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Chings Notes > JM Chapter 14 > Flashcards

JM Chapter 14 Flashcards

1
Q

TSH receptor antibodies (TR Ab):

A

Graves disease

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2
Q

Thyroid peroxidase antibodies (TPO Ab):

A

Hashimoto disease

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3
Q

Thyroglobulin antibody (Tg Ab):

A

Hashimoto disease

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4
Q

The term refers to the accumulation of mucopolysaccharide in subcutaneous
tissues.

Tiredness +HUSKY VOICE + cold intolerance

A

Myxoedema

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5
Q

Common causes of primary hypothyroidism include

A

radioactive iodine treatment, thyroid surgery
and Hashimoto 1thyroiditis

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6
Q

Patients at risk for primary hypothyroidism

A

Previous Graves disease

Autoimmune disorders (e.g.autoimmune lymphocytic thyroiditis, rheumatoid arthritis, type 1
diabetes)

Down syndrome

Turner syndrome

Drug treatment: lithium, amiodarone, interferon, iodine

Previous thyroid or neck surgery

Previous radioactive iodine treatment of the thyroid

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7
Q

Clinical Features of Primary hypothyroidism

A

Constipation
Cold intolerance
tiredness/lethargy/somnolence
physical slowing
mental slowing
depression
huskiness of voice
puffiness of face and eyes
pallor
loss of hair
weight gain

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8
Q

is an autoimmune thyroiditis, is the
commonest cause of bilateral non-thyrotoxic goitre in Australia.

firm and rubbery
patients may be hypothyroid or euthyroid

A

Hashimoto thyroiditis, or lymphocytic thyroiditis

Confirmatory Teats:
(TPO Ab) titre
and/or fine-needle aspiration cytology.

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9
Q

Most common cause
of hyperthyroidsim
(Thyrotoxicosis)

A

Graves disease
Followed by nodular thyroid disease

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10
Q

What are the other causes of Hyperthryoidism ?

A

Graves disease (typical symptoms with a diffuse goitre and eye signs)

Autonomous functioning nodules/toxic adenoma

Subacute thyroiditis (de Quervain thyroiditis) viral origin (suspect if painful thyroid and
malaise)

Excessive intake of thyroid hormones thyrotoxicosis factitia

Exogenous iodine excess, e.g. food contamination
Amiodarone (beware of this drug)

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11
Q

What are the Clinical features of Hyperthyroidsm?

A

Heat intolerance

Sweating of hands

Muscle weakness

Weight loss despite normal or increased appetite

Emotional lability, especially anxiety, irritability

Palpitations

Frequent loose bowel motions

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12
Q

Physical examinations
Hyperthyroidism
Signs are (usually):

A

agitated, restless patient
warm and sweaty hands
fine tremor (place paper on hands)
goitre
proximal myopathy
hyperactive reflexes
bounding peripheral pulse
+ atrial fibrillation

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13
Q

DxT anxiety + weight loss + weakness

A

Thyrotoxicosis

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14
Q

Eye signs of
Hyperthyroidism

A

Lid retraction (small area of sclera seen above iris)
Lid lag
Exophthalmos
Ophthalmoplegia in severe cases

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15
Q

Investigations
Hyperthyroidism

A

T4 (and T3) elevated
TSH level suppressed
Radioisotope scan
Antithyroid peroxidase (TPO Ab) often positive

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16
Q

Treatment for Hypothyroidism

A

Levothyroxine (thyroxine) 50-100 mcg daily up to 200 mcg daily

Aim TSH levels of 0.5-2mUL

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17
Q

Treatment of Hyperthyroidism

A

Radioactive iodine therapy

Thionamide antithyroid drugs (initial doses)
*carbimazole 10-45 mg (o) daily starting with 10-20 mg in divided doses depending on
disease activity
or
*propylthiouracil 200-600 mg (0) daily in divided doses or methimazole

Adjunctive drugs:
beta blockers propranolol 10-40 mg, 6 to 8
hourly); diltiazem or atenolol are alternatives

Lithium carbonate (rarely used when there is intolerance to thionamides)

Lugol’s iodine: mainly used prior to surgery
Surgery
Page 140

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18
Q

What are the surgical treatment for Hyperthyroidism

A

Subtotal thyroidectomy or Total Thyroidectony

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19
Q

Thyroid enlargement may be diffuse or multinodular. Diffuse causes include physiological,
Graves disease, thyroiditis (Hashimoto or de Quervain), iodine deficiency or it can be hereditary

A

Goitre

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20
Q

Investigations include
Goitre

A

TFTs, needle biopsy, ultrasound and CXR.

