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Pathology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What does the anterior pituitary gland produce?

A 
Growth Hormone
Adenocortico-tropic Hormone
Follicle Stimulating Hormone
Luteinizing Hormone
Prolactin
TSH
Melanocyte Stimulating Hormone
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2
Q

What does the posterior pituitary gland produce?

A

ADH (vasopressin)

Oxytocin

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3
Q

HPA Axis includes?

A

Hypothalamus
Anterior Pituitary
Adrenal Cortex

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4
Q

Types of pituitary neoplasms?

A

Adenomas
Carcinomas (v rare)
Mets (breast, lung, GIT)

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5
Q

Features of pituitary adenomas?

A

most are small/incidental
functioning: effects vary
non-functioning: pressure effects, hypopituitarism

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6
Q

Most common cause of hyperpituitarism?

A

Pituitary adenoma

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7
Q

Most common pituitary adenomas?

A

Prolactinomas
GH adenomas
ACTH cell adenomas

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8
Q

Who are prolactinomas most frequently diagnosed in?

A

most commonly in menstruating women- their period stops

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9
Q

What is the most common pituitary adenoma?

A

Prolactinoma

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10
Q

Symptoms of GH adenomas?

A

Inc. growth- bone and soft tissue

‘sausage digits’

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11
Q

ACTH adenoma causes what?

A

Cushing’s Disease

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12
Q

Causes of hypopituitarism?

A

surgery
irradiation
apoplexy/ischaemia
pressure effects of neoplasm

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13
Q

Diagnosis of hypopituitarism?

A

low serum corticosteroid levels

normal response to ACTH

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14
Q

Deficiency of ADH causes?

A

Diabetes Insipidus

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15
Q

Excess of ADH causes?

A

SIADH

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16
Q

Most common cause of goitre?

A

Dietary iodine deficiency

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17
Q

2 types of goitre are?

A

Diffuse (non-toxic) simple goitre

Multi-nodular goitre

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18
Q

Abrupt enlargement of goitre most likely cause?

A

Haemorrhage

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19
Q

Symptoms of hyperthyroidism?

A

palpitations, weight loss, inc. appetite, nervousness, sweating, heat intolerance, diarrhoea, arrhythmias, osteoporosis, exophthalmos (Grave’s)

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20
Q

Hyperthyroidism presentation in bloods?

A

Elevated T3, T4

Low TSH

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21
Q

Causes of hyperthyroidism?

A

Grave’s Disease
Multi-Nodular Goitre with toxic nodule
Toxic adenoma

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22
Q

Most common cause of hyperthyroidism?

A

Grave’s Disease (85%)

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23
Q

Grave’s Disease symptoms?

A

Hyperthyroidism
Exophthalmos
Pretibial myxoedema

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24
Q

Grave’s Disease mechanism?

A

Anti TSH receptor antibodies

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25
Q

Histological appearance of Grave’s Disease?

A 
hyperplasia
hypertrophy
papillary infoldings
scalloping of colloid
lymphoid infiltrate
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26
Q

Causes of hypothyroidism?

A

Autoimmune- Hashimoto’s Disease
Post-ablative- surgery, radiation, radioactive iodine
Others- severe iodine deficiency, metabolism errors, drugs

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27
Q

Symptoms of hypothyroidism?

A

tiredness, cold intolerance, mental and physical slowing, weight gain, constipation, depression, muscle aches, dry and scaly skin, brittle nails and hair, cretinism

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28
Q

Hypothyroidism on blood tests?

A

Low T3, T4

High TSH

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29
Q

Hashimoto’s Thyroiditis presentation?

A

Painless Diffuse enlarged gland (early)

Shrunken fibrosed gland (late)

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30
Q

Histology of Hashimoto’s?

A

lymphocytic infiltrate with germinal centres
hurthle cell change
fibrosis

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31
Q

What appears as a hot nodule on radioactive iodine scan?

A

toxic adenoma

toxic nodule in MNG

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32
Q

What appears as a cold nodule on radioactive iodine scan?

A

neoplasms

cysts

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33
Q

What appears as a diffuse increased uptake?

