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Pathology Term 3 > Week 2 - ENDOCRINE > Flashcards

Week 2 - ENDOCRINE Flashcards

Pituitary, Thyroiditis

1
Q

From what does the anterior and posterior pituitary develop from?

A

Anterior:
-rathke’s pouch (epithelium of nasal cavity)

Posterior:
-diencephalon (neural crest)

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2
Q

What are the 3 types of cells present in the anterior pituitary?

A
  1. basophilic (blue cells)
  2. acidophilic (red cells)
  3. chromophobes (clear cells)
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3
Q

What structures are present in the posterior pituitary?

A
  • astrocytes

- axons

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4
Q

What is the commonest pituitary disorder (hyperpituitarism)?

A 
prolactinoma --> lactotroph
-adenoma
galactorrhoea
-amenorrhoea (females)
-sexual dysfunction/infertility

*no. 2 = somatotroph (GH) –> gigantism/acromegaly

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5
Q

What are the 6 cells/adenomas in pituitary, there respective hormones, and associated Sx.?

A
  1. lactotroph –> prolactin –> glactorrhoea, amenorrhoea, infertility
  2. somatotroph –> GH –> gigantism (kids), acromegaly (adults)
  3. mammosomatotroph –> GH + PRL –> combined PRL + GH Sx.
  4. corticotroph –> ACTH –> cushing’s, nelson’s syndrome
  5. thyrotroph –> TSH –> secondary hypothyroidism
  6. gonadotroph –> FSH/LH –> hypogonadism + hypopituitarism
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6
Q

What is the commonest cause of hypopituitarism?

A
  • injury
  • trauma
  • tumour
  • infarction
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7
Q

Why will women typically have increased hormone-related features and men have increased tumour-related features in prolactinomas? and what are these features?

A
  • microadenomas increased in females (90%) - <10mm
  • macroadenomas increased in males (10%) - >10mm
  • micro = functional/macro = non-functional
  • F –> hormone –> amenorrhoea, galactorrhoea, infertility
  • M –> tumour –> headache, visual loss, hypogonadism, infetility
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8
Q

What is the microscopy of pituitary adenomas?

A

-uniform ONE type of cells –> compared to normal when there are 3 types of cells (acidophilic, basophilic, chromophobes)

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9
Q

How does GH cause clinical features in somatotroph adenoma?

A

GH induces insulin-like growth factor 1 (somatomedin C) –> clinical features

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10
Q

What are the clinical features of acromegaly?

A
  • long arms/legs
  • prominent lower jaw
  • large hands/feet
  • DM, CCF, arthritis, HTN
  • increased head circumference
  • prominent supraorbital ridges
  • organomegaly/cardiomegaly
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11
Q

True or False?

Physiologically, during pregnancy there is hypertrophy of anterior pituitary

A

True

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12
Q

What is Sheehan’s syndrome, its Sx and Tx.?

A

Post-partum anterior pituitary necrosis
-shock/bleeding –> necrosis of hypophyseal portal system –> hypopituitarism

Sx: - inability to breastfeed, severe fatigue/depression, lack of menstrual bleeding, loss of pubic/axillary hair, decreased BP

Tx: replace ant. pituitary hormones

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13
Q

What % of anterior pituitary loss leads to hypopituitarism?

A

75% (with or wihtout post. pituitary loss)

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14
Q

What are the clinical features of hypopituitarism?

A

*BASED ON HORMONE INVOLVED

GH: - pituitary dwarfism (proportional)
FSH/LH: - infertility, impotence
TSH: - hypothyroidism
MSH: - pallor (melanocytes)
ACTH: - hypo-adrenalism

Post. pituitary: - diabetes insipidus (decr. ADH)

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15
Q

When do we suspect hypothalamic disorder in hypopituitarism?

A

When there is COMBINED anterior and posterior features (i.e. including D. insipidus)

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16
Q

What are the 2 main posterior pituitary disorders?

