Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y2S2 > Adrenal and Thyroid Conditions > Flashcards

Adrenal and Thyroid Conditions Flashcards

1
Q

What is the shape of the thyroid gland?

A

Bow tie

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give two secretions of the thyroid gland and what are they for?

A

Thyroxine- metabolise energy
Calcitonin- metabolise Ca2+ production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give a secretion of the parathyroid gland and what is it for?

A

Parathyroid hormone- effects extracellular Ca2+ fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give a secretion of the thymus gland and what is it for?

A

Thymosins- immune system, T lymphocyte production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name two sections of the adrenal gland and their secretions and function:

A

Adrenal cortex- coritsol -stress and BG, aldosterone for salt water balance
Adrenal medulla- produces adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the gland called for sex hormones?

A

Gonads

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give a secretion of the pineal gland and what is it for?

A

Melatonin- sleep wake cycle, circadian rhythms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe how the hypothalamus and the pituitary are involved in controlling secretion:

A

Hypothalamus ->releasing hormone (1)-> anterior pituitary-> stimulating hormone (2)-> target gland-> target gland hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are three classes of hormones and give an example of each:

A

Peptide hormones: insulin, oxytocin
Steroid hormones: cortisol, sex hormones
Modified a.a: adrenaline, thyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why are peptide hormone receptors on the cell and why?

A

Peptide hormones are hydrophilic and therefore can’t cross the cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does a peptide hormone signal?

A

Bind to GPCR at cell membrane causing a 2º messenger cascade, this means it converts ATP to cAMP, which cAMP then activates an enzyme cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does a steroid hormone signal?

A

Steroid hormone diffuses through membrane (as its a lipophille), it binds to receptors in nucleus causing a hormone- receptor complex which activates DNA and protein synthesis which leads to a change in gene expression, can also act through second messenger systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the main glands in the endocrine system?

A

Hypothalamus
Pituritary
Pineal
Thymus
Pancreas
Testes
Ovaries
Adrenal
Thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the structure of the pituitary gland:

A

Extension of the hypothalamus
Anterior lobe (adenohypophysis)- consists of glandular epithelial tissue connects by a unique vascular link
Posterior lobe (neurohypophysis)- consists of nervous tissue connects by neural pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does the posterior pituitary release?

A

Oxytocin and anti-diuretic hormone (ADH)=vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe how the hypothalamus and the posterior pituitary are linked to produce ADH and oxytocin?

A

Cell bodies of neurones are in the hypothalamus in the supraoptic and paraventricular nuclei
Axons pass through pituitary stalk and the terminals are on capillaries on the posterior pituitary
Neuronal cell bodies in the hypothalamus produce 2 small peptide hormones, oxytocin and ADH, which are packaged in secretory granules, transported down the axon cytoplasm and stored in the neuronal terminals in the posterior pituitary until excretion of neuron causes their release
Each terminal stores one or the other but not both, so they can be released independently into the BS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which nuclei in the hypothalamus is vasopressin and oxytocin produced by?

A

Supraoptic= vasopressin
Paraventricular= oxytocin
Although both can produce both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the functions of oxytocin in women?

A

Contraction of the uterine muscle to help expel infant during birth- increase in secretion by reflexes in birth canal
Promotes ejection of milk from mammary glands during breastfeeding- increased secretion by suckling
Influences social behaviour- mating/ bonding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can oxytocin be used in childbirth?

A

Injection of Syntocinon used to induce labour and prevent post-partum haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the functions of vasopressin?

A

Enhances retention of water by nephrons during urine formation:
-primary regulator of water balance
-binds to V2 receptors so an increase in water permeability in distal tubule and collecting ducts leading to increase in water reabsorption
Contraction of the arteriolar smooth muscle:
-minor role in regulating BP
-binds to V1 receptor causing an increase in vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is diabetes insipidus?

A

Caused by a lack of ADH or a lack or response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the symptoms of diabetes insipidus?

A

Main symptoms are polyuria and polydipsia
If left untreated can lead to shock like symptoms, hypotension, tachycardia and tachypnea, dehydration, hypernatrena (increase sodium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the treatment for diabetes insipidus?

A

Vasopressin injection
Desmopressin injection/tab/nasal spray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does desmopressin not cause vasoconstriction?

A

Has no effect on the V1 receptors so no vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What causes nephrogenic diabetes insipidus?