A

Grave’s Disease

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34
Q

What appears as a diffuse decreased uptake?

A

Thyroiditis

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35
Q

How does a MNG appear on radioactive iodine scan?

A

Patchy, irregular uptake

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36
Q

Neoplasms of the thyroid?

A

Adenomas- follicular
Carcinomas- follicular, papillary, medullary, anaplastic
Others- lymphoma, mets

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37
Q

What percentage of follicular adenomas are toxic?

A

1%

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38
Q

Presentation of follicular adenoma?

A

Encapsulated follicular lesion

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39
Q

Reasons to favour follicular adenoma as a diagnosis rather than adenomatoid nodule?

A 
single
completely encapsulated
dissimilar to adjacent thyroid
composed of follicles smaller than adjacent thyroid
compresses adjacent tissue
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40
Q

What differentiates follicular adenoma from follicular carcinoma?

A

No capsular or vascular invasion in follicular adenoma

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41
Q

Follicular Carcinoma features?

A 
follicular pattern
looks like follicular adenoma
vascular invasion
capsular invasion
mets
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42
Q

Spread of follicular carcinoma?

A

doesn’t usually spread to LNs

liver, lung, brain, bone

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43
Q

Treatment of follicular carcinoma?

A

Surgery, Iodine 131, thyroxine

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44
Q

Papillary Carcinoma features?

A

Presents from 20yrs onwards
LN mets early
blood spread uncommon and late
good prognosis

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45
Q

Papillary carcinoma histologically?

A

papillary or follicular pattern

nuclear features key to diagnosis

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46
Q

Treatment of papillary carcinoma?

A

Surgery, Iodine 131, thyroxine

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47
Q

Nuclear features of papillary carcinoma?

A 
enlargement
overlapping
grooves
nuclear inclusions
smooth chromatin pattern
'Orphan Annie' nuclei
Psammoma bodies/calcifications
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48
Q

What percentage of thyroid malignancies are medullary carcinomas?

A

5-10%

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49
Q

What cells do medullary carcinomas evolve from?

A

neuroendocrine C cells

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50
Q

What is elevated in medullary carcinomas?

A

Calcitonin

51
Q

What does elevated calcitonin indicate?

A

Medullary Carcinoma

52
Q

Causes of medullary carcinoma?

A

80% sporadic
MEN 2A or 2B
Familial medullary carcinoma

53
Q

Outcome of thyroid cancers?

A

Papillary carcinoma- fatality 5%
Follicular carcinoma- fatality 20%
Medullary carcinoma- fatality 50%

54
Q

What percentage of thyroid malignancies are anaplastic?

A

5-10%

55
Q

Prognosis for anaplastic carcinoma?

A

Dismal, mortality >95%

56
Q

Mutations involved in thyroid malignancies?

A

BRAF
RAS
RET/PTC
PAX8/PPAR

57
Q

Does RAS mutation distinguish between benign and malignant?

A

No
20% of follicular adenomas have RAS mutation
40% of follicular carcinomas have it too

58
Q

What does PTH do?

A

Increases blood calcium levels

59
Q

How does PTH increase blood calcium levels?

A 
increase resorption of bone
increase Ca absorption from GIT
increase Ca reabsorption from kidneys
increase urinary excretion of PO4
enhances action of Vit D
60
Q

What happens if blood calcium level is too high?

A

Thyroid releases calcitonin

61
Q

What happens if blood calcium level is too low?

A

Parathyroid releases PTH

62
Q

Primary causes of hyperparathyroidism?

A

Adenoma (80%)
Hyperplasia
Carcinoma (rare)

63
Q

Secondary causes of hyperparathyroidism?

A

CKD

response to hypocalcaemia

64
Q

Tertiary cause of hyperparathyroidism?

A

Autonomous production of PTH

65
Q

How do primary, secondary and tertiary hyperparathyroidism present?

A

Primary- elevated Ca and PTH
Secondary- normal Ca, elevated PTH
Tertiary- elevated Ca and PTH

66
Q

Symptoms of primary hyperparathyroidism?