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21
Q

Management
Goitre

A

Supportive thyroxine if TSH elevated (may lead to marked regression) and subtotal or total thyroidectomy

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22
Q

It is defined as a discrete lesion on palpation and/or ultrasonography that is distinct from the rest of the thyroid gland.

A

Thyroid nodules

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23
Q

Causes of Thyroid Nodules

A

Dominant nodule in a multinodular goitre (most likely)

Colloid cyst

True solitary nodule: adenoma, carcinoma (papillary or follicular)
Investigations

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24
Q

Investigations of Thyroid Nodule

A

Ultrasound imaging
Fine-needle aspiration cytology
Thyroid function tests

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25
Q

The main presentations of Thyroid carcinoma are

A

painless nodule,
a hard nodule in an enlarged gland or
lymphadenopathy.

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26
Q

Most common thyroid malignancy

A

Papillary carcinoma

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27
Q

is the investigation of choice of Thyroid Carcinoma

A

Fine-needle aspiration

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28
Q

Hyperprolactinaemia”
main causes (of many) are a pituitary adenoma (prolactinoma; micro- or macro),
pituitary stalk damage, drugs - such as

A

antipsychotics, various antidepressants, metoclopramide,
cimetidine, oestrogens, opiates, marijuana - and physiological causes such as pregnancy and
breastfeeding.

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29
Q

Clinical features
Hyperprolactinaemia

A

Symptoms common to males and females: reduced libido, subfertility, galactorrhoea (mainly
females)
Females: amenorrhoea/oligomenorrhoea
Males: erectile dysfunction, reduced facial

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30
Q

Hyperprolactinaemia
Diagnosis

A

Serum prolactin and macroprolactin assays
MRI:if there is headache

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31
Q

DxT nasal problems + fitting problems (e.g. rings, shoes) + sweating -
acromegaly

A

Acromegaly

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32
Q

Symptoms of Acromegaly

A

Symptoms suggestive of acromegaly include:
excessive growth of hands (increased glove size)

excessive growthof tissues (e.g. nose, lips, face)

excessive growth of feet (increased shoe size)

increased size of jaw and tongue; kyphosis
general: weakness, sweating, headaches

sexual changes, including amenorrhoea and loss of libido

disruptive snoring (sleep apnoea)

deepening voice

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33
Q

What is the key test fpr investigating Acromegaly?

A

IGF-1

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34
Q

Diagnosis of
Acromegaly:

:

A

Plasma growth hormone excess

Elevated insulin-like growth factor 1 (IGF-1) (somatomedin) the key test

X-ray skull and hands

MRI scanning pituitary

Consider associated impaired glucose tolerance/diabetes

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35
Q

Treatment options of
Acromegaly

A

Transsphenoidal pituitary microsurgery, drugs and radiotherapy

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36
Q

DxT weakness + polyuria + polydipsia -

A

diabetes insipidus

37
Q

impaired secretion of vasopressin (antidiuretic hormone) from the posterior pituitary leads to
polyuria, nocturia and compensatory polydipsia, resulting in the passage of 3-20 L of dilute
urine per day.

A

Diabetes insipidus

38
Q

Causes of diabetes insipidus (DI)

A

The commonest being
postoperative (hypothalamic-pituitary), which is usually transient only. Other causes of cranial
DI include tumours, infections and infiltrations.

39
Q

is caused by
cancer (e.g. lung,lymphomas, kidney, pancreas), pulmonary disorders, various intracranial
lesions and drugs such as carbamazepine and many antipsychotic agents.

A

The syndrome of secretion of inappropriate antidiuretic hormone (SIADH)

40
Q

Management of
SIADH is essentially

A

Fluid restriction

41
Q

The treatment of DI is

A

Desmopressin, usually given twice daily intranasally.