A
  1. SIADH:
    - increased ADH (decreased urine output)
    - water intoxication
    - hyponatremia
    - high urine osmolality
  2. Diabetes Insipidus:
    - decreased ADH (increased urine output)
    - dehydration
    - hypernatremia
    - high serum osmolality
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17
Q

What are C cells?

A
  • calcitonin producing cells found in between thyroid gland follicles
  • calcitonin = bone forming (opposite to PTH)
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18
Q

What are the normal morphological features of the thyroid?

A
  • cuboidal cells
  • plenty of colloid (location of thyroglobulin protein)
  • few vacuoles –> reflect levels of activity
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19
Q

What do presence of vacuoles on microscopy of thyroid reflect?

A

ACTIVITY

  • increased vacuoles = hyperthyroid
  • no vacuoles = hypothyroid
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20
Q

What is microscopic features of hyper and hypothyroidism?

A

HYPER:

  • reabsorption of colloid
  • markedly increased vacuolisation –> therefore increased T3/T4 release

HYPO:

  • no vacuoles (no activity)
  • colloid becomes solid with no vacuolisation
  • epithelial cell degeneration
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21
Q

What is the pathogenesis of exopthalmos in hyperthyroidism?

A
  • autoimmune-mediated inflammatory process of the orbital tissues, predominantly affecting the fat and extraocular muscles
  • deposition of glycosaminoglycans (GAG) and water infulx increases the orbital contents
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22
Q

What are the clinical features of hyperthyroidism?

A
  • anxiety
  • exopthalmos
  • hypermetabolism (wt. loss, diarrhoea, osteoporosis, myopathy)
  • goitre
  • hair loss
  • CVS –> tachycardia, palpitations, AF
  • menorrhagia
  • warm, moist palms; fine tremor
  • pretibial myxoedema
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23
Q

What are the commonest causes of hyperthyroidism?

A
  1. primary, autoimmune (GRAVES)

2. iodine excess; toxic change in a tumour

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24
Q

What is thyroid storm?

A

acute, sudden severe complication of hyperthyroidism

  • fever
  • tachycardia
  • AF
  • arrhythmias
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25
Q

What are the clinical features of hypothyroidism?

A
  • hypometabolism –> wt. gain, apathy/depression, constipation, weakness
  • non-pitting oedema –> pretibial myxoedema
  • dry hair, loss of outer 1/3 of eyebrows
  • CVS –> bradycardia, IHD, ECG changes
  • decreased sweating
  • goitre/deafness ?
  • dry, cold skin –> cold insensitivity
  • myxoedemic face
  • hoarseness (gruff voice)
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26
Q

What is the commonest cause of hypothyroidism?

A
  1. primary, autoimmune (destructive) thyroiditis (HASHIMOTO’S)
  2. iodine deficiency
    - common in Himalayan/mountainous regions (decreased iodine in water)
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27
Q

What is cretinism and its features?

A

Hypothyroidism in infancy/childhood

  • mental retardation (severe)
  • protruding tongue
  • short stature (dwarf)
  • umbilical hernia
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28
Q

What are the characteristic features of hashimotos thyroiditis?

A
  1. thick, firm subcutaneous tissue
  2. non-pitting oedema (increased pretibial)
  3. dermatitis
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29
Q

What is the pathogenesis of Hashimoto’s thyroiditis?

A

Genetic: -HLA DR3/5, CTLA4, PTPN22
Environmental: -viral?
Autoimmunity: -TSI, anti-thyroglobulin and anti-thyroid peroxidase antibodies
-T cell mediated cytotoxicity
-thyrocyte injury (via activated macrophages)
-Ab-dependent cell-mediated cytotoxicity

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30
Q

What are the gross and microscopic features of Hashimoto’s thyroiditis?

A

Gross:

  • less vascular
  • pale
  • grey
  • lymph node-like
  • firm

Micro:

  • atrophy of thyroid follicles
  • plenty of lymphocytes
  • lymphoid follicles
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31
Q

What is the triad of clinical features seen in Graves disease and the causative antibody?

