid cells

Excess administration of thyroxine (e.g. abuse for weight loss)

Pituitary adenoma

Other hormones acting as TSH - hCG

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63
Q

Which symptoms are specific to graves’ disease?

A

Graves’ Ophthalmopathy - autoimmune inflammatory disorder of the orbit and periorbital tissues

Dermopathy

  • red, swollen skin, usually on the shins and tops of the feet.
  • texture may be similar to an orange peel
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64
Q

Characteristics of Graves’ Ophthalmopathy

A 
o	Lid retraction / lag and periorbital oedema 
o	Proptosis (30%) = Exophthalmos
o	Diplopia (10%) = double vision
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65
Q

Pathophysiology of of Graves’ Ophthalmopathy

A

Autoantibodies target the fibroblasts in the eye muscles, which can differentiate into adipocytes.

Fat cells and muscles expand and become inflamed.

inflammation causes deposition of collagen / glycosaminoglycans in the muscles -> enlargement and fibrosis

increase in volume of the intraorbital contents within the confines of the bony orbit

Veins become compressed, and are unable to drain fluid, causing oedema

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66
Q

Thyroid acropachy

A

soft-tissue swelling of the hands and clubbing of the fingers

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67
Q

Treatment of hyperthyroidism

A
  • Antithyroid drugs
  • Surgery – will lead to hypothyroidism
  • Radioiodine - will probably lead to hypothyroidism
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68
Q

How does thyroid hormone circulate in the blood?

A

Free (0.5%) / bound (99.5%)

Bound to thyroid binding globulin, transthyretin and albumin

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69
Q

Primary hypothyroidism

A

High TSH and low T4

Disease is in the thyroid gland

Treat with thyroxine

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70
Q

Secondary hypothyroidism

A

Low TSH and low T4

Pituitary cause of disease
May also have other pituitary axis hormone deficits

NB: Make sure their cortisol is okay before commencing thyroxine treatment

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71
Q

Primary hyperthyroidism

A

Low TSH and high T4

72
Q

Sick euthyroidism

A

low TSH and low T4

Effect on thyroid hormones with other illness (e.g. malignancy), but not fundamental thyroid disease

73
Q

Investigation of thyroid function

A 
Measure: 
o	TSH
o	free T4
o	total T3 
o	TSH receptor antibodies 
o	TPO - thyroid peroxisomal antibody
  • Primary hypothyroidism – High TSH and low T4
  • Secondary hypothyroidism – Low TSH and low T4
74
Q

radioiodine uptake scan

A

Used for investigation of hyperthyroidism

different conditions will cause different uptake patterns

75
Q

Causes of hyperthyroidism

A

Auto-immune (Graves’ disease)

Toxic adenoma – solitary nodule over secreting thyroid hormones

Multinodular goitre - can be either:
o toxic multinodular goitre (causes hyperthyroidism)
o non-toxic (does not make too much thyroid hormone)

Thyroiditis (acute early phase) - generally caused by an attack on the thyroid, resulting in inflammation and damage to the thyroid cells

Excess administration of thyroxine (e.g. abuse for weight loss)

Pituitary adenoma

Other hormones acting as TSH - hCG

76
Q

Thyrotoxicosis symptoms

A 
o	Weight loss 
o	Tachycardia 
o	Tremor 
o	Hypertension
o	Heat intolerance 
o	Palpitations 
o	Diarrhoea 
o	Sweating
77
Q

Which symptoms are specific to graves’ disease?

A

Graves’ Ophthalmopathy - autoimmune inflammatory disorder of the orbit and periorbital tissues

Dermopathy

  • red, swollen skin, usually on the shins and tops of the feet.
  • texture may be similar to an orange peel
78
Q

Characteristics of Graves’ Ophthalmopathy

A 
o	Lid retraction / lag and periorbital oedema 
o	Proptosis (30%) = Exophthalmos
o	Diplopia (10%) = double vision
79
Q

Pathophysiology of of Graves’ Ophthalmopathy

A

Autoantibodies target the fibroblasts in the eye muscles, which can differentiate into adipocytes.