A

Bones, stones, groans and moans

67
Q

How to distinguish between adenoma and hyperplasia?

A

Adenoma- normal gland, compressed rim of parathyroid gland at the periphery

68
Q

What causes T1DM?

A

autoimmune destruction of the beta cells in the islets of langerhan in the pancreas

69
Q

What HLAs are associated with T1DM?

A

HLA-DR3 and HLA-DR4

70
Q

Clinical features of T1DM?

A 
young patient
thin
polydipsia
polyuria
visual blurring
dehydration
DKA
71
Q

2 key components to T2DM?

A

reduced ability of tissues to respond to insulin (obesity)

beta cell dysfunction (initially qualitative, followed by quantitative)

72
Q

Clinical features of T2DM?

A 
middle-aged
high BMI
sedentary lifestyle
HTN
Hypercholesterolaemia
may be asymptomatic (GP screening)
may present with advanced complications
73
Q

Complications of DM?

A 
Macrovascular
Microvascular
DKA
HONK
Hypoglycaemia
74
Q

Macrovascular complications of DM?

A

atherosclerosis
MI
stroke
peripheral vascular disease

75
Q

Microvascular complications of DM?

A

Diabetic retinopathy
Diabetic nephropathy
Diabetic neuropathy

76
Q

Features of diabetic retinopathy?

A 
thickening of BM
leaky capillaries
oedema
microhaemorrhages
exudate
77
Q

Two types of DR?

A

Non-proliferative (early)

Proliferative (later, angiogenesis)

78
Q

3 main lesions in diabetic nephropathy?

A

Glomerular lesions
Renal vascular lesions
Pyelonephritis

79
Q

What type of glomerular lesion is seen in DNephropathy?

A

nodular glomerulosclerosis/Kimmelsteil-Wilson lesions

80
Q

What is seen in renal vascular lesions due to diabetes?

A

hyaline arteriosclerosis

81
Q

What is seen in diabetic pyelonephritis?

A

Papillary necrosis

82
Q

What causes diabetic neuropathy?

A

toxic effects on neurons due to oxidative stress related to hyperglycaemia

83
Q

3 types of Diabetic Neuropathy?

A

Diffuse- Distal symmetrical sensorimotor polyneuropathy
Focal- mononeuropathy (cranial)
Diabetic autonomic neuropathy

84
Q

What causes HONK?

A

decrease in extracellular fluid level, may be precipitated by infection, dehydration etc.

85
Q

Treatment of HONK?

A

Fluid resuscitation with K and insulin

86
Q

Risk factors for hypoglycaemia?

A 
Tight glucose control
Alcohol
Insulin prescription error
Long history of diabetes
renal dialysis
malabsorption
drugs
lack of anti-insulin hormone function (Addison's, hypothyroidism)
87
Q

Hypoglycaemia treatment?

A

If conscious, oral glucose

If unconscious, IV glucose

88
Q

What does the adrenal cortex produce?

A

aldosterone, cortisol, sex hormones

89
Q

What does the adrenal medulla produce?

A

catecholamines (adrenaline, noradrenaline)

90
Q

What is Addison’s disease?

A

primary adrenal insufficiency

91
Q

When does Addison’s disease become symptomatic?

A

When >90% of the cortex has been destroyed

92
Q

Presentation of Addison’s disease?

A 
insidious onset
progressive weakness, fatigue
GI disturbances
hyperpigmentation
Hyperkalaemia, hyponatremia, volume depletion
hypotension
93
Q

Pathology of Addison’s Disease?

A

adrenal gland is shrunken in autoimmune disease

adrenal gland is enlarged in infection, mets

94
Q

How does acute adrenal insufficiency present?

A

intractable vomiting, abdominal pain, hypotension, coma, vascular collapse

95
Q

Treatment of acute adrenal insufficiency?

A

Steroid ASAP

or else death

96
Q

What causes secondary hypoadrenalism?

A

any cause if hypothalamic or pituitary loss of function

97
Q

What distinguishes primary from secondary hypoadrenalism?