A
  • HYPERTHYROIDISM; vascular enlarged thyroid
  • infiltrative ophthalmopathy - EXOPTHALMOS
  • dermatopathy, PRETIBIAL MYXOEDEMA

*TSH receptor stimulating Ig (TSI/LATS)

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32
Q

What are the gross and microscopic features of Graves disease?

A

Gross:

  • increased vascularity (bruit on auscultation)
  • soft, smooth, red
  • hyperaemic
  • enlarged gland

Micro:

  • cells become prominent and columnar (cluster rather than single line of cuboidal cells)
  • marked vacuolisation within colloid
  • large follicles with papillary epithelial hyperplasia
  • pale, scanty, vacuolated colloid (increased activity)
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33
Q

What is subacute granulomatous thyroiditis?

A
  • subacute, PAINFUL, fever, fatigue
  • viral/post-viral
  • De Quervain thyroiditis
  • hyperthyroidism - but decr. iodine uptake (release)
  • heals with normal thyroid function
  • granulomas on microscopy
34
Q

What is subacute lymphocytic thyroiditis?

A
  • subacute, SILENT/PAINLESS
  • females, middle age, increased risk post-partum
  • initial thyrotoxicosis –> euthyroid in months
  • minority progress to hypothyroidism
35
Q

What will the TSH, free T3 and free T4 levels be like in Graves and Hashimotos?

A

Graves:
TSH - low
T3 - high/normal
T4 - high

Hashimoto’s
TSH - high
T3 - low/normal
T4 - low

36
Q

True or False?

TSH is most sensitive test and earliest subclinical abnormality

A

True

-do serum TSH levels over T3/T4 if thyroid abnormality is suspected

37
Q

Clinically, what is the most common thyroid tumour?

A 
Multinodular Goitre (MNG)
-hormone induced hyperplasia in response to decreased hormone
38
Q

What is the pathogenesis of multinodular goitre and why is there no change in thyroid function?

A

-sporadic (enzymes, drugs, food)
-endemic (iodeine deficiency)
*both result in decreased T3/T4 levels
THEREFORE –> increased TSH levels (proliferative hormone) –> gland HYPERPLASIA –> compensates for function –> EUTHYROID state

39
Q

What are clinical presentations for multinodular goitre?

A
  • mass effect (disfigurement)
  • dysphagia
  • SVC syndrome (if retrosternal expansion present)
40
Q

What is Plummer’s syndrome?

A

toxic change in one of the nodules in multinodular goitre whereby it begins to produce increased T3/T4

41
Q

What is the microscopy and characteristic feature on scan of multinodular goitre?

A

Micro:

  • nodular hyperplasia (which compresses BVs)
  • inflammation, haemorrhage, fibrosis, calcification

Scan:
-uneven iodine uptake

Prognosis –> small risk of follicular cancer

42
Q

What are 3 key microscopic features of multinodular goitre?

A
  1. nodules of hyperplastic follicles
  2. colloid-rich follicles
  3. inflammation, haemorrhage, fibrosis, necrosis, calcification
43
Q

Is multinodular goitre non-neoplastic or neoplastic?

A

non-neoplastic

44
Q

What is the commonest cause of thyroid enlargement?

A

multinodular goitre

45
Q

What is meant by thyroid adenomas being hot or cold?

A

When we do a radio-iodine scan:

  • if activity shown –> HOT nodule (usually benign)
  • if no activity shown –> COLD nodule (can also be malignant)
46
Q

What is the commonest thyroid carcinoma? and what are the others?

A 
Papillary carcinoma (85%)
-young (males), solitary nodule, good prognosis

also: -follicular carcinoma, medullary carcinoma, anaplastic carcinoma

47
Q

What is microscopy of papillary carcinoma?