Fat cells and muscles expand and become inflamed.

inflammation causes deposition of collagen / glycosaminoglycans in the muscles -> enlargement and fibrosis

increase in volume of the intraorbital contents within the confines of the bony orbit

Veins become compressed, and are unable to drain fluid, causing oedema

80
Q

Thyroid acropachy

A

soft-tissue swelling of the hands and clubbing of the fingers

81
Q

Treatment of hyperthyroidism

A
  • Antithyroid drugs (carbimazole, PTU)
  • Surgery – will lead to hypothyroidism
  • Radioiodine - will probably lead to hypothyroidism
82
Q

Radioiodine therapy for Graves’ Disease

A
  • Destroys thyroid tissue by beta emission
  • May worsen eye disease – ensure steroid cover and avoid hypothyroidism
  • Defer conception for at least 4 months
  • Hypothyroidism is main side effect. May be transient in first 6 months
83
Q

Causes of hypothyroidism

A

Autoimmune thyroid disease (Hashimotos)

Thyroiditis – Viral and often painful

Thyroidectomy

Following radio iodine therapy

Drug-induced
o Amiodarone
o Lithium
o Sunitinib

Pituitary disease – secondary hypothyroidism

Severe iodine deficiency

84
Q

Signs and Symptoms of hypothyroidism

A 
Symptoms of hypothyroidism 
•	Weight gain
•	Depression 
•	Lethargy 
•	Constipation 
•	Cold intolerance 
•	Poor concentration 
•	Hoarseness 
•	Menorrhagia - menstrual periods with abnormally heavy or prolonged bleeding
Signs of hypothyroidism 
•	Weight gain 
•	Bradycardia 
•	Lethargy 
•	Dry skin 
•	Coarse, thin hair 
•	Anaemia 
•	Slow relaxing reflexes 
•	May have goitre
85
Q

Treatment of hypothyroidism

A

Mainstay is levothyroxine
o usually 75-150 mcg per day
o Generally need 1.7-2.0 micrograms / kg / day (with no gland whatsoever)
o Best taken on an empty stomach

86
Q

Signs/symptoms of Neonatal hypothyroidism/cretinism

A 
o	Coarse facial features
o	Large fontanelles
o	Umbilical hernia
o	Mottled, cool, and dry skin
o	Developmental delay
o	Pallor
o	Myxedema
o	Goitre
87
Q

Jod Basedow phenomenon

A

iodine induced hypERthyroidism

88
Q

Wolff Chaikoff effect

A

iodine induced hypOthyroidism

89
Q

Amiodarone thyroid disease

A

type 1: autoimmune thyrotoxicosis
o treatment with high dose carbimazole

type 2: destructive thyroiditis
o treatment with glucocorticoids

90
Q

What does hypertension + hypokalaemia suggest?

What tests would you perform and what results do you expect?

A

Primary Aldosteronism (CONN’S SYNDROME)

Aldosterone - high
Renin - low
ARR = aldosterone renin ratio - increased. Disproportionate amount of aldosterone to renin in the blood

suppression testing: IV saline load will fail to suppress aldosterone
Adrenal CT scan

91
Q

CONN’S SYNDROME

A

Primary Aldosteronism

most common cause of secondary HTN. Usually caused by single adrenal adenoma (or bilateral hyperplasia)

Patients present with severe HTN and hypokalaemia

92
Q

Management of primary aldosteronism

A

Surgical
• Unilateral laparoscopic adrenalectomy if the patient has an adrenal adenoma

Medical
• Use MR antagonists (spironolactone or eplerenone)

93
Q

Cushing’s Syndrome

A

Excess cortisol secretion

ACTH dependent (ACTH will be high)
• Pituitary adenoma = Cushing’s Disease
• Ectopic ACTH
• Ectopic CRH

ACTH independent (ACTH will be low)
• Adrenal adenoma
• Adrenal carcinoma
• Nodular hyperplasia

94
Q

Clinical features of cortisol excess

A
  • Centripetal obesity
  • Prone to HTN/hyperglycaemia
  • Easy bruising (thin skin)
  • Moon face
  • Striae
  • Proximal myopathy - muscle wasting in arms/legs
  • buffalo hump
  • abdominal striae
95
Q

Diagnosis of Cushing’s syndrome

A

1) Establish cortisol excess:

Perform two of the following:
• 24 hr Urinary free cortisol
• Dexamethasone suppression test
• Late night salivary cortisol

2) Determine underlying cause. If cortisol is abnormal, determine the origin -> CRH stimulation test
• low ACTH - problem with the adrenal gland (ACTH-independent)
• high ACTH - ACTH dependent Cushing’s (pituitary)