A

Collecting ducts don’t respond to ADH
Can be used by drugs e.g Lithium, genetic or intrinsic kidney disease and electrolyte imbalance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is cranial diabetes insipidus?

A

Hypothalamus doesnt produce ADH
Can be caused by brain tumours, infections or idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How do you test for both types of diabetes insipidus?

A

Measure urine osmolality without fluid or food for 8 hours, then give desmopressin, then measure urine osmolality 8 hours after
Cranial DI- higher urine osmolality
Nephrogenic DI- same (low) urine osmolality
Primary polydipsia (no DI) after initial 8 hour deprivation there should still be a high osmolality so no diabetes insipidus so don’t give desmopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Name the 5 main cell types in the anterior pituitary and which hormones do they secrete?

A

Somatotropes- GH- growth hormone
Thyrotropes- TSH- thyroid stim hormone
Corticotropes- ACTH- adrenocorticotrophic hormone
Gonadotropes- FSH follicle stim hormone -LH luteinizing hormone
Lactotropes- PRL- prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are hypothalamic hormones called?

A

Releasing factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the hypothalamic pituitary (hypophyseal) portal system?

A

A unique vascular link between hypothalamus and anterior pituitary
There is a direct capillary to capillary bed so the hypothalamic hormone just travel locally within this
Upon arrival to the pituitary, the hypothalamic hormones bind to specific receptor on specific cells in the anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How is growth hormone released?

A

GHRH from the hypothalamus binds to receptors on the somatotroph cells in the anterior pituitary, triggering the release of GH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the purpose of GH?

A

Stimulates growth and development resulting in:
-net synthesis of proteins
-lengthening of long bonds
- increase in size and number of cells in soft tissues
Doesn’t directly affect tissues but works by stimulating insulin like growth factor (IGF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What other factors are growth influenced by?

A

Genetics
Adequate diet
Chronic disease
Other growth influencing hormones; thyroid, insulin etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe primary and secondary GH deficiency:

A

Primary- deficiency is due to pituitary effect
Secondary- deficiency is due to hypothalamic or target dysfunction e.g lack of GHRH or IGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

State and describe the symptoms of growth hormone deficiency?

A

Short stature due to reduced skeletal growth
Decrease in muscle protein synthesis and increase in fat deposition
If it occurs in adult hood, results in muscle effects e.g at risk of heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the treatment for GH deficiency?

A

Potential risk of cancer
Treatment is somatotropin (recombinant GH)
Given for short stature
Also somatorelin, a 44a.a can be given if relevant
Also Mecasermin (recombinant IGF-1) where is growth failure in children lacking adequate IGF-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What can cause and happen in GH excess?

A

Most often benign tumour of somatotrophs
Results in giantism
No distortion to body proportions but person is taller
Can result in acromegaly- pts have thicker bones and soft tissue proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the treatment for a pt having GH excess?

A

Surgery
Medicines- somatostatin analogues given as an adjunct to surgery
Somostatinn acts on all the SST1-5 receptors
Different analogues acts on specific set receptors:
-octreotide -lanreotide -pasireotide
Other drugs:
-dopamine agonists, bromocriptine
-GHRH antagonists, pegvisomant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the structure and function of somatostatin:

A

14 a.a residue peptide
Produced in hypothalamus
Inhibits release of GH, TSH, insulin and glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe octreotide drug as a SST1-5 agonist:

A

A long lasting analogue of somatostatin
Treatment for other hormone secreting tumours, acromegaly, usually given SC
SEs: GI disturbances and pain at site of injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe lanreotide drug as an SST1-5 agonist:

A

Has similar effects to octreotide and is also used in the treatment of thyroid tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe pasireotide drug as a SST1-5 agonist:

A

Has similar effects and is also used in Cushing’s syndrome when surgery is inappropriate or ineffective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Where are the adrenal glands found?

A

Above the left and right kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Describe the structure of the adrenal gland:

A

Consists of the outer cortex and the inner medulla and divided into three zones:
Zona Glomerulosa- outermost
Zona Fasciculata- middle
Zona Reticularis- inner zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where is aldosterone produced in the adrenal gland?

A

Zona Glomerulosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Where are cortisol and corticosteroids produced in the adrenal gland?

A

Zona Fasciculata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How is cholesterol made into other steroids?