A

papillary structures with fibrovascular cores

48
Q

True or False?

commonest type of thyroid ca. in pts with endemic goitre is follicular carcinoma

A

True

49
Q

Outline structure of adrenal gland

A

CORTEX: -glands

  1. Zona glomerulosa –> mineralocorticoids (aldost.)
  2. Zona fasciculata –> glucocorticoids (cortisone)
  3. Zona reticularis –> gonadocorticoids (andro/estro)

1–>3 (sup. –> deep) (GFR) - salty, sweet, sexy

MEDULLA: -neural

  • catecholamines
  • chromaffin cells + sympathetic nerve endings
50
Q

What is cushings syndrome vs. cushings disease? and what is the difference between resultant adrenal gland structure?

A

Cushings Syndrome:
-exogenous cause of increased glucocorticoids (i.e. chronic steroid therapy)

Cushings Disease:
-endogenous cause of increased glucocorticoids (i.e. pituitary ACTH adenoma - 70%)

Exogenous (syndrome) –> adrenal gland atrophy
Endogenous (disease) –> adrenal gland hypertrophy

51
Q

Besides pituitary ACTH adenoma (70%) what are the other causes of Cushings disease?

A
  • ectopic ACTH –> SCLC paraneoplastic synd. (10%)

- adrenal adenoma (10%), ca. (5%)

52
Q

What are the clinical features of Cushings disease?

A
  • HTN
  • central adiposity
  • myopathy
  • hyperglycemia (DM)
  • osteoporosis
  • moon face/buffalo hump
  • hair thinning
  • striae; easy bruising
  • tendency to infections
  • menstrual disturbance
  • renal stones
  • peptic ulcer
53
Q

What are diagnostic tests for Cushings syndrome and disease?

A
  • increased 24hr urine cortisol
  • loss of diurnal variation
  • SERUM ACTH* –> used to distinguish between exogenous (syndrome) and endogenous (disease)
  • exogenous = low ACTH
  • endogenous = high ACTH
54
Q

What are the 2 most common causes of primary hyperaldosteronism?

A
  1. idiopathic (60%)
    - nodular hyperplasia
    - later age, moderate HTN
  2. aldosterone adenoma (35%)
    - Conn syndrome
    - middle age, F:M (2:1), severe HTN
55
Q

What are the effects of primary hyperaldosteronism and how is it diagnosed?

A
  • suppression of RAAS mechanism
  • increased Na+ retention –> common secondary HTN
  • increased K+ loss

Dx: - hypokalemia, increased aldosterone

56
Q

Why do you get adrenal hyperplasia in adrenogenital syndrome?

A

21-hydroxylase deficiency –> decreased mineralo/glucocorticoids –> decreased cortisol –> increased compensatory ACTH via negative feedback –> adrenal hyperplasia

57
Q

What is the commonest adrenogenital syndrome?

A

21-hydroxylase deficiency

58
Q

What are the clinical types of adrenogenital syndrome and what is the most common?

A
  • simple virilizing –> increased testosterone *COMMON
  • salt wasting synd. –> Na loss, K ret (decreased aldost.)
  • late onset adult virilism –> partial deficiency
59
Q

What are the causes of acute adrenocortical insufficiency?

A
  • sudden withdrawal from long term steroid therapy
  • crisis in a chronic insufficiency pt. (Addison’s)
  • Waterhouse-Friderichsen Syndrome (acute haemorrhagic necrosis (apoplexy); secondary to DIC, meningoccal meningitis, new born, trauma)
60
Q

What are the clinical features of acute adrenocortical insufficiency?

A
  • shock, DIC, purpura, septicemia
  • salt + water loss (decreased aldost.)
  • hypoglycemia, fatigue
  • hypovolemic shock
61
Q

What is primary chronic adrenal insufficiency known as?

A

Addison’s Disease

  • decreased serum cortisol
  • increased ACTH
62
Q

What are the clinical features of Addison’s Disease?

A
  • anorexia, wt. loss
  • vomiting
  • weakness, lethargy
  • hypotension (low Na, high K –> low aldost.)
  • skin pigmentation in primary (increased MSH)
  • GI disturbances
  • chronic dehydration and sexual dysfunction
  • changes in body hair distribution
63
Q

True or False?

