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Endocrine Flashcards

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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
Histological appearance of Grave's Disease?
``` hyperplasia hypertrophy papillary infoldings scalloping of colloid lymphoid infiltrate ```
26
Causes of hypothyroidism?
Autoimmune- Hashimoto's Disease Post-ablative- surgery, radiation, radioactive iodine Others- severe iodine deficiency, metabolism errors, drugs
27
Symptoms of hypothyroidism?
tiredness, cold intolerance, mental and physical slowing, weight gain, constipation, depression, muscle aches, dry and scaly skin, brittle nails and hair, cretinism
28
Hypothyroidism on blood tests?
Low T3, T4 | High TSH
29
Hashimoto's Thyroiditis presentation?
Painless Diffuse enlarged gland (early) | Shrunken fibrosed gland (late)
30
Histology of Hashimoto's?
lymphocytic infiltrate with germinal centres hurthle cell change fibrosis
31
What appears as a hot nodule on radioactive iodine scan?
toxic adenoma | toxic nodule in MNG
32
What appears as a cold nodule on radioactive iodine scan?
neoplasms | cysts
33
What appears as a diffuse increased uptake?
Grave's Disease
34
What appears as a diffuse decreased uptake?
Thyroiditis
35
How does a MNG appear on radioactive iodine scan?
Patchy, irregular uptake
36
Neoplasms of the thyroid?
Adenomas- follicular Carcinomas- follicular, papillary, medullary, anaplastic Others- lymphoma, mets
37
What percentage of follicular adenomas are toxic?
1%
38
Presentation of follicular adenoma?
Encapsulated follicular lesion
39
Reasons to favour follicular adenoma as a diagnosis rather than adenomatoid nodule?
``` single completely encapsulated dissimilar to adjacent thyroid composed of follicles smaller than adjacent thyroid compresses adjacent tissue ```
40
What differentiates follicular adenoma from follicular carcinoma?
No capsular or vascular invasion in follicular adenoma
41
Follicular Carcinoma features?
``` follicular pattern looks like follicular adenoma vascular invasion capsular invasion mets ```
42
Spread of follicular carcinoma?
doesn't usually spread to LNs | liver, lung, brain, bone
43
Treatment of follicular carcinoma?
Surgery, Iodine 131, thyroxine
44
Papillary Carcinoma features?
Presents from 20yrs onwards LN mets early blood spread uncommon and late good prognosis
45
Papillary carcinoma histologically?
papillary or follicular pattern | nuclear features key to diagnosis
46
Treatment of papillary carcinoma?
Surgery, Iodine 131, thyroxine
47
Nuclear features of papillary carcinoma?
``` enlargement overlapping grooves nuclear inclusions smooth chromatin pattern 'Orphan Annie' nuclei Psammoma bodies/calcifications ```
48
What percentage of thyroid malignancies are medullary carcinomas?
5-10%
49
What cells do medullary carcinomas evolve from?
neuroendocrine C cells
50
What is elevated in medullary carcinomas?
Calcitonin
51
What does elevated calcitonin indicate?
Medullary Carcinoma
52
Causes of medullary carcinoma?
80% sporadic MEN 2A or 2B Familial medullary carcinoma
53
Outcome of thyroid cancers?
Papillary carcinoma- fatality 5% Follicular carcinoma- fatality 20% Medullary carcinoma- fatality 50%
54
What percentage of thyroid malignancies are anaplastic?
5-10%
55
Prognosis for anaplastic carcinoma?
Dismal, mortality >95%
56
Mutations involved in thyroid malignancies?
BRAF RAS RET/PTC PAX8/PPAR
57
Does RAS mutation distinguish between benign and malignant?
No 20% of follicular adenomas have RAS mutation 40% of follicular carcinomas have it too
58
What does PTH do?
Increases blood calcium levels
59
How does PTH increase blood calcium levels?
``` 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
What happens if blood calcium level is too high?
Thyroid releases calcitonin
61
What happens if blood calcium level is too low?
Parathyroid releases PTH
62
Primary causes of hyperparathyroidism?
Adenoma (80%) Hyperplasia Carcinoma (rare)
63
Secondary causes of hyperparathyroidism?
CKD | response to hypocalcaemia
64
Tertiary cause of hyperparathyroidism?
Autonomous production of PTH
65
How do primary, secondary and tertiary hyperparathyroidism present?
Primary- elevated Ca and PTH Secondary- normal Ca, elevated PTH Tertiary- elevated Ca and PTH
66
Symptoms of primary hyperparathyroidism?
Bones, stones, groans and moans
67
How to distinguish between adenoma and hyperplasia?
Adenoma- normal gland, compressed rim of parathyroid gland at the periphery
68
What causes T1DM?
autoimmune destruction of the beta cells in the islets of langerhan in the pancreas
69
What HLAs are associated with T1DM?
HLA-DR3 and HLA-DR4
70
Clinical features of T1DM?
``` young patient thin polydipsia polyuria visual blurring dehydration DKA ```
71
2 key components to T2DM?
reduced ability of tissues to respond to insulin (obesity) | beta cell dysfunction (initially qualitative, followed by quantitative)
72
Clinical features of T2DM?
``` middle-aged high BMI sedentary lifestyle HTN Hypercholesterolaemia may be asymptomatic (GP screening) may present with advanced complications ```
73
Complications of DM?
``` Macrovascular Microvascular DKA HONK Hypoglycaemia ```
74
Macrovascular complications of DM?
atherosclerosis MI stroke peripheral vascular disease
75
Microvascular complications of DM?
Diabetic retinopathy Diabetic nephropathy Diabetic neuropathy