A

Cholesterol-> pregnenelone and then a series of enzyme reactions occurs to produce different steroid molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the 3 steroid categories and give an example of each:

A

Mineralocorticoids- aldosterone
Glucocorticoids- cortisol
Sex hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where does aldosterone act on and what does it do?

A

Acts on the distal and collecting tubules of the kidney
Promotes Na reabsorption in kidney
Na retention induces water retention
Increase in K+ and H+ excretion in urine
This increases BP long term

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How is aldosterone secretion increased?

A

By activation of the renin angiotensin aldosterone system or direct stimulation of adrenal cortex by a rise in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the functions of cortisol?

A

Role in metabolism to increase BG conc at the expense of protein and fat stores
Stimulate hepatic gluconeogenesis
Inhibits glucose uptake by several tissues
Stimulates protein breakdown in several tissues, especially muscle
Stimulates lipolysis in adipose tissue to provide alternative source of three fatty acids to tissue rather than using up glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How is cortisol involved in stress?

A

Stress increases cortisol secretion
Cortisol in flight/flight situation favours providing glucose and amino acids/free fatty acids as immediate source of energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How is cortisol involved in anti-inflammatory effects?

A

Inhibits phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How is cortisol secreted?

A

Cortisol is released in response to ACTH from the pituitary, which in turn is released in response to CFR from the hypothalamus
There is negative feedback mechanism that decreases secretion once sufficient hormone has been made

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Which factors influence cortisol release?

A

Cortisol has a diurnal rhythm, highest in the morning and lowest at night
This is important when interpreting blood samples at different times of the day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What does cortisol stimulate during stress?

A

Stimulates protein catabolism
Stimulates gluconeogenesis by liver
Inhibits glucose uptake by tissues, not brain
Stimulates lipolysis to free fatty acids
Inhibit inflammation and specific immune responses
Inhibits nonessential functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What does CRH stand for?

A

Corticotrophin releasing hormone

58
Q

What does ACTH stand for?

A

Adrenocorticotrophic hormone

59
Q

What can be the causes of aldosterone hyper secretion and give symptoms?

A

Primary- hyper secreting adrenal tumour made of aldosterone secreting cells, Conn’s syndrome
Secondary- High activity of renin angiotensin aldosterone system causing a narrowing of the blood vessels
Results in hypernatraemia, hyperkalaemia and high blood pressure (due to any and H2O retention)

60
Q

What is the treatment for aldosterone hypersecretion?

A

Usually surgery to remove a tumour and spironolactone

61
Q

What are the pharmacological causes of Cushing’s syndrome?

A

Cortisol hypersecretion, excess CRH and/or ACTH and adrenal tumours secreting excess cortisol it can also occur from ACTH secreting tumours located in places other than the pituitary, usually the lung

62
Q

State and describe the symptoms of Cushing’s syndrome:

A

Results in glucose excess and protein shortage, abnormal fat distribution resulting in ‘buffalo hump’ and ‘moonfaced’
Fragile thin skin- from muscle breakdown leading to tiredness and weakness
Inhibits immune system- adequate protein production for wound healing
osteoporosis, hirsutism, hypertension, psychosis and depression, hyperglycaemia

63
Q

What are the causes of Cushing’s disease?

A

Exogenous steroids, treating patients with steroids
Pituitary adenoma (tumour) producing ACTH excess cortisol

64
Q

What are the causes of adrenal Cushing’s?

A

Adrenal adenoma producing excess cortisol

65
Q

What are the causes of paraneoplastic Cushing’s?

A

Ectopic ACTH

66
Q

State and describe the treatment for Cushing’s syndrome:

A

Surgery or radiotherapy for tumours
Corticosteroid inhibitors:
-metyrapone- a competitive inhibitor of 11B hydroxylation in the adrenal cortex
-ketoconazole- acts as a potent inhibitor of cortisol and aldosterone synthesis by inhibiting the activity of a17-hydroxylase, 11 hydroxylation steps and at higher doses the cholesterol sidechain cleavage enzyme, may have direct effect on corticotropic tumour cells in patients with Cushing’s disease
-mitotane- inhibits glucocorticoid synthesis by an unknown direct effect on the adrenal gland
-carbenexone- inhibits hydrocortisone conversion to cortisone

67
Q

Describe Addison’s disease:

A

Deficiency in glucocorticosteroids and in mineralcorticoids
Due to atrophy in the adrenal cortex

68
Q

What are the symptoms of Addison’s disease?

