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Metabolic and Endocrine > Pituitary, adrenal and thyroid disease > Flashcards

Pituitary, adrenal and thyroid disease Flashcards

1
Q

give physiological examples that cause positive feedback the hypothalamus?

A

cold, acute psychosis, circadian rhythm

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2
Q

describe the feedback system of the thyroid?

A
  • hypothalamus releases TRH which acts on the anterior pituitary
  • the anterior pituitary releases TSH which acts on the thyroid which in turn releases T4 and T3
  • causing inhibitor feedback to the anterior pituitary and hypothalamus
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3
Q

give physiological examples that cause negative feedback the hypothalamus?

A

severe stress

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4
Q

what causes negative feedback to the anterior pituitary?

A

corticosteroids, dopamine

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5
Q

how long will changes to thyroid medication take to have an affect on feedback loops?

A

4-6 weeks

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6
Q

TSH, T3/T4 all high (or low)

A

pituitary issue

secondary

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7
Q

TSH varied

normal T3/T4

A

subclinical

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8
Q

TSH and T3/T4 opposite

A

primary hypo/hyper thyroidism

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9
Q

give examples of primary hyperthyroidism?

A

graves, multinodular gitre, adenoma, subacute thyroiditis (post partum thyroiditis)

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10
Q

give examples of secondary hyperthryoidism?

A

pituitary TSHoma

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11
Q

give examples of primary hypothryoidism?

A

hashimoto thyroiditis, atrophic hypothyroidism

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12
Q

give examples of secondary hypothyroidism?

A

hypopituitarism

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13
Q

give examples of thyroid hormone resistance?

A

thyroid hormone resistance syndrome, 5’-monodeiodinase deficiency

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14
Q

give examples of primary non functioning tumours causing thyroid disease?

A

differential carcinoma, medullary carcinoma, lymphoma

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15
Q

TSH high

T3, T4 high

A

TSH producing pituitary adenoma

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16
Q

high TSH

low T3, T4

A

primary hypothyroidism

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17
Q

TSH high

T3, T4 normal

A

subclinical hypothyroidism

recovery from euthyroid sick syndrome

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18
Q

low TSH
low T3, T4
potential conditions?

A

euthyroid sick syndrome

central hypothyroidism

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19
Q

low TSH
high T4
normal T3

A

THYROIDITIS
T4 ingestion
hyperthyroidism in elderly or comorbidity

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20
Q

low TSH
normal T4
high T3

A

T3 toxicosis

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21
Q

low TSH

normal T3, T4

A

subclinical hyperthyroidism

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22
Q

low TSH

high T3, T4

A

hyperthyroidis

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23
Q

what are the signs and symptoms of hyperthyroidism?

A 
Weight loss
Heat intolerance
Fatigue/apathy
Anxiety
Irritability
Psychosis
Emotional
Tremor
Muscle weakness
Goitre with bruit
Tremor
Hyperreflexia
Diarhheoa 
Hyperdefecation
Anorexia vomiting
Swaeting
Pruritis
Alopecia
Palpitations
Dyspnoea
Angina
Ankle swelling
AF
HT
Cardiac failure
Gynaecomastia
Lymphadenopathy
Palpar erythema
Spider nivase
Ankle swelling
Asthma exascerbation
Amenorrhoea
Oligomenorrhoea
Infertility
Abrtion
Loss of libido
Crittiness
Red eyes
Diplpia
Loss of visual acuity
Tachycardia
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24
Q

what is the medical management for hyperthyroidism?

A

Control symptoms, BB or CCB caution in asthma

Control of hyperthyroidism
Thionamides (carbimazole, methimazole, propylthiuroacil) caution-agranulocytosis

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25
Q

what are the management options for hyperthyroidism?

A

medication
radioactive iodine
surgery

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26
Q

describe the use of surgery in treating hyperthyroidism?

A

For CI to medical therapy, relapsed GD and TED, large disfiguring goiter, suspicious thyroid nodules, patient preference

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27
Q

what are the causes of hypothyroidism?

A

Hashimotos

Spontaneous atrophic

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28
Q

what are the signs and symptoms of hypothyroidism?