A

no hyperpigmentation in secondary
normal aldosterone synthesis-> K and Na are normal
low levels of both ACTH and cortisol
rise is seen in cortisol levels after exogenous ACTH given

98
Q

What causes Cushing’s syndrome?

A

cortisol excess

99
Q

Symptoms of Cushing’s syndrome?

A 
moon facies
buffalo hump
hirsutism
easy bruising
HTN
proximal muscle weakness
menstrual abnormalities
DM
osteoporosis
100
Q

Most common cause of Cushing’s syndrome?

A

Exogenous steroids

101
Q

Endogenous causes of Cushing’s syndrome?

A

pituitary adenoma (Cushing’s disease)
cortisol hypersecretion due to adrenal tumour or hyperplasia
ectopic ACTH secretion due to neoplasm e.g., lung

102
Q

Diagnosis of Cushing’s Syndrome?

A

increased free cortisol in urine
lack of diurnal rhythm
failure to suppress cortisol (low dexamethasone suppression test, high dexamethasone suppression test)

103
Q

Results of dexamethasone suppression test?

A 
pituitary adenoma (initial serum levels of ACTH- high, urine steroids following high dose dex.- suppressed)
ectopic ACTH (initial serum levels of ACTH- v high, not suppressed)
adrenocortical neoplasm (initial serum levels of ACTH- v low, not suppressed)
104
Q

Adrenal appearance in Cushing’s syndrome?

A 
cortical atrophy (exogenous steroids)
diffuse or nodular hyperplasia (endogenous causes)
mass present (adenoma or carcinoma)
105
Q

Main cause of primary hyperaldosteronism?

A

cortical adenoma (>90% are Conn’s syndrome)

106
Q

What is Conn’s syndrome?

A

primary hyperaldosteronism

most often caused by adrenal adenoma

107
Q

Features of Conn’s syndrome?

A

Low K
Inc. Na
Oedema
HTN

108
Q

Causes of secondary hyperaldosteronism?

A

activation of RAS
renal artery stenosis
arterial hypovolemia/oedema

109
Q

Causes of adrenogenital syndromes?

A

Excess production of adrenal androgens:
adrenocortical neoplasms
congenital adrenal hyperplasia
bilateral nodular hyperplasia (e.g., Cushings)

110
Q

What causes congenital adrenal hyperplasia?

A

21 hydroxylase deficiency

111
Q

Adrenal neoplasms?

A

Cortex- adenoma, carcinoma

Medulla- neuroblastoma, pheochromocytoma

112
Q

What score is used to differentiate between adenoma and carcinoma?

A

WEISS score

>3 indicates carcinoma

113
Q

WEISS score criteria?

A 
mitotic activity
atypical mitoses
nuclear pleomorphism
absence of clear cells
diffuse architecture
necrosis
capsular invasion
venous invasion
sinusoidal invasion
114
Q

When do the majority of neuroblastomas occur?

A

<5 years of age

115
Q

Prognosis of neuroblastoma is related to?

A

Age (younger=better)
Stage
Histological features
Genetic factors

116
Q

What genetic factors indicate a poorer prognosis for neuroblastomas?

A

N-Myc gene amplification

Chr 17q gain, 1p loss

117
Q

How does a neuroblastoma present?

A

small round blue cell tumour

neurosecretory granules

118
Q

What do pheochromocytomas produce?

A

Catecholamines

119
Q

Presentation of pheochromocytomas?

A

HTN, palpitations, flushing

120
Q

Diagnosis of pheochromocytomas?

A

Elevated serum catecholamine

Elevated urine catecholamines and VMA

121
Q

What percentage of pheochromocytomas are malignant?

A

10%

122
Q

What percentage of pheochromocytomas are familial related and what conditions are involved?

A 
10%
MEN 2a and 2b
Von Hippau Lindel syndrome
neurofibromatosis
sturge weber
familial SDH mutations
123
Q

What is Sheehan Syndrome?

A

maternal hypopituitarism caused by excessive blood loss during or after the delivery of a baby

124
Q

What bone condition is associated with hyperparathyroidism?

A

Osteo fibrosa cystica

Pathology (13 decks)

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