A

Lethargy, depression, anorexia and weight loss

69
Q

What is Addison’s crisis?

A

Where it can first present as a severe adrenal deficiency and is a medical emergency
Symptoms of vomiting, abdominal pain, weakness, hypertension, hyperpigmentation and eventually coma

70
Q

What is a treatment for Addison’s disease?

A

Lifelong steroid replacement
Hydrocortisone- replaces cortisol, 20 to 30 mg daily and divided dose, larger dose in morning to mimic diurnal rhythm of cortisol secretion
Fludrocortisone- replaces aldosterone, 50 to 300 µg daily

71
Q

What is a treatment for Addison’s crisis?

A

Treat with IV hydrocortisone
100mg every 6-8 hours

72
Q

What are the inhaled and topical side-effects of corticosteroids?

A

Topical: skin thinning, skin infections, folliculitis, stretch marks
Inhaled: hoarseness, throat irritation, dysphonia, candida

73
Q

What are the side effects of systemic corticosteroids and what rules are put in place to decrease these?

A

Adrenal suppression, occurs during long-term therapy, lack of production of endogenous steroids
Patients should carry a steroid card

74
Q

What are the sequels for long-term steroid use?

A

Inter-current illness, trauma or surgery- need to temporarily increase days to compensate (temporarily double)

75
Q

Why shouldn’t you withdraw steroids abruptly?

A

Cause acute adrenal insufficiency as adrenal glands can’t switch back on
Hypotension, confusion, coma, death

76
Q

What is a steroid treatment card?

A

Blue card- allows healthcare professionals to not stop abrupt withdrawal
Contains the drugs name, dose, strength etc

77
Q

Under which conditions would gradual withdrawal of steroids be needed:

A

More than 40mg prednisolone OD for more than a week
More than 3 week treatment
Recently received repeated short courses
Needed short course within 1 year of stopping long term therapy

78
Q

Under which conditions would gradual withdrawal of steroids not be needed:

A

If disease is unlikely to relapse
And not in the rules where gradual withdrawal is needed

79
Q

What are the rules of infection for patients on prolonged steroid therapy?

A

Prolonged causes increase susceptibility to infection
If never had chickenpox, avoid contact with people who have had shingles or chickenpox
Avoid exposure to measles
Seek medical advice if exposure occurs

80
Q

What are psychiatric reactions of steroid therapy?

A

High doses:
-euphoria, nightmares, insomnia, irritability, suicidal thoughts (especially if history)
Usually subside on dose reduction or withdrawal

81
Q

What are other side-effects of corticosteroid treatment?

A

Mineral corticoid:
- hypertension (Na and water retention)
Glucocorticoid:
-diabetes/ glucose intolerance, osteoporosis, GI disturbances, Cushing’s syndrome, growth suppression in children

82
Q

Give an example of a prophylaxis treatment of corticosteroids:

A

Bisphosphonates, prophylaxis for osteoporosis

83
Q

Describe the thyroid hormone:

A

Contains iodine
There are two forms, thyroxine (T4) and tri-iodothyronine (T3)
Involved in growth and development

84
Q

Where are thyroid hormones made and stored?

A

Thyroid hormones are synthesised in the follicular (epithelial) cells and stored in the extracellular colloid (lumen) of the follicles of the thyroid gland
Colloid is extracellular but it isn’t in direct contact with the extracellular fluid

85
Q

Where is calcitonin synthesised?

A

In the parafollicular cells (C cells)

86
Q

Explain the structure and transport of the thyroid hormone:

A

Thyroxine (T4) contains 4 iodines where as Tri-iodothyronine (T3) contains 3 iodines
T3 and T4 are synthesised by the iodination of tyrosine, a non-essential amino acid synthesised in the body
The ratio of T4 to T3 secretion is 10:1 in the blood and T4 (inactive) is converted to T3 (active) in the target tissue by de-iodinases
They are hydrophobic so require a transporter called ‘Thyroxine binding globulin’ (TBG)
They also bind onto albumin and transthyretin

87
Q

How do humans obtain iodine and how much is the daily dose?