A 
Hypothrmia
Bradycardia
Periorbtal oedema
Tongue enlargement 
Diastolic hypertension
Hair loss
Fatigue
Weakness
Constipation
Cold intolerance
Dry skin
Hoarse
Voice
Oedema
Congnitive dysfunction
Dreession
Muscle ccramps
Paresthesias
Menorrhagia 
Dry, gritty feeling eyes
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29
Q

describe the basic anatomy of the thyroid?

A

2 lobes connected by isthmus
Each lobe is about 5x3x2cm
Usually palpable and moves with swallowing

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30
Q

describe thyroid physiology?

A

Negative feedback loop
T3 is 5x more bioactive than T4
T4 is converted to T3 in peripheral tissues
Majority of plasma hormone is bound to transport proteins and is biologically inactive
Only free hormone is bioactivei

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31
Q

describe graves disease?

A 
Younger age
F:M 10:1
Often familial
Autoimmune disorder (positive thyroid antibodies-TPO and TSH receptor Ab)
May be self limiting
Thyrotoxicosis may be severe
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32
Q

describe the features of multinodular goitre/single functioning nodule?

A 
Older age
F:M 1:1
Rarely familial
No autoantibodies 
Gradual onset
Persistent
Usually mild
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33
Q

how may older patients present with thyrotoxicosis?

A

may present with only weight loss or symptoms of heart failure

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34
Q

what are the clinical signs of thyrotoxicosis?

A

Rapid speech, agitation
Eyes – lid retraction and lag (sympathetic overactivity), orbital inflammation (graves)
Skin – warm and moist, pre-tibial myxedema (graves)
Pulse – tachycardia or AF
Neuromuscular – tremor, proximal muscle weakness
Neck – presence and size of goiter depend on cause

35
Q

what laboratory tests are useful to diagnose thyrotoxicosis?

A

Raised thyroid hormones – free T3 and T4
TSH usually suppressed below detection limit of assay
Thyroid peroxidase antibodies and TSH receptor antibodies
Imaging may be helpful but isn’t routine

36
Q

what is the treatment of hyperthyroidism?

A

Medical therapy – carbimazole or propylthiouracil – block thyroid hormone production
Surgery – partial or total thyroidectomy
Radiotherapy- radioactive iodine
Beta blockers – symptomatic relief

37
Q

what lab tests are important in hypothyroidism?

A

Raised TSH
Reduced FT4 and FT3
TPO positive in autoimmune disease
Imaging rarely needed

38
Q

what are the causes of hypothyroidism?

A

Autoimmune (hashimoto’s thyroiditis)
Iatrogenic (surgery, radioiodine treatment)
Drugs (Directly causing hypothyroidism , Affecting hormone metabolism, Affecting GI absorption)

39
Q

what are the mechanisms leading to symptoms of hypothyroidism?

A

General slowing of metabolic processes (cold intolerance, fatigue weight gain etc)
Tissue deposition of matrix glycosaminoglycans (skin changes, hoarse voice, tongue enlargement etc)

40
Q

what are the potential extremes of thyroid dysfunction?

A

Myoedema coma – extreme hypothyroidism
Thyroid storm – extreme thyrotoxicosis
Both have high mortality and rare

41
Q

what is the treatment of hypothyroidism?

A

Relatively straightforward with levothyroxine 75-175mcg
Lifelong treatment
Be careful in treatment of hypothyroid patients with cardiac dysfunction.

42
Q

describe subclinical thyroid disorders?

A

Subclinical hyperthyroidism - reduced TSH but normal FT4 and ft3
Subclinical hypothyroidism – raised TSH but normal FT4 and FT3
No symptoms
Common
May need further investigation depending on circumstances (age, presence of autoantibodies, possible symptoms )

43
Q

describe the features of goitre?

A

Palpable swelling of the thyroid
thyroid lobes grow outward and even very goiters rarely cause compressive symptoms
Asymmetric lobe enlargement or a substernal goitre may cause compressive problems
Substernal goiters are rare
Patients may be; euthroid, hyperthyroid, hypothyroid

44
Q

what are the investigations for goitre?

A

fine needle aspiration, ultrasound, radionucleotide imaging, computed tomography/MRI

45
Q

what are the most common symptoms of substernal goitre?

A

wheeze, dyspnea and cough (multinodular goiter or large follicular adenoma)

46
Q

describe thyroid nodules?

A

When person notices a neck swelling or incidentally when detected during radiological examination of neck performed for another reason (carotid ultrasound, CT, MRI)
Need to exclude thyroid cancer

47
Q

what are the investigations for thyroid nodule?