42
Q

This rare disorder (acute or chronic) should be considered with:
a history of postpartum haemorrhage or head injury

symptoms of hypothyroidism

symptoms of adrenal insufficiency

symptoms suggestive of a pituitary tumour

thin, wrinkled skin: ‘monkey face’

pale ‘alabaster’ skin/hairlessness

A

Hypopituitarism

43
Q

Causes: of
HYPOPITUITARISM

A

Pituitary adenoma, other parasellar tumours and inflammatory/infiltratie lesions.

44
Q

DXT (female): amenorrhoea + loss of axillary and pubic hair + breast
atrophy -

A

hypopituitarism

45
Q

DXT (male): ! libido + impotence + loss of body hair -

A

hypopituitarism

46
Q

Investigation of
hypopituitarism

A

Serum pituitary hormones

imaging (MRI) and

triple stimulation test

47
Q

Treatment of
hypopituitarism

A

HRT,

surgery or

radiotherapy

48
Q

Mineral corticoids, especially aldosterone

A

Zona glomerulosa

49
Q

Glucocorticoids

A

Zona fasciculata

50
Q

Androgens, especially DHEA

A

Zona reticularis

51
Q

epinepherine, norepinephrine

A

Catecholamines

52
Q

deficiency of cortisol and aldosterone

A

chronic adrenal insufficiency (Addison disease

53
Q

cortisol excess

A

Cushing syndrome

54
Q

DXT fatigue + a/n/v + abdominal pain (+/-Skin discolouration)

A

Addison
disease

55
Q

The most common cause of Addison
disease

A

Autoimmune destruction of the adrenals

others are infection, e.g. TB
or fungal

56
Q

Clinical features of Addison’s Disease

A

Lethargy/excessive fatigue/weakness

Anorexia and nausea

Diarrhoea/abdominal pain

Weight loss

Dizziness/funny turns, syncope:

hypoglycaemia (rare); postural hypotension (common)

Hyperpigmentation, especially mucous membranes of mouth and hard palate, skin creases of
hands

57
Q

Diagnosis of Addison’s

A

Elevated serum potassium, low serum sodium

Low plasma cortisol level (fails to respond to synthetic adrenocorticotropic hormone [ACTH])

The short synacthen stimulation test is the definitive test

Consider adrenal autoantibodies and imaging? calcification of adrenals

58
Q

Treatment of Addison’s

A

Corticosteroid replacement-hydrocortisone/fludrocortisone acetate, other options.

59
Q

It develops because of an inability to increase cortisol in response to stress
which may include intercurrent infection, surgery or trauma.

A

Addisonian crisis

60
Q

Clinical features
Addisonian crisis

A

Nausea and vomiting
Acute abdominal pain
Severe hypotension progressing to shock
Weakness, drowsiness progressing to coma

61
Q

Urgent management
Addisonian crisis

A

Establish IV line with IV fluids

Hydrocortisone sodium succinate 100 mg IV initially and 50-100 mg 4-6 hourly until stable

Arrange urgent hospital admission

62
Q

Clinical features of Cushings

A

Proximal muscle wasting and weakness

Central obesity, buffalo

hump on neck

Cushing facies: plethora, moon face, acne

Weakness

Hirsutism

Abdominal striae

Thin skin, easy bruising

Hypertension

Hyperglycaemia (30%)

Menstrual changes (e.g. amenorrhoea)

Osteoporosis

Psychiatric changes, especially depression

Backache

63
Q

DxT plethoric moon face + thin extremities + muscle weakness -

A

Cushing
syndrome

64
Q

Cushing syndrome
The five main causes are:

A

iatrogenic- chronic corticosteroid administration

pituitary ACTH excess (Cushing disease)

bilateral adrenal hyperplasia

adrenal tumour (adenoma, adenocarcinoma)

ectopic ACTH or (rarely) corticotrophin-releasing hormone (CRH) from non-endocrine
tumours (e.g. oat cell carcinoma of lung).

65
Q

Diagnosis (apart from iatrogenic cause
Cushing syndrome

A

Cortisol excess (plasma or 24-hour urinary cortisol)

Dexamethasone suppression test

Late night salivary cortisol (2 measurements)

Inferior petrosal sinus sampling

Serum ACTH

Radiological localisation; MRI for ACTH-producing pituitary tumours; CT scanning for
adrenal tumours

66
Q

Management
Cushing syndrome

A

Transsphenoidal excision of pituitary tumour

Ketoconazole (o) is first line.
.