In Addison’s Disease, plasma Na is high and K is low

A

False

-other way around

64
Q

What is the commonest etiology of Addison’s disease, and what are the others?

A 
Commonest = autoimmune (70%)
Also:
-APS1, APS2
-infections (TB, fungal)
-tumours
65
Q

How is Addison’s disease diagnosed?

A

Serum ACTH

  • high = primary
  • low = secondary
66
Q

What is a pheochromocytoma?

A
  • benign tumour of adrenal medulla chromaffin cells
  • young age –> fluctuating secondary HTN
  • increased catecholamines –> HTN
  • 25% familial (MEN2 syndrome, NF1, VH2)
  • 10% extraadrenal, bilat. (MEN), malig, no HTN
67
Q

What is the Dx. of pheochromocytoma?

A

increased urinary VMA ( vanillylmandelic acid)

-epinephrine metabolite

68
Q

What does PTH do?

A
  • releases Ca from bone
  • reabsorbs Ca in kidneys
  • absorbs Ca in small intestine (+phosphate)

***INCREASE SERUM CALCIUM

69
Q

What is the main cause for hyperparathyroidism?

A

Primary: - ADENOMA (90%)

-F:M = 4:1

70
Q

What are the Sx. of hyperparathyroidism?

A
  • hypercalcemia
  • renal calculus
  • bone resorption –> osteoporosis
  • depression
  • seizures
  • osteitis fibrosa cystica (brown tumour of bone) –> in severe form
71
Q

What is secondary, tertiary and quaternary hyperparathyroidism?

A 
#2: -Chronic Renal Failure --> Ca loss --> increase PTH
#3: -#2 + hyperplasia, not responding to Ca levels
#4: -#3 + adenoma
72
Q

What does MEN1 consist of and what is the most common?

A 
PPPP
-Pituitary adenoma
-Parathyroid adenoma --> MOST COMMON*
-Pancreatic adenoma
(-Peptic ulcers)
73
Q

What does MEN2 consist of and what are the subclasses 2A + 2B?

A

PTAG

  • Parathyroid adenomas –> MEN2A
  • Thyroid medullary carcinoma –> MEN2
  • Adrenals (pheochromocytoma) –> MEN2B
  • GIT (neuromas + ganglioneuromas) –> MEN2B
74
Q

What is APS1 and what does it consist of?

A

Autoimmune Polyendocrine Syndrome
*APECED:
Autoimmune Polyendocrinopathy, Candidiasis and Ectodermal Dystrophy
Sx: -alopecia, anemia, cataract, vitiligo, malabsorption, hypoparathyroidism
-childhood, Addisons, Pernicious anemia, hypoPTH, etc
-Ab against IL-17 (increased fungal inf.)

75
Q

What does APS2 consist of?

A

Sx: -nausea, polyuria, wt. loss, hypotension, hypoparathyroidism, anorexia, myalgia

  • early adult
  • adrenal insufficiency (Addison’s) with autoimmune thyroiditis and T1DM
  • NO infections (unlike in APS1)
76
Q

What is the likely Dx. of 18yr old boy with sudden severe episodes of fluctuating episodes of hyper and hypotension?

A

Pheochromocytoma

77
Q

What type of MEN does pheochromocytoma fit into?

A

MEN2(B)

-adrenal medullary adenoma

78
Q

What is the commonest type of thyroid adenoma and its microscopy?

A

Follicular adenoma

-plenty of small follicles

79
Q

What is Waterhouse-Friederechsen Syndrome?

A
  • large blood clot replacing adrenal gland
  • severe stress –> adrenal haemorrhage –> necrosis
  • acute loss of adrenal function –> shock, haemorrhage, hypoglycemia, hypovolemia, DIC, etc.

N.B. severe stress: -meningococcal meningitis, speticemia, multi organ failure, DIC

80
Q

What are 3 microscopic features of papillary carcinoma?

A
  1. irregular cells forming papillary structures
  2. dense fibrous stroma
  3. microcalcifications

Pathology Term 3 (6 decks)

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