A

Thyroid function tests (if abnormal suggest benign lesion) and autoantibodies
Thyroid ultrasound and fine needle aspiration cytology
Scintigraphy (thyroid isotope scan)- increased uptake more likely benign

48
Q

what are the potential causes of thyroid nodules?

A 
overgrowth of normal thyroid tissue
thyroid cyst
chronic inflammation
multinodular gitre
thyroid cancer
iodine deficiency
49
Q

what tests are used to make a diagnosis of adrenal insufficiency?

A

Random cortisol

9am cortisol (<100nmol confirms adrenal insufficiency)

Short synacthen/ACTH stimulation test (definitive test)

  • Test cortisol then inject synthetic ACTH (synacthen) then test cortisol response after 30 minutes
  • Normal response is 30 min cortisol >550nmol/L
50
Q

what is the acute management for adrenal insufficiency?

A

Fluids 1-3L of 0.9% saline in first 12-24 hours
Hypoglycaemia: IV dextrose
Glucocorticoids:hydrocortisone 100mg stat, 100mg iv 8 hourly
Treat precipitating cause
Adrenal crisis is life threatening emergency and requires immediate treatment

51
Q

what is the long term management for adrenal insufficiency?

A

Hydrocortisone
10mg morning
5mg lunch
5mg evening

Fludrocortisone 100mcg daily

Androgen replacement: DHEA 25-50mg daily

52
Q

what are the sick day rules of adrenal insufficiency treatment?

A

Never stop steroids
Double dose during illness/infection
if unable to take PO hydrocortisone, need IM/IV hydrocortisone
Carry steroid card/medicAlert bracelet

53
Q

what are the causes of secondary adrenal insufficiency?

A

HPA axis suppression-long term steroid use

Pituitary/hypothalamic disease

54
Q

what is the clinical presentation of secondary adrenal insufficiency?

A

No hyperpigmentation
No dehydration or hyperkalaemia
Hypoglycamia more common
Clinical manifestations of tumour

55
Q

how is a diagnosis of secondary adrenal insufficiency made?

A

Failed SST
ACTH low or suppressed
History of exogenous steroid use
Other pituitary hormone dysfunction

56
Q

what is the long term management for secondary adrenal insufficiency?

A

Hydrocortisone
No need for fludrocortisone
Taper steroids gradually
Sick day rules

57
Q

describe the management of hypopituirarism?

A

Visual field test – bi-temporal hemianopia
Macroprolactinoma with hypopituitarism
Other pituitary hormone profile
Treatment with dopamine agonists (cabergoline or bromocriptine)
transphenoidal surgery

58
Q

name pituitary hormones?

A 
Growth Hormone (GH)
Adrenocorticotropin (ACTH)
 Thyrotropin (TSH) 
Prolactin 
Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) 
Antidiuretic hormone (ADH) 
Oxytocin
59
Q

name pituitary cell types?

A

Somatotropes – 30-40%
Corticotropes 20%
Thyrotropes, gonadotropes, lactotropes – 3-5%

60
Q

what are the symptoms of hypopituitarism?

A 
Tiredness
Weight loss 
Decreased libido
Increased sensitivity to cold
Loss of appetite
Infertility 
Irregular periods
Loss of body or facial hair 
Short stature
61
Q

what is the presentation of acromegaly?

A

Opthalmologists –bi-temporal hemianopia
Respiratory physicians-sleep apnoea
Dentists- poor dentition
Diabetologists – poorly controlled T2DM, insulin resistance
Cardiologist – HTN, cardiomyopathy, heart failure

62
Q

how is a diagnosis of acromegaly made?

A

Screening tests – IGF-I, random GH
Confirmatory test- glucose tolerance test
Imaging MRI pituitary

63
Q

describe the role of random GH level in diagnosing acromegaly?

A

Little value in diagnosis
GH secretion is pulsatile
Stimulated by variety of factors like fasting, exercise, stress and sleep

64
Q

describe the role of IGF-I in diagnosing acromegaly?

A 
Long half life
-Assess GH secretion
-Screen for acromegaly
-Monitor response to treatment
IGF-I concentrations vary with age
Starvation, obesity and diabetes mellitus-decreased IGF-1
Pregnancy increased IGF-I1
65
Q

describe the role of glucose tolerance test in diagnosing acromegaly?