A

From the diet
0.15 mg a day

88
Q

Describe actions of the thyroid hormone:

A

Increase in basal metabolic rate
Increase in heat production
Influence of synthesis and degradation of major fuels in the body
Increase in cell responsiveness to catecholamines
Stimulates GH and IGF-1 secretion so essential for normal growth
Is essential for development and activity of the CNS

89
Q

Describe the synthesis of the thyroid hormone:

A

I- ions are actively transported into the follicle cells from the blood by the Na+/I- co transporter 2
Iodide ions are oxidised to iodine by thyroid peroxidase
Thyroglobulin is a large glycoprotein forming in the colloid in the follicle lumen, it contains a large amount of tyrosine
Iodine is attached to tyrosine residues of thyroglobulin a stepwise manner
+I- monoiodotyrosine (MIT), +2I- diiodotyrosine (DIT) and then two more tyrosine molecules T3 or T4
2 x DIT= T4
1x MIT and DIT= T3
Protease cleaves the T4 and T3 off the peptidoglobulin out of the cell by the monocarboxylate transporter (MCT) into the plasma

90
Q

What does the thyroid hormone do once cleaved into the plasma?

A

70% binds to TBG
15% bound to albumin
Less than 15% bonded to thyroxine binding pre-albumin (TBPA)

91
Q

Describe how the synthesis and release of thyroid hormones are controlled:

A

T3 and T4 synthesis is controlled by TSH, which is secreted from the anterior pituitary
TSH binds to cAMP-coupled receptors on epithelial cells and stimulates iodine uptake, which increases synthesis
Plasma iodine levels also control synthesis:
Increase [I-], increase in T3 and T4 synthesis so decrease in TSH release
Decrease [I-], decrease in T3 and T4 synthesis so increase in TSH release

92
Q

What type of receptors are T3 receptors and name them:

A

Nuclear receptors
alpha 1, alpha 2, Beta 1 and Beta 2

93
Q

What are the symptoms of too much thyroid hormone?

A

Weight loss, increase heart rate, fatigue etc

94
Q

What are the symptoms of too little thyroid hormone?

A

Swelling, weight gain etc

95
Q

How is thyroid secretion regulated by genomic control?

A

Thyroid hormone up taken by MCT (MCT8 AND MCT10)
Once in cell perodinase removes I from T4 to form T3
5’/3’ deiodinase removes I from outer ring
Type 1 5’/3’ deiodinase generates circulating T3 in liver
Type 2 5’/3’ deiodinase generates pituitary, CNS and placenta, controls when TSH is released

96
Q

What is the major presenting symptom of thyroid disease/ dysfunction and give reasons for this:

A

Goitre= enlargement of the thyroid as swelling in the neck
This occurs in:
-Thyroid cancer
-Hypothyroidism often due to Hashimoto’s thyroiditis
-Hyperthyroidism often due to Graves disease

97
Q

Describe the aetiology of thyroid cancer:

A

Quite rare
More common in women 35-39 than in men 70+
Over 85% of pts survive

98
Q

Name and describe the five types of thyroid cancer:

A

Papillary – most common, slow-growing (80 to 85%)
Follicular – More aggressive and is generally found in countries where there is iodine deficiency (5 to 10%)
Hurthle cell – Carcinoma is a subtype of follicular cancer (4%)
Medullary – Originates from the C cells, is more aggressive and more likely to metastasis (3%)
Anaplastic – an undifferentiated form, very aggressive and metastasises quickly (1 to 3%)

99
Q

What are the risk factors of thyroid cancer?

A

Presence of benign disease
Increased weight
Genetic factors
Radiation exposure (KI can potentially prevent radioactive iodine being absorbed)

100
Q

What are the symptoms of thyroid cancer?

A

Lump in neck
Hoarse voice
Sore throat
Difficulty swallowing

101
Q

What are the invasive treatments for thyroid cancer?

A

Surgery to remove thyroid
Radiotherapy
Chemotherapy- doxorubicin or cisplatin
Targeted chemotherapy when other options aren’t available

102
Q

What are the drug treatments for thyroid cancer and describe where they work:

A

Most target vascular endothelial growth factor receptor pathway as thyroid is vascular rich
-vandetanib (medullary)
-cabozantinib (medullary)
-lenvatinib (papillary/ follicular)

103
Q

What is primary hypothyroidism?

A

Failure of the thyroid gland- 95% of cases
A lack of dietary iodine is most common cause

104
Q

What is Hashimoto’s thyroiditis?