76
Features of diabetic retinopathy?
``` thickening of BM leaky capillaries oedema microhaemorrhages exudate ```
77
Two types of DR?
Non-proliferative (early) | Proliferative (later, angiogenesis)
78
3 main lesions in diabetic nephropathy?
Glomerular lesions Renal vascular lesions Pyelonephritis
79
What type of glomerular lesion is seen in DNephropathy?
nodular glomerulosclerosis/Kimmelsteil-Wilson lesions
80
What is seen in renal vascular lesions due to diabetes?
hyaline arteriosclerosis
81
What is seen in diabetic pyelonephritis?
Papillary necrosis
82
What causes diabetic neuropathy?
toxic effects on neurons due to oxidative stress related to hyperglycaemia
83
3 types of Diabetic Neuropathy?
Diffuse- Distal symmetrical sensorimotor polyneuropathy Focal- mononeuropathy (cranial) Diabetic autonomic neuropathy
84
What causes HONK?
decrease in extracellular fluid level, may be precipitated by infection, dehydration etc.
85
Treatment of HONK?
Fluid resuscitation with K and insulin
86
Risk factors for hypoglycaemia?
``` 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
Hypoglycaemia treatment?
If conscious, oral glucose | If unconscious, IV glucose
88
What does the adrenal cortex produce?
aldosterone, cortisol, sex hormones
89
What does the adrenal medulla produce?
catecholamines (adrenaline, noradrenaline)
90
What is Addison's disease?
primary adrenal insufficiency
91
When does Addison's disease become symptomatic?
When >90% of the cortex has been destroyed
92
Presentation of Addison's disease?
``` insidious onset progressive weakness, fatigue GI disturbances hyperpigmentation Hyperkalaemia, hyponatremia, volume depletion hypotension ```
93
Pathology of Addison's Disease?
adrenal gland is shrunken in autoimmune disease | adrenal gland is enlarged in infection, mets
94
How does acute adrenal insufficiency present?
intractable vomiting, abdominal pain, hypotension, coma, vascular collapse
95
Treatment of acute adrenal insufficiency?
Steroid ASAP | or else death
96
What causes secondary hypoadrenalism?
any cause if hypothalamic or pituitary loss of function
97
What distinguishes primary from secondary hypoadrenalism?
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
What causes Cushing's syndrome?
cortisol excess
99
Symptoms of Cushing's syndrome?
``` moon facies buffalo hump hirsutism easy bruising HTN proximal muscle weakness menstrual abnormalities DM osteoporosis ```
100
Most common cause of Cushing's syndrome?
Exogenous steroids
101
Endogenous causes of Cushing's syndrome?
pituitary adenoma (Cushing's disease) cortisol hypersecretion due to adrenal tumour or hyperplasia ectopic ACTH secretion due to neoplasm e.g., lung
102
Diagnosis of Cushing's Syndrome?
increased free cortisol in urine lack of diurnal rhythm failure to suppress cortisol (low dexamethasone suppression test, high dexamethasone suppression test)
103
Results of dexamethasone suppression test?
``` 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
Adrenal appearance in Cushing's syndrome?
``` cortical atrophy (exogenous steroids) diffuse or nodular hyperplasia (endogenous causes) mass present (adenoma or carcinoma) ```
105
Main cause of primary hyperaldosteronism?
cortical adenoma (>90% are Conn's syndrome)
106
What is Conn's syndrome?
primary hyperaldosteronism | most often caused by adrenal adenoma
107
Features of Conn's syndrome?
Low K Inc. Na Oedema HTN
108
Causes of secondary hyperaldosteronism?
activation of RAS renal artery stenosis arterial hypovolemia/oedema
109
Causes of adrenogenital syndromes?
Excess production of adrenal androgens: adrenocortical neoplasms congenital adrenal hyperplasia bilateral nodular hyperplasia (e.g., Cushings)
110
What causes congenital adrenal hyperplasia?
21 hydroxylase deficiency
111
Adrenal neoplasms?
Cortex- adenoma, carcinoma | Medulla- neuroblastoma, pheochromocytoma
112
What score is used to differentiate between adenoma and carcinoma?
WEISS score | >3 indicates carcinoma
113
WEISS score criteria?
``` mitotic activity atypical mitoses nuclear pleomorphism absence of clear cells diffuse architecture necrosis capsular invasion venous invasion sinusoidal invasion ```
114
When do the majority of neuroblastomas occur?
<5 years of age
115
Prognosis of neuroblastoma is related to?
Age (younger=better) Stage Histological features Genetic factors
116
What genetic factors indicate a poorer prognosis for neuroblastomas?
N-Myc gene amplification | Chr 17q gain, 1p loss
117
How does a neuroblastoma present?
small round blue cell tumour | neurosecretory granules
118
What do pheochromocytomas produce?
Catecholamines
119
Presentation of pheochromocytomas?
HTN, palpitations, flushing
120
Diagnosis of pheochromocytomas?
Elevated serum catecholamine | Elevated urine catecholamines and VMA
121
What percentage of pheochromocytomas are malignant?
10%
122
What percentage of pheochromocytomas are familial related and what conditions are involved?
``` 10% MEN 2a and 2b Von Hippau Lindel syndrome neurofibromatosis sturge weber familial SDH mutations ```
123
What is Sheehan Syndrome?
maternal hypopituitarism caused by excessive blood loss during or after the delivery of a baby
124
What bone condition is associated with hyperparathyroidism?
Osteo fibrosa cystica

Pathology (13 decks)

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