96
Q

Management of Cushing’s syndrome

A

Surgical
o Trans-sphenoidal pituitary surgery
o Laparoscopic adrenalectomy
o Removal of ACTH source

97
Q

IATROGENIC CUSHING’S SYNDROME

A
  • COMMONEST CAUSE OF CORTISOL EXCESS
  • Cushingoid appearance but low plasma cortisol
  • Due to prolonged high dose steroid therapy

• Causes chronic suppression of pituitary ACTH production and adrenal atrophy. Patients become steroid dependent

98
Q

Clinical presentation and management of secondary adrenal insufficiency

A

Skin pale (no elevated ACTH, therefore no pigmentation)

No electrolyte abnormalities as aldosterone production is intact (regulated by RAAS)

Treat with hydrocortisone replacement (fludrocortisone unnecessary)

99
Q

symptoms of Congenital Adrenal Hyperplasia

A

Female
• masculinisation of female genitalia due to excess exposure to androgens in utero
• Usually presents earlier in girls

Male
• Adrenal crisis (Hypotension, hyponatraemia)
• Early virilization

100
Q

treatment of Congenital Adrenal Hyperplasia

A

mineralocorticoid and glucocorticoid replacement with the aim to normalize androgen production

101
Q

PHAEOCHROMOCYTOMA

A

Catecholamine secreting tumours of the adrenal medulla

102
Q

Symptoms/ signs of phaeochromocytoma

A

Hypertension (intermittent in 50%)

Episodes of headache, palpitations, pallor and sweating

Also tremor, anxiety, nausea, vomiting, chest or abdo pain

  • Crises last about 15 minutes
  • Often well in between crises
103
Q

Paraganglioma

A

extra-adrenal neural crest cell tumours. Can secrete catecholamines

e.g. sympathetic ganglia

104
Q

Phaeochromocytoma diagnosis and treatment

A

Measure 24 hour urinary catecholamines and metabolites

CT scan of adrenals

Adrenalectomy is treatment of choice

NB: Need pre-operative treatment with α1 +/- β1 antagonists to block effects of catecholamine surge

Alpha-blockade initially - doxazosin

Then beta blocker if tachycardic - bisoprolol

105
Q
  • 21-year-old female
  • ‘unwell’ for few months
  • Weight loss
  • Amenorrhoea
  • Acutely unwell over past 48 hours with vomiting and diarrhoea
On examination: 
•	Dark skin
•	Dehydrated 
•	Hypotensive 
•	Low Na, high K
A

Adrenal insufficiency

106
Q

Causes of Primary adrenal insufficiency

A

o Addison’s disease
o Adrenal TB/malignancy
o Congenital Adrenal Hyperplasia = neonatal form
o Autoimmune destruction

107
Q

Causes of secondary adrenal insufficiency

A

Due to lack of ACTH stimulation of the adrenal glands
 Iatrogenic (excess administration of exogenous steroid)
 Pituitary/hypothalamic disorders (tumours, surgery, radiotherapy)

108
Q

Treatment Issues (Androgen Replacement)

A
  • Mood (aggression/behaviour change)
  • Libido issues
  • Increased haematocrit
  • Possible prostate effects
  • Acne, sweating
  • Gynaecomastia
109
Q

Clinical Features of Addison’s Disease

A 
o	Anorexia, weight loss 
o	Fatigue/lethargy 
o	Dizziness and low BP 
o	Abdominal pain, vomiting, diarrhoea 
o	Skin pigmentation
110
Q

Diagnosis of adrenal insufficiency

A

SHORT SYNACTHEN TEST

very elevated ACTH levels
High renin -> renin activation due to hypotension
low aldosterone -> Low Na, high K

Adrenal autoantibodies may be present

111
Q

Management of primary adrenal insufficiency

A
  • Untreated, this is a fatal condition
  • Do not delay treatment to confirm diagnosis
  • Hydrocortisone as cortisol replacement
  • Fludrocortisone as aldosterone replacement

Patient education:
o ‘sick day rules’ – double oral hydrocortisone for 3 days when unwell
o Cannot stop suddenly - will cause adrenal crisis
o Need to wear identification

112
Q

Clinical presentation and management of secondary adrenal insufficiency

A

Skin pale (no elevated ACTH, therefore no pigmentation)

No electrolyte abnormalities as aldosterone production is intact (regulated by RAAS)

Treat with hydrocortisone replacement (fludrocortisone unnecessary)

