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Endocrine Flashcards

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1
Q

Causes/origins of hyperpituitarism:

A
  1. Adenoma of the pituitary gland-> overproduction of hormones
  2. Carcinoma (rare)
  3. Hyperplasia (rare)
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2
Q

Causes/origins of hypopituitarism:

A
  1. Sheehan’s syndrome (also known as postpartum pituitary gland necrosis)
    - blood loss/lowbp after labour -> deprive body of O2
    - ischaemic necrosis of anterior pituitary
  2. Pituitary adenoma
    - non-functioning adenoma compress normal gland -> necrosis
    - may result in infarction (apoplexy)
  3. Iatrogenic causes: radiation, surgery
  4. Head trauma
  5. Infections
    - TB, inflammation, sarcoid (granulomas develop)
    - post-meningitis
    Or decreased levels of GH-> pituitary dwarfism (failure of growth)
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3
Q

Types of pituitary tumours:

A
  1. Adenoma (benign) (usually this)
  2. Carcinoma (rare)
  3. Craniopharyngioma: cystic tumour derived from embryonal remnants
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4
Q

Effects of hyperpituitarism

A
  1. Increased ACTH -> Cushing’s
  2. Increased GH -> gigantism in children, acromegaly in adults
  • gigantism is when the long bones can still grow n become damn long
  • acromegaly is when the hands and legs become big, long bone epiphyseal plates alr fused, dont elongate
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5
Q

What hormones do the pituitary gland secrete?

A

Anterior lobe: ACTH, TSH, FSH, LH, PRL, GH
Posterior lobe: Vasopressin (ADH), oxytocin

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6
Q

Effects of hypopituitarism:

A

Decreased GH-> pituitary dwarfism (failure of growth)

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7
Q

Effects of pituitary tumours:

A

Mass effect:
1. Compress optic pathway -> visual defects
2. Compress hypothalamus
3. Increased intracranial pressure -> compresses brain

+ hormone effect (depends, could potentially cause hyper or hypo pituitarism)

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8
Q

How is the thyroid gland regulated?

A
  1. Regulated by TSH produced by the pituitary gland.
  2. -ve feedback: thru Ca2+ levels
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9
Q

What does the thyroid gland produce?

A
  1. Follicular cells produce T3 (tri-iodothyronine), T4 (thyroxine)
  2. Parafollicular cells produce calcitonin (which opposes PTH to decrease Ca2+)
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10
Q

What is a goitre?

A
  • lump/swelling at the front of neck due to swollen thyroid

could be:
1. Localised nodule
Due to multinodular goitre (hyperplasia) or neoplasms (tumours)
2. Diffuse
Due to hyperplasia, graves disease or thyroiditis

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11
Q

Name the primary causes of hyperthyroidism:

A
  1. Graves disease (diffuse)
  2. Toxic multinodular goitre (localised nodules)
  3. Toxic neoplasm (tumour)
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12
Q

Name a secondary cause of hyperthyroidism:

A

Pituitary hyperfunction.

Increased pituitary action -> increased TSH pdn -> increased thyroid function

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13
Q

Name the primary causes of hypothyroidism:

A
  1. Hashimoto’s disease (autoimmune, destruction of follicular epithelial cells)
  2. Iatrogenic (e.g. surgery, overdose of hyperthyroidism medicine)
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14
Q

Name a secondary cause of hypothyroidism:

A

Pituitary failure

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15
Q

Signs of Hyperthyroidism:

A

Signs (what physician can see):

  1. Weight: Thin
  2. Face: staring gaze, lid lag, exophthalmos (abnormal protrusion of eyeball)
  3. Skin: warm, sweaty
  4. CVS: tachycardia, atrial fibrillation
  5. Lower limbs: proximal myopathy(muscle weakness), pituitary myxoedema (lesions in skin due to accumulation of glycosaminoglycans in skin)
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16
Q

Difference between signs and symptoms:

A

Signs: what physician can see of the bat
Symptoms: what patient himself can feel, subjective experience, over time

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17
Q

Symptoms of hyperthyroidism

A

Symptoms (subjective experience by patient)

  1. Weight: loss
  2. Temp: heat intolerance
  3. Menstrual: oligomenorrhea (infrequent)
  4. Bowel: diarrhoea (cuz digestion is sped up)
  5. Mental state: irritable
  6. Appetite: increases
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18
Q