67
Q

Most commonly due to an adrenal adenoma

A

Primary hyperaldosteronism

68
Q

Conn syndrome
Usually asymptomatic and hypertensive but any symptoms are features of hypokalaemia:

A

weakness, headaches
palpitations
cramps
paraesthesia
polyuria and polydipsia

69
Q

Investigations
Conn syndrome

A

Aldosterone (serum and urine) 1
Plasma renin !
Plasma aldosterone to renin activity ratio
Na t, K !, alkalosis
Imaging (MRI or CT scan) of adrenals

70
Q

Treatment
Conn syndrome

A

Spironolactone to prepare for
surgery.

71
Q

DxT episodic headache + sweating + tachycardia -

A

Phaeochromocytoma

72
Q

Investigations
Phaeochromocytoma

A

Series of three 24-hour free catecholamines 1 VMA
Abdominal CT or MRI scan (both highly sensitive)

73
Q

Treatment
Phaeochromocytoma

A

Excise tumour cover with alpha and beta blockers

74
Q

An AR condition with 21-hydroxylase deficiency being the most common of several forms,.

There is inadequate synthesis of cortisol and aldosterone with increased androgenisation.

Major
problem is adrenal failure + salt-losing state (SLS).

In females, ambiguity of external genitalia
and hirsutism before puberty usually occurs.

Males may have normal urogenital development but
SLS is a concern.

Infants of either sex may present with failure to thrive or vomiting and
dehydration (SLS).

A

Congenital adrenal hyperplasia (adrenogenital
syndrome)

75
Q

Treatment
Congenital adrenal hyperplasia (adrenogenital
syndrome)

A

Lifelong glucocorticoid treatment (e.g. prednisolone) is required.

76
Q

DXT weakness + constipation + polyuria

A

hypercalcaemia

77
Q

DXT cramps + confusion + tetany

A

hypocalcaemia

78
Q

is caused by an excessive secretion of parathyroid hormone and is usually
due to a parathyroid adenoma.

The classic clinical features
Due to the
effects of hypercalcaemia.

Classic mnemonic: bones, moans, stones, abdominal groans

A

Primary hyperparathyroidism’

79
Q

Diagnosis
Primary
hyperparathyroidism

A

Exclusion of other causes of hypercalcaemia

Serum parathyroid hormone (elevated)

TC-99m Sestamibi scan to detect tumour

80
Q

Causes include parathyroid injury, autoimmune hyperparathyroidism, severe vitamin D
deficiency and neonates of mothers with hypercalcaemia,

This usually presents with tetany or
more generalised neuromuscular hyperexcitability and neuropsychiatric manifestations.

The
sensory equivalents are paraesthesia in the hands, feet and around the mouth (distinguish from
tetany seen in the respiratory alkalosis of hyperventilation).
There may be seizures and cramps.

A

Hypocalcaemia

81
Q

Hypocalcaemia
The diagnosis is by

A

measurement of serum total calcium concentration in relation to serum
albumin (s. calcium <2.10 mmol/L).

82
Q

Hypocalcaemia
Two important signs are:

occlusion of the brachial artery with BP cuff precipitates carpopedal spasm
(wrist flexion and fingers drawn together

A

Trousseau sign: )

83
Q

Hypocalcaemia
Two important signs are

tapping over parotid (facial nerve) causes twitching in facial muscles

A

Chvostek sign:

84
Q

It is the most common cause of hypocalcaemia.

Causes include postoperative
thyroidectomy and parathyroidectomy, congenital deficiency (DiGeorge syndrome) and
idiopathic (autoimmune) hypoparathyroidism.

The main features are neuromuscular
hyperexcitability, tetany and neuropsychiatric manifestations.

A

Hypoparathyroidism

85
Q
A

Hypernatreamia >145mmol/L

86
Q
A

Hyponatreamia <135mmol/L

87
Q
A

Hyperkalemia >5.5 mmol

88
Q
A

Hypokalemia <3.5 mmol

89
Q
A

Chings Notes (39 decks)

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