113
Q

Clinical Features of Male Hypogonadism

A 
Child/Young Adult
•	Slow growth in teens
•	No pubertal growth spurt
•	Small testes &amp; phallus
•	Lack of 2° sexual development
Adult
•	Depression/low mood
•	Poor libido
•	Erectile problems
•	Poor muscle bulk/power
•	Poor energy
  • Sparse body/facial hair
  • Gynaecomastia
  • Gynoid weight gain
  • Great head hair
  • Short phallus
  • Small testes – abnormal consistency to palpation
114
Q

Orchidometer

A

tool used to determine at what point in development the testes are. 20-25ml = adult

115
Q

Testing for male hypogonadism

A

Sex steroid deficiency?
• Testosterone - measure in early morning
• LH & FSH - possible pituitary cause

Fertility?
• Semen analysis

116
Q

Hypogonadal hypogonadism

A

Primary Gonadal Failure

i.e. testicular cause of hypogonadism

117
Q

Hypogonadotrophic Hypogonadism

A

Secondary gonadal failure

i.e. Hypothalamic-Pituitary Problem

Characterised by:
• Low testosterone
• Low LH/FSH

NB: Determine prolactin levels – possible prolactinoma
• Prolactin suppresses LH and FSH

118
Q

Kallmann’s Syndrome

A

Commonest form of isolated gonadotrophin deficiency
• Isolated LH and FSH deficiency

Failure of cell migration of GnRH cells to hypothalamus from Olfactory placode

characterized by delayed or absent puberty and an impaired sense of smell (aplasia/hypoplasia of olfactory lobes)

119
Q

PRIMARY GONADAL DISEASE: DIFFERENTIAL DIAGNOSIS

A

Klinefelters syndrome
Cryptorchidism
Trauma/chemotherapy/radiotherapy causing leydig cell/seminiferous tubule failure
Myotonic dystrophy

120
Q

Klinefelter’s Syndrome

A

Commonest genetic cause of male hypogonadism

XXY

Clinically manifests at puberty
• Poor growth and delayed puberty
• Increased LH & FSH – but seminiferous tubules regress & Leydig cells do not function normally

low testosterone and elevated oestrogen levels

121
Q

Male Hypogonadism Treatment

A

Androgen Replacement Therapy
• Oral
• IM = sustanon
• Topical – NB: need to be careful to make sure that other people don’t come into contact with the testosterone gel

NB: will not reach high enough testicular androgen levels to treat infertility

Fertility Treatment
• Need to stop androgen replacement therapy
• hCG
• Recombinant LH & FSH
• GnRH pumps – overstimulate pituitary to get enough endogenous testosterone production

122
Q

Treatment Issues (Androgen Replacement)

A
  • Mood (aggression/behaviour change)
  • Libido issues
  • Increased haematocrit
  • Possible prostate effects
  • Acne, sweating
  • Gynaecomastia
123
Q

24 yr old female
• Complains of facial hair growth / male pattern
• No periods in last 6 months, acne worse recently
• No prescribed or OTC medications
• Weight going up
• FHx Type 2 Diabetes

A

PCOS

124
Q

Causes of primary amenonorrhoea

A

GU malformations
Chromosomal abnormalities - Turner’s syndrome (XO)
Pituitary/hypothalamic disorders- secondary hypogonadism

125
Q

Causes of secondary amenonorrhoea

A 
Premature ovarian failure
PCOS
Pituitary tumour (prolactinoma)

Weight loss
drugs (opiates)
stress
thyroid dysfunction

126
Q

Hirsutism

A

Excess hair growth in a male pattern due to increased androgens and increased skin sensitivity to androgens

Vast majority of cases are due to PCOS

127
Q

symptoms of anovulation

A

o Amenorrhoea
o Oligomenorrhoea – infrequent periods
o irregular cycles

128
Q

symptoms of hyperandrogenism in women

A

o Hirsutism
o Acne
o Alopecia

129
Q

Symptoms of PCOS

A

Classic presentation is with symptoms of anovulation
o Amenorrhoea
o Oligomenorrhoea – infrequent periods
o irregular cycles

Associated with symptoms of hyperandrogenism
o Hirsutism
o Acne
o Alopecia

Polycystic ovaries on USS

Typically presents during adolescence

130
Q

PCOS

A

Commonest cause of anovulatory infertility

Typical endocrine features are raised testosterone and LH

Associated with metabolic abnormalities and increased risk of type 2 diabetes

Defined by:

  • Clinical and/or biochemical signs of hyperandrogenism
  • Oligo- and/or anovulation
131
Q

GONADOTROPHINS in PCOS

A

Increased LH concentration

  • Increased androgen production from theca cells under influence of LH
  • I.e. LH drives some of the phenotype that we see

Decreased FSH

  • Low constant levels result in continuous stimulation of follicles without ovulation
  • Decreased conversion of androgens to oestrogens in granulosa cells
132
Q

Which androgen is predominantly produced in the adrenal glands in females?

A

DHEA-s (95%)

133
Q

What would cause high calcium and suppressed PTH?

A

malignancy

drugs

granulomatous disease

134
Q

What would cause high calcium and high PTH?

A

primary hyperparathyroidism

lithium

Familial hypocalciuric hypercalcemia

135
Q

What is the significance of decreased sex-hormone binding globulin (SHBG) in PCOS?

A

Insulin resistance causes increased insulin production to maintain glucose homeostasis

This results in decreased SHBG and increased androgen levels

Results in increased free testosterone
o SHBG is a carrier protein produced in liver
o binds testosterone in the circulation, stopping it from becoming biologically active

Increased testosterone leads to clinical symptoms of PCOS

136
Q

Treatment of PCOS

A

weight loss is main strategy. Other strategies have limited efficacy and more side effects.

Insulin sensitizers (metformin):
• Decreased LH levels
• Increased SHBG
• and hence decreased FAI (free androgen index)

Ovarian Androgen Suppression:

  • OCP
  • AR antagonists (spironolactone)

-Finasteride for 5 alpha reductase inhibition to reduce peripheral conversion

137
Q

24 yr old female
• Complains of facial hair growth / male pattern
• No periods in last 6 months, acne worse recently
• No prescribed or OTC medications
• Weight going up
• FHx Type 2 Diabetes

A

PCOS

138
Q

Functions of calcium

A 
muscle contraction
bone growth/remodelling
hormone secretion
second messenger in signalling
enzyme cofactor
139
Q

what is the effect of albumin on plasma calcium levels?

A

If a patient has a low albumin concentration, the TOTAL [Calcium] will also be low but the FREE [Calcium] may be quite normal

Albumin is a negative acute phase reactant, i.e. it decreases in inflammation

Many ill people thus have decreased albumin, and therefore decreased total [calcium]

Calcium is thus adjusted for the low [albumin]

140
Q

What impact does acid-base balance have on plasma calcium?

A

Alkalosis causes ionized calcium to bind to albumin more strongly.

This causes a decrease in the ionized calcium and may trigger symptoms of hypocalcemia.

  • cramps
  • paraesthesia
  • perioral numbness
141
Q

Effect of PTH

A

In response to a decrease in iCa, PTH:

1) Stimulates calcium REABSORPTION in renal tubule (DCT) and excretion of phosphate
2) Stimulates formation of 1,25 DHCC in kidney, which enhances calcium ABSORPTION from gut and bone RESORPTION
3) Promotes bone RESORPTION

Overall effect → rise in iCa back to normal

142
Q

Role of vitamin D

A 
increases absorption of calcium from the gut
increases bone resorption
reduces insulin resistance
immunomodulation
increased muscle strength
143
Q

What form of vitamin D is measured in Clinical Vitamin D Assays?

A

25-hydroxycholecalciferol (25HCC)

144
Q

Hypercalcaemia symptoms

A

Remember: Bones, stones, abdominal moans, and groans

Moans = depression/confusion, fatigue

Bones = bone pain, muscle weakness, osteopaenia

Stones = predisposed to nephrocalcinosis/nephrolithiasis

Abdominal Groans = vomiting, constipation

Also increased thirst and polyuria
Bradycardia and hypertension

145
Q

ECG changes in hypercalcaemia

A
  • Can predispose to dysrhythmia
  • Shortened QTc interval
  • Bradycardia
146
Q

Causes of Hypercalcaemia

A

1) Hyperparathyroidism – adenoma of parathyroid gland (in rare cases a carcinoma)
- high calcium and high PTH

2) Malignancy
- Tumour produces PTH related peptide
- Lung cancer, breast cancer, multiple myeloma
- high calcium and suppressed PTH

3) vitamin D toxicity
- Least common cause

147
Q

What would cause high calcium and suppressed PTH?

A

production of PTHrP by a tumour
-Lung cancer, breast cancer, multiple myeloma

drugs

granulomatous disease

148
Q

What would cause high calcium and high PTH?

A

primary hyperparathyroidism

lithium

Familial hypocalciuric hypercalcemia

149
Q

By what mechanisms can malignancy lead to hypercalcaemia?

A

1) Osteolytic metastases and myeloma
- bone metastases break down bone and release calcium

2) Tumour secretion of PTHrP
- squamous cell lung cancer; oesophageal cancer; renal cell carcinoma; breast cancer

3) Tumour production of 1,25 dihydroxycholecalciferol
- Occurs in lymphoma

150
Q

Management of hypercalcaemia

A

Stop offending / contributing medications

1) Rehydration - isotonic (0.9%) saline infusion
• hypovolaemic -> exacerbates hypercalcemia by impairing renal clearance of calcium
• see if this works before starting other treatments

2) loop diuretic -> Promote calciuria

3) Bisphosphonate Therapy
• Inhibit bone resorption
• useful in hypercalcaemia of malignancy
• Zolendronic acid is most commonly used

4) Steroids
• Inhibit vitamin D production

151
Q
  • 62-year-old female
  • Sees GP with polyuria, polydipsia, constipation
  • History spans several months
  • Previous hospital admission with renal colic
  • BP/HR normal
  • Glucose /eGFR normal
  • Calcium 2.9 mmol/L (NR 2.2-2.58)
  • PTH 28 pmol/L (N=1.0-6.8)
A

Primary Hyperparathyroidism

152
Q

Management of Primary Hyperparathyroidism

A

Observation if no end-organ damage or unfit for surgery
• Annual bone profile
• renal function + urinary calcium
• DEXA and renal US every 3 years

Surgery - Parathyroidectomy in patients who have:
• Calcium > 3.0 mmol/L
• Hypercalciuria
• age under 50 years
• end organ damage - Osteoporosis, renal stones

Medical treatment only indicated if not fit for surgery
• Calcium sensing receptor agonists (Cinacalcet)

153
Q

Complications of parathyroidectomy

A

Mechanical
• Vocal cord paresis
• Haematoma causing tracheal compression

Metabolic
• Transient hypocalcaemia

154
Q

Causes of Vitamin D Deficiency

A

Primary / Nutritional causes
o Lack of sunlight exposure
o nutritional deficit

Secondary causes
1) Deficient absorption
o	Partial gastrectomy

o	Small bowel malabsorption 
o	Pancreatic disease (fat-soluble vitamin)

2) Chronic Renal Failure
o Impaired conversion to 1,25-DHCC

3) Enzyme inducing drugs, e.g. anticonvulsants

155
Q

Osteomalacia

A

Failure to ossify bones in adulthood as a result of Vitamin D deficiency

156
Q

Signs/symptoms of osteomalacia

A

bone pain - can be localised or generalised, but is particularly prevalent in the groin/lower legs

proximal myopathy
 Waddling gait
 Difficulty rising from a chair

hypocalcaemia

157
Q

Findings in osteomalacia

A
  • Low calcium
  • low phosphate
  • High alkaline phosphate = high bone turnover
  • Low 25HCC = vitamin D deficiency
  • elevated PTH

• Looser zones on xray = pseudofractures

158
Q

Vitamin D Deficiency - treatment

A

Cholecalciferol (D3)

Alfacalcidol (i.e. active Vit D)

  • In renal impairment, cannot activate vitamin D stores
  • In hypoparathyroidism (cannot activate Vit D in gut)
  • Higher risk of hypercalcaemia
159
Q

Amiodarone and TFTs

A

1) inhibits T4→T3 conversion – which in the pituitary results in a mild raise in TSH
2) can induce hypothyroidism- in 1st year of treatment
3) can induce hyperthyroidism – due to increased iodine intake or destructive thyroiditis

patients on amiodarone have:
 elevated/high normal fT4
 low normal fT3
 initially a high TSH – normalises within a few months.

160
Q

Thyrotoxicosis vs hyperthyroidism

A

Thyrotoxicosis = syndrome resulting from excessive free t4 and/or T3.

Can occur without hyperthyroidism – e.g. stored hormone released from a damaged gland or excess hormone replacement

Hyperthyroidism = thyroid over activity resulting in thyrotoxicosis.

161
Q

Thyrotoxicosis causes

A

Primary – i.e. driven by the thyroid
 Graves’ disease
 Toxic Multinodular Goitre
 Toxic Adenoma

Secondary
 TSH secreting pituitary adenoma (rare) – ‘TSHoma’
 Gestational Thyrotoxicosis – high levels of hCG in 1st trimester (resembles TSH)

162
Q

What investigations can help determine the cause of thyrotoxicosis?

A

Antibodies +/- nuclear medicine scan (=Thyroid scintigraphy)

163
Q

Thyroid scintigraphy patterns

A

1) Diffuse uptake with suppression of background activity = Graves’
2) Irregular Uptake – Multi Nodular Goitre
3) Hot Nodule – Toxic Adenoma
4) Reduced uptake- thyroiditis eg viral.

164
Q

What are the 2 treatment regimens for thyrotoxicosis?

A

1) A reducing regimen where higher doses are started at initiation of treatment, then as the patient becomes euthyroid the dose is reduced, maintaining a euthyroid state.
2) Block and Replace – Commence with blocking medication, then when patient is euthyroid add in Thyroxine. Smoother biochemical control, ideal where there is concern of hypothyroidism with thyroid eye disease. Avoid in pregnancy.

165
Q

What are features of thyroid eye disease are specific to Graves’ disease?

A

1) Grittiness and redness
2) Conjunctival oedema
3) Periorbital oedema
4) Proptosis and exophthalmos (proptosis secondary to endocrine cause). Lower sclera visible
5) Ophthalmoplegia (paralysis of the muscles within or surrounding the eye)

NB: Lid lag (slowed lid closing) and lid retraction (upper sclera visible) are the result of excess sympathetic activity and are not specific to Graves’ disease.

166
Q

What factors increase the risk of developing Graves’ opthalmopathy?

A 
 Smoking 
 Male Sex
 Age
 Radioactive iodine treatment
 Signs of thyroid eye disease
167
Q

Treatment of Graves’ ophthalmopathy

A

 Grittiness – artificial tears

 Eyelid – tape eyelids at night to avoid corneal damage, surgery if risk of exposure keratopathy

 Proptosis – steroids, radiotherapy may need orbital decompression

 Optic neuropathy - steroids, radiotherapy may need orbital decompression

 Ophthalmoplegia – orbital decompression, orbital
muscle surgery.

168
Q

Myxoedema

A

denote severe hypothyroidism

there is accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues

Leads to the thickened facial features and doughy skin.

Other tissues also affected:
 Dull, expressionless face, sparse hair, periorbital puffiness, macroglossia
 Pale, cool, skin which is rough and doughy
 Pericardial effusion
 Megacolon/ intestinal obstruction
 Cerebellar ataxia
 Prolonged relaxation phase of deep tendon reflexes
 Peripheral neuropathy

169
Q

Myxoedema Coma

A

state of decompensated hypothyroidism

occurs in patients with long-standing, undiagnosed hypothyroidism and is usually precipitated by infection, cerebrovascular disease, heart failure, trauma, or drug therapy

170
Q

Subclinical hyperthyroidism

A

low levels ofTSH but normal levels of T3 and T4

171
Q

Subclinical hypothyroidism

A

elevated TSH value (on at least 2 occasions) with

normalT4 hormone levels.

172
Q

Autoimmune Polyendocrine Syndrome Type 2

A

Autoimmune condition affecting several endocrine glands

Triad of:
o Addison’s
o AI thyroiditis
o T1DM

 More common in females
 Presents in adulthood
 Polygenic

173
Q

DKA diagnosis

A

1) hyperglycaemia (blood glucose >11.1)
2) metabolic acidosis (bicarbonate <15mmol/L) = anion gap metabolic acidosis.
3) ketosis/ketonuria

174
Q

What could cause high ketone levels other than DKA?

A

starvation

175
Q

DKA pathophysiology

A

Insulin deficiency results inlipolysis -provides the substrate for ketone production from the liver.

Ketones (β hydroxyl butyrate, acetoacetate, acetone) are excreted by the kidneys and buffered in the blood initially but eventually this system fails and acidosis develops.

Hyperglyceamia occurs due to unregulatred gluconeogensis and glycogenolysis.

Reduced peripheral glucose utilisation associated with Insulin deficiency exacerbates hyperglycaemia -> activation of counterregulatory hormones

osmotic diuresis produced by hyperglycaemia and ketonuria causes hypovolaemia

J3 (18 decks)

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