A 
Baseline GH level
Ingestion of 75g oral glucose
GH measured at 30, 60, 90 and 120 mins
Failure to suppress GH levels to <1ug/L
Parodoxical rise (15-20%)
66
Q

what are the treatment options for acromegaly?

A

Surgery
Medical (GH receptor antagonist, dopamine agonists, somatostatin analogues)
Radiotherapy

67
Q

what is cushings syndrome caused by?

A

Caused by prolonged exposure to elevated levels of glucocorticoids
Most common cause is exogenous steroids

68
Q

what are the effects of glucocorticoids?

A 
Increase glucose production
Inhibit protein synthesis 
Increase protein breakdown
Stimulate lipolysis
Immunologic and inflammatory responses
69
Q

in cushings disease hat are the mortality and morbidity related to?

A

excess glucocorticoids

70
Q

who is more likely to get cushings syndrome?

A

Female to male incidence is 1:5

Peak age of incidence is 25-40 years

71
Q

what are the causes of cushings syndrome?

A

Exogenous steroids
Cushings disease 70%
Ectopic ACTH secretion 15%
Adrenal tumour 15%

72
Q

what are the signs of cushings syndrome?

A 
steroid encephalopathy
depression
growth retardation
central obesity
moon face
thin neck
fat trunk/abdomen
atrophy of skin/ striae
muscle wasting/weakness
easy bruising 
diabetes melitus 
hypertension
hypokalaemic alkalosis 
infertility
menstrual irregularity
acne
73
Q

what is cushings syndrome?

A

symptoms+signs +biochemical hypercortisolism

74
Q

what is cushings disease?

A

pituitary ACTH dependent syndrome

75
Q

what is pseudo cushings?

A

activation of CRH

76
Q

what are the potential screening tests for cushings syndrome?

A

24hr urine free cortisol
1mg overnight dexamethasone suppression test
Late night salivary cortisols

77
Q

what are the steps to perform once cushings syndrome has been confirmed?

A
  1. check ACTH level
    if;
    -low -ACTH independent (adrenal cushings) -> CATscan/MRI abdo to determine if adrenal adenoma or bilateral adrenal hyperplasia
    -borderline - CRH stimulation test to determine if low or high ACTH
    -high - ACTH dependent ->inferior petrosal sinus sampling and MRI brain to determine if either pituitary tumour or ectopic ACTH producing tumour.
78
Q

give examples of primary hypersecretion syndromes?

A

acromegaly and gigantism

79
Q

describe acromegaly and gigantism?

A

Growth hormone stimulates skeletal and soft tissue growth. GH excess produces gigantism in children (if acquired before epiphyseal fusion) and acromegaly in adults
Both due to GH secreting pituitary tumour (somatotroph adenoma) in almost all cases

80
Q

what are the investigations for pituitary hypersecretion syndromes?

A

GH levels – may xclude acromegaly if undetectable
Glucose tolerance test – diagnostic if there is no suppression of GH
IGF-1 levels – usually raised in acromegaly
Visual field examination- defects are common
MRI scan of pituitary –pituitary ademona
Pituitary function – primary or complete anterior hypopituitarism is common
Prolactin – occasionally hyperprolactinaemia

81
Q

why is treatment of acromegaly important?

A

If untreated can result in reduced survivial due to heart failure, CAD and hypertension related issues. Increase deaths due to neoplasia
Aim of treatment is to achieve a growth hormone level below 2.5ug/L

82
Q

describe surgery for acromegaly?

A

trans-sphenoidal surgery causes clinical remission in most patients

83
Q

describe the role of pituitary radiotherapy in treating acromegaly?

A

normally used after pituitary surgery to normalize GH levels. Usually combined with medium term treatment with somatostatin analogue, dopamine agonist or GH antagonist

84
Q

describe the medical therapy used in acromegaly?

A
  • Somatostatin receptor agonist – octreotide and ianreotide act on sst2/sst5 which are highly expressed in growth hormone secreting tumours. Short term treatment. Both drugs are administered as monthly depot injections
  • Dopamine agonists – D2 receptors and shrink tumours prior to therapy
  • Growth hormone antagonist – pegvisomat, binding and preventing dimerization of GH receptor. Daily injecion

Metabolic and Endocrine (12 decks)

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