A

An autoimmune disease where the body makes antibodies to thyroglobulin and causes primary hypothyroidism, preventing thyroid hormone from being made

105
Q

What is secondary hypothyroidism?

A

Hyper secretion of hormones that stimulate it or target tissue dysfunction
Pituitary dysfunction from tumours/infections can result in low levels of TSH

106
Q

What is tertiary hypothyroidism?

A

Hypothalamic dysfunction in low levels of thyrotropin-releasing hormone (TRH) or peripheral effects resulting in tissue insensitivity to thyroid hormone

107
Q

Name foods which contain iodine:

A

Sea fish, shellfish, some cereals, dairy foods, eggs and some fruits

108
Q

What can an iodine deficiency in pregnancy cause and why?

A

Neurological abnormalities e.g congenital myxoedema or cretinism- caused by a deficiency of thyroid hormone during prenatal development
Characterised by dwarfed stature, mental retardation, dystropy of bones and a low basal metabolism

109
Q

What are the symptoms and signs of hypothyroidism?

A

Metabolism slows down so everything is slower and weaker resulting in a low metabolic rate, generalised weakness, slow speech, cold and intolerance, memory loss, depression, constipation, weight gain, dry skin, sparse thin hair, growth failure in children, amenorrhea

110
Q

What is myxoedema coma?

A

A life-threatening complication of chronic thyroid hormone deficiency resulting in brain damage and death if not treated

111
Q

What is the diagnosis for primary hypothyroidism?

A

Confirm by checking a patient’s thyroid function test (TFTs) and testing blood TSH and T3 and free T4 levels
Ideally all levels and thyroid antibodies should be checked but not available in all hospitals
Hypothyroidism will be confirmed by high TSH levels and low free T4 and T3 levels, raise TSH levels is a gold standard for diagnosis

112
Q

Give the reference range values for the optimum TSH, free T4 and T3 in the blood:

A

TSH (0.4-4.5µlu/ml)
FT4 (10-24pmol/L)
T3 (4-7.8pmol/L)

113
Q

Why are there high TSH levels in primary hypothyroidism?

A

Due to insufficient T4 and T3 produced by thyroid and resulting negative feedback causing anterior pituitary to produce more TSH

114
Q

What is the diagnosis for secondary hypothyroidism?

A

All TSH, T4 and T3 will be low

115
Q

What is the treatment for hypothyroidism?

A

Levothyroxine (thyroxine) orally, a synthetic form of T4

116
Q

Describe the treatment for hypothyroidism:

A

Levothyroxine starting dose 50 to 100mcg, 1.6mcg/kg in the morning, 25µg for the elderly
Should be taken on an empty stomach
Can take a few months to have an effect, the aim is to maintain TSH levels in reference range, can take up to 6 months
Initially check levels after 2-3 months, if TSH levels still raised, increase dose by 25-50mcg
Usual maintenance dose 100-150mcg daily, very rare to see a dose higher than 200mcg

117
Q

Why do you have to take levothyroxine on an empty stomach?

A

Food can decrease reabsorption by 40 to 80% and reduced by iron, antacids, calcium containing products and soya milk

118
Q

What is a treatment for severe hypothyroid states including hypothyroid coma?

A

Liothyronine (T3)- IV
Acts rapidly but has a shorter duration of action
Need to be monitored in the blood to minimise risk of hyperthyroidism
Iodine can also be given in iodine deficiency

119
Q

Give the aetiology of hyperthyroidism:

A

Most common is Graves’ disease (80-90%)
Most patients present between 30 to 60 years and is 10% more common in women than men

120
Q

What is Graves’ disease?

A

An autoimmune condition with a genetic predisposition, where the body makes thyroid-stimulating antibodies that mimic TSH, stimulating the TSH receptor

121
Q

Apart from graves disease, what else causes hyperthyroidism and describe:

A

Toxic nodular goitre
When new follicles are formed, increased thyroid hormone secretion, which develops into nodules
Thyroid adenomas, benign tumours that secrete thyroid hormones can cause disorder

122
Q

What are the symptoms and signs of hyperthyroidism?