Biochemical manifestations of hyperthyroidism:

A
  1. Total T4 & Free T4,T3: high
  2. TSH: low (primary)
  3. Auto-antibodies: Graves (TSH mimic antibodies)
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19
Q

Signs of hypothyroidism:

A

Signs (what physician can see right off the bat)

  1. Weight: Fat
  2. Face: swollen & puffy
  3. Skin: dry, cool
  4. CVS: bradycardia, pericardial effusion (buildup of fluid in pericardium)
  5. Lower limbs: proximal myopathy (weakness in limbs)
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20
Q

Symptoms of hypothyroidism:

A

Symptoms: (subjective experience by patient)

  1. Weight: gain
  2. Temp: cold intolerance
  3. Menstrual: menorrhagia (heavy)/oligomenorrhea (infrequent)
  4. Bowel: constipation
  5. Mental state: mental slowness
  6. Appetite: poor
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21
Q

Biochemical manifestations of hypothyroidism:

A
  1. Total T4 & Free T4, T3: low
  2. TSH:
    Primary: high
    Secondary: low
  3. Auto-antibodies: hashimoto’s (autoimmune: cytotoxic destruction of follicular epithelial cells)
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22
Q

What is thyrotoxicosis?

A

Excess T3/T4 action at tissue level in the body due to any cause
(Hyperthyroidism is a form of thyrotoxicosis)

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23
Q

What is opthalmopathy?

Study These Flashcards
A

Presents as 1. Lid lag 2. Eyelid retraction 3. Exophthalmos(bulging eyes)

  • just think of the disturbing graves disease eye photo
  • due to overproduction of glycosaminoglycans within orbit
24
Q

Name the effects of Graves disease:

Study These Flashcards
A
  1. Hyperthyroidism (go back to the signs and symptoms)
  2. Thyrotoxicosis
  3. Opthalmopathy
  4. Diffuse goitre
25
Pathogenesis of Graves disease:
- primary hyperthyroidism - production of autoantibodies similar to TSH - binds & activates TSH receptor - increased cellularity & hyperplasia of gland -> goitre - follicular cells stimulated to release T3/T4 - high T3/T4 leads to low TSH (-ve feedback)
26
The most common cause of hypothyroidism in SG is…
Hashimoto’s thyroiditis
27
Hashimoto’s thyroiditis is more common in..?
Females, familial clustering
28
Pathogenesis of Hashimoto’s thyroiditis:
- autoimmune disease - primary hypothyroidism - immune-mediated cytotoxic destruction of follicular epithelial cells - destruction of thyroid-> failure to produce T3/T4 - low T3/T4 -> leads to high TSH (-ve feedback)
29
Lymphoma of the thyroid gland is related to..
Hashimoto’s thyroiditis
30
What are hurthle cells?
Hurthle cells are a particular type of thyroid cell that can be found in both benign and cancerous thyroid nodules. - related to hashimoto’s thyroiditis
31
Gross features of hashimoto’s thyroiditis:
Histology: - lymphoid follicles - hurthle cell changes
32
Subacute (granulamatous) thyroiditis/ DeQuervain thyroiditis
-post-viral inflammatory process - self-limiting - short history - more common in females - linked to viral, bacterial & autoimmune etiologies
33
Symptoms of Subacute (granulamatous) thyroiditis/ DeQuervain thyroiditis
- flu-like - inflammation of thyroid gland - painful goitre (other goitre conditions dont result in pain)
34
Histology of Subacute (granulamatous) thyroiditis/ DeQuervain thyroiditis
- granulomatous - acute & chronic inflammation in thyroid
35
Gross features of follicular adenoma:
- rounded, encapsulated well-demarcated nodule - bulging from cut surface
36
Histology of follicular adenoma:
- completely surrounded by intact capsule - follicles - resembles normal thyroid
37
Types of thyroid carcinomas:
Well differentiated: 1. Follicular (metastasises to organs) 2. Papillary (metastasises to to lymph nodes) Poorly/undifferentiated: 3. Anaplastic (undifferentiated) 4. Medullary (parafollicular C cells)
38
Characteristics of follicular thyroid carcinomas (well-differentiated):
- well differentiated - similar to follicular adenoma, BUT, has CAPSULAR/VASCULAR INVASION - more common in women Prognosis: - depends of degree of invasion - metastasis: via bloodstream to organs (e.g. lungs, bones, liver) Effects: slow growing, painless, cold nodule
39
Characteristics of papillary thyroid carcinomas (well-differentiated):
- well differentiated - may be multifocal (additional tumours arising from original tumour) -> remove entire thyroid in surgery - associated w ionising radiation Metastasises to: LN (lymph nodes) Diagnosis: - based on nuclear features - finely dispersed chromatin, nuclear grooves, pseudo inclusions Classical features: - nuclear features - papillae w fibrovascular cores - psammoma bodies
40
Papillary thyroid carcinomas metastasise to?
Lymph nodes
41
Follicular thyroid carcinomas metastasise to?
Organs via bloodstream e.g. lungs, bone, liver
42
Characteristics of anaplastic thyroid carcinomas:
- rapidly enlarged - undifferentiated - more common in elderly - poor prognosis (months)
43
Effects of anaplastic thyroid carcinomas
- compressive symptoms (squeezes trachea) - often spread beyond thyroid - metastasises to lungs
44
Characteristics of medullary thyroid carcinoma:
- arises from parafollicular C cells => elevated calcitonin production - 80% sporadic (occurs in solitary, older px), 20% hereditary (MEN syndrome/familial MTC) (multifocal, younger px) - MEN: multiple endocrine neoplasia - MTC: malignant thyroid cancer w hereditary risk factor
45
What does the parathyroid gland do?
Produce PTH, increases Ca levels in plasma via: 1. Increasing bone resorption by osteoblasts 2. Increasing renal tubular absorption 3. Increasing absorption (mediated by Vit D, PTH increases its synthesis)
46
Causes of hyperparathyroidism:
Primary: 1. Parathyroid adenoma/carcinoma: 1 gland enlarged => 1 nodule - adenoma is the most common cause 2. Parathyroid hyperplasia: > 1 gland enlarged Secondary: 3. Renal failure (kidney too much phosphate reabsorption => form insoluble calcium phosphate => decreased serum Ca2+ => increased PTH
47
Causes of hypoparathyroidism:
1. Iatrogenic: thyroidectomy (surgical removal of all/part of thyroid) 2. Autoimmune 3. Congenital absence/dysfunction: DiGeorge syndrome - decreased PTH => decreased serum Ca2+, hypocalcemia
48
Complications from hyperthyroidism:
1. Renal & urinary calculi, nephrocalcinosis 2. Osteitis fibrous cystica (skeletal disorder) 3. Hypertension 4. Pancreatitis 5. Peptic ulcers 6. Metastatic calcification
49
Complications from hypoparathyroidism:
- muscle twitching, cramps, tetany - mental changes: irritability, depression, confusion - eye problems: cataracts, opacification of lens - heart: ECG changes, arrhythmia, pump weakness - dental anomalies: enamel hypoplasia, hypodontia, root defects, disturbances in eruption
50
What are the adrenal glands regulated by?
ACTH released by pituitary glands -> stimulates release of adrenal cortical hormones
51
What does the cortex of the adrenal glands produce?
1. Aldosterone - regulates bp, Na+/water retention, K+ excretion 2. Cortisol - maintain homeostasis 3. Androgens - for sexual development & function
52
What does the medulla of the adrenal glands produce?
Catecholamines (adrenaline, noradrenaline)
53
Name the causes of adrenal hyperfunction:
Primary 1. Adrenal adenoma/carcinoma 2. Adrenal hyperplasia Secondary: 3. Pituitary adenoma: increased ACTH-> increased adrenal hormones Iatrogenic: 4. Steroids (same effect as cortisol) Paraneoplastic: 5. Ectopic hormone production E.g. small cell carcinoma in lung produces ACTH
54
Increased aldosterone levels lead to:
Conn’s syndrome
55
Increased cortisol levels lead to:
Cushing’s syndrome
56
What syndromes can adrenal hyperfunction lead to?
1. Conn’s syndrome (elevated aldosterone) 2. Cushing’s (elevated cortisol)
57
List the clinical features of Cushing’s syndrome:
1. Adrenal tumours/hyperplasia 2. Emotional disturbance 3. Enlarged sella turcica 4. Moon face, buffalo bump, obesity 5. Thin wrinkled skin, abdominal stress 6. Skin ulcers ( poor wound healing) 7. Osteroporosis 8. Muscle weakness 9. Hypertension 10. Amenorrhea (no period)

Y2 Patho (9 decks)

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