A

The metabolism speeds up with an increase in sympathetic activity, resulting in a higher metabolic rate
Palpitations, sweating, trauma, anxiety, diarrhoea, inability to tolerate heat and weight loss
In addition patients experience goitre and eye problems:
-Exophthalmus (bulging eyes)
-swelling of eyelids
-irritation, lid retraction
-ophthalmoplegia (weakness of eye muscles)
-diplopia

123
Q

What is a diagnosis for hyperthyroidism?

A

Low TSH levels and high free T4 and T3 levels due to too much T4 and T3 produced by thyroid and resulting negative feedback causing anterior pituitary to cut off production of TSH

124
Q

What is primary hyperthyroidism?

A

The thyroid behaves abnormally and produces thyroid hormone

125
Q

What is secondary hyperthyroidism?

A

Thyroid producing excessive thyroid hormone due to over stimulation of thyroid stimulating hormone in hypothalamus or pituitary

126
Q

What is exophthalmos and how is it caused?

A

Causes buldging of eyes due to graves disease due to inflammation, swelling and hypertrophy of muscle behind eyeball, forcing it forward

127
Q

What is pretibial myxoedema?

A

Deposits of mucin under the skin
Discoloured, waxy, oedematous
Specific to Grave’s disease

128
Q

What is De Quervain’s thyroiditis?

A

Viral infection in thyroid gland- fever, neck pain and tenderness, dysphagia and hyperthyroidism
Hyperthyroid phase followed by a hypothyroid phase and then the thyroid return back to normal

129
Q

What is a thyroid storm?

A

Thyrotoxic crisis
Rare presentation of hyperthyroidism
Acute, severe presentation, pyrexia, tachycardia delirium
Admission for monitoring, fluid resuscitation

130
Q

Describe the first line treatment for hyperthyroidism?

A

Carbimazole (thioureylenes)
Normal thyroid function after 4 to 8 weeks
Continue maintaining dose or titrated down to maintain all levels ‘titration block’
Or block all production of thyroid hormone and replace with levothyroxine ‘block and replace’
Complete remission after 18 months

131
Q

Describe the second line treatment for hyperthyroidism:

A

Propylithiouracil
Small risk of hepatic reactions- death

132
Q

How can radioactive iodine be used in hyperthyroidism?

A

I-131
Drink it and radiation destroys thyroid cells which decreased thyroid hormone as selectivities taken up by thyroid gland, can take up to 6 months, can lead to hypothyroidism

133
Q

What can’t you do when taking radioactive iodine for hyperthyroidism?

A

Can’t get pregnant
Stay away from children
Limit contact with anyone few days after treatment

134
Q

What are other drug treatments for hyperthyroidism?

A

Beta blockers (propranolol, non selective for thyroid storm), doesn’t treat hyperthyroidism but blocks adrenaline related symptoms:
-tachycarida, anxiety, sweating, tremor
Surgery

135
Q

Give the mechanism of action of carbimazole for hyperthyroidism:

A

Inhibits thyroperoxidase, thus inhibiting the iodination of tyrosine and subsequently the sysnthesis of thyroid hormone
Propylthiouracil inhibits T4 to T3 conversion

136
Q

What are side-effects in drugs used for hyperthyroidism?

A

Rashes (5%) and agranulocytosis, rare but life-threatening in 0.3% of patients- Ab mediated, resulting in complete depletion of neutrophils and increase susceptibility to bacterial infections, as well as the depletion of RBCs so increase risk of bleeding

137
Q

What are the monitoring parameters for drugs used in hyperthyroidism and why?

A

All patients should be told to report any signs of sore throat, mouth ulcers, fever, malaise, bruising or bleeding due to the risk of agranulocytosis

138
Q

When are high doses of iodine/iodide given in hyperthyroidism?

A

Lugol’s iodine
Sometimes given to temporarily inhibit the release of thyroid hormones
Given as oral solution
Symptoms decrease after 1-2 days
Max effect at 10-15 days then effect decreases
Sometimes given to patients are waiting for surgery and acute throtoxiccrisis

139
Q

Describe drug induced thyroid dysfunction and what should be the monitoring parameters?

A

Amiodarone (for cardiac arrhythmias) can cause thyroid dysfunction (hypo/hyper) as molecule contains a significant amount of iodine
Patients taking amiodarone should have the baseline TFT’s measured at start of treatment and six months thereafter

140
Q

What is the role of CRH for stress?

A

ACTH release by CRH from hypothalamus and stimulates cortisol secretion in the adrenal cortex

